Cuccurullo Flashcards
Gait cycle
Single sequence of functions of one limb
One gait cycle = 1 stride
1 stride = 2 steps
Stride
Linear distance between successive points of contact of same foot (heel strike to heel strike of same foot)
Step
Linear distance between successive contact points of opposite feet (heel strike of one foot to heel strike of other foot)
Normal step length
15-20 inches (~40 cm)
Gait cycle phases
Stance phase & swing phase
Gait cycle at normal walking speed
60% stance
40% swing
Walking faster decreases the time spent in stance phase (increasing time in swing phase)
Double limb support
Occurs at beginning & end of stance phase
20% of normal gait cycle (vs 80% of single limb support)
When is a person considered to be running?
When there is no longer a double support period
Cadence
Number of steps per unit time
Center of Gravity (CoG)
5-cm anterior to the S2 vertebra
CoG is displaced 5-cm (<2 inches) horizontally & 5-cm vertically during an average step
Stance Phase sub-divisions
I Like My Tea Pre-sweetened:
I: Initial contact
L: Loading response (body has lowest CoG during this)
M: Mid-stance (time period from lift of the contralateral extremity from the ground to the point where ankles of both extremities are aligned in frontal (or coronal plane) (body has the highest CoG during this)
T: Terminal stance
P: time period from initial contact of contralateral extremity to just prior to lift of the ipsilateral extremity from the ground (unloading weight)
Base of support
Space outlined by the feet & any assistive device in contact with the ground
Falling is avoided if the CoG remains positioned over the base of support
Normal base of support (distance between heels): 6-10 cm
Swing Phase
In My Teapot:
I: Initial swing (lift of the extremity from the ground to position of maximum knee flexion)
M: Midswing (knee flexion to vertical tibia position)
T: terminal Swing (vertical tibia position to just prior to initial contact)
Determinants of gait
- Pelvic rotation: rotates anteriorly on swinging leg side, lengthening limb as it prepares to accept weight
- Pelvic tilt: pelvis on side of swinging leg lowered 4-5 degrees, which lowers CoG at mid-stance
- Knee flexion in stance: early knee flexion at foot strike (15 degrees). Bending of the knee reduces the vertical elevation of the body at mid-stance. This lowers the CoG (by minimizing its vertical displacement), decreasing energy expenditure. Also tends to absorb shock of impact at heel strike by lengthening contraction of quadriceps
- Foot mechanisms (ankle flexion/extension): at heel strike, ankle PF smoothens the curve of the falling pelvis. A/w controlled PF during the first part of the stance. 3 pivot points (rockers) at the heel, ankle, & forefoot help to functionally lengthen the stance limb at initial contact & pre-swing, & shorten the limb at mid-stance
- Knee mechanisms: after mid-stance, the knee extends as the ankle PF & the foot supinates to restore the length to the length & diminish the fall of the pelvis at the opposite heel strike
- Lateral displacement of the pelvis: displacement toward the stance limb
1-5 reduce displacement on the vertical plane. 6 reduces displacement on the horizontal plane
Why does foot slap occur at initial contact?
Moderately weak dorsiflexors (grade 3/5)
Why does genu recurvatum occur from initial contact through mid-stance??
- Weak, short, or spastic quadriceps
- Compensated hamstring weakness
- Achilles tendon contracture
- PF spasticity
Why does excessive foot supination occur from initial contact through mid-stance?
- Compensated forefoot valgus deformity
- Pes cavus
- Short limb
Why does excessive trunk extension occur from initial contact through mid-stance?
- Weak hip extensor or flexor
- Hip pain
- Decreased knee ROM
Why does excessive trunk flexion occur from initial contact through mid-stance?
- Weak glut max & quadriceps
- Hip flexion contracture
Why does excessive knee flexion occur from initial contact through pre-swing?
- Hamstring contracture
- Increased ankle DF
- Weak PF
- Long limb
- Hip flexion contracture
Why does excessive medial femur rotation occur from initial contact through pre-swing?
- Tight medial hamstrings
- Anteverted femoral shaft
- Weakness of opposite muscle group
Why does excessive lateral femur rotation occur from initial contact through pre-swing?
- Tight lateral hamstrings
- Retroverted femoral shaft
- Weakness of opposite muscle group
Why does wide base of support occur from initial contact through pre-swing?
- Hip abductor muscle contracture
- Instability
- Genu valgum
- Leg length discrepancy
Why does narrow base of support occur from initial contact through pre-swing?
- Hip adductor muscle contracture
- Genu varum
Why does excessive trunk lateral flexion (compensated Trendelenburg gait) occur from loading response through pre-swing?
- Ipsilateral glut med weakness
- Hip pain
Why does pelvic drop (uncompensated Trendelenburg gait) occur from loading response through pre-swing?
Ipsilateral glut med weakness
Why does waddling gait occur from loading response through pre-swing?
Bilateral glut med weakness
Why does excessive foot pronation occur from mid-stance through pre-swing?
- Compensated forefoot or hindfoot varus deformity
- Uncompensated forefoot valgus deformity
- Pes planus
- Decreased ankle DF
- Increased tibial varum
- Long limb
- Uncompensated internal rotation of tibia or femur
- Weak tibialis posterior
Why does bouncing or exaggerated motion occur from mid-stance through pre-swing?
- Achilles tendon contracture
- Gastroc-soleus spasticity in PF
Why does inadequate hip extension occur from mid-stance through pre-swing?
- Hip flexor contracture
- Weak hip extensor
Why does steppage gait/foot drop occur in swing phase?
- Severely weak dorsiflexors
- Equinus deformity
- PF spasticity
Why does circumduction occur in swing phase?
- Long limb
- Abductor muscle shortening or overuse
- Stiff knee
Why does hip hiking occur in swing phase?
- Long limb
- Weak hamstring
- QL shortening
- Stiff knee
Gait impairment in Parkinson disease
Stooped posture, festinating gait, shuffling, decreased arm swing, reduced trunk rotation, “start hesitation,” freezing while walking/turning (when severe)
Primary disturbance: reduced step length
Gait impairment with hip flexion contracture
Decreased hip extension ROM results in compensation with anterior pelvic tilt, decreased contralateral step length, & increased knee flexion
Increases energy consumption. A 35-degree contracture due to iliopsoas tightness results in a 60% increase in energy consumption
Energy expenditure during wheelchair propulsion
Only 9% increased compared to ambulation in normal subjects
Energy expenditure during crutch walking
Requires more energy than walking with a prosthesis
Muscles that need strengthening in preparation for crutch walking
Latissimus dorsi, triceps, pec major, quads, hip extensors, hip abductors
What type of amputation has higher energy expenditure?
Vascular > traumatic (usually sicker)
What is a major risk factor for LE amputation?
DM- contributes to 67% of all LE amputations
55% of those will require amputation of contralateral LE within 2-3 years
Since 1996, rate of LE amputation from DM is actually declining- prevention is key
What is the leading cause of UE amputations?
Trauma- 80% of UE amputations
Majority are limited to digital amputations
Mostly male between ages 15-30
MVC is most common cause
UE amputations account for 67% of all trauma-related amputations
What is a mangled hand?
An amputation causing irreparable damage when 4 of the following 6 basic parts are not salvageable: skin, vessels, skeleton, nerves, extensor tendons, flexor tendons
Initial goal: save all feasible length
What is the most common terminal device for a body-powered device (hook or hand)
Voluntary opening
Prosthetic wrist units
Wrist units are used for attaching terminal devices to prostheses & providing pronation/supination to place the terminal device in its proper position
What does a wrist flexion unit allow for terminal device?
For TD to be in the flexed position, facilitating ability to perform activities close to the body, which is important for bilateral UE amputees
What are the two types of wrist units?
Friction control or locking
What is a friction control wrist unit?
Permits pronation & supination of the TD & hold it in a selected position by means of friction derived from a compressed rubber washer or from forces applied to the stud of the TD
What is a locking wrist unit?
Prevents inadvertent rotation of the TD in the wrist unit when a heavy object is grasped
What are the two types of wrist flexion units?
Add-on & combination
What is an add-on wrist flexion unit?
Worn between wrist & TD, allowing manual positioning of the TD in either the straight or the flexed position
What is the combination type wrist flexion unit?
Combines a friction wrist & a wrist flexion component in one & provides for setting & locking in one position
What is a Muenster socket (self-suspended socket)?
Alternative to the split socket (for short trans-radial amputees)
Socket & forearm are set in a position of initial flexion & the socket encloses the olecranon & epicondyle of the humerus
The intimate residual limb encapsulation, flexion attitude, & high trim lines provide suspension
Although there is some limitation in flexion-extension ROM, this is compensated by pre-flexing the socket
When this type of suspension is used, a figure-9 harness can be used for control purposes only
With these prostheses, the patient can operate the TD in common positions & still apply full torque about the elbow. Although these techniques yield less EF than the split socket, the reduction in force requirements & ease of use more than compensate for this limitation
What is a Figure-8 (O-ring) harness?
Most commonly used harness
The axilla loop, worn on the sound side, acts as a reaction point for the transmission of body force to the TD
The anterior suspension strap on the involved side gives additional support for pulling or lifting, & acts as the attachment point for the elbow loading strap on a body-powered above-elbow prosthesis
What is an elbow disarticulation prosthesis?
Variation of a trans-humeral prosthesis
Socket is flat & broad distally to conform to epicondyles of distal humerus, which provides self-suspension & allows for IR & ER of humerus
Length of residual limb requires use of external elbow joint with cable-operated locking mechanism
Harness and control system are the same as for trans-humeral prostheses
What harness designs are used most frequently for trans-humeral prostheses?
Modifications of the basic figure-8 & chest strap patterns used with trans-radial prostheses
Dual-control cable mechanism operation in the trans-humeral amputee
Elbow flexion: humeral flexion & bi-scapular abduction –> dual-control cable
Lock elbow (in desired degree of flexion): shoulder depression, extension, & abduction (down, back, & out) –> single-control cable (elbow-lock cable)
TD operation (open & close): further humeral flexion & bi-scapular abduction –> dual-control cable
Unlock elbow: shoulder depression, extension, & abduction (down, back, & out) –> single-control cable (elbow-lock cable). After desired TD function is accomplished, the elbow is unlocked & the elbow extends by gravity
Body-powered vs myo-electric control systems
Body-powered devices: less expensive, lighter, more durable, easier to repair, higher sensory feedback. Disadvantages: mechanical appearance, difficult to use for some people, dependent on motor strength
Myo-electric devices: better cosmesis, less harnessing, stronger grasp force. Disadvantages: more expensive, heavier, decreased durability due to electronic components & the need for daily recharging of batteries
Trans-radial amputee training (myo-electric)
Myo-electric trans-radial prostheses use muscle contractions to activate the prosthesis (such as activation of wrist flexors closing TD & activation of wrist extensors opening TD)
Diagnostic testing for PAD
ABI, Doppler velocity waveform analysis, intra-arterial contrast angiography
ABI
Ratio of brachial systolic pressure to ankle systolic pressure
Accuracy is limited for large vessels & for calcified vessels, which can occur in diabetic, elderly, or renal failure patients
Not a reliable tool for determining level of amputation
0.91 - 1.30 –> normal
0.71 - 0.90 –> mild PAD
0.41 - 0.70 –> moderate PAD
0.00 - 0.40 –> severe PAD
>1.30 –> calcified, non-compressible vessels (false negative)
Doppler velocity waveform analysis
Performed when screening ABI is abnormal, done to localize lesion
Obtained at multiple sites. Change in waveform from one level to next is indicative of PAD
Intra-arterial contrast angiography
Gold standard testing for PAD
Invasive test & should not be used for screening purposes
Myodesis
Muscles & fascia are sutured directly to bone through drill holes
Residual limb is more structurally stable
Contra-indicated in severe dysvascularity- blood supply to the bone may be compromised
Myoplasty
Opposing muscles are sutured to each other & to the periosteum at the end of the cut bone with minimal tension
Less operating time, procedure of choice in severely dysvascular residual limbs
Where does Lisfranc amputation occur?
Tarsometatarsal junction
What is a Chopart amputation?
Removes all tarsals & metatarsals. Only talus & calcaneus remain
What occurs after both the Lisfranc & Chopart amputation?
Remaining foot often develops a significant equinovarus deformity resulting in excessive anterior WB with breakdown
Adequate dorsiflexor tendon re-attachment with Achilles tendon lengthening can be used to prevent this deformity
Syme’s amputation
Essentially an ankle disarticulation with attachment of the distal heel pad to the end of the tibia; may include removal of the malleoli and/or distal tibial/fibular flares
Indications: trauma of the foot, congenital anomalies, tumors, & deformities that necessitate amputation
Disadvantages: healthy plantar heel skin is necessary for WB in this area. Patient also must have good perfusion in this area, so difficult procedure for the dysvascular patient
Pros: functionally, this procedure represents an excellent level of amputation because:
- maintains length of limb
- preservation of heel pad, excellent WB residual limb
- early fitting of prosthesis is possible with excellent results
- partial WB of residual limb is possible almost immediately after the procedure with a proper rigid casting (within 24 hours)
Cons:
- decreased cosmesis (bulky, bulbous residual limb)
- fitting for a prosthesis may be more difficult than for other amputation levels
Functional ability after BKA in the elderly
50% of patients have worse functional ability
Ideal shape for trans-tibial residual limb
Cylindrical
Ideal shape for trans-femoral residual limb
Conical
Medicare’s functional levels of ambulation for amputees (K levels)
K0: non-ambulatory (bed-bound), no prosthesis allowed
K1: limited to transfers or limited household ambulator –> manual lock or stance-control knee, SACH, or single-axis foot
K2: unlimited household but limited community ambulator –> pneumatic or polycentric knee, multi-axis foot
K3: unlimited community ambulator, VARIABLE CADENCE –> hydraulic knee, micro-processor knee, energy-storing foot
K4: high-energy activities (sports work) –> same as K3
Prosthetics for Syme’s amputation
Patient can stand easily & walk on the end of the residual limb without wearing a prosthesis for short household distances
Prosthesis either has a posterior or medial opening. Both require removal of a portion of the socket wall to get the bulbous residual limb in. Major disadvantage is poor cosmesis. Newer socket designs that incorporate an expandable air suspension chamber inside the socket or a thin removable expandable inner socket liner provide a more cosmetically acceptable prosthetic design. Pros: thinner, tighter, stronger prosthetic socket, maintain structural integrity of prosthesis
Prosthetic feet available for a Syme’s amputation:
- SACH
- SAFE (syme stationary ankle flexible endoskeleton)
- Energy-storing carbon fiber foot (low profile)
Patellar tendon bearing socket
Standard socket used for the average BKA –> total contact PTB socket
PTB socket is a custom-molded thermoplastic or laminated socket that distributes weight through convex build-ups (bulges) over pressure-tolerant areas & provides concavities (relief areas) on pressure-sensitive areas
Bar in anterior wall designed to apply pressure on the patellar tendon
Trim line extends anteriorly to the mid-patellar level, may extend medially & laterally to the femoral condyles, & extends posteriorly to level of the PTB bar
Pressure should be equally distributed over pressure-tolerant areas
Pressure-tolerant areas
- Patella tendon
- Pre-tibial muscles
- Popliteal fossa (gastroc-soleus muscles via gastroc depression)
- Lateral shafter of fibula
- Medial tibial flare
Pressure-sensitive areas (relief areas)
- Tibial crest, tubercle, & condyles
- Fibular head
- Distal tibia & fibula
- Hamstring tendons
- Patella
How is PTB socket aligned to relieve pressure on pressure-sensitive areas?
Socket is aligned on the shank on slight flexion (5-8 degrees) to enhance loading of the patellar ligament, prevent genu recurvatum, resist the tendency of the residual limb to slide down the socket, & to place quadricep in a more efficient & mechanically advantageous position, facilitating its contraction
A maximum of 25 degrees of flexion is possible to accommodate knee flexion contracture
Alignment of socket also includes a slight lateral tilt to reduce pressure on fibular head
Liner added to socket to protect fragile or insensate skin, reduce shear forces, provide a more comfortable socket for tender residual limbs, or accommodate for growth
Custom gel liners without the suspension pin are helpful in managing shear problems that can occur with residual limbs covered with split-thickness skin grafts, or boney prominences
Suction suspension for BKA
Silicone or other gel insert with use of a one-way expulsion valve in the distal aspect of the socket. Valve allows air to escape from the socket but not enter
Advantages: does not create pressure distributions that are likely to disturb normal circulation & soft tissue fluid balance as much as pin suspension. Provides excellent suspension for amputees with greater suspension demands (like athletes), & for those with short residual limbs, as well as excellent skin protection for the scarred residual limb
Elevated vacuum socket systems use a mechanical or electric pump to generate negative pressure between the limb & socket for enhanced suspension & contact
Disadvantage: expensive because gel liners are typically replaced annually
What are different types of prosthetic feet?
Rigid keel, single-axis foot, multi-axis foot, flexible keel, Seattle foot (energy-storing/dynamic response), Flexfoot (carbon fiber or fiberglass foot; energy-storing/dynamic response)
What are examples of a rigid keel?
- SACH (solid ankle cushion heel)
- Wooden keel
- Compressible heel
What are main uses of rigid keel?
For general use, kids-durable, limited ambulation needs, & K1 users
Advantages: inexpensive, light (lightest foot available), durable, reliable
Disadvantages: energy-consuming, rigid, best on flat surface
What is a single-axis foot?
Movement in one plane (DF/PF). Heel-height adjustable versions available
What is the main use of a single-axis foot?
To enhance knee stability
AKA who needs greater knee stability (goes to flat foot quick before knee buckles); knee goes back into extension (gives stability in early stance)
K1 users
Advantages: adds stability to prosthetic knees
Disadvantages: increased weight (70% heavier than SACH), increased cost, increased maintenance
What is function of a multi-axis foot?
Allows PF, DF, inversion, eversion, & rotation
What is the main use of a multi-axis foot?
Used for ambulation on uneven surfaces, absorbs some of the torsional forces created in ambulation, K2 users
Advantages: multi-directional motion, permits some rotation, accommodates uneven surfaces, relieves stress on skin & prosthesis
Disadvantages: relatively bulky, heavy, expensive, increased maintenance, greater latitude of movement may create instability in patients with decreased coordination
What are examples of a flexible keel?
- SAFE (stationary ankle flexible endoskeleton) - used in Syme’s amputation
- STEN (stored energy)
What are main uses for a flexible keel?
Used for ambulation on uneven surfaces, K2 users
Advantages: multi-directional motion, moisture & grit resistance, accommodates uneven surfaces, absorbs rotary torques, smooth rollover
Disadvantages: heavy, increased cost, not cosmetic, does NOT offer inversion/eversion
Why would you specifically use a STEN for flexible keel?
Used when smooth rollover needed. Has an elastic keel & accommodates numerous shoe styles. The ML stability is similar to SACH
Major disadvantage: cannot be used with Syme amputation
Seattle foot (energy-storing foot/dynamic response)
Consists of a canti-levered plastic C- or U-shaped keel, which acts as a compressed spring
Used for jogging, general sports, conserves energy. Used for K3 & K4 users
Advantages: energy storing, smooth rollover
Disadvantages: high cost, no SACH heel makes it difficult to change compressibility of heel
Flexfoot (carbon fiber or fiberglass foot) (energy-storing foot/dynamic response)
Pylon & foot incorporated into one unit. The dynamic keel extends to the bottom of the trans-tibial socket (& in AKA, to the level of the knee unit). Flex-walk is a shorter version of the Flexfoot, attaching to the shank at the ankle level
Used for running, jumping, vigorous sports, conserves energy. K3 & K4 users
Advantages: very light, most energy-storing most stable ML, lowest inertia
Disadvantages: very high cost, alignment can be cumbersome
Why is polycentric knee different than single-axis knee?
Polycentric knee has an instantaneous center of rotation that changes & is proximal & posterior to the knee unit itself. This allows greater knee stability, more symmetrical gait, & equal knee length when sitting
Ischial containment socket
Also known as a narrow ML socket or contoured adducted trochanteric-controlled alignment method (CAT-CAM) socket
ML dimension is narrower than the AP measurement
ML design provides a more normal anatomic (adducted) alignment of the femur inside the socket
Ischial tuberosity is contained inside the socket, providing a bony lock between the ischium & greater trochanters
WB is concentrated in the medial aspect of the ischium & ischial ramus
Socket is pre-flexed 5-7 degrees to maximize hip extensor muscle control. Maximum 20 degree flexion is allowed to accommodate flexion contracture
Fabricated with a flexible inner thermoplastic liner & a rigid outer frame. Cutouts can be made in the outer frame to accommodate bony or sensitive areas
What are advantages of an ischial containment socket?
- Stabilizes relationship between pelvis & proximal femur since the ischial tuberosity is controlled inside socket rather than on top of posterior brim like in quad socket
- Narrow ML design keeps femur in adduction during stance phase, permitting hip abductors to be in a more stretched & efficient position
- More energy-efficient ambulation at high speed
- Increased comfort in groin area compared to quad socket (in which WB is done primarily on the ischial tuberosity)
- Less lateral thrust of prosthesis at midstance
- Higher trim line results in better control of the residual limb especially for short AKA amputation
- Able to accommodate smaller residual limb
- Greater ML control of pelvis with this design
What are disadvantages of ischial containment socket?
- More expensive & difficult to fabricate than quad socket
- Wider AP dimension at level of ischial ramus leads to increased movement in AP plane
What are the different types of knee units available for AKA?
- Constant friction knee (single axis with constant friction unit)
- Stance control knee/Safety knee/Weight-activated friction brake
- Polycentric/Four-bar knee
- Manual locking knee
- Fluid-controlled knee units- hydraulic (oil), pneumatic (air)
- Microprocessor-control hydraulic knee
Constant Friction Knee (Single axis with constant friction unit)
Friction mechanisms are devices used in swing control knee to dampen the pendular action of the prosthetic knee during the swing phase, to decrease the incidence of high heel rise in early swing & decrease terminal impact in late swing
Single walking speed when used, may be used in kids
Does NOT give stance control; a screw is used to adjust the friction to determine how fast or slow the knee swings
Good for a K1 ambulator
Inexpensive, durable, & reliable
Disadvantages: low stability (in early stance the single axis has the lowest zone of stability), fixed single cadence, too much friction prevents knee from flexing, too little friction causes the knee to swing too easily so patient needs to vault, no stance control
Stance-Control Knee/Safety Knee/Weight-Activated Friction Brake
Single axis knee with stance control. Stance control acts as a brake system
Indications: geriatrics, short residual limb, general disability, uneven surfaces, amputees with weak hip extensors
Good for K1 ambulator & for preparatory prosthesis. Provides improved knee stability. Braking mechanism if weight applied with knee flexed 0-20 degrees
Disadvantages: slightly increased weight, increased cost, increased maintenance, must unload fully to flex, cannot use in b/l AKA since knees would not bend with loading & cannot bend both knees at same time (patient cannot sit down), activities that require knee motion under WB (such as step over step stair descent) are incompatible with this knee
Polycentric/Four-Bar Knee
No stance control, but inherently stable.
Short knee unit, so can be used in knee disarticulation & long residual limb
Good for K1 ambulator. Excellent knee stability & improved cosmesis in knee disarticulation & long residual limb patients
Disadvantages: greater weight, bulk, cost, & maintenance. Although durable, needs maintenance every 3-6 months
Manual Locking Knee
Knee of last resort used in the blind or CVA patient with amputation
Uses a spring-loaded pin that automatically locks the knee when the amputee stands or extends the knee
Knee is kept extended throughout the entire gait cycle to increase stability
Good for K1 ambulator. Ultimate knee stability in stance phase
Disadvantages: abnormal gait, awkward sitting, cannot use in b/l AKA because (like in stance-control knee), patient cannot sit. Knees lock on loading; therefore, person cannot bend both knees at same time to sit down
Fluid-Controlled Knee Units
Hydraulic (oil) & Pneumatic (air)
Pneumatic (air): cadence-responsive knee units through cadence-dependent resistance. Allows for either swing phase, or swing & stance phase control. Indications: For patients who vary cadence frequency, active walkers, ambulation in uneven terrain, K3 & K4 ambulators
Advantages: variable cadence, smoothest gait, stable (will not lock unless at full extension). Pneumatic units are lighter but hydraulic units tolerate more weight (can support the heavier & more athletic amputee), can unlock for some activities (biking0
Disadvantages: greatest weight, increased cost, increased maintenance
Microprocessor-Control Hydraulic Knee
Function similar to other hydraulic swing & stance phase knees. Has additional features of computer-programmed custom settings for each individual. Microprocessor re-calibrates stability of the knee 50x/second to adapt to changing conditions & ultimately prevent falls
Advantages: computer-adjusting knee for variable gait cycles, energy-saving
Disadvantages: highest cost, heavy, increased maintenance, inconvenience of daily charging, unproven track record for dependability
Swim prostheses
Waterproof prosthesis or special swim leg
Peg leg with or without fin attached for BKA or AKA
Rubber suspension sleeve used for BKA that prevents water from entering the socket
Hollow-chambered leg for BKA or AKA
Exoskeletal leg with knee lock for AKA
Waterproof suspension belt for AKA
Flatfoot for barefoot walking for BKA or AKA
What is choke syndrome?
Caused by proximal prosthetic socket being too tight & lack of total contact between residual limb & socket leads to impairment of venous return.
Occurs most commonly at the distal trans-tibial residual limb due to atrophy over time & use of additional socks or when the residual limb becomes larger (excessive weight gain)
Exam findings a/w choke syndrome
Initially with wearing a prosthesis, patient develops a well-circumscribed indurated area; if acute, edema can have weeping/blistering of skin
Area is TTP & prone to cellulitis
When chronic, skin becomes thickened & hyper-pigmented due to hemosiderin accumulation
What is the treatment for choke syndrome?
Relieving proximal constriction & restoring total contact between the socket & residual limb by reducing number of socks & modification of the distal end pad. Often a new total contact socket is needed
What is verrucous hyperplasia?
Wart-like skin overgrowth, usually of the residual distal limb resulting from inadequate socket wall contact with subsequent edema formation
Chronic choke syndrome can lead to this
Reversible by re-establishing total contact with the socket
Trans-tibial amputee gait deviations: excessive knee flexion (increased knee flexion at moment of initial contact)
Increased ankle dorsiflexion
Excessive anterior displacement of the socket over the foot
Excessive posterior displacement of the foot in relation to the socket
Too hard heel cushion (or plantar flexion bumper)
Knee flexion contracture
Trans-tibial amputee gait deviations: excessive knee extension (recurvatum; increased knee extension at moment of initial contact)
Increased ankle plantarflexion
Moving socket too posteriorly in relation to the foot
Moving foot anteriorly in relation to the socket
Too soft heel cushion (or plantarflexion bumper)
Quad weakness (excessive knee extension used as a stabilizing technique)
Distal anterior tibial discomfort
Habit
Trans-femoral amputee gait deviations
- Lateral trunk bending
- Abducted gait
- Circumduction
- Vaulting
- Medial & lateral whips (swing pase)
- Foot rotation at heel strike
- Foot slap
- Uneven heel rise
- Terminal impact
- Uneven step length
- Exaggerated lordosis
- Instability of prosthetic knee during stance
- Drop-off at end of stance phase
Trans-femoral gait deviation: lateral bending of trunk
Excessive bending occurs laterally from midline, generally to prosthetic side
Prosthetic causes:
- Prosthesis may be too short
- Improperly shaped lateral wall may fail to provide adequate support for femur
- High medial wall may cause amputee to lean away to minimize discomfort
- Prosthesis aligned in abduction may cause wide-based gait, resulting in this defect
Amputee causes:
- May not have adequate balance
- May have hip abduction contracture
- Residual limb may be over-sensitive & painful
- Very short residual limb may fail to provide a sufficient lever arm for pelvis
- Habit pattern
Trans-femoral gait deviation: abducted gait
Very wide-based gait with prosthesis held away from midline at all times
Prosthetic causes:
- Prosthesis may be too long
- Too much abduction may have been built into prosthesis
- High medial wall may cause amputee to hold prosthesis away to avoid ramus pressure
- Improperly shaped lateral wall can fail to provide adequate support for femur
- Pelvic band may be positioned too far away from patient’s body
Amputee causes:
- Hip abduction contracture
- Habit
Trans-femoral gait deviation: circumducted gait
Prosthesis swings laterally in wide area during swing phase
Prosthetic causes:
- May be too long
- May have too much alignment stability or friction in knee, making it difficult to bend knee in swing-through
Amputee causes:
- Inadequate suspension
- Abduction contracture of residual limb
Trans-femoral gait deviation: vaulting
Rising on toe of sound foot permits amputee to swing prosthesis through with little knee flexion
Prosthetic causes:
- Prosthesis may be too long
- Socket suspension may be inadequate
- Excessive stability in alignment or some limitation of knee flexion, such as knee lock or strong extension aid, may cause this deficit
Amputee causes:
- Vaulting is a fairly frequent habit pattern
- Fear of stubbing toe may cause this defect
- Residual limb discomfort may be a factor
Trans-femoral gait deviation: medial or lateral whips
Best observed when patient walks away from observer. Medial whip is present when heel travels medially on initial flexion at beginning of swing phase. Lateral whip exists when heel moves laterally
Prosthetic causes:
- Lateral whips may result from excessive IR of prosthetic knee
- Medial whips may result from excessive ER of knee
- Socket may fit too tightly, thus reflecting residual limb rotation
- Excessive valgus in prosthetic knee may contribute to this defect
- Badly aligned toe break in a conventional foot may cause twisting on toe-off
Amputee causes:
- Improper donning of socket or socket rotated on limb
Trans-femoral gait deviation: foot rotation at heel strike
As heel contacts ground, the foot rotates laterally, sometimes with vibrating motion
Prosthetic causes:
- Too hard heel cushion or plantar flexion bumper
Amputee causes:
- Weakness at hip muscles
Trans-femoral gait deviation: foot slap
Foot PF too rapidly & strikes the floor with a slap
Prosthetic causes:
- PF bumper is too soft, offering insufficient resistance to foot motion as weight is transferred to the prosthesis
Amputee causes:
- None
Trans-femoral gait deviation: uneven heel rise
Prosthetic heel rises markedly & rapidly when knee is flexed at beginning of swing phase
Prosthetic causes:
- Knee joint may have insufficient friction
- Extension aid may be inadequate
Amputee causes:
- May be using more power than necessary to force knee into flexion
Trans-femoral gait deviation: terminal swing impact
Rapid forward movement of shin piece allows knee to reach maximum force before heel strike
Prosthetic causes:
- Knee friction is insufficient
- Knee extension aid may be too strong
Amputee causes:
- Amputee may try to assure that knee is in full extension by deliberately & forcibly extending the residual limb
Trans-femoral gait deviation: uneven step length
Length of the step taken with the prosthesis differs from that of the sound leg
Prosthesis causes:
- Insufficient socket flexion
- Insufficient friction at the prosthetic knee or too loose an extension aid
Amputee causes:
- Pain or insecurity causing amputee to transfer weight quickly from the prosthesis to the sound leg
- Hip flexion contracture
Trans-femoral gait deviation: exaggerated lordosis
Exaggerated when the prosthesis is in stance phase, & the trunk may lean posteriorly
Prosthetic causes:
- Knee joint may be too far ahead of trochanter-knee-ankle line
- Socket is mounted with excess flexion
- PF resistance may be too great, causing knee to buckle at heel strike
- Failure to limit DF can lead to incomplete knee control
Amputee causes:
- May have hip extensor weakness
- Severe hip flexion contracture may cause instability
Trans-femoral gait deviation: drop-off at end of stance phase
Downward movement of trunk as body moves forward over prosthesis
Prosthetic causes:
- Limitation of DF of prosthetic foot is inadequate
- Heel of a SACH-type foot may be too short, or toe break of a conventional foot may be too far posterior
- Socket may have been placed too far anterior in relation to foot
Amputee causes:
- None
Bony overgrowth in amputation
Much more common in acquired amputations in children than in adults
Bone usually grows faster than overlying skin & soft tissue in the distal end of amputated long bones (residual limb)
Formation of bursa may occur over the sharp end & at times the bone may actually protrude through the skin
Seen most frequently in: humerus –> fibula –> tibia –> femur
Has been reported in congenital limb deficiencies, but very rarely
May require surgical revision several times before skeletal maturity. Capping the end of the involved long bone with a cartilage epiphysis to eliminate overgrowth is an option
Avoided in through-joint disarticulation; epiphyseal growth is preserved in through-joint disarticulation
Cane measurement for ambulation
20-30 degree EF or height of the greater trochanter of the hip for cane height
Cane typically goes on opposite side of weak extremity for bigger base of support
Indications for a walker
- Bilateral weakness and/or incoordination of the lower limbs or whole body
- Whenever a firm, free-standing aid is appropriate to increase balance (like MS or Parkinsonism)
- Relieve WB either fully or partially on a LE (allow the UE to transfer body weight to the floor)
- Unilateral weakness or amputation of the lower limb where general weakness makes the greater support offered by the frame necessary (OA or fractured femur)
- General support to aid mobility & confidence (after prolonged bedrest & sickness in the elderly)
Advantages of a walker
- Provide wider base of support
- More stable base of support
- Sense of security for patients fearful of ambulation
Disadvantages of a walker
- More conspicuous in appearance
- Interferes with development of a smooth reciprocal gait pattern (decreased step length with step-to gait pattern)
- Interferes with stair negotiation/difficult to maneuver through doorways or bathrooms
UCBL orthosis (internal modification)
University of California Biomechanics Lab orthosis
Custom-molded orthosis used to control flexible calcaneal deformities (rear-foot valgus or varus) & transverse plane deformities of the mid-tarsal joints (forefoot abduction or adduction)
Encompasses the heel & hindfoot & holds the mid-foot with high medial & lateral trim lines
Provides effective longitudinal arch support & realigns a flexible flat foot
Allows for sub-talar supination, holds the calcaneus in place, & prevents sub-talar pronation
What is a rocker bar (external sole modification?)
Convex strip placed across the sole just posterior to the metatarsal heads. Longer than the metatarsal bar
Can be used to relieve metatarsal pain (by relieving pressure), quicken the gait cycle (by assisting rollover during stance), or assist DF or decrease demand on weak PF (push-off)
Rigid rocker-bottom shoes are recommended for use in cases of plantar fasciitis, neuropathic ulceration, & trauma to mid-foot or metatarsal region
Can include entire heel & sole to become a rocker-bottom sole
Rocker bottom is good for a Charcot foot –> minimize forces the foot sees during standing/ambulatory activity; minimizes plantar area in contact with ground at any one time
Line of gravity (weight line)
Line passing through the COG to the ground
Behind the cervical vertebrae, in front of the thoracic vertebrae, & behind the lumbar vertebrae
Slightly posterior to hip joint & tends to passively extend the hip joint
Anterior to knee joint & tends to passively extend the knee
Passes 1-2 inches anterior to ankle joint & tends to DF the ankle. Resisted by the soleus & gastroc
While standing, the COG is midline & just anterior to S2 vertebra
Line of gravity (weight line) during quiet standing passes through:
Posterior to hip joint –> extension
Anterior to knee joint –> extension
Anterior to ankle joint –> ankle DF
What are thermoplastics?
Soften & become moldable when heated & harden when cooled so they can be molded & re-molded by heating
Low-temperature thermoplastics:
- Molded at temperatures just above body temperature (<80C or < 180F)
- Can be shaped directly to the body without the need for a cast
- Cannot be used effectively when high stress is anticipated, as in spasticity or in many LE applications
- Main use is UE limb orthotics
High-temperature thermoplastics:
- Used to manufacture permanent orthotic devices using vacuum-forming techniques
- Major types: acryclic, polyethylene, polypropylene, polycarbonate, ABS, vinyl polymers, & co-polymers
Thermosetting plastics: develop a permanent shape when heat & pressure are applied & maintain a memory. More difficult to use than thermoplastics & cause more body irritation & allergic reactions
Carbon fiber- advantages: lightweight, high strength. Disadvantages- very expensive, difficult to shape or modify
Single channel ankle joint
Three options:
1. Inserting spring in the channel for dorsiflexion assist
2. Inserting a steel pin for plantarflexion stop
3. Inserting both a pin & a spring for dorsiflexion assist & plantarflexion stop
Dual channel ankle joints
Have both anterior & posterior channels
Posterior channel functions exactly the same as single channel ankle joint
Anterior channel has additional option of an adjustable steel pin to block the forward progression of the tibia at mid-stance (dorsiflexion stop), or to lock the joint in a fixed position. Can be useful when quad muscle is weak or when there is a Charcot joint deformity at the ankle
What is the best type of knee joint for an obese patient with quadriceps weakness?
KAFO with double metal uprights & a posterior offset knee joint (single axis knee joint)
Offset knee joint
Places the hinge posterior to the knee joint so patient’s weight line falls anterior to the offset joint, stabilizing the knee early during stance phase
Allows sitting without needing to manipulate the lock
Should not be used in patients with knee or hip flexion contractures, or with a PF stop at the ankle
Must be careful when walking on a ramp as the knee may flex inadvertently
Scott Craig orthosis
Bilateral KAFOs designed for standing & ambulation in adults with paraplegia
Provides patient with a complete neurological level at L1 or lower with a more functional & comfortable gait
Eliminates unnecessary hardware to reduce weight & facilitate donning/doffing (eliminates lower thigh & calf band)
Components:
- Sole plate extending to the met heads w/a crossbar added to the met heads for ML stabilization
- Ankle joint set at 10 degrees of DF
- Anterior rigid tibial band (patellar tendon strap)
- Offset knee joint with bail lock
- Proximal posterior thigh bind
Is unsupported standing possible with a Scott Craig orthosis?
Yes!
With the ankles & knees locked, hip stabilization can be achieved by leaning the trunk backward so that the CoG of the trunk rests posterior to the hip joint, resulting in tightening of the anterior hip capsule & the Y ligament
Can paraplegic patients ambulate with Scott Craig orthosis?
Yes!
If they also use crutches or walker using a swing-to or swing-through gait pattern
Reciprocal Gait Orthosis (RGO)
A special design of the HKAFO used for upper lumbar paralysis in which active hip flexion is preserved
Consists of bilateral HKAFO’s with offset knee joints with drop locks, posterior plastic AFO’s, thigh pieces, custom-molded pelvic girdle, hip joints, & a thoracic extension with Velcro straps in addition to the control mechanism
Several designs are available, such as cord & pulley design, single cable, dual cable, & isocentric (IRGO, latest design)
In all RGO’s, the hip joints are coupled together with cables (or to the pivoting band in the IRGO), which provides mechanical assistance to hip extension while preventing simultaneous bilateral hip flexion
As a step is initiated & hip flexion takes place on one side, the cable coupling induces hip extension on the opposite side, producing a reciprocal walking pattern
Forward stepping is achieved by active hip flexion, lower abdominal muscles, and/or trunk extension
Using two crutches & an RGO, paraplegics can ambulate with a four-point gait. A walker may also be used
Isocentric RGO (IRGO)
Cord is substituted by a pelvic band attached to the posterior surface of the molded thoracic section
Advantages: less bulky appearance (no protruding cables in the back), may be more cost-efficient than cable RGO (no energy loss due to cable friction)
What does adding a footplate to a knee immobilizer do?
Decreases rotational instability of the knee
Opponens orthosis
Immobilizes the thumb & first MCP joint to promote tissue healing and/or protection, or for positioning of the weak thumb in opposition to other fingers to facilitate three-jaw chuck pinch
Long opponens orthosis with wrist-control attachments
Similar to short opponens orthosis but crosses the wrist
Stabilizes 1st MCP while forearm bar maintains wrist in extension & prevents radial & ulnar deviation deformities
Examples: long opponens splint, thumb spica splint
Wrist-driven prehension orthosis (tenodesis orthosis, flexor hinge splint)
Used in C6 complete tetraplegia (no muscles to flex or extend; fingers remain innervated, but wrist extension, through the ECR, is intact) to provide prehension through tenodesis action & maintain flexibility of the hand, wrist, & elbow
Wrist extensors should be 3+ or better to use body-powered tenodesis
PIP & DIP joints of fingers 2 & 3 and the CMC & MCP joints of the thumb are immobilized
May interfere with manual wheelchair propulsion
Rarely accepted by C7 & C8 tetraplegics who prefer to use their residual motor power or utensil holders
RIC Tenodesis Splint (Rehabilitation Institute of Chicago)
Made of low-temperature thermoplastics in 3 separate pieces (wristlet, short opponens, & dorsal plate over index & middle finger)
Easily & quickly fabricated; made as a training & evaluation splint for patients; lightweight
Uses a cord/string running from the wrist piece, across the palm, & up between the index & ring fingers. String is lax when wrist is flexed & tightens with wrist extension, bringing the fingers close to the immobilized thumb, accomplishing three-jaw chuck prehension
Balanced forearm orthosis
Shoulder-elbow-wrist-hand orthosis that consists of a forearm trough (attached by a hinge joint to a ball-bearing swivel mechanism) & a mount (which can be mounted on the WC, on a table or working surface, or onto the body jacket)
Helps support the forearm & arm against gravity & allows patients with weak shoulder & elbow muscles to move the arm horizontally & flex the elbow to bring hand to the mouth
What are the requirements of the balanced forearm orthosis?
- Some residual muscle strength of biceps & pec (at least grade 2 or better) & coordination of elbow flexion (can be used for C5 tetraplegia)
- Adequate trunk stability & balance
- Adequate endurance in sitting position
- Preserved ROM of the shoulder & elbow joints
- Other uses: may be used in spastic patients to allow self-feeding by dampening muscle tone through a friction device
Soft cervical collar
Made of polyethylene foam or sponge rubber
Provides no significant control of motion of the C-spine, but does provide a kinesthetic reminder (through sensory feedback) to limit motion
Retains body heat, which may help reduce muscle spasm & aid in healing of soft-tissue injuries
Indications: symptomatic tx of soft tissue injuries of the neck (like whiplash injury)
Maximum amount of time should be worn: 10 days
Risks with prolonged use: muscle atrophy, psychological dependency
Sterno-Occipital Mandibular Immobilizer (SOMI)
Cervico-thoracic orthosis with chest piece connected by uprights (going from anterior to posterior) to occipital plate
Can easily be applied to a supine patient
Has removable mandibular piece so patient can eat, wash, or shave while lying supine
Indications: cervical arthritis, post-surgical fusions, stable cervical fractures
Minerva CTO/Thermoplastic Minerva Body Jacket
Encloses the entire posterior skull, includes a band around the forehead, & extends downward to the inferior costal margin
Forehead band provides good control of all cervical motions
Advantages: lighter weight than the halo vest; no pins (no invasive supports that carry risks of infection & slippage)
Disadvantages: less restriction of motion compared to a halo vest
Indications: management of unstable cervical spine (although halo vest is usually preferred for maximum motion control)
May be the preferred orthosis (over halo) in management of cervical spine instability in preschool age children due to increased comfort, decreased weight, & allows for early mobilization of the patient for rehabilitation, in addition to providing the necessary stability
Halo vest CTO
Provides the best control of motion (in all planes) in the C-spine of all the cervical CTO
Permits early mobilization without risk of compromising spinal alignment
Non-removable
Consists of a rigid halo ring secured to the skull with 4 external fixation pins (anterolateral above the orbital rim & posterolateral below the largest diameter of the skull). Pins are placed where they are to prevent cephalad pin migration, piercing the temporalis muscle, frontal & temporal fossae, or injury to CN’s)
Halo supports 4 posts attached to the anterior & posterior part of the vest (thoracic component)
Indications: management of unstable fractures of the C-spine (especially high cervical fractures); non-surgical alternative in cases where surgery is contraindicated or refused
Complications: risk of pressure ulcers with bedrest- especially scapula & sternum
TLSO
Extend from sacrum to above the inferior angle of the scapulae & are used to support & stabilize the trunk & to prevent progression of moderate scoliosis (20-45 degrees) until patient reaches skeletal maturity, & used for thoracic kyphosis
Except for thoracolumbosacral flexion-control orthoses, TLSO’s can increase intra-abdominal pressure (which in turn decreases load on spine/IVD by transmission of the load to the surrounding soft tissues)
Cause an increase in O2 consumption & EE
During ambulation, with axial rotation between the pelvis & shoulders, there may be increased motion at the unrestrained segments cephalad & caudal to the orthosis
Jewett Brace (flexion-control TLSO)
Consists of a sternal pad, suprapubic pad, & anterolateral pads connected by oblique lateral uprights counteracted by a dorsolumbar pad
Suprapubic band may be substituted by a boomerang band, which applies force on the iliac crests (used in females to avoid direct pressure on the bladder)
Indications:
- Used to permit the upright position while preventing flexion after compression fracture of the TL spine (use in tx of compression fractures in osteoporotic elderly patients is controversial because it can place excessive hyper-extension forces on the lower lumbar vertebrae, which can induce posterior element fractures or exacerbate a degenerative arthritis condition)
- TL Scheurmann’s disease
- Thoracic osteoporotic kyphosis (limited efficacy)
Milwaukee brace
CTLSO used for scoliosis
Consists of a rigid plastic pelvic girdle connected to a neck ring over the upper thorax by one anterior, broad aluminum bar & 2 paraspinal bars
The cervical ring has mandibular & occipital bars, which rest 20-30 mm inferior to occiput & mandible
Pads strapped to the bars apply a transverse load to the ribs & spine to correct scoliotic curvatures
Indications:
- Idiopathic or flexible congenital scoliosis with curves 25-40 degrees if curve apex is located superior to T8, the scoliosis shows signs of progression, & puberty has not finished
- Thoracic Scheuermann’s disease kyphosis
Definition of CVA
Rapidly developing clinical signs of focal or global disturbances of cerebral function lasting 24 hours or longer OR leading to death with no apparent cause other than of vascular origin
If <24 hours –> TIA
What are the 2 categories of CVA risk factors?
Non-modifiable & modifiable
Non-modifiable risk factors for CVA
- Age (most important; after age 55, incidence increases (risk more than doubles each decade after 55))
- Sex (male > female)
- Race (AA»_space; white > asian)
- Family h/o CVA
Modifiable risk factors for CVA
- HTN (most important for both ischemic & hemorrhagic; 7-fold increased risk)); lower rates of recurrent CVA with lower BP’s. Target SBP <130
- H/o prior TIA/CVA
- Heart disease (CHF, CAD)
- Valvular heart disease, arrhythmias (increased risk of embolic stroke for these)
- AF
- DM
- Cigarette smoking (for ischemic CVA & SAH)
- Carotid stenosis (& carotid bruit)
- EtOH/cocaine abuse
- High-dose estrogens (birth control pills) (considerable increased risk when combined with cig smoking)
- Systemic diseases a/w hyper-coagulable states (elevated RBC, hematocrit, fibrinogen; Protein C & S deficiencies; sickle cell anemia; CA)
- HLD (LDL-C a/w increased risk of CVA & has stronger association for large artery atherosclerotic subtype)
- Migraine HA
- OSA
- PFO
- Sedentary physical activity
- Nutrition (Mediterranean diet reduces incidence of CVA)
Where is CSF produced?
In the brain mostly by modified ependymal cells in the choroid plexus in the lateral, 3rd, & 4th ventricles, with the remainder formed around blood vessels & along ventricular walls
CSF circulation
From the lateral ventricles to the foramina of Monro (IVF), 3rd ventricle, aqueduct of Sylvius (cerebral aqueduct), 4th ventricle, foramen of Magendie (Median aperture) & foramina of Luschka (lateral apetures), & sub-arachnoid space over brain & spinal cord
Types of CVA
Ischemic (87%)
Hemorrhagic
Subtypes of ischemic:
- Thrombotic
- Embolic
- Lacunar
Subtypes of hemorrhagic:
- ICH- hypertensive
- SAH- ruptured aneurysm
Thrombotic CVA’s (large artery thrombosis)
- 48% of all CVA’s
- Usually occurs during sleep (patient awakens unaware of deficits)
- May have stuttering, intermittent progression of neuro deficits, or be slowly progressive (over 24-48 hours)
- Profound LOC is rare except when area of infarction is large or when brainstem is involved
- Perfusion failure distal to site of severe stenosis or occlusion of major vessels
- Emboli from incompletely thrombosed artery may precipitate an abrupt deficit. May have embolism from extra-cranial arteries affected by stenosis or ulcer
Embolic CVA’s
- 26% of all CVA’s
- Immediate onset of neuro deficits, usually occurs during waking hours
- Seizures may occur at onset of CVA
- Most commonly due to cardiac source: mural thrombi & platelet aggregates
- Emboli most commonly originate from cardiac thrombus caused by AF. Also occur in rheumatic heart disease (like MS), post-MI, & vegetations on heart valves in bacterial/marantic endocarditis) or prosthetic heart valves
- Emboli may dislodge spontaneously or after invasive CV procedures (like cath)
- 75% of cardiogenic emboli go to the brain
- Embolus can consist of fat (from fractured long bones, air (decompression sickness), or venous clot that passes through a PFO with shunt (paradoxical embolus)
- Rarely, a subclavian artery thrombosis may embolize to the VA or its branches
Lacunar CVA’s
- 13% of all CVA’s
- Onset may be abrupt or gradual; up to 30% develop slowly over 36 hours
- Lacunes are small infarcts (<15 mm) seen in the putamen, pons, thalamus, caudate, & internal capsule
- Due to occlusive arteriolar or small artery disease (occlusion of deep penetrating branches of large vessels)
- Occlusion occurs in small arteries of 50-200 mm in diameter
- Strong correlation with HTN; also a/w microatheroma, micro-embolism, or rarely arteritis
- CT shows lesion is about 2/3 of cases (MRI more sens)
- Often relatively pure syndromes (motor or sensory)
- Absence of higher cortical function involvement (language, praxis, non-dominant hemisphere syndrome, vision)
What is the most common cause of occlusion of the superior division of the MCA?
Embolus
*Superior division of the MCA supplies Rolandic & pre-rolandic areas (AKA horizontal M1)
What happens with occlusion of one ACA DISTAL to an anterior communicating artery?
- Contralateral weakness & sensory loss, affecting mainly the distal contralateral leg (foot/leg more affected than thigh)
- Mild/no UE involvement
- Head & eyes may be deviated toward side of lesion acutely
- Urinary incontinence with contralateral grasp reflex & paratonic rigidity (Gegenhalten) may be present
- May produce transcortical motor aphasia if left side is affected
- Gait apraxia: disturbances in gait & stance
What occurs if both ACA’s arise from one stem & there is a CVA distal to anterior communicating arteries?
Major disturbances occur with infarction occurring at the medial aspects of both cerebral hemispheres –> aphasia, paraplegia, incontinence, & frontal lobe/personality dysfunction (emotional instability, disinhibition, apathy)
Clinical presentation in PCA CVA
- Occlusion can produce a variety of clinical effects because PCA supplies the upper brainstem & inferior parts of the temporal lobe, as well as medial parts of the occipital lobe
- 70% of time, both PCA’s arise from the basilar artery & are connected to the ICA’s through the posterior communicating artery
- 20-25% of the time, one PCA comes from basilar & other comes from ICA
- 5-10% of time, both PCA’s come from carotids
- Visual field cuts –> when bilateral, may have denial of cortical blindness (Anton syndrome)
- May have prosopagnosia (cannot read faces)
- Palinopsia (abnormal recurring visual imagery)
- Alexia (cannot read)
- Alexia without agraphia (patient able to write but not read or recognize written words)
- Transcortical sensory aphasia (loss of power to comprehend written or spoken words; patient can repeat)
What structures are supplied by the inter-peduncular branches of the PCA?
CN 3 (oculomotor nerve) & CN 4 (trochlear) nuclei & nerves
What is Weber syndrome?
Clinical syndrome caused by occlusion of the inter-peduncular branches of the PCA: oculomotor palsy with contralateral hemiplegia
What else can happen with occlusion of the inter-peduncular branches of the PCA?
Trochlear nerve palsy (vertical gaze palsy)
What are symptoms in CVA with vetebro-basilar system involvement?
- Nystagmus
- Vertigo, Abnormalities of motor function, often b/l
- Ipsilateral CN dysfunction
- Crossed signs: motor or sensory deficit on ipsilateral side of face & contralateral side of body; ataxia, dysphagia, dysarthria
What is the main difference between symptoms in CVA comparing vetebro-basilar system involvement to anterior circulation involvement?
There is absence of cortical signs when there is involvement of the vertebro-basilar system (such as aphasia or cognitive deficits)
Vertigo in vertebro-basilar insufficiency
Isolated attacks can be the initial & only symptom, however attacks of vertigo in vertebro-basilar insufficiency usually lasts <30 minutes & have NO associated hearing loss
Wallenberg (lateral medullary syndrome)
- AKA PICA syndrome or vertebral artery syndrome
- Occurs due to occlusion of the one of the following: vertebral arteries (involved in 8 of 10 cases), PICA, superior lateral/middle lateral/inferior lateral medullary artery)
- Signs & symptoms:
Ipsilateral: Horner syndrome (ptosis, anhidrosis, miosis); decrease in pain & temp sensation on face; cerebellar signs such as ataxia on ipsilateral extremities (patient falls to side of lesion)
Contralateral: decreased pain & temp on body, dysphagia/dysarthria/hoarseness/vocal cord paralysis, vertigo/n/v, hiccups, nystagmus, diplopia
There is NO facial or extremity muscle weakness in this syndrome
Symptoms & site of lesion of Wallenberg syndrome
- Ipsilateral Horner’s syndrome: Pupillodilator (sympathetic) fibers)
- Ipsilateral face pain & temp loss: Spinal trigeminal tract
- Ipsilateral ataxia (UE > LE): Spinocerebellar tract
- Contralateral arm/leg pain & temp loss: Spinothalamic tract
- Dysphagia, hiccups, hoarseness: nucleus ambiguus, CN 9, CN 10 nerves
- Vertigo, n/v: Vestibular nuclei
Gross locations of CN brainstem nuclei
Midbrain: 1-4 (CN1 & 2 nuclei are located in forebrain)
Pons: 5-8
Medulla: 9-12 (CN 11 has 2 divisions- the cranial & spinal division; the spinal division arises from the ventral horns of CN1-6 levels)
Weber syndrome
- Clinical syndrome caused by occlusion of the inter-peduncular branches of the PCA: oculomotor palsy with contralateral hemiplegia
- Paramedian (medial) brainstem syndrome
Millard-Gubler syndrome
- Paramedian (medial) brainstem syndrome
- Obstruction of circumferential branches of basilar artery
- Ipsilateral CN (abducens; LR) 6 paralysis (often 7 involved- facial)
- Contralateral hemiplegia (if extends into medial lemniscus –> Raymond-Foville syndrome with gaze palsy to side of lesion)
- Contralateral lemniscus (tactile sensation) sensory loss 2/2 damage to medial lemniscus with analgesia, hypoesthesia
Medial medullary syndrome AKA “another lesion”
- Paramedian (medial) brainstem syndrome
- Caused by infarction of the medial medulla due to occlusion (usually athero-thrombotic) of penetrating branches of the VA’s (upper medulla) or anterior spinal artery (lower medulla & medullocervical junction)
- Rare; much less common than lateral medullary syndrome
Ipsilateral hypoglossal (CN 12) palsy with deviation toward side of lesion - Contralateral hemiparesis
- Contralateral lemniscal sensory loss (proprioception & position sense)
Region of brainstem syndromes
Midbrain:
- Main artery: PCA
- Paramedian: Weber
- Lateral: N/a
Pons:
- Main artery: Basilar artery
- Paramedian: Millard-Gubler syndrome
- Lateral: N/a
Medulla:
- Main artery: VA (or ASA)
- Paramedian: medial medullary synrome
- Lateral: Wallenberg syndrome
Locked-in syndrome
- Quadriparesis with patients who are only able to move eyes vertically or blink
- Patient remains fully conscious due to sparing of RAS (which is located primarily in midbrain)
- Caused by b/l lesions of the ventral pons (basilar artery occlusion)
What is dysarthria/clumsy hand syndrome?
Lacunar CVA at location of basis pontis & anterior limb of internal capsule
Where is the most common location for a hypertensive ICH?
Putamen
Hemiplegia occurs 2/2 compression of adjacent internal capsule
Vomiting occurs in half of cases
HA is frequent but not constant
With smaller hemorrhages –> HA leading to aphasia, hemiplegia, eyes deviate away from paretic limbs
Where do most saccular aneurysms occur?
Anterior part of circle of Willis
What makes saccular arterial aneurysms more likely to rupture?
If 10 mm or larger
What is peak age for rupture of saccular arterial aneurysm?
40’s-50’s
Hunt & Hess Scale for Atraumatic SAH
Grade 1: asx, mild HA, slight nuchal rigidity
Grade 2: moderate to severe HA, nuchal rigidity, no neuro deficit other than CN palsy
Grade 3: drowsiness/confusion, mild focal neuro deficit
Grade 4: stupor, moderate-severe hemiparesis
Grade 5: coma, decerebrate posturing
Clinical presentation of saccular aneurysm/SAH
Compression of adjacent structures such as CN3 with a posterior communicating-internal carotid junction aneurysm or posterior communicating-PCA aneurysm
Signs of CN3 involvement:
- Deviation of ipsilateral eye to lateral side (lateral or divergent strabismus)
- Ptosis
- Mydriasis & paralysis of accommodation due to interruption of parasympathetic fibers in CN3
What is a sentinel HA?
Sudden, intense, & persistent HA, preceding SAH by days or weeks in half of patients
What is mortality in rupture of aneurysm producing SAH with or without ICH?
25% during first 24 hours
What is the risk of re-bleeding in rupture of aneurysm producing SAH with or without ICH?
Within 1 month: 30%
2.2% per year during first decade
What are AVM’s?
Low-pressure systems; larger the shunt, the lower the interior pressure. With these large dilated vessels, there needs to be an occlusion distally to raise luminal pressures to cause hemorrhage
Clinical presentation of AVM rupture
- Hemorrhage is the initial presentation in half of cases
- May be parenchymal (41%), subarachnoid (23%), or intra-ventricular (17%) hemorrhage
- Seizures occur in 30% of cases
- HA occurs in 20% of cases, 10% overall with migraine-like HA
- Neurologic deficit varies according to area affected
Ischemic CVA BP Management
IV Labetalol, Nicardipine, & Clevidipine
Can also consider Hydralazine & Enalapril
If BP remains uncontrolled or DBP >140, consider IV sodium nitroprusside
Hemorrhagic CVA BP Management
IV Labetalol (does not cause cerebral vasodilation, which could worsen increased ICP)
What is the best indication for AC in CVA?
Cardiac emboli
- Primarily from non-valvular AF & mural thrombus from MI
- There is a probable risk of inducing cerebral hemorrhage or hemorrhagic infarction within large infarcts if AC in the first 24-36 hours
- If neuro deficit is mild (& CT shows no hemorrhage), may begin AC immediately
- If deficit is severe (clinically and/or with CT), wait 3-5 days before starting AC
- Most common cause is chronic AF
Who should get CEA?
Symptomatic lesions with 70-90% stenosis is effective in reducing the incidence of ipsilateral hemisphere CVA (moderate, symptomatic carotid stenosis)
What decreases cerebral vasospasm after SAH & has been shown to improve outcome after SAH?
PO Nimodipine 60 mg q4h for 21 days; should initiate therapy within 4 days of onset of hemorrhage
Rehabilitation methods for motor deficits
- PNF (Proprioceptive NM facilitation)
- Bobath/Neurodevelopmental Technique (NDT)
- Brunnstrom/Movement Therapy
- Sensorimotor/Rood
- Motor Relearning Program/Carr & Shepherd
PNF (Proprioceptive NM Facilitation)
Uses spiral & diagonal components of movement rather than the traditional movement in cardinal planes of motion with the goal of facilitating movement patterns that will have more functional relevance than the traditional technique of strengthening individual group muscles
Bobath approach/NDT
Goal is to normalize tone, inhibit primitive patterns of movement, & facilitate automatic, voluntary reactions & subsequent movement patterns
Abnormal patterns are modified at the proximal key points of control (shoulder & pelvic girdle)
Brunnstrom approach/Movement therapy
Uses primitive synergistic patterns in training in an attempt to improve motor control through central facilitation
Sensorimotor/Rood
Modification of muscle tone & voluntary motor activity using cutaneous sensorimotor stimulation
Motor Relearning program/Carr & Shepherd Approach
Goal is for patient to relearn how to move functionally & how to problem-solve during attempts at new tasks
Constraint-induced movement therapy (CIMT)
Restrain the less affected arm (like Brunnstrom)
In the EXCITE Trial, participants were required to have at least 10 degrees active wrist extension, 10 degrees thumb abduction/extension, & 10 degrees extension in at least two additional digits
Post-CVA shoulder pain
70-84% of CVA patients with hemiplegia have shoulder pain with varying degrees of severity
Majority (85%) will develop it during the spastic phase of recovery
Most common causes of hemiplegic shoulder pain are CRPS Type 1 & soft-tissue lesions (including plexus lesions)
CRPS (Complex Regional Pain Syndrome)
Neuropathic pain c/b exaggerated response to a traumatic lesion or peripheral nerve that results in severe neuropathic pain & sensory, autonomic, motor, & trophic impairments
Includes sympathetic-maintained pain & related sensory abnormalities, abnormal blood flow, abnormalities in motor system, & changes in both superficial & deep structures with trophic changes
CRPS Type 1: RSD, shoulder-hand syndrome, Sudeck’s atrophy. Follows an injury without nerve injury in affected limb
CRPS Type 2: develops following peripheral nerve injury to affected limb
Stages of CRPS
Stage 1 (acute): burning pain, diffuse swelling/edema, exquisite tenderness, hyperpathia &/or allodynia, vasomotor changes in hand/fingers (increased nail & hair growth, hyperthermia or hypothermia, sweating). Lasts 3-6 months
Stage 2 (dystrophic): pain becomes more intense & spreads proximally, skin/muscle atrophy, brawny edema, cold insensitivity, brittle nails/nail atrophy, decreased ROM, mottled skin, early atrophy, & osteopenia (late). Lasts 3-6 months
Stage 3 (atrophic): pain decreases, trophic changes occur, hand/skin appear pale & cyanotic with a smooth, shiny appearance, feeling cool & dry; bone demineralization progresses with muscular weakness/atrophy, contractures/flexion deformities of shoulder/hand, tapering digits. No vasomotor changes in this stage
Diagnostic approaches to CRPS
XR: normal in initial stages; periarticular osteopenia may be seen in later stages. Need 30-50% demineralization for detection
Triple phase bone scan: high sens, only 56% spec. High NPV. Main thing to look for is juxta-articular tracer activity on delayed images (most sensitive for Type 1)
EMG: association between spontaneous activity & eventual development of CRPS
Clinical exam: shoulder pain with ROM (flexion/abduction/ER), absence of pain in elbow & with forearm pronation/supination; wrist DF pain with dorsal edema; pain in MCP/PIP flexion with fusiform PIP edema. Shoulder/hand pain preceded by rapid ROM loss. Most valuable is MCP tenderness to compression
Skeletal scintigraphy (bone scan): delayed image showing increased uptake in wrist, MCP, & IP joints
Stellate ganglion block: successful when patient develops an ipsilateral Horner syndrome. Alleviation of pain following sympathetic blockage of the stellate ganglion using local anesthetic is the gold standard for diagnosis of sympathetically-mediated CRPS Type 1
Treatment for CRPS
ROM exercises of involved joint, passive stretch
Systemic corticosteroids (high doses tapered over 2 weeks). More effective in CRPS Type 1 confirmed by bone scan than in clinical CRPS Type 1 with a negative bone scan
Other meds:
- NSAIDs
- TCA’s
- Bisphosphonates
- Calcitonin
- Anti-convulsants (gabapentin, carbamazepine)
- Alpha-adrenergic blockers (clonidine, prazosin)
- BB
- CCB
- Topical capsaicin
Modalities:
- Edema control measures
- TENS
- Desensitization techniques
- Contrast baths
- Ultrasound
Injections:
- IA CSI
- Local injections
- Sympathetic stellate ganglion blocks may be diagnostic & therapeutic
Other:
- RFA, surgical sympathectomy
Treatment for shoulder subluxation in CVA
Friedland (1975): slings do not prevent/correct subluxation & are not necessary to support pain-free shoulder
Hurd er al (1974): no difference in shoulder ROM, subluxation, or shoulder pain in patients with or without slings
Brachial plexus/peripheral nerve injury in CVA
Etiology: traction injury to plexus/nerve
Diagnosis: atypical functional return, segmental muscle atrophy, finger extensor contracture, delayed onset of spasticity
EMG will show LMN findings of a brachial plexopathy
Treatment:
- Proper bed positioning to prevent patient from rolling onto paretic arm, trapping it behind the back or through bed rails & causing traction stress
- ROM to prevent contracture while traction avoided
- 45 degree shoulder abduction sling for nighttime positioning
- Sling for ambulation to prevent traction by gravity
- Armrest in wheelchair as needed
Prognosis: may require 8-12 months for re-innervation
Other ddx for post-CVA shoulder pain
Inferior subluxation, RTC tear, adhesive capsulitis, RTC impingement, biceps tendinopathy
Shoulder subluxation in CVA diagnostic test & treatment
Testing: XR in standing position, scapular plane view
Treatment: sling when upright, FES
Adhesive capsulitis in CVA exam, diagnostic test, & treatment
Exam: ER < 15 degrees, early decrease in scapular motion, spastic
Diagnostic test: arthrogram
Treatment: PT/ROM, debridement manipulation, SAS/GH CSI (large distention), oral steroids, reduction of internal rotator cuff tone
Diagnosis of dysphagia in CVA
Bedside swallow to evaluate gag reflex or pharyngeal sensation, observing for overt signs of cough or other difficulty during swallowing trials
VFSS (videofluorographic swallowing evaluation) AKA MBS (modified barium swallow): gold standard for evaluation & treatment of dysphagia
FEES (fiberoptic endoscopic evaluation of swallowing): used as a comprehensive functional evaluation of the pharyngeal stage of swallowing; visualizes anatomic structures that might cause potential bolus obstruction & natural bolus flow & containment
Aspiration
Entry of a substance through the vocal folds (true vocal cords) into the trachea
Missed on bedside swallowing evaluations in 40-60% of patients (silent aspiration)
Can be reliable diagnosed on VFSS, showing penetration of contrast material below true vocal cords
Predictors of aspiration on bedside swallowing exam
- Abnormal cough
- Cough after swallow
- Dysphonia
- Dysarthria
- Abnormal gag reflex
- Voice change after swallow (wet voice)
Aspiration PNA
Risk factors include:
- Decreased level of consciousness
- Trach
- Emesis
- GERD
- NGT feeds
- Dysphagia
- Prolonged pharyngeal transit time
Four phases of swallowing
- Oral prep
- Oral
- Pharyngeal
- Esophageal
Oral preparatory phase of swallowing
Voluntary
Variable duration, influenced by consistency of material ingested, number of chews, etc
Hallmark of phase: preparation of bolus
Requires:
- Tension in labial & buccal musculature to close the anterior & lateral sulci
- Rotatory jaw motion for mastication/grinding
- Lateral tongue movement to position food on the teeth during mastication (tongue moves food back to teeth)
- Depression & forward movement of the soft palate to seal the oral cavity posteriorly & widen the nasal airway
- Saliva
Problems seen in this phase: drooling, pocketing
Oral phase of swallowing
Voluntary
Lasts usually <1 second
Hallmarks of this phase:
- Tongue that elevates & occludes the anterior oral cavity & compresses the bolus toward the oropharynx
- Contraction of the palato-pharyngeal folds
- Elevation of the soft palate
Phase requires:
- Tension in the labial & buccal musculature to close the anterior & lateral sulci
- Anterior-posterior tongue movement to transport the bolus to the pharynx
- Soft palate elevation & velo-pharyngeal port closure (also seen in pharyngeal phase) to close off the nasal cavity & prevent regurgitation into the nasopharynx
Problems seen in this phase: drooling, pocketing, head tilt
Pharyngeal phase of swallowing
Reflex
Lasts 0.6-1 second
Hallmarks of this phase:
- Bolus propelled from mouth to esophagus
- Aspiration is most likely to occur during this phase
- With initiation of pharyngeal phase, inhibition of breathing occurs to prevent aspiration
Phase requires:
- Soft palate elevation & velo-pharyngeal port closure to close off the nasal cavity & prevent regurgitation into naso-pharynx
- Laryngeal elevation, with forward movement of the hyoid bone & folding of epiglottis to protect airway
- Adduction of ventricular & true vocal cords to protect airway
- Coordinated pharyngeal constriction & cricopharyngeal (UES) relaxation to facilitate bolus transport into esophagus
Esophageal phase of swallowing
Reflex
Longest phase- lasts 6-10 seconds
Hallmarks of this phase:
- Bolus pass from pharynx –> esophagus –> stomach
- Esophageal clearance is assisted by gravity but requires relaxation of the GES
Phase requires:
- Cricopharyngeal muscle contraction
- Coordinated peristalsis & LES relaxation
Problems seen in this phase: heartburn, food sticking
Compensatory strategies for treatment of dysphagia/prevention of aspiration
Chin tuck: provides airway protection by preventing entry of liquid into larynx by facilitating forward motion of the larynx; also decreases the space between the base of the tongue & the posterior pharyngeal wall, creating increased pharyngeal pressure to move the bolus through the pharyngeal region
Head rotation: closes ipsilateral pharynx, forces bolus into contralateral pharynx, & decreases cricopharyngeal pressures. Turn the head TO the paretic side
Recovery of dysphagia in CVA
Ickenstein et al (2012): subjects 72 hours post-CVA rated at a level 1-3 on the Functional Communication Measure (FCM) of Swallowing & level 5-8 on the Penetration-Aspiration Scale (PAS) were 11.8x less likely to be orally fed 90 days post-stroke
Nasal speech
Hyper-nasality caused by partial or complete failure of soft palate to close off the nasal cavity from the oral cavity or by incomplete closure of the hard palate
Uplifting the soft palate prevents nasal speech
Anatomic location of major speech areas: Wernicke’s aphasia
Posterior part of superior (first) temporal gyrus of the dominant (usually left) hemisphere
Anatomic location of major speech areas: Broca’s aphasia
Posterior-inferior frontal lobe (3rd frontal convolution) of dominant (usually left) hemisphere –> anterior to motor cortex areas that supply the tongue, lips, & larynx
Anatomic location of major speech areas: Global aphasia
Vary in size & location but usually involve the distribution of the left MCA (entire peri-sylvian region)
Anatomic location of major speech areas: Anomic aphasia
Temoro-parietal injury, angular gyrus. At the lateral Sylvian fissure
Anatomic location of major speech areas: Conduction aphasia
Lesion of the parietal operculum (arcuate fasciculus) or insula or deep to the supra-marginal gyrus (usually left side)
Anatomic location of major speech areas: Transcortical motor aphasia
Frontal lobe, anterior or superior to Broca’s area or in the sub-cortical region deep to Broca’s area
Anatomic location of major speech areas: Transcortical sensory aphasia
Watershed lesion isolating perisylvian speech structures (Broca & Wernicke areas) from the posterior brain; angular gyrus or posterior-inferior temporal lobe
Errors in speech: paraphasia
Incorrect substitution of words or parts of words
Literal or phonemic: similar sounds (sound for found)
Verbal or semantic: words substituted for another from same class (fork for spoon)
Errors in speech: anomia (aka nominal aphasia)
Difficulty recalling words; word-finding difficulty
Unimpaired comprehension & repetition
Errors in speech: echolalia
Repetition of words or vocalizations made by another person
Errors in speech: circumlocution
Roundabout way of describing a word that cannot be recalled
Often seen with anomia
Errors in speech: neologism
A “new word” that is well-articulated but has meaning only to the speaker
Errors in speech: jargon
Well-articulated but mostly incomprehensible, unintelligible speech
A/w Wernicke’s aphasia
Errors in speech: stereotype
Repetition of non-sensical syllables (no, no no) during attempts at conversation
Melodic intonation therapy
Recruits the right hemisphere for communication by incorporating melodies or rhythms with simple statements
May be useful in patients with non-fluent (Broca’s) aphasia
Post-CVA aphasia recovery
Greatest improvement occurs in first 2-3 months
After 6 months, there is a big drop in rate of recovery
Usually, spontaneous recovery does not occur after 1 year (but can get better many years later with therapy)
Negative risk factors for return to work post-CVA
Low score on Barthel index at time of rehab discharge
Prolonged rehab length of stay
Aphasia
Prior alcohol abuse
Barthel index
Functional assessment tool that measures independence in ADLs on 0-100 scale
What is the single most common cause of death & injury in MVAs
Ejection of occupant from vehicle
TBI based on marital status
Single (46%) > married (33%) > divorced (16%) > widowed/separated (5%)
What substance is attributed to 50% of all TBI?
Alcohol, likely under-estimated/reported
Examples of primary brain injury
- Contusion (bruising of cortical tissue) +/- DAI
- Impact depolarization: massive surge in extracellular K & glutamate release (excitatory) occurring after severe head injury leading to excitotoxicity (secondary injury)
Diffuse axonal injury definition
Immediate disruption of the axons due to acceleration-deceleration & rotational forces that cause shearing upon impact
Evidence of a secondary axotomy due to increased axolemmal permeability, calcium influx, & cytoskeletal abnormalities that propagate after the injury
Leads to white matter punctate petechial hemorrhages characteristic of DAI
Focal brain hemorrhages
Epidural hematoma, SDH, SAH
Epidural hematoma
90% occur with skull fracture in the temporal bone crossing MMA (60-90%) or veins (MMV, diploic veins, or venous sinus; 10-40%)
Hematoma expansion is slowed by the tight adherence of the dura to the skull
Lucid interval presentation happens 50% of the time. Biconvex acute hemorrhagic mass seen on CTH
Subdural hematoma
Occurs in 30% of severe head trauma
Result from shearing of the bridging veins between the pia-arachnoid & the dura
Usually larger in the elderly due to generalized loss of brain parenchyma
High density, crescentic, extra-cerebral masses seen on CTH
Acute: immediately symptomatic lesions
Subacute: 3 days-3 weeks
Chronic: >3 weeks
Subarchnoid hemorrhage
Closely a/w ruptured cerebral aneurysms & AVMs creating blood around the cisterns, although they could also result from leakage from an IPH & trauma
CT shows blood within the cisterns around the brainstem & the sub-arachnoid space within 24 hours
CT sensitivity decreases to 30% 2 weeks after the initial bleed
What is the most common cause of unconsciousness during & following the first 24 hours of injury after TBI
Axonal injury (DAI)
Brain plasticity (PUN)
Plasticity = Unmasking + Neuronal Sprouting
What is brain plasticity?
Represents the capability of the damaged brain to “repair” itself by means of morphologic & physiologic responses
Influenced by the environment, complexity of stimulation, repetition of tasks, & motivation
Brain plasticity: collateral (neuronal) sprouting
Intact axons establish synaptic connections through dendritic & axonal sprouting in areas where damage has occurred
May enhance recovery of function, may contribute to unwanted symptoms, or may be be neutral (with no increase or decrease of function)
Occurs weeks to months post-injury
Brain plasticity: unmasking neural re-organization (functional re-organization)
Healthy neural structures not formerly used for a given purpose are developed (or reassigned) to do functions formerly subserved by the lesioned area (vicariation)
What are synaptic alterations that occur after TBI?
Diaschisis & increased sensitivity to neurotransmitter levels
Diaschisis
Mechanism to explain spontaneous return of function
Lesions/damage to one region of the CNS can produce altered function in other areas of the brain (at a distance from the original site of injury) that were not severed if there is a connection between the 2 sites (through fiber tracts)
Function is lost in both injured & in morphologically intact brain tissue
There is some initial loss of function 2/2 depression of areas of the brain connected to the primary injury site, & resolution of this functional de-afferentation parallels recovery of the focal lesion
What is consciousness?
Function of the ascending RAS & cerebral cortex
RAS is composed of cell bodies in the central reticular core of the upper brainstem (mainly midbrain) & their projections to widespread areas of the cerebral cortex via both the thalamic & extra-thalamic pathways
Lesions that interrupt the metabolic or structural integrity of the RAS or enough of the cortical neurons receiving RAS input can cause DOC
Vegetative state (unresponsive wakefulness syndrome)
C/b the resumption of the sleep-wake cycle on EEG
No awareness of self/environment, no purposeful behavior
There is presence of verbal or auditory startle but no localization or tracking
Patient opens eyes (either spontaneously or with noxious stim)
Related to diffuse cortical injury
Bilateral thalamic lesions are prominent findings
Persistent: Present for 1 months or more after TBI or non-traumatic BI
Permanent: Present for >3 months after non-traumatic & 12 months for TBI
When is decerebrate posturing seen?
With midbrain lesions/compression. Also with cerebellar & posterior fossa lesions
When is decorticate posturing seen?
Seen in cerebral hemisphere/white matter, internal capsule, & thalamic lesions
What is a simple scale for assessing depth of coma?
GCS
Severity of TBI based on GCS score
Severe: 3-8
Moderate: 9-12
Mild: 13-15
What is the best predictor of outcome in GCS?
Best motor response 2 weeks post-injury
What is the second-best acute predictor of outcome in GCS?
Verbal response
Glasgow Outcome Scale (GOS)
- Death: self-evident criteria
- VS (UWS)
- Severe disability (conscious but dependent): patient unable to be independent for any 24-hour period by reason of residual mental and/or physical disability
- Moderate disability (independent but disabled): patient with residual deficits that do not prevent independent daily life; patient can travel by public transport & work in a sheltered environment
- Good recovery (mild to no residual effects): return to normal life; may be minor or no residual deficits
What does resolution of PTA correspond with?
Period when incorporation of ongoing daily events occurs in the working memory
Galveston Orientation & Amnesia Test (GOAT)
Developed by Harvey Levin & colleagues, it is a standard technique for assessing PTA
Brief, structured interview that quantifies the patient’s orientation & recall of recent events
Assesses orientation to person, place, time; recall of circumstances of hospitalization; & last pre-injury & first post-injury memories
When is the end of PTA using GOAT?
When patient scores 75 or higher for 2 consecutive days
Period of PTA is defined as the number of days beginning at the end of the coma to the time the patient attains the first of two successive GOAT scores 75 or higher
Attempts at more involved neuropsych assessment are usually unproductive until patient consistently obtains 70 or greater
Post-traumatic amnesia & severity of TBI based on time
0-1 days: mild
1-7 days: moderate
>7 days: severe
Functional Independence Measure (FIM)
Ordinal scale with 18 items & 7 levels to assess physical & cognitive function with documented validity & reliability
Motor items: self-care, sphincter control, mobility
Cognition items: communication, psychosocial adjustment, cognitive function
Level of function scoring:
- Independent: 7 for complete independence (timely, safe), 6 for mod-I (extra time, devices)
- Modified dependence: 5 for supervision (cueing, coaxing, prompting), 4 for min-A (patient performs 75% of task), 3 for mod-A (patient performs 50-75% of task)
- Complete dependence: 2 for max-A (patient performs 25-50%), 1 for total assist (patient performs <25%)
Neuropsychosocial testing
Halstead-Reitan Neuropsychological Battery (HRNB): diagnostic test for all kinds of brain damage. Original battery was used to assess frontal lobe disorders by Halstead (1947) & then used by Reitan (1970-1974) who added tests & expanded to all brain damage
Most examiners use HRNB in conjunction with the Weschler Adult Intelligence Scale (revised WAIS-R) & Weschler Memory Scale (WMS) or the Minnesota Multiphasic Personality Inventory (MMPI)
What is the WAIS-R?
Weschler Adult Intelligence Scale-Revised
Sub-tests (6 determine verbal IQ & 5 determine performance IQ)
Most frequently used measure of general IQ
The revised version of WAIS-R is called WAIS-III:
- Verbal IQ: vocab, similarities, arithmetic, digit span, information, comprehension, letter-number sequencing
- Performance IQ: picture completion, digit-symbol coding, block design, matrix reasoning, picture arrangement, object assembly
What is the MMPI?
Minnesota Multiphasic Personality Inventory
550 T/F questions that yield info about aspects of personality
What is the Token test?
Correlates with scores on tests of auditory comprehension & language production
Comprised of 20 tokens (circles/squares, big/little, five colors), laid out horizontally
Increasingly complex oral commands (touch the white circle –> before touching the yellow circle, pick up the red square)
90% sens discriminating people with aphasias from people without
Evaluation of ICP
In a normal adult, reclining with the head & trunk elevated to 45 degrees, normal ICP is 2-5 mmHg
ICP levels up to 15 mmHg are considered harmless
Elevated ICP
ICP >20 mmHg for >5 minutes
Common after severe TBI
A unilateral mass lesion causes distortion of the brain, a reduction of CSF volume, increased ICP in the closed skull –> formation of internal hernias (including tentorial/uncal herniation)
If unchecked, increased ICP leads to death because of deformation of tissue, brain herniation, & cerebral ischemia
ICP > 40 mmHg –> neuro dysfunction & impairment of brain’s electrical activity
ICP > 60 mmHg –> fatal
Fever, hyperglycemia, hyponatremia, & seizures can worsen cerebral edema by increasing ICP
It is more important to maintain an adequate CPP then controlling only ICP
Indications for continuous monitoring of ICP & for MV
- Patient in coma (GCS <8) & with CTH showing elevated ICP (absence of 3rd ventricle & CSF cisterns)
- Deep coma (GCS <6) without hematoma
- Severe chest & facial injuries AND mod/severe head injury (GCS <12)
- After evacuation of intracranial hemorrhage if patient in coma (GCS <8) beforehand
Factors that may increase ICP
- Turning head, especially to left side if completely horizontal or head down
- Loud noise
- Vigorous PT
- Chest physiotherapy
- Suctioning
- Elevated BP
What type of seizures are majority of post-traumatic seizures?
Simple, partial
Risk factors a/w late post-traumatic seizures
- Penetrating head injury (biggest risk factor)
- ICH
- Early PTS (>24 hours-7 days)
- Depressed skull fracture
- Prolonged coma or PTA (>24 hours)
- Other: dural tearing, presence of foreign bodies, focal signs (aphasia, hemiplegia), age, EtOH abuse, use of TCA’s
When are therapeutic anti-convulsant medications started?
Once late seizures occur
What AED’s are preferred in TBI population?
Carbamazepine (partial) & valproic acid (generalized) are preferred over meds that are more sedating or a/w cognitive impairment (such as phenobarb & phenytoin) (although carbamazepine may be as sedating as phenytoin)
AED’s: Carbamazepine
Uses: Partial seizures, tonic-clonic (generalized) seizures, stabilization of agitation & psychotic behavior, bipolar affective disorder, neuralgia
ADRs:
- Acute: stupor/coma, hyper-irritability, convulsions, respiratory depression, SJS
- Chronic: drowsiness, vertigo, ataxia, diplopia, blurred vision, n/v, aplastic anemia, agranulocytosis, hypersensitivity reactions (dermatitis, eosinophilia, splenomegaly, lymphadenopathy), transient mild leukopenia, transient thrombocytopenia, water retention with decreased serum osmolality & Na, transient elevation of LFTs
AED’s: Gabapentin
Use: partial seizures
ADRs: somnolence, dizziness, ataxia, fatigue
AED’s: Levetiracetam (Keppra)
Uses: partial seizures, myoclonic seizures
ADRs:
- Acute: hyperirritability, depression
- Chronic: drowsiness, vertigo, ataxia, hallucinations, flu-like symptoms, poor coordination, rash, BPD, suicidality
AED’s: Phenobarbital
Uses: partial seizures, tonic-clonic; generalized seizures
ADRs: sedation, irritability, & hyperactivity in children; rash; exfoliative dermatitis; hypothrombinemia with hemorrhage in newborns whose mothers took phenobarbital; megaloblastic anemia; osteomalacia; nystagmus & ataxia at toxic doses
AED’s: Phenytoin (Dilantin)
Uses: partial seizures, tonic-clonic (generalized) seizures, neuralgia
ADRs:
- IV: cardiac arrhythmias, hypotension, CNS depression
- PO: disorders of cerebellar & vestibular systems, cerebellar atrophy, blurred vision, mydriasis, diplopia, ophthalmoplegia, behavioral changes (hyperactivity, confusion, dullness, drowsiness, hallucination), increased seizure frequency, GI sx, gingival hyperplasia, osteomalacia, megaloblastic anemia, hirsutism, transient elevation in LFT’s, decreased ADH secretion, hyperglycemia, glycosuria, hypocalcemia, SJS, SLE, neutropenia, leukopenia, red cell aplasia, agranulocytosis, thrombocytopenia, lymphadenopathy, hypothrombinemia in newborns whose mothers received phenytoin, drug allergy (skin, BM, liver function involvement)
AED’s: Valproic Acid (Depakote)
Uses: partial seizures, tonic-clonic (generalized) seizures, myoclonic seizures, absence seizures, stabilization of agitation & psychotic behavior
ADRs: transient GI sx (anorexia, n/v), increased appetite, sedation, ataxia, tremor, rash, alopecia, LFT elevation, fulminant hepatitis (rare but fatal), acute pancreatitis, hyperammonemia
AED’s drug interactions: Carbamazepine
- Increased metabolism (decreased levels) with co-use of phenobarb, phenytoin, & valproic acid
- Enhances metabolism of phenobarb
- Enhances metabolism of primidone into phenobarb
- Reduces concentration & effectiveness of Haldol
- Metabolism inhibited by propoxyphene & erythromycin
AED’s drug interactions: Lamotrigine
- When used with carbamazepine, may increase levels of 10,11-epoxide (an active metabolite of carbamazepine)
- Half-life is reduced to 15 hours when used with carbamazepine, phenobarb, or primidone
- Reduces valproic acid concentration
AED’s drug interactions: Levetiracetem (Keppra)
When used with anti-histamines, or meds that potentiate GABA, may cause AMS and/or respiratory depression
AED’s drug interactions: Phenobarbital
- Increased levels when valproic acid or phenytoin given concurrently
- Variable reaction with phenytoin levels
AED’s drug interactions: Phenytoin (Dilantin)
- Levels may increase with concurrent use of chloramphenicol, cimetidine, dicumarol, disulfiram, isoniazid, & sulfonamides
- Free phenytoin levels may increase with concurrent use of valproic acid & phenobarb
- Decreased total levels may occur with sulfisoxazole, salicylates, & tolbutamide
- Decreased levels with concurrent use of carbamazepine (& vice versa)
- When concurrently used with theophylline, levels may be lowered & theophylline metabolized more rapidly
- May decrease effectiveness of OCP’s
- Enhances metabolism of corticosteroids
AED’s drug interactions: valproic acid (Depakote)
- Increases level of phenobarb
- Inhibits metabolism of phenytoin
- Rare development of absence status epilepticus a/w concurrent use of clonazepam
When is it reasonable to consider withdrawal of AED’s in post-traumatic epilepsy?
2-year, seizure-free interval
CN 1 (olfactory nerve) injury in TBI
Most often CN damaged by blunt head trauma due to tearing of the olfactory nerve filaments in or near the cribiform plate through which they traverse
Sx: anosmia, apparent loss of taste
Overall incidence: 7% & increases with severity of TBI
Injury to this nerve is the only CN neuropathy present in mild TBI
Often a/w: CSF rhinorrhea, anosmia, dysnosmia, hyposmia, parosmia (sensation of smell in absence of stimulus), cacosmia (awareness of foul odor that does not exist; may be aura)
In higher level patients –> decrease in appetite, weight loss, and/or altered feeding pattern
Recovery occurs in more than one-third of cases, usually during the first 3 months
Agitated Behavioral Scale
Designed for serial assessment of agitated patients after TBI
Ratings are based on behavioral observations made after an 8-hour nursing shift or therapy treatment session
Consists of 14 items or behaviors rated from 1 (absent) to 4 (present to an extreme)
Scoring:
- Below 21: normal
- 22-28: mild agitation
- 29-35: moderate agitation
- 35-54: severe agitation
Enteral feeding after TBI
Preferred when oral feeding is compromised because it directly uses the GI tract (distal to the site of tube placement), provides the most physiologic approach in nutritional administration & absorption, low in cost, & lower risk of metabolic complications
What is the primary risk in tube feeding?
Aspiration (increased if patient has GERD, or with more proximal tube placement)
Risks with distal tube placement include decreased absorptive capacity & tolerance of the remaining gut
What are enteral feeding products composed of?
Pureed foods, liquid nutritional supplements, elemental nutritional supplements, or a combination of products
Options for enteral routes of feeding
NG, naso-enteric, esophago-gastric, PEG, PEJ, & more surgically invasive tubes (Janeway gastrotomy, esophago-gastrotomy
When should feeding tube be placed after TBI?
No current guidelines (also no guidelines as to where it should be placed)
Factors to consider for enteral tube placement
- Direct gastrostomy or jejunostomy has decreased risk of aspiration or GERD-related problems; preferred when there is a potentially prolonged length of time of non-oral nutrition
- Direct routes should be in place at least 30 days to avoid complications on removal
- Perc placement has added advantages of decreased surgical risks & ability to start tube feeds within 24 hours of placement, whereas more surgically placed tubes have mechanical parts that can more easily be inserted (during mealtimes only) & removed (especially when in therapy)
- Enteral routes that allow for bolus feeding are advantageous because they more closely approximate natural feeding, making daily routines & therapies more manageable, especially in patients more likely to go home
Associated problems with enteral feeding
- In patients with GERD, recurrent PNA, or possible aspiration, distal tube placement is preferred
Patients suspicious for aspiration or aspiration PNA should have a gastric source of aspirate confirmed to rule out aspiration of oral secretions
- GERD has a high prevalence in TBI patients & can also lead to aspiration & esophagitis
- Head elevation may reduce the risk of aspiration, & antacids may improve esophagitis
- High level of gastric residue was the most common feeding intolerance found in TBI patients & the delivery of erythromycin by NGT may control GI disorders
- Although Metoclopramide (Reglan) increases gastroesophageal sphincter tone & can aid in GERD, it should be avoided due to its ability to cause sedation & EPS
Parenteral feed in TBI
IV-delivered nutrition, usually through a central venous line, or in limited circumstances, a peripheral line
Can be either supplemental or primary (TPN)
Utilized when there is a temporary interruption of GI function or in any condition with an increased metabolic demand
TPN is preferred when a segment of GI tract is non-functional or must be free of food for a prolonged period of time
Because parenteral feeding products bypass essential GI metabolism, they are made of nutrients that must be in elemental form. Optimal portions vary widely & should be frequently re-assessed
Risks of parenteral feeding: central/peripheral line complications (infection, clot formation, edema); electrolyte & metabolic abnormalities are common with parenteral feeding & should be closely monitored
What drug is a common cause of SIADH?
Carbamazepine
Treatment for SIADH
Fluid restriction to about 1.0 L/day, either alone or with a loop diuretic
Careful daily monitoring of weight changes & serum Na until Na level > 135 mmol/L
Hypertonic saline: 200-300 mL should be infused over 3-4 hours in patients with severe symptoms as confusion, convulsions, or coma
Na may not be corrected more than 10 mEq/L over 24 hours until Na reaches 125. NaCl repletion with salt tablets
Chronic SIADH maybe treated with demeclocycline, which normalizes serum Na by inhibiting ADH action in the kidney
Lithium carbonate acts similar to demeclocycline, but is rarely used because it is more toxic
Why does DI occur?
Severe injuries; often a/w fractures of the skull
A fracture in or near the sella turcica may tear the stalk of the pituitary gland, with resulting DI (due to disruption of ADH secretion from posterior pituitary) in addition to other clinical syndromes, depending on extent of lesion
What is cognitive remediation in TBI?
Includes visuospatial rehabilitation, executive control, self-monitoring, pragmatic interventions, memory retraining, & strategies to improve attention
Post-concussive syndrome
Reduced alcohol intolerance was included in old criteria
DSM-5: neuro-cognitive disorder within spectrum of mild or major TBI (ICD refers to this as a syndrome, DSM-5 refers to it as a state, not syndrome). Noted to resolve within days to weeks after the injury, with complete resolution by 3 months
Loss of consciousness is NOT included in DSM-5
A/w social & vocational difficulties that appear out of proportion to severity of neurologic insult
Persistent PCS has been used to describe sx lasting over 3-6 months
What is pannus formation in RA?
Most important destructive element in RA
Pannus is a membrane of granulation tissue that covers the articular cartilage at joint margins. It is a synovial membrane-derived tissue that overgrows cartilage
Fibroblast-like & macrophage-like cells invade & destroy the peri-articular bone & cartilage at joint margins
Osteoclasts invade bone, leading to marginal erosions at the pannus-bone interface
What is vascular granulation tissue composed of in pannus in RA?
- Proliferating fibroblasts
- Numerous small BV
- Various inflammatory cells, but mainly CD-4 T-lymphocytes
- PMN’s predominate in the synovial fluid
- Occasionally, collagen fibers are seen within phagolysosomes of cells at the leading edge of pannus
Pannus is vascular
- CD4 & T-cells predominate in pannus (but PMNs are in synovial fluid)
- Cytokines mediate inflammation (IL-1, TNF-a, IL-6, IL-17, GM-CSF, & TGF-beta)
Clinical Diagnosis of RA
Based on 2010 ACR/EULAR classification criteria
Patient must have at least one joint with definite clinical synovitis (swelling) that is not best explained by another disease process
A score of 6/10 or greater is needed for classification of a patient having definite RA
2010 ACR/EULAR Classification Criteria for RA
A. Joint Involvement
- 1 large joint: 0
- 2-10 large joints: 1
- 1-3 small joints: 2
- 4-10 small joints: 3
- >10 joints (with at least one small joint): 5
B. Serology (at least one test result is needed for classification)
- Negative RF & negative Anti-CCP: 0
- Low positive RF or low-positive Anti-CCP: 2
- High positive RF or high-positive Anti-CCP: 3
C. Acute-phase reactants (at least one test result is needed for classification)
- Normal CRP & normal ESR: 0
- Abnormal CRP or abnormal ESR: 1
D. Duration of sx
- <6 weeks: 0
- > 6 weeks: 1
Insidious onset in RA
Occurs in 50-70% of patients. Initial symptoms can be systemic or articular
Slow onset from weeks to months
Constitutional symptoms: fatigue, malaise
Diffuse MSK pain may be the first non-specific complaint with joint involvement later. Most commonly symmetric involvement although asymmetric involvement may be seen early
Morning stiffness in involved joints lasting 1 or more hours
Joint swelling, erythema. Muscle atrophy around affected joints
Low-grade fever without chills
Morning stiffness of major arthritides: duration & location
RA: MCP, PIP, MTP joints. >1 hour
OA: DIP, knees, hips. <30 mins
AS: LS spine. ~3 hours
Synovial fluid analysis in RA
Low viscosity
WBC: 1K-75K
>70% PMN’s
Transparent-cloudy
RF in RA
70-80% of patients with RA are RF+
RF+ is a/w increased severity of disease with increased systemic manifestation
Serial titers are of no value
RF+ can be seen in other disease: rheumatic (SLE, scleroderma, Sjogren’s), viral, parasitic, bacterial infections, neoplasms, hyperglobulinemic, cryoglobulinemia, Hep C
Radiographic findings in RA
Early findings: soft tissue swelling, joint space narrowing
Late findings: uniform joint space narrowing due to loss of articular cartilage, axial migration of the hip (protrusio acetabuli), malalignment & fusion of joints
Marginal bone erosions near attachment of joint capsule
Juxta-articular osteopenia (bone washout)
Predilection of swelling of joints in wrists (MCPs, PIPs, MTPs, but not DIPs)
Erosion of ulnar styloid & met head of MTP joint
C-spine involvement may lead to cervical A-A subluxation (>2.5-3 mm)
Radial deviation of the radiocarpal joint
Hallux valgus
Hand & Wrist Deformities in RA
- Boutonniere
- Swan neck
- Ulnar deviation of fingers
- Flexor tenosynovitis
- Instability of carpal bones
- Floating ulnar head (piano key sign)
- Resorptive arthropathy
- Pseudobenediction sign
Hand & Wrist Deformities in RA: Boutonniere
Weakness or rupture of the terminal portion of the extensor hood (tendon or central slip) at the PIP joint, which holds the lateral bands in place
Initially caused by PIP synovitis
Lateral bands of the extensor hood slip downward (sublux) from above the axis of the PIP joint to below axis, turning them into flexors at the PIP joint
The PIP then protrudes through the split tendon as if it were a buttonhole, hyper-extending the distal phalanx
Hand & Wrist Deformities in RA: Swan neck
May be due to synovitis at the MCP, PIP, or DIP (rare) joint
Flexor tenosynovitis –> MCP flexion contracture
Contracture of the intrinsic (lumbricals, interosseous) –> PIP hyperextension
Contracture of deep finger flexor muscles & tendons –> DIP flexion
Hand & Wrist Deformities in RA: ulnar deviation of the fingers
Synovitis & weakening of the ECU, UCL, RCL results in radial wrist deviation, increasing the torque of the stronger ulnar finger flexors
Flexor/extensor mismatch causes ulnar deviation of the fingers as the patient tries to extend the joint
Hand & Wrist Deformities in RA: flexor tenosynovitis
Early RA may be confused with deQuervain’s disease
Diffuse swelling of the extensor & flexor tendon sheaths
One of the most common manifestations of the hands in RA, can be a major cause of hand pain & weakness
Hand & Wrist Deformities in RA: instability of the carpal bones
Ligament laxity, carpal bone erosions, radial deviation of the wrist, ulnar styloid deviates dorsally, & carpal bones rotate (proximal row: volar, distal row: dorsal, rotating in a zig-zag pattern)
Hand & Wrist Deformities in RA: floating ulnar head (piano key sign)
Synovitis at the ulnar styloid leads to rupture/destruction of the UCL, which results in laxity of the radioulnar joint
Ulnar head floats up dorsally in the wrist
Easily compressible elevated ulnar styloid
Hand & Wrist Deformities in RA: resorptive arthropathy
Digits are shortened & phalanges appear retracted with skin folds
Possible mechanism via osteoclastogenesis & osteoclastic bone resorption
Telescoping appearance of digits
Most serious arthritic involvement
Hand & Wrist Deformities in RA: pseudobenediction sign
stretched radioulnar ligaments allow the ulna to drift upward
Extensor tendons of the 4th & 5th digits are subject to abrasion from rubbing on the sharp, elevated ulnar styloid & can rupture
Result: extensor tendon rupture, inability to fully extend the 4th & 5th digit
C-Spine instability in RA
A-A joint subluxations –> most common are anterior subluxations
With cervical flexion, the A-A space normally should not increase significantly. Any space >2.5-3 mm is considered abnormal
What diseases are subcutaneous nodules found in?
RA & gout
Cardiac findings in RA
Pericarditis, may lead to constrictive pericarditis with right-sided HF
May be found in about half of RA patients, but rarely symptomatic
Can also see valvular heart disease
Felty syndrome
Triad: RA, splenomegaly, leukopenia, often a/w leg ulcers
Exercise in treatment of RA
Mild disease (moderate synovitis) requires an ISOMETRIC program
Isometric exerise:
- Least amount of peri-articular bone destruction & joint inflammation/pain, especially during an acute flare
- Restores & maintains strength
- Generates maximal muscle tension with minimal work, fatigue, & stress
- Isotonic & isokinetic exercise may exacerbate the flare & should be avoided
What is therapeutic range for ASA in RA?
15-25 mg/dL. Toxic >30 mg/dL
Non-biological DMARDs in RA
Hydroxychloroquine, Sulfasalazine, Methotrexate, Leflunomide, Cyclosporine, Gold, Azathioprine
Non-biological DMARDs in RA: Hydroxychloroquine
Retinopathy, hyperpigmentation
Non-biological DMARDs in RA: Sulfasalazine
Myelosuppression, GI disturbances
Non-biological DMARDs in RA: Methotrexate
Stomatitis, myelosuppression, hepatic fibrosis, cirrhosis, pulmonary involvement, worsens rheumatoid nodules, teratogenicity
Non-biological DMARDs in RA: Leflunomide
Hepatotoxicity, nausea, diarrhea, HTN, teratogenicity
Non-biological DMARDs in RA Cyclosporine
Renal dysfunction, tremor, hirsutism, HTN, gum dysplasia
Non-biological DMARDs in RA: Gold IM, oral
Myelosuppression, renal –> proteinuria
Diarrhea (#1 oral), rash (#1 IM)
Non-biological DMARDs in RA: Azathioprine
Myelosuppression, hepatotoxicity, lymphoproliferative disorders
Pathology in OA
Early: hypercellularity of chondrocytes
- Cartilage breakdown: swelling & loosening of collagen framework
- Increased proteoglycan synthesis
- Minimal inflammation
Late: cartilage fissuring, pitting, & destruction
- Hypocellularity of chondrocytes
- Inflammation secondary to synovitis
- Osteophyte spur formation seen at joint margins
- Subchondral bone sclerosis (eburnation)
- Cyst formation in the juxta-articular bone
Increased water content of OA cartilage leads to damage of the collagen network –> increased chondrocytes, collagen, & enzymes
Hallmark of DISH
Ossification spanning 4 contiguous vertebral bodies (3 or more IVD’s)
Can see dysphagia with cervical involvement
NOT a/w sacroiliitis, apophyseal joint ankylosis, or HLA-B27 positivity (distinguishes from ankylosing spondylitis)
Oligoarticular JIA
Knee is the most common joint involved, followed by ankle, wrist, & then elbows
ANA+, RF-
HLA B27+
Iridocyclitis
No erosions
When diagnosing Oligoarticular JIA, must refer to ophtho as they need slit lamp exam 4x/year for 4-5 years
Key points of juvenile arthritides
JIA:
A. Multi-systemic involvement: RF- in 98%, Stills disease, high fever, rheum rash, lymphadenopathy, HSM, anemia
B. Polyarticular (5+ joints involved): no extra-articular manifestations of systemic onset disease, gradual onset of swelling, stiffness affecting c-spine & hip, growth retardation with early closure of epiphyseal plates. This group has worst prognosis when disease is unremitting
C. Oligoarticular (1-4 joints involved): RF- 98%, chronic iridocyclitis (<6 y old occurs in 20-40%; more frequently in females ANA+, must have ophtho referral, HLA B27+, no bony erosions on XR
Juvenile spondyloarthropathies (all present like adult):
- AS
- Reiter syndrome
- Psoriatic arthritis
- IBD-associated
Juvenile spondyloarthropathy unique to kids:
- SEA syndrome (seronegative enthesopathy & arthropathy) with RF-, ANA-, enthesitis/arthritis/arthralgia, may have uveitis (painful & acute)
Inflammatory vs non-inflammatory arthritis
Inflammatory:
- Increase in WBC & ESR, acute painful onset, erythema, warmth, & tenderness
- CTD- SLE, polymyositis/dermatomyositis, PSS, RA
- Crystal: gout & pseudogout
- Infectious
- Seronegative spondyloarthoprathies
Non-inflammatory:
- DJD- OA, AVN
- Traumatic
- Joint tumors
- Hemophilia
- Metabolic- hemochromatosis, alkaptonuria, rheumatic fever, Wilson’s disease
Crystal-induced synovitis
Gout & pseudogout
Gout: monosodium urate crystals, acute synovitis in synovial membrane & joint cavity
Pseudogout: articular chondrocalcinosis, CPPD crystals, hyaline cartilage & fibrocartilage joints
Gout: negative birefringence (moderate-severe inflammation WBC 15-20K- neutrophils)
Pseudogout: positive birefringence
What is a/w pseudogout?
Hypothyroid, hyperparathyroid, hemochromatosis, amyloidosis, hypomag, hypophos
Most common site for pseudogout
Knee
Drugs that may precipitate gout flare
Thiazides, ASA, loop diuretics, niacin
Lab finding in gout vs pseudogout
Gout: hyperuricemia
Pseudogout: uric acid normal
Seronegative spondyloarthropathies
HLA B27+, but no RF positivity
AS
Reactive arthritis
Psoriatic arthritis (HLA Cw6)
Enteropathic arthropathy
Pauci/oligoarticular JIA
Ankylosing spondylitis
Chronic, inflammatory rheumatic disorder of the axial skeleton affecting the SIJ & spine
Most common sx are back pain & significant stiffness, notably in AM & night
Symptoms worsen with rest & improve with activity
Hallmark: bilateral sacroiliitis
Onset as late adolescent & early adulthood, males»_space; females, more common in whites
Synovitis & inflammation with intimal cell hyperplasia- lymphocyte & plasma cell infiltrate
Will see pre-spinous calcifications
Clinical manifestations of AS: skeletal involvement
Insidious onset of back/gluteal pain: first site of involvement is SIJ. Initially asymmetric but eventually b/l
Persistent sx of pain for at least 3 months
Decreased lumbar lordosis & increased thoracic kyphosis
Cervical ankylosis develops in 75% of patients who have AS for 16 years or longer
L- or C-spine is the most common site of fracture
Enthesitis: tenderness over ischial tuberosity, greater trochanter, ASIS, & iliac crests
Hip & shoulder involvement is more common in juvenile onset, <16 years old
Respiratory restriction with limited chest expansion:
- Normal is 7-8 cm; if less, risk of restrictive lung disease
- Once restrictive lung disease ensues, chest expansion decreases, patient develops diaphragmatic breathing, & T-spine involvement (costovertebral, costosternal, manubriosternal, sternoclavicular)
Clinical manifestations of AS: extra-skeletal involvement
Fatigue, weight loss, low grade fever
Acute iritis/iridocyclitis (anterior uveitis that involves the iris & ciliary body) –> most common extra-skeletal manifestation. More progressive in Reiter syndrome (Reiter has unilateral, recurrent & pain/photophobia/blurred vision)
Cardiac: aortitis leading to fibrosis, conduction defects
Apical pulmonary fibrosis: dyspnea, cough
Amyloidosis
Neuro: CES, C1-C2 subluxation
Clinical manifestations of AS: radiographic findings
SI joint narrowing: symmetric, erosions & sclerosis may lead to ankylosis of the SIJ
Pseudo-widening of the joint space:
- Sub-chondral bone resorption, blurring of joint line
- Erosion sclerosis
- Calcification leading to ankylosis
Bamboo spine:
- Ossification of the annulus fibrosis, resulting in bridging syndesmophytes that completely bridge adjacent VB’s
Interspinous ligament ossification can give dagger sign appearance on XR
Along with above, ankylosis of facet joints leads to complete spinal fusion:
- Squaring of lumbar vertebrae’s anterior concavity
- Reactive bone sclerosis
- Squaring & fusion of the VB’s secondary to ossification of the outer annulus fibrosis at the dorsolumbar & lumbosacral area
Associated osteoenia/osteoporosis (bone washout)
Loss of cervical lordosis
Hip & shoulder involved to lesser extent
Treatment for AS (bed)
Firm mattress, sleep in position to keep spine straight/prevent spine flexion deformity- lie prone
Triad of reactive arthritis
Conjunctivitis, arthritis, non-gonococcal urethritis
How many patients with reactive arthritis progress to AS?
3-10%
Clinical manifestation in reactive arthritis
Asymmetric
May be confused with plantar fasciitis
Radiographic findings in reactive arthritis
Lover’s heel: erosion & periosteal changes at the insertion of the plantar fascia & Achilles tendons
Ischial tuberosities & greater trochanter with similar findings
Asymmetric SIJ involvement
Syndesmophytes
Pencil-in-cup deformities of hands & feet (more common in psoriatic arthritis)
Psoriatic arthritis
Male:female equal
Age of onset 30-55
More common in whites, a/w HIV:
- Foot & ankle involvement is most common & severe
- Treatment is same as psoriatic: first line NSAIDs, no oral corticosteroids, no MTX
Unknown pathogenesis, may be environmental like infectious or trauma, or immunologic
Stiffness of spine lasting about 30 mins
Asymmetric mono or oligoarticular involvement:
- Large joints –> knee
- DIP involvement –> arthritis mutilans: osteolysis of phalanges & metacarpals of the hand resulting in “telescoping of the finger”
Enthesopathy, spondylitis, sacroiliitis
1/3 experience conjunctivitis
Aortic insufficiency
Radiographic findings:
- Pencil in cup appearance of the DIP
- Asymmetric sacroiliitis –> fusion
- Fluffy periostitis –> hands, feet, spine, & SIJ
Clinical manifestations of enteropathic arthropathy
Large joints: knees, ankles, feet. 2 types can occur: enteropathic arthritis or AS
A/w ANCA+ (antimyeloperoxidase)
What do all the seronegative spondyloarthopathies have in common?
Mucocutaneous lesions, frequent inflammation of the enthesitis, spondylitis with SIJ involvement
Causes of Raynaud’s
Collagen vascular disease- PSS, SLE, RA, dermato/polymyositis
Arterial occlusive disease
Pulmonary HTN
Neurologic- SCI, CVA
Blood dyscrasia
Trauma
Drugs: ergots, BB, cisplatin
Eosinophilic fasciitis
Precipitated by strenuous exercise
Exercise should be done in a non-inflammatory state
Pain & swelling
Treatment: steroids
What area of upper GI system is involved with poly/dermatomyositis
Pharynx –> dysphagia
Type III poly/dermatomyositis
Can be either poly or dermatomyositis
5-8% a/w malignancy
Male >40 years old
Poor prognosis
Type IV poly/dermatomyositis
Childhood
Severe joint contractures, more disabling in a child. Rapid, progressive weakness, respiratory weakness
Muscle biopsy in poly/dermatomyositis
- Perifascicular atrophy
- Evidence of necrosis of Type 1 & 2 fibers
- Variation in fiber size
- Large nuclei
Clinical features/ACR Criteria for poly/dermatomyositis
Hips involved first then shoulders, +/- respiratory muscle involvement, dysphagia
Must have minimum 5.5 for diagnosis:
Age at onset: 18-40- 1.3
Age at onset: >40- 2.1
Symmetric weakness of proximal UE: 0.7
Symmetric weakness of proximal LE: 0.8
Neck flexors weaker than extensors: 1.9
Proximal legs weaker than distal legs: 0.9
Heliotrope rash: 3.1
Gottron’s papules: 2.1
Gottron’s sign: 3.3
Dysphagia/esophageal dysmotility: 0.7
Anti-Jo-1+: 3.9
Elevated CPK or LDH or AST/ALT: 1.3
Muscle bx w/ endomysial infiltration of mononuclear cells surrounding but not invading myofibers: 1.7
Muscle bx with perimysial and/or perivascular infiltration of mononuclear cells: 1.2
Muscle bx with peri-fascicular atrophy: 1.9
Muscle bx with rimmed vacuoles: 3.1
EMG in poly/dermatomyositis
Myopathic changes, PSW, fibs, CRDs
Juvenile dermatomyositis
Seen more commonly than polymyositis in children
A/w generalized vasculitis (unlike adult form)
Slight female preponderance
heliotrope is predominant feature
Presence of clumsiness often unrecognized
Transient arthritis, elevated rsh
80-90% respond well to steroids
No a/w malignancy in children
Arthridites: ANA & RF status
MCTD: Both +
RA: Both +
SLE: ANA+, RF -
PSS: ANA+, RF -
Polymyositis: ANA+, RF -
Sjogren’s: Both +
Treatment for temporal arteritis
High-dose steroids ASAP imperative to preventing permanent vision loss
ASA 325 mg qD improves prognosis
PMR
Some feel it is an expression of temporal arteritis (a vasculitidy)
Symptoms:
- Fever, weight loss, malaise
- Morning stiffness, muscle tenderness
- Hallmark: difficulty abducting shoulders above 90
- Affects proximal muscles- neck, pelvic
- Diagnosis: ESR >50
- Treatment: steroids
What can polyarteritis nodosa be seen in?
RA, SLE, Sjogren’s
Sjogren’s clinical presentation (sicca symptoms)
Dry eyes, dry mouth, skin lesions, parotid involvement
Primary: no other rheum diseases
Secondary: commonly a/w RA & SLE
Most common organisms in septic arthritis
Neonates: Staph, GBS
6 months-2 years: H flu
Children >2: Staph, GBS
Adults: Neisseiria gonorrhea
RA: Staph
Other causes of septic arthritis: TB
TB arthritis affecting hips & knees
Monoarticular
Radiologic findings: Phemister’s triad
1. Juxta-articular osteoporosis
2. Marginal erosions
3. Joint space narrowing
Other causes of septic arthritis: Lyme
Intermittent migratory episodes of polyarthritis
Arthritis in hemophilic arthropathy
Arthritis caused by remaining blood in the joint depositing hemosiderin into the synovial lining –> synovial proliferation & pannus formation
Treatment for hemophilic arthropathy
Joint aspiration as a last resort. Blood in joint acts as a tamponade to prevent further bleeding
Causes of Charcot joint (STD –> SKA)
Syringomyelia –> Shoulder
Tabes dorsalis (syphilis) –> Knee
Diabetic neuropathy –> Ankle
Charcot joint vs OA
Both have soft tissue swelling, osteophytes, joint effusion
Charcot joints have:
- Bony fragments
- Subluxation
- Peri-articular debris
What is a/w SCFE?
Endocrinopathies:
- Hypothyroidism (most common)
- GH abnormalities
- Down syndrome
ACR criteria for fibromyalgia
1990: widespread pain in all 4 quadrants of body, axial involvement: cervical, anterior chest, thoracic, & low back, pain in 11-18 tender points (occipital, lower cervical, trap, supraspinatus, 2nd rib, lateral epicondyle, gluteal, greater troch, knee)
2010: non-tender point diagnostic criteria based on:
- Widespread pain index score
- Symptom severity score (includes fatigue, cognitive & somatic symptoms)
- Sx must be present consistently for 3 or more months
- Must rule out other disorders that could cause pain syndrome
Clinical stages of CRPS
Acute: few weeks- 6 months
- Allodynia, hyperpathia, hypersensitivity, swelling, vasomotor changes
- Increased blood flow creating temperature & skin color changes
- Hyperhidrosis
Dystrophic: 3-6 months
- Persistent pain, disability, atrophic skin changes
- Decreased blood flow, decreased temp
- Hyperhidrosis
Atrophic
- Atrophy & contractures
- Skin glossy, cool, dry
Radiographic findings in CRPS
Plain XR: Sudeck’s atrophy: patchy osteopenia, ground-glass appearance
Triple phase bone scan: first 2 phases are non-specific, third phase is abnormal with enhanced uptake in peri-articular structures
Treatment in CRPS
Advise patients to continue activities as tolerated to avoid disuse atrophy
CRPS in children vs adults
Children/adolescents:
- Common in LE
- 4:1 female > male
- Three phase bone scan has mixed results & mostly used to rule out other pathology; will see decreased uptake of the extremity & decreased atrophic changes; occasionally normal; will have increased uptake normally secondary to bone growth
- Tx: PT alone, non-invasive TENS, biofeedback, TCA’s, blocks in UE are more common
- Good prognosis
Adults:
- UE more common
- Gender ratio equal
- Sympathetic blocks more common
- Poor prognosis
Sympathetically-mediated CRPS
4 tests used:
1. Sympathetic block with local (proper response to stellate ganglion block is ipsilateral Horner’s, anhidrosis, conjunctival injection, nasal congestion, vasodilation, increased skin temp
- Guanethidine test: injection of this into extremity distal to a suprasystolic cuff. Test is + if pain is reproduced after injection & immediately relieved after cuff released
- Phentolamine test: IV of this will reproduce pain
- Ischemia test: inflation of suprasystolic cuff decreases pain
Dupuytren’s contracture
Abnormal fibrous hyperplasia & contracture of the palmar fascia, causing a flexion contracture at the MCP & PIP joints
More common in white men 50-70 years old
A/w epilepsy, pulmonary TB, alcoholism, & DM
Mechanism: palmar fascia is a continuation of the palmaris longus tendon attaching to the sides of the PIP & middle phalanges as well as to the skin. Fibromatosis of the palmar fascia & contracture of the fibrous bands that develop into nodules can lead to development of a finger flexion contracture & skin dimpling
Most commonly 4th & 5th digits
Treatment: trpsin, chymotrypsin, lidocaine injection followed by forceful extension, rupturing the contracture & improving ROM
Mallet finger
Most common extensor tendon injury
Rupture of the extensor tendon into the distal phalanx 2/2 forceful flexion
DIP joint remains in a flexed position & cannot be actively extended
Treatment: DIP splint immobilizes the distal phalanx in hyperextension
- Acute: 6 weeks
- Chronic: 12 weeks
Surgical indications: poor healing, volar subluxation, avulsion >1/3 of bone
How is arm abduction achieved?
GH & scapulothoracic motion. You get 2 degrees of GH for every 1 of scapulothoracic (120 GH to 60 degrees scapulothoracic)
The scapulothoracic motion allows the glenoid to rotate & permits GH abduction without acromial impingement
Rockwood classification for AC separations
Type 3: clavicle elevated above superior border of acromion
Type 4: clavicle displaced posteriorly through the trapezius, can see skin tenting
Type 5: CC distance >100% of contralateral side, severe shoulder droop that does not improve with shrug
Type 6 (rare): distal clavicle inferior to coracoid
Direction of GH instability
Anterior: most common direction, common direction in younger population with high recurrence rate; mechanism is arm abduction & ER; complication: axillary nerve injury
Posterior: less common, may occur as result of seizure; patient may p/w arm in adducted & IR position; landing on a forward flexed adducted arm
Multidirectional: rare; patient may display laxity in other joints
Bankart lesion
Labral tear off the anterior glenoid allows the humeral head to slip anteriorly
Most commonly a/w anterior instability
May be a/w avulsion fracture off glenoid rim
Hill-Sachs lesion
Compression fracture of the posterolateral humeral head caused by abutment against the anterior rim of the glenoid fossal
A/w anterior dislocations
A lesion that accounts for >30% of the articular surface may cause instability
A notch occurs on the posterior lateral aspect of the humeral head
O’Brien’s test
Used to detect SLAP lesions
2 parts: typical part, then apply a downward force to patient’s supinated arm
Positive test: deep shoulder pain that improves when downward force is applied with hand in supination
Where is the critical zone of hypovascularity in supraspinatus?
About 1 cm from insertion site
Pain in shoulder (RTC) from swimming
Occurs at the “catch” phase of the overhead swimming stroke via flexion abduction, IR
More commonly: freestyle, backstroke, butterfly
Less common: breast stroke
How many degrees of abduction can be achieved with thumb pointing down?
120
Shoulder arthrogram
Beneficial in assessing full thickness tears of RTC but unable to delineate the size of the tear or partial tears
Functional phase of RTC rehab
Happens after acute phase (up to 4 weeks) & recovery phase (months)
Continue strengthening, increasing power & endurance (plyometrics), activity-specific training, rehab in swimmers focuses on strengthening RTC muscles & scap stabilizers (including serratus anterior & lower trap)
CSI can be considered (although too much may weaken the collagen tissue, leading to more microtrauma)
Shoulder arthrodesis fusion position
50 degrees abduction
30 degrees flexion
50 degrees IR
Biceps tendon rupture
Most common site of rupture is at proximal end of long head of biceps tendon
Medial scapular winging
Serratus anterior weakness, long thoracic nerve palsy
Bench pressing very heavy weights or wearing heavy pack straps can also impinge the nerve
Scapula is elevated & retracted
Winging of the medial border of the scapula away from the ribs, more evident when patient flexes arms or does a wall push-up
Lateral scapular winging
Trap weakness, due to spinal accessory nerve lesions
Nerve injury occurs in the posteiror triangle of the neck
Scapula is depressed & protracted
Rotary lateral winging of scapula around thorax
Upper trap muscles can be tested by resisted shrug; mid & lower trap fibers can be tested by prone rowing exercise
Most common location for proximal humerus fracture
Surgical neck
When fractures at surgical neck occur, the supraspinatus is the principal abductor, which causes abduction of proximal fragment of humerus
Complications from proximal humerus fracture
Brachial plexus injury
Axillary nerve injury with surgical neck fractures
Fusion position for elbow arthrodesis
Unilateral: flexion to 90 degrees
Bilateral: flexion to 110 in one arm & 65 for the other
Cozen’s test
Examiner stabilizes the elbow with a thumb over the extensor tendon origin just distal to lateral epicondyle
Pain in the lateral epicondyle is seen with patient making a fist, pronating the forearm, & radially deviating & extending the wrist against resistance by the examiner
Test may be more sensitive when done in full extension at the elbow
Racket adjustments for lateral epicondylalgia
Decrease string tension, increase grip size
Valgus extension overload (VEO) test
Provocative maneuver
Flex elbow to 30 degrees & repeatedly extend the elbow fully while applying a valgus stress
Pain may be elicited, particularly at the last 5 degrees to 10 degrees of extension
Valgus stress should also be performed at >90 degrees to rule out UCL injury
What are potential sites for median nerve compression at the elbow?
Ligament of Struthers, lacterus fibrosis, pronator teres, between the 2 heads of the FDS
Radial nerve injury with fracture at humeral shaft
Patients may exhibit weakness of radial nerve innervated muscles with sparing of triceps
Testing CMC for OA of wrist
Axial compression of the metacarpal on the trapezium giving a painful grinding sensation
Osteonecrosis of the lunate
Kienbock’s disease (AVN)
Where is majority of blood supply to scaphoid?
Distal one-third of the bone
Therefore, the middle & proximal portion of the bone have a large non-union rate, with 1/3 developing ostenecrosis
Most fractures occur at the scaphoid waist
Hamate fractures
Body fractures often from direct trauma; can occur involving axial loading through 4th or 5th metacarpal
Fractures of hook of hamate can occur as result of direct trauma on the palmar surface of wrist/hand or due to avulsion from shear forces from adjacent/attached tendons during forceful twisting motion of wrist (Mike Trout swing)
Hamate is located slightly distal & radial to the pisiform & forms radial border of the tunnel of Guyon, through which ulnar nerve traverses
Vascular supply at radial base & ulnar tip
Pain may occur over the hook of hamate or over dorsal ulnar hamate
Imaging for hamate fractures
PA, lateral, carpal tunnel, & 45 degrees supinated oblique
CT may be needed for fractures at the base of the hook
Treatment for hamate fractures
Non-displaced body fractures:4-6 weeks short arm cast
Displaced body fractures: surgical referral
Acute hook fractures: 50% heal after prolonged casting (6 weeks-4 months)
Most acute hook fractures should have adequate vascular supply to heal if immobilized within first week
Cast should maintain slight wrist flexion & slight MCP flexion to reduce shear forces from 4th & 5th digit flexor tendons
Injuries older than 2 weeks may require excision
Stenosing tenosynovitis (trigger finger)
Repetitive trauma that causes an inflammatory process to the flexor tendon sheath of the digits
Forms a nodule in the tendon, resulting in abnormal gliding through the A1 pulley system. As the digit flexes, the nodule passes under the pulley system & gets caught on the narrow annular sheath; as a result, the finger is locked in a flexed position
Skier’s/Gamekeeper’s thumb
May occur with chronic lateral laxity or acute disruption of the UCL
UCL attaches dorsally at the metacarpal head & runs distally to insert on the volar side of the proximal phalanx base
Most acute tears occur at the distal insertion point
Complete tears can lead to entrapment of the adductor aponeurosis between the ruptured portions of the ligament –> Stener’s lesion & will impair healing. Avulsion or avulsion fracture can also occur; both are surgical indications
Will see instability of the MCP joint
To examine, stabilize the radial portion of the MCP & position joint in about 30 degrees of flexion –> radial deviation force to stress the UCL
Fullness at MCP may indicate a Stener’s lesion:
- Grade I: pain, no increased motion
- Grade 2: increased opening with pain on stressing
- Grade 3: no pain, continued motion while stressing
Stress radiographs should be done comparing both hands. Instability is indicated by radial deviation >40 degrees in extension & >20 degrees in flexion on XR
Treatment:
- Short arm cast with thumb spica splint for 4-6 weeks. RTP when thumbs is painless, with firm end point on radial deviation stress & at least 80% recovery or ROM & pinch strength
Jersey Finger
Unable to flex the DIP joint due to complete or incomplete injury to the FDP tendon, most commonly at 4th digit
Internal rotators of the hip (TAGGGSS)
T: TFL
A: Adductor magnus/longus/brevis
G: Glut med
G: Glut min
G: Gracilis
S: Semitendinosus
S: Semimembranosus
Iliofemoral ligament
Y-ligament of Bigelow, strongest ligament in body
Extends from AIIS to inter-trochanteric line
Functions to limit extension, abduction, & ER of hip
Ischiofemoral ligament
Extends from ischium behind the acetabulum to blend with the capsule
Function is to limit IR of the hip
Pubofemoral ligament
Extends from superior pubic ramus & joints the iliofemoral ligament
Limits hip abduction
OA of the hip
Limits IR first
True leg length discrepancy
Measure from ASIS to medial mal (both fixed bony landmarks)
True leg length has many causes, including fractures crossing epiphyseal plate in childhood or polio
Hamstring strain
Normal strength hamstring:quad is 3:5
Hamstring placed under maximal stress when hip is forced into flexion & knee into extension
Injuries typically occur during the eccentric phase of muscle contraction & at the myotendinous junction, most commonly in the lateral hammy
Hip flexor strain
Occurs due to eccentric overload of psoas or as athlete tries to flex the fully extended hip
Imaging: AP & frog leg lateral views are used to exclude bony injury such as an apophyseal avulsion fracture
Posterior hip dislocation
Most common type, occurring during trauma when hip is flexed, adducted, & medially rotated , driving hip posteromedially
Head of the femur is covered posteriorly by the capsule & not bone
Sciatic nerve may be stretched or compressed (anterior hip dislocations may cause femoral nerve compromise)
AVN in 10-20%
Hip will be flexed, adducted, IR (unlike in hip fracture)
Imaging in AVN of femoral head
MRI of both hips is indicated. MRI is most sensitive to early changes & is more specific than a bone scan
Low signal intensity on T1 that appears as rings, wedges, or irregular configurations
T2 may show a double line sign with a high signal intensity zone inside of a low signal intensity margin
Posterior approach hip precautions
Total hip precautions: avoid hip flexion over 90 degrees, hip adduction past midline, & extreme hip IR
A high chair height is preferred to reduce hip flexion & potential for posterior hip dislocation
Anterior approach hip precautions
Avoid hip extension & ER (opposite of posterior approach)
Inter-trochanteric fractures
Most common type of hip fracture
Highly fragmented fractures may result in significant blood loss/hypovolemia
Post-op, a leg length discrepancy may result due to comminution s/p fixation
Moderately high forces are generated in this area, & a strong fixation is required
Fractures may be non-displaced, displaced 2-part, or unstable 3-part
Myositis ossificans
Formation of HO within muscle
Ossification within an area of muscle forms from encapsulated blood 2/2 a hematoma
Usually the result of repeated trauma to that area of muscle or can be due to a direct blow to the hip
Quad is the most common location. Other areas: brachialis, deltoid, intercostal space, erector spinae, pec, glut
U/s, heat, or repeated trauma at onset of myositis ossificans can exacerbate the process
If the ossifying mass involves a nerve, related nerve impingement symptoms may occur
Imaging:
- Initially, XR will reveal a soft tissue mass
- Calcific flocculations can develop within 2 weeks
- Ossification can be seen between 2-3 weeks
- Bone scan & MRI are more sensitive than XR in early stages. U/s can be helpful for office or bedside diagnosis of a hematoma & myositis ossificans
Treatment: gentle ROM, prevention of contractures, strengthening involved muscles progressively. Surgery may be necessary in cases resulting in nerve entrapment, decreased ROM, or loss of function; if possible, surgery should be delayed until the lesion matures at 10-12 months. Radiation therapy can be trialed for recalcitrant symptoms
ACL functional anatomy
Primary function is to limit anterior tibial translation
Also prevents posterior translation of the femur & hyperextension of knee
Limits IR of femur when foot is fixed & knee is locked
Tightens with full extension & loosens in flexion
Femoral ER loosens the ACL, & IR tightens it
In flexion, it draws the femoral condyles anteriorly
ACL-deficient knees create increased pressures on the posterior menisci
PCL functional anatomy
Primary function is to restrain posterior tibial translation
Ligament is looser in extension & tighter in flexion
In extension, the PCL pulls the femur posteriorly
PCL-deficient knees pace more force on the patellofemoral joint
MCL functional anatomy
Has an attachment to medial meniscus
In full extension, the MCL tightens to full tension. Tension is increased with abduction stress at increasing positions of flexion
LCL functional anatomy
Does NOT have an attachment to lateral meniscus
Restrains varus stresses. Peak stress with adduction when knee is at 70 degree flexion
Arcuate popliteal ligament complex (APLC)
Provides attachment for the posterior horn of the lateral meniscus
Reinforces the lateral aspect of the knee & gives posterior lateral rotary stability
Also provides restraint to posterior tibial translation
Its attachment can be mistaken for a tear of the posterior horn of the lateral meniscus on MRI
Menisci of the knee
2 menisci (medial & lateral) are composed of crescent-shaped fibrocartilaginous tissue
Deepen the articular surface area of the tibia to provide more stability for the femoral condyles & increased force dispersion to the tibial plateau
Peripheral outer 1/3 of meniscus is well-vascularized. Inner 2/3 is not & cannot be surgically reparied
Medial C –> longer & larger
Lateral O –> covers a larger area. Jointed to the MFC by the posterior meniscofemoral ligament
Why is anterior drawer test for knee not very sensitive?
Hemarthrosis, hamstring spasm, & other structures (like posterior capsule) can limit forward movement of the tibia
What test is more sensitive: Lachman or anterior drawer?
Lachman
What test has high specificity for ACL tear?
Pivot shift test. 5-mm of motion is considered a Grade I tear
Treatment for meniscal tears
Meniscectomy: WBAT in 1-2 days
Repair: NWB 4-6 weeks, followed by strengthening
Mechanism of injury for ACL tear
Cutting, deceleration, & hyperextension of the knee
Sudden pop & anterior knee pain with posterior lateral joint line pain
What is the most sensitive marker for acute ACL injury?
Severe effusion in the 2-12 hours following injury
Lachman test
May be positive but can yield a false negative in about 10% of cases. Examiner-dependent & influenced by muscle guarding
Grading criteria:
- Translation Grade I: <5 mm translation
- II: 5-10 mm translation
- III: >10 mm translation
Endpoint Grade:
- A: firm, sudden endpoint to passive anterior translation of tibia on fixed femur
- B: absent, ill-defined, or softened endpoint to passive anterior translation of tibia on a fixed femur
ACLR post-op rehab
PWB initially –> ROM to regain flexion over first 2 weeks –> progress to closed chain kinetics –> avoid open chain exercises, especially in full extension
Resistive exercises between 0-45 degrees flexion is AVOIDED during first 3-6 months
Lenox Hill de-rotation orthosis is used to control knee axial rotation as well as AP & medial-lateral control
Sport-specific exercises at 6-12 weeks
MCL tears
Opening of 5-8 mm compared to opposite side may indicate complete tear
Instability in slight flexion of 30 degrees is specific for MCL injury, whereas instability in full extension may indicate injury to the MCL & posterior capsule
Epiphyseal fractures may present with or without MCL tears
Patellofemoral pain syndrome
Runner’s/biker’s knee
Most common cause of anterior knee pain
Overuse injury caused by repeated microtrauma, leading to peripatellar synovitis
Patellar tracking problem
Treatment: adjust saddle position on bicycle. Having saddle too forward or low will stress anterior knee, but too high will stress posterior knee. Minimize hyperflexion of cyclist knee in force generation phase of pedaling. Adjust rotation of cleats; anterior knee is stressed with internally rotated cleats, whereas medial knee is stress with externally rotated cleats
Therapeutic exercise:
- Quad strengthening, especially VMO
- Short arc quad activities (0-15) used to strengthen VMO
- Isotonic quad strengthening with eccentric loading occurs in a non-painful ROM
- Isometric quad contractions are used
- SLR for iliopsoas strengthening occurs
- Stretching of hammies, ITB, adductors, & vastus lateralis
- Proprioceptive exercises
- Increase activity when ROM full & pain-free & strength is 80% of normal
Possible surgeries (rarely needed):
- Lateral release of knee capsule & retinaculum
- Patellar realignment
- Patellar tendon transfer
- Patellectomy
Q angle
Normal in females: 18 degrees, males should be 13 degrees
Factors that increase Q angle: internal torsion of femur, lateral insertion of the infrapatellar tendon on the tibia, genu valgum
Most common site of patellar tendonitis
Inferior pole of the patella
Osteochondritis dissecans
2/2 small stresses to sub-chondral bone that disrupt blood supply to that area of bone
Localized segmental area of AVN at the end of a long bone –> formation of dead sub-chondral bone covered with articular hyaline cartilage
Overlying cartilage degenerates around the defect & an entire piece may detach from the rest of the bone, entering the joint space as a loose body. Usual area is MFC
Other areas of involvement: distal femur, patella, elbow, talus, & distal humerus
Most commonly affects adolescents
Gradual onset of joint pain & irritation, synovial effusion, & buckling sensation
Walking with the foot rotated outward may relieve pain
To palpate the MFC, have knee flexed to 90 with pressure directed medial to the inferior pole of the patella
“Shark bite” on MRI
Healing of defect may occur if diagnosis is made before fragment separates –> knee must be placed at rest & NWB
Popliteus tendonitis
Popliteus arises from lateral face of the LFC & inserts into the triangular area in the posterior tibia
Main function is IR of the tibia (laterally rotates femur on the tibia = medially rotating the tibia with respect to the femur, depedning on which bone is fixed)
Assists in unlocking knee by laterally rotating femur
With the ACL, limits anterior translation of the femur
Lateral knee pain with downhill activities & excessive pronation
Stress to popliteus is caused by forward femoral displacement, such as running downhill
Point tenderness anterior to the fibular colalateral ligament & LCL
Pain with legs in figure 4 or cross-legged
Treatment: may require arch supports or MEDIAL heel wedges
Pain pattern in CECS
Pain will typically increase with exercise & progress as the activity increases in intensity
What is the main predisposing factor to shin splints (MTSS)?
Hyperpronation
Clinical feature of MTSS
Pain may improve with exercise but worsens AFTER the completion of activity & can last until next morning
Ligaments of the ankle (lateral)
ATFL (primary lateral ankle ligament stabilizer), CFL, PTFL (posterior talofibular)
Indications for surgery in lateral ankle sprains
Large bony avulsions, severe ligamentous damage on the medial & lateral sides of the ankle, & severe recurrent injuries
Clinical features of tibialis posterior tendon injury
Insidious onset of posteromedial ankle pain increased by activity, medial hindfoot swelling, increased pain with push-off, weakness with inversion & PF, too many toes sign 2/2 collapse of medial longitudinal arch
Can be a/w malignant malalignment syndrome –> broad pelvis, increased femoral anterversion, squinting patellae, excessive Q angle, & excess pronation of the foot. Hyperpronation can lead to tibialis posterior pain
Where is there inadequate vascularization in Achilles tendon?
2-6 cm proximal to insertion of the tendon, which is where most ruptures occur
Do not perform CSI into Achilles tendon as it may cause rupture –> decreases metabolic rate of chondrocytes & fibrocytes, weakening structural integrity of the tendon & articular cartilage
Sinus tarsi syndrome
Talocalcaneal sprain
Occurs via excessive foot pronation causing adduction of the talus
Usually h/o arthritis: RA, gout, & seronegative spondyloarthropathies
Usually h/o prior ankle injury: inversion sprain or fracture of the tibia, calcaneus, or talus
Pain on anterolateral aspect of foot/ankle
Diagnosis made with block into sinus tarsi. If pursuing surgical management (can be done conservatively), decompression of tunnel contents
SPLATT procedure
Split Anterior Tibial Tendon Transfer
Used for TA spasticity (inversion)
TA tendon is split, & portion of tendon is transferred to lateral foot. Half remains attached to its site of origin, while distal end of lateral half of tendon is tunneled into the 3rd cuneiform & cuboid bones
Provides an eversion force to counteract the dynamic varus deformity to provide a flat base for WB
Often done along with Achilles tendon lengthening to decrease PF
Over-correction is a possible complication
Talar neck fractures
Shear force on the anterior lateral surface of talus –> shallow lesion
Compressive force on posterior medial surface –> deep lesion
MoI: eversion & DF, inversion & PF
Hawkin’s classification:
Type I: non-displaced vertical fracture of talar neck
Type II: displaced fracture of talar neck of subtalar joint with ankle joint intact
Type III: displaced fracture of talar neck with dislocation of the body of the talus from the subtalar & ankle joints
Complications: AVN, most commonly of the talar body. Risk increases as amount of displacement increases
Fracture of the talar dome may form a subchondral fragment that can detach & become displaced in the joint space
Conservative treatment: NWB, surgical is ORIF if indicated
What is a/w plantar fasciitis?
Tight Achilles tendon
What should be avoided in treatment of plantar fasciitis?
Do not inject anesthetic/corticosteroid into the subq tissue or fascial layer. Stay away from superficial fat pad to avoid fat necrosis
Can use nighttime dorsiflexion splints if other measures fail
Morton’s neuroma
Irritation & degeneration of the distal interdigital nerves in the toes from the plantar nerve with eventual enlargement due to perineural fibrosis. Mass can produce pain in the web spaces between met heads
Most commonly affects 3rd intermetatarsal space (between 3rd & 4th toes), followed by 2nd intermetatrsal space
Females > males
To examine, apply direct pressure to the interdigit web space with one hand & then apply lateral & medial foot compression to squeeze met heads together
Hammer toe
Deformity of the lesser toes in which there is flexion of the PIP joint
Passive extension of the MTP joint occurs when the toe is flat on the ground. DIP joint is usually not affected
Caused by chronic, tight shoe wear that crowds the toes, but may be seen after trauma
Treatment:
- Shoe with high toe box
- Shoe should be 1/2 inch longer than longest toe
- HEP of passive manual stretching
Fifth metatarsal fractures
Most common metatarsal to fracture
Fractures at the base are classified by zone:
- Zone 1: pseudo-Jones- avulsion fracture of tuberosity
- Zone 2: Jones- metaphyseal-diaphyseal junction, risk of non-union
- Zone 3: diaphyseal stress fractures from repetitive loading, risk of non-union
Dancer’s: distal shaft fracture
Nutcracker: cuboid fracture
March: metatarsal stress
Treatment:
- Jones: NWB cast for 6 weeks, ORIF if non-union occurs
- Nutcracker: ORIF
- March: relative rest with immobilization, cast if needed, may require surgical fixation due to increased risk of fracture displacement
What steroid is more likely to cause tissue atrophy than methylprednisolone when injecting superficial structures?
Triamcinolone
Viscosupplementation
HA is a large, linear glycosaminoglycan. Benefit derived from enhanced endogenous HA synthesis by synovial cells, proteoglycan synthesis by chondrocytes, anti-inflammatory effects, & analgesic effects
Use caution with patients with allergy to products from birds such as feathers, eggs, or poultry
Clinical course of LBP
Disability & ability to return to work generally improve in 1 month, but 1/3 may have persistent discomfort for up to a year after injury, with 20% of those reporting limitation in activity
Approximately 50% resolve in 1-2 weeks
Approximately 90% resolve in 6-12 weeks
Approximately 85% recur in 1-2 years
Absenteeism in regard to LBP
Missed 6 months –> 50% RTW
Missed 1 year –> 25% RTW
Missed 2 years –> 0% RTW
Cervical uncinate processes
Raised spondylotic margins along the lateral aspect of the superior surface of a cervical vertebral body due to disc degeneration
These raised margins approximate with the body of the superior vertebra, creating a degenerative joint known as the uncovertebral joint (joint of Luschka)
Joints of Luschka limit lateral translation
Sacral vertebrae
Triangular shaped bone consisting of 5 fused vertebrae (S1-S5)
Four pair of foraminae (anterior & posterior), sacral promintory, sacral ala, hiatus, cornua, medial, intermediate, & lateral crests, which are analogous to spinous processes
Contains sacral ligaments
Facet joint orientation
Cervical:
- AA & AO joints have no true facet joints due to their atypical anatomy
- C3-7 facets –> frontal (coronal) plane
Thoracic: frontal (coronal) plane
Lumbar: sagittal plane in upper lumbar, frontal plane at L5-S1
Intervertebral disc
Nucleus pulposus: viscous gel mixture of water & proteoglycans in a network of Type II collagen that braces annulus to prevent buckling
Annulus fibrosis: Type I collagen fibers arranged in obliquely running lamellae that encase the nucleus pulposus & are attached to the vertebral endplates. This orientation withstands distraction forces & bending but is more susceptible to injury with torsional stresses
Vertebral endplate: cartilaginous covering of the VB apophysis, forming the interface between the disc & VB (forming the top & bottom of the disc)
Vascular supply: supplied by cartilaginous VB endplates; IVD’s are essentially avascular by adulthood
Innervations of IVD
Outer 1/3 of annulus –> sinuvertebral nerve & gray ramus communicans, both from b/l ventral rami
Nucleus pulposus –> no innervation
Anterolateral part of annulus –> ventral rami & gray rami communicans
Posterior part of annulus –> sinuvertebral nerves (recurrent branches off the ventral rami)
Innervations of spine/IVD
Ventral primary rami –> trunk musculature, plexus contributions
Dorsal primary rami:
- Lateral: iliocostalis, skin
- Intermediate: longissimus
- Medial: multifidi, rotators, interspinalis, intertransversarii, posterior spinal ligaments, Z-joints
Sinuvertebral nerve: PLL, posterior disc, anterior dura, VB
Aging effects in spine
Decreases:
- Nuclear water content
- Ratio of chondroitin:keratin
- Proteoglycan molecular weight
Increases:
- Fibrous tissue
- Cartilage cells
- Amorphous tissue
Interspinous & supraspinous ligaments
Run from spinous process to spinous process. The supraspinous ligament runs from C7-L3. Functions to weakly resist both spinal separation & flexion
The superior continuation of the supraspinous ligament extending from occipital protuberance to C7 –> ligamentum nuchae (functions to form boundary of the deep muscle in the cervical region)
Disc herniation
May initiate the release of enzyme phospholipase A2, which activates inflammatory mediators, such as leukotrienes, prostaglandins, platelet-activating factors, bradykinins, & cytokines
Higher prevalence for L-spine at L4-5 or L5-S1, followed by C5-6
Disc herniation classifications
Bulge: no annulus defect, disc convexity is beyond vertebral margins
Prolapse: nuclear material protrudes into annulus defect
Extruded: nuclear material extends to the PLL
Sequestered: nuclear fragment free in the canal
Disc herniation location
Central: may p/w axial spinal pain with or without radicular symptoms. Possible multiroot involvement if cauda is affected or myelopathy if SC is involved
Posterolateral: more common in L-spine due to tapering of PLL. A posterolateral L4-5 herniation can impinge the L5 nerve root
Lateral/foraminal: may p/w axial spinal pain with or without radicular sx. Affects the exiting root of that IV level; for example, a lateral L4-5 herniation can impinge the L4 nerve root
Vertebral distraction for relieving nerve compression
Cervical: 20-30 degrees flexion with 25 lb resistance. Less flexion is required for treatment of muscle spasm
Lumbar: may require increased force or a split table to overcome friction
Chymopapain injections
Dissolves sub-ligamentous herniations contained by the PLL
Complication/ADR: anaphylactic reaction, chronic pain, poor efficacy
Where is LSS most common when it affects nerve roots?
L4-5 levels
Classification of LSS
Central spinal stenosis: causes include facet & ligamentum flavum hypertrophy, disc herniation, epidural lipomatosis, or degenerative spondylolisthesis; C-spine AP dimensions: normal SC is 10-mm in diameter, spinal canal is 17 mm. Neuro sequelae may begin when central canal is <12 (relative stenosis) to 10 mm (absolute stenosis)
Lateral recess stenosis: subdivided into 3 areas of entrapment across motion segment:
- Lateral recess
- Midzone (lateral/far lateral)
- IVF (lateral/far lateral)
Spinal stenosis location & borders
Entrance zone (lateral recess):
- Borders: posterior- SAP; anterior- posterior body & disc; medial & lateral walls- open
- Contents: descending nerve root
- Etiology: hypertrophic facet joints
- Root level: nerve root exiting below (L3-4 lateral recess involves L4 nerve root)
Foraminal stenosis: mid-zone (pars region):
- Borders: posterior- pars; anterior- posterior VB; medial wall- open
- Contents: DRG, ventral motor root
- Etiology: osteophytes under the pars
- Root level: same as vertebrae (L3 pars involves L3 roots)
Foraminal stenosis: exit zone (IVF):
- Borders: posterior- Z-joint (inferior level); anterior- posterior disc (inferior level)
- Contents: spinal nerve
- Etiology: hypertrophic facet joints
- Root level: one level up from the vertebrae (L4 SAP or L3-4 disc involve L3 roots)
Etiology of spondylolisthesis
Class II: Isthmic –> most common type in adolescents & young adults, age 5-50
Criteria: pars fracture (subtype A), which is most common at L5-S1 or an elongation (subtype B)
Scheuermann’s disease (juvenile kyphosis)
Adolescent disorder of the vertebral endplates & apophysis resulting in an increased thoracic kyphosis, usually involving 3 sequential vertebrae & generally >45 degrees
Imaging: XR, CT, MRI
- VB wedging, irregular endplate, Schmorl’s nodes with increased kyphosis angulation (Schmorl’s nodes is a herniation of disc material through the vertebral endplate into the spongiosa of the VB, & vertebral wedging (~5 degrees)
VB burst fractures
Compression fractures of the VB involving the anterior & middle columns of the spine from significant trauma, typically fall from height
Most commonly seen in TL region
Treatment is based on stability:
- Stable: neurologically intact. Posterior column remains intact. <50% collapse of anterior VB height
- Unstable: neuro deficits present, >50% loss of anterior VB height
SIJ
Ear-shaped articulation between the sacrum & ilium that has a synovial joint anteriorly & syndesmosis posteriorly
Innervated by the L4/5 dorsal ramus & lateral branches of the S1-3 (S4) dorsal rami
VB OM & discitis
Embolic infection of the VB metaphysis causing ischemia, infarct, & bony destruction with disc involvement
Risk factors: advanced age, DM, immunodeficiency, penetrating trauma, dental infections, GU procedures, & invasive spinal procedures
Most commonly seen in L-spine with IVDA & in the TL junction with TB
Staph: most common
Pseudomonas: IVDA
Mycobacterium tuberculi: Pott’s (needs 12 months of treatment)
Waddell’s signs
Distraction: +SLR but negative slump (should both be +)
Overreaction
Regionalization
Simulation: leg or lumbar pain with light axial load on skill, or presentation of lumbar pain with simultaneous pelvis & shoulder rotation in unison
Tenderness
Where is SCS placed?
Electrodes are placed over the area of the dorsal columns into the epidural space
Muscles of shoulder flexion
Anterior deltoid
Pec major, clavicular portion
Biceps brachii
Coracobrachialis
Muscles of shoulder extension
Posterior deltoid
Lat
Teres major
Triceps, long head
Pec major, sternocostal portion
Muscles of shoulder abduction
Middle deltoid
Supraspinatus
Muscles of shoulder adduction
Pec major
Lat
Teres major
Coracobrachialis
Infraspinatus
Long head of triceps
Anterior & posterior deltoid
Muscles of shoulder IR
Subscapularis
Pec major
Lat
Anterior deltoid
Teres major
Muscles of shoulder ER
Infraspinatus
Teres minor
Deltoid, posterior portion
Supraspinatus
Muscles of elbow flexion
Brachialis
Biceps
Brachioradialis
Pronator teres
Muscles of elbow extension
Triceps
Anconeus
Muscles of forearm supination
Supinator
Biceps
Muscles of forearm pronation
Pronator teres
Pronator quadratus
FCR
Muscles of wrist flexion
FCR
FCU
Palmaris longus
FDS
FDP
FPL
Muscles of wrist extension
ECRL
ECRB
ECU
EDC
EDM
EIP
EPL
Muscles of ulnar deviation of the wrist (adduction)
FCU
ECU
Muscles of radial deviation of the wrist (abduction)
FCR
ECRL
Muscles of finger flexion
FDP
FDS
Lumbricals
Dorsal & palmar interossei
Flexor digiti minimi
Muscles of finger extension
EDC
EIP
EDM
Muscles of finger abduction
Dorsal interossei
Abductor digiti minimi
Muscles of finger adduction
Palmar interossei
Muscles of thumb flexors
FPB
FPL
Opponens pollicis
Adductor pollicis
Muscles of thumb extensors
EPL
EPB
APL
Muscles of thumb abduction
APL
APB
Muscles of thumb adduction
Adductor pollicis
Muscles of opposition of the thumb to 5th digit
Opponens pollicis
FPB
APB
Opponens digiti minimi
Muscles of hip flexion
Iliopsoas
Sartortius
Rectus femoris
Pectineus
TFL
Adductor brevis/longus/magnus
Gracilis
Muscles of hip adductors (anterior)
Gracilis
Pectineus
Adductor longus/brevis/magnus
Muscles of hip adduction (posterior)
Glut max
Obturator externus
Gracilis
Long head of biceps femoris
Semimem
Semiten
Muscles of hip abduction
Glut med
Glut min
Muscles of abductors & IR of the hip
TFL
Sartorius
Piriformis
Glut max, superior fibers
Muscles of hip extension
Glut max
Glut med, posterior fibers
Glut min, posterior fibers
Piriformis
Adductor magnus
Hamstring muscles
Muscles of hip ER
Piriformis
Obturator internus
Superior & inferior gemellus
Obturator externus
Quadratus femoris
Glut max
Muscles of knee extension
Rectus femoris
Vastus lateralis
Vastus intermedius
VMO
Muscles of knee flexion
Hamstrings
Sartorius
Gracilis
Gastroc
Muscles of medial rotation of knee
Semiten
Semimem
Sartorius
Gracilis
Muscles of lateral rotation of knee
Biceps femoris (long & short heads)
Muscles of ankle dorsiflexion
TA
EHL
Muscles of ankle dorsiflexion & foot evertors
EDL
Peroneus tertius
Muscles of foot evertors & weak PF
Peroneus brevis
Peroneus longus
What is an innervation ratio?
Amount of muscle fibers belonging to 1 axon. Ratio varies depending on function of the motor unit
Muscles of gross movement & greater force generated have a high ratio (axons innervating leg muscles can have a 600:1 ratio, meaning 600 muscle fibers are innervated by 1 axon)
Innervation ratio of the eye muscles can be 1:1 (1 muscle fiber to 1 axon) –> finer movements
Endoneurium
Connective tissue surrounding each individual axon & its myelin sheath
Perineurium
Strong, protective connective tissue surrounding bundles of fascicles of myelinated & unmyelinated nerve fibers
Helps strengthen the nerve & acts as a diffusion barrier
Individual axons may cross from one bundle to another along the course of the nerve
Epineurium
Loose connective tissue surrounding the entire nerve that holds the fascicles together & protects it from compression
What type of nerves does EMG study?
Type Ia (large, myelinated) fibers
Temperature effects on Na channels
Na channels normally remain open for about 25 microseconds
Decrease in temp affects the protein configuration & causes a delay in opening & closing of the gates –> changes waveform appearance
Although amplitude is expected to increase as a result of gates being open longer, it can still decrease due to increased temporal dispersion or phase cancellation
In focal cooling, will see prolonged onset & peak latencies, increased amplitude, & decreased CV
In generalized cooling, will see even longer onset & peak latencies, & even slower CV. However, amplitude is about normal because the increased temporal dispersion & phase cancellation knocks down any increase in amplitude from temp alone
Waveform changes due to a decrease in temperature
Latency –> prolonged 1 ms
Amplitude –> increased by 20%
Duration –> increased
CV –> decreased by 10 m/s
Phases –> increased
Propagation of a nerve current
As Na goes into the cell from a depolarization, it moves away from the membrane & spreads the current down the path of least resistance along length of the axon
Affinity to flow back out through the membrane is low due to the myelin sheath covering –> potential jumps to next group of Na channels, located between the myelin to nodes of Ranvier (saltatory conduction)
Skeletal muscle fiber
Cylindrical, multinucleated cell containing contractile elements composed of actin & myosin
Sarcomere is a basic unit of a muscle’s myofibril. Sarcomere runs from Z-line to Z-line. Its size changes during contraction
M line: runs down center of sarcomere, through the middle of the myosin filaments
I band: contains only thin filaments
H zone: contains only thick filaments
A band: contains both thin & thick filaments & is the center of the sarcomere that spans the H zone
During contraction, the H zone, I band, distance between Z lines, & distance between M lines all become smaller. However, the A band’s size remains constant during contraction
Muscle fiber contraction & relaxation
Contraction:
- An action initiated by muscle fiber depolarization
- Stimulus spreads in both directions on the fiber at 3-5 m/s
- Stimulus penetrates deeper into muscle through the T-tubule system, which causes Ca to be released from the SR
- Ca binds to the troponin-tropomyosin complex & exposes actin’s active sites
- Myosin heads, powered by ATP, bind with the active sites
- Actin & myosin filaments slide over each other to shorten the muscle
Muscle fiber contraction & relaxation
Contraction:
- An action initiated by muscle fiber depolarization
- Stimulus spreads in both directions on the fiber at 3-5 m/s
- Stimulus penetrates deeper into muscle through the T-tubule system, which causes Ca to be released from the SR
- Ca binds to the troponin-tropomyosin complex & exposes actin’s active sites
- Myosin heads, powered by ATP, bind with the active sites
- Actin & myosin filaments slide over each other to shorten the muscle
Etiologies of demyelinating injuries
Focal compression causing a transient ischemic episode, edema, or myelin invaginations with paranodal intussusceptions
Axonal regrowth after axonal nerve injury
Process of repair- axon will regrow down its original pathway toward its muscle fibers, travelling approximately 1 mm/day or 1 inch/month (35 mm/month) if the supporting connective tissue remains intact. These axons will have a decreased diameter, thinner myelin, & shorter internodal distance
With reinnervation, low-amplitude, long-duration, & polyphasic potentials known as nascent potentials are formed
If connective tissue is NOT in tact to guide proper nerve regrowth –> neuroma with failure to reach end organ
Shorter the distance from injury to end organ, the higher the likelihood for a better prognosis
Needle electrodes
If used for NCS, the waveform’s amplitude & CV cannot be assessed because the needle samples only a few fibers
Monopolar (what we use): 22-30 gauge Teflon-coated needle; inexpensive, omni-directional recording, less painful (Teflon decreases friction), larger recording area (2x that of concentric), records more PSW’s & more abnormal activity in general. Disadvantages: requires separate reference, non-standardized tip area, Teflon can fray, may have more interference if the reference is not near recording electrode
Concentric (coaxial): 24-26 gauge reference needle with a bare inner wire (active); standardized exposed area, fixed location from reference with less interference, used for quantitative EMG. Disadvantages: beveled tip so unidirectional recording, smaller recording area, MUAPs have smaller amplitudes, more painful
Bipolar concentric: needle with the active & reference wires within its lumen; best for isolating MUAP with less artifact. Disadvantages: expensive & more painful
Single fiber needle: needle (reference) consisting of an exposed 25 micrometer diameter wire (active); looks at individual muscle fibers, used to assess fiber type density, jitter, & fiber blocking, helpful in assessing NMJ disorders & MND. Disadvantages: not used for traditional EMG, expensive
Anodal block
Theoretical local block that occurs when reversing the stimulator’s cathode & anode. It hyperpolarizes the nerve, thus inhibiting the production of an AP
What happens with volume conduction? (Stim intensity too high)
- Decreased conduction times & shortened latencies
- Altered waveforms
- Amplitudes remain unchanged
Signal:noise ratio
Process of averaging improves this ratio by a factor that is the square root of the number of averages performed
The # of averages must be increased by a factor of 4 to double the S:N
S:N = Signal amplitude x square root of # of averages performed, then all of that divided by noise amplitude
Types of NCS Filters
High-frequency filter (HFF) = Low pass
Low-frequency filter (LFF) = High pass
HFF (Low pass): removes signals with frequencies higher than its cutoff setting (beLOW this number can pass); affects faster portions of the waveform
LFF (High pass): removes signals with frequencies lower than its cutoff setting (the high can pass). Affects slower portions of the waveform
Elevating the LFF (High pass):
- Reduces peak latency (but does not change onset latency) –> gets faster
Reduces amplitude –> less overall getting through
Changes potentials from bi to tri –> sexually gets faster
Reducing the HFF (Low pass):
- Prolongs peak & onset latency latency –> gets slower
- Reduces amplitude –> less overall getting through
- Creates a longer negative spike
CV variations with aging
Newborn is 50% that of an adult
80% of adult by 1 year
Adult values at 3-5
Once in 50’s, CV decreases by 1-2 m/s per decade
CV differences with temp
Normal is 32 C in UE & 30 C in LE
CV decreases 2.5 m/s per 1 degree C dropped
Once below 29 degrees C, there is a 5% decrease in CV for every degree dropped
SNAP in relation to DRG
DRG is located in the IVF & contains the sensory cell body. Lesions proximal to it (injuries to sensory nerve root or to the SC) preserve the SNAP despite clinical sensory abnormalities. This is because axonal transport from the cell body to the peripheral axon remains intact. SNAPs are considered more sensitive than CMAPs in detection of an incomplete peripheral nerve injury
Pre-ganglionic injury to motor fibers –> will see NCS abnormalities. But for sensory, will see above
Post-ganglionic injury –> will see NCS abnormalities for both sensory & motor, since there is physical separation of the axon from the cell bodies in the DRG & the ventral portion of the SC
Results when electrodes are <4 cm apart
All decrease: peak latency, amplitude, duration, rise time
H-reflex
Late response analogue to a monosynaptic reflex
Initiated with a SUB-MAX stim at long duration (1.0 ms), preferentially activating Ia afferent nerve fibers –> orthodromic sensory response to SC with orthodromic motor back to recording electrode
Can be potentiated with agonist muscle contraction or abolished with antagonist contraction increased stimulation causing collision blocking
Morphology & latency remain constant with each stim at the appropriate intensity
A mean of 10 F waves can substitute for one H-reflex
Typically used for S1 radic (soleus) or C7 radic (FCR)
Formula: 9 + 0.5 (Leg length in cm from medial mal to pop fossa) + 0.1(age). If >60 years, add 1.8 ms
Normal latency is 28-30 ms
Side to side difference: Anything >0.5-1ms is significant
Waveforms can still be picked up in someone with UMN lesion or even infants
Limitations:
- Evaluates a long neural pathway, which can dilute focal lesions & hinder specificity of injury location Can be normal with incomplete lesions
- Cannot distinguish between acute & chronic lesions. Once abnormal, it is always abnormal
- NOT specific –> can also be seen in generalized peripheral neuropathies, plexopathies, & UMN lesions
- Can be normally abnormal in older adults
F-wave
Small late motor response occurring after the CMAP, representing response from 1-5% of the CMAP amplitude
Produced using a short duration, SUPRAMAX stim, which initiates an antidromic motor response to the anterior horn cells in the SC, which in turn produce an orthodromic motor response to the recording electrode
Pure motor response & does NOT represent a true reflex as no synapse along the nerve pathway occurs
Configuration & latency change with each stim due to activation of different groups of anterior horn cells with each stim
May be helpful in polyneuropathies & plexopathies but not overly useful in radiculopathies
Latency:
Normal: UE: 28 ms, LE: 56 ms
Side to side difference: >2 is significant in UE, >4 is significant in LE
Decreased persistence (occurrence) on repetitive stim correlates with potential abnormality
Can be obtained from any muscle
Limitations:
- Evaluates a long neural pathway, which can dilute focal lesions & hinder specificity of injury location
- Only assesses motor fibers
A-wave (axon)
Response evoked when you are SUBMAX (abolished when SUPRAMAX)
Stim travels antidromically along the motor nerve & becomes diverted along a neural branch formed by collateral sprouting due to a previous denervation & reinnervation process
Occurs between CMAP & F wave at a constant latency (M –> A –> F)
Waveform represents collateral sprouting following nerve damage
Blink reflex
NCS technique electrically evoking an analogue to the corneal reflex
Initiated by stimulating the supra-orbital branch of the trigeminal nerve (CN V). G1 placed inferior & slightly lateral to pupil at mid-position, G2 placed just lateral to lateral canthus. For each side, the ipsilateral supra-orbital nerve is recorded over the medial eyebrow
The response propagates into the pons & branches to the lateral medulla –> then branches to innervate the ipsilateral & contralateral orbicularis oculi via the facial nerve
3 responses are evaluated –> ipsilateral R1 & bilateral R2
Blink response –> a/w R2 response
Latencies (normals):
- R1: <13 ms
- Ipsilateral R2 (direct): <40 ms
- Contralateral R2 (consensual): <41 ms
Afferent loop of the blink reflex is mediated by V1, which synapses with both the main sensory nucleus of CN V in the mid-pons & the nucleus of the spinal tract of CN V in the medulla. The earlier R1 potential is mediated by a di-synaptic connection between the main sensory nucleus & ipsilateral facial motor nucleus (CN VII). The later R2 responses are mediated by a multi-synaptic pathway between the nucleus of the spinal tract of CN V & both ipsilateral & contralateral CN VII. The efferent pathway for both R1 & R2 is mediated via CN VII to the orbicularis oculi muscles
R1 (Early) –> through the pons
R2 (Late) –> through the pons & lateral medulla
R1 is affected by lesions of the:
- CN V
- Pons
- CN VII
R2 is affected by:
- Consciousness level
- PD
- Lateral medullary syndrome
- Valium
- Habituation
Synkinesis
Aberrant regeneration of axons can occur with facial nerve injuries, leading to reinnervation of inappropriate muscles
May present as lip twitching when closing an eye or crocodile tears when chewing
Direct facial nerve NCS (CMAP in relation to amplitude & prognosis)
CMAP <10% of unaffected side –> poor outcome, likely to have incomplete recovery. Recovery >1 year
CMAP 10-30% of unaffected side –> fair prognosis, recovery within 2-8 months
CMAP >30% of unaffected side –> good prognosis, recovery within 2 months
Nerves most commonly used for SSEPs
Median for UE, tibial for LE
What does SSEP monitor for?
Peripheral nerve injuries, CNS lesions such as MS, or intra-operative monitoring of spinal surgery
SSEP evaluates time-locked responses of the nervous system to an external stimulus, representing function of ascending sensory pathways using an afferent potential, which travels from peripheral nerve to the plexus, root, spinal cord (posterior column), contralateral medial lemniscus, thalamus, to the somatosensory cortex
Most common abnormality in MS is prolonged peak latencies (can also see amplitude reduction or absence); more common to see issues in LE
During spinal cord surgery, loss of tibial nerve potentials with preservation of median nerve potentials can indicate nerve injury at the level of intervention. Anesthesia will affect SSEP potentials in both the upper & lower limbs
Median nerve SSEP
N9- Erb’s point (reflects brachial plexus integrity)
N11- roots
N13- cervicomedullary junction (nucleus cuneatus)
P14- lower brainstem
N18- rostral brainstem
N20- primary cortical somatosensory receiving area
Insertional activity on EMG
Represents discharge potentials that are mechanically provoked by physically disrupting the muscle cell membrane with a needle electrode. This is an electrical injury potential
Increased insertional activity may be seen in both neuropathic & myopathic conditions
In rare conditions where significant muscle atrophy has occurred, insertional activity may be decreased. Severe, acute ischemia of muscle due to vascular occlusion or compartment syndrome may also produce decreased or absent insertional activity
Normal duration: 300 ms via muscle depolarization
Increased insertional activity: >300-500 ms via denervation or irritable cell membrane
Decreased insertional activity: via fat, fibrosis, edema, or electrolyte abnormalities
Normal spontaneous activity: MEPP
Occurs spontaneously at the NMJ, referred to as endplate noise
Results from the normal spontaneous exocytosis of individual quanta of ACh travelling across the NMJ, leading to a non-propagated, sub-threshold EPP
Distinct small amplitude of 10-50 microvolts & monophasic negative morphology
The endplate noise is due to spontaneous quanta release (100-200 quanta), which normally occurs every 5 seconds regardless of stimulus
IRREGULAR baseline
Seashell murmur
Normal spontaneous activity: EPP
Endplate spikes due to an increased ACh release, provoked by needle irritation of the muscle fiber or synchronization of several MEPP’s
Results in a propagated single muscle fiber AP
Hallmark sign: irregularity with negative deflection (biphasic)
Sputtering fat in a frying pan
Abnormal spontaneous activity
Nerve resting membrane potential becomes less negative & unstable, causing it to approach the threshhold more easily to activate an AP
Abnormal via muscle fibers:
- Fibs
- PSWs
- CRDs
- Myotonic discharges
Abnormal via motor unit:
- Neuromyotonic discharges
- Myokimia
- Fasciculations
Notes on the abnormal spontaneous activities
Motor fiber source
Fibs & PSWs: can be seen in nerve disorders, NMJ disorders, or muscle disorders (hyperkalemic periodic paralysis, acid maltase deficiency included)
CRDs: can be seen in anterior horn cell disease, chronic radic, peripheral neuropathy; muscle disorders (limb-girdle dystrophy & myxedema incldued); can be a normal variant
Motor unit (neural) source
Fasciculations: if a/w fibs or PSWs, they care considered pathological. A/w anterior horn cell disease, tetany, Mad Cow, radic, mononeuropathy, thyrotoxicosis, or could be a normal variant
Myokimic discharges: facial- MS, brainstem neoplasm, polyradiculopathy, Bell’s palsy; extremity- radiation plexopathy (most common), compression neuropathy, rattle-snake venom
Cramp discharges: NOT muscle in origin; they originate from high-frequency discharges from motor axons. A/w painful, involuntary muscle contractions & are synchronous. Etiology: electrolyte disturbances, uremia, pregnancy, myxedema, strenuous exercises, prolonged muscle contraction, liver cirrhosis, myotonia congenita, myotonic dystrophy, stiff-man’s syndrome
Firing rate
Number of times a MUAP fires per second, expressed in Hz
Calculation: 1000/distance between 2 successive spikes in ms
Normal: 20 Hz or below. Above 20 –> neuropathic process
Recruitment frequency
Firing rate of the first MUAP when a second begins to fire
Initiated by an increase in the force of a contraction
Normal: 20 Hz or below
Anything above 20 –> neuropathic
This increases due to a loss of MOTOR UNITS restricting additional motor unit activation to increase contractile force. This causes the first motor unit to fire more rapidly until a second motor unit finally joins in. This shortens the interval between successive MUAPs from one motor unit
Recruitment Interval
Interspike interval (in ms) between two discharges of the same MUAP when a second MUAP begins to fire
Initiated by an increase in the force of a contraction
Normal is about 100 ms
This increases due to a loss of MUSCLE FIBERS causing a second motor unit to join in early to help increase contractile force. This occurs before the first motor unit has the opportunity to increase its firing frequency. This lengthens the interval between successive MUAPs from one motor unit
Firing pattern of recruitment frequency vs recruitment interval in neuropathy & myopathy
Neuropathy: recruitment frequency increases, interval decreases
Myopathy: recruitment frequency decreases, interval increases
Recruitment ratio
Used to represent recruitment capabilities, especially when a patient demonstrates difficulty in controlling a contractile force
Calculated by dividing the firing rate of the first MUAP by # of different MUAPs on the screen
A motor unit firing at 10 Hz when 2 different MUAPs are viewed on the screen –> RR of 5 (10 Hz/2 different MUAP)
Normal RR: <10
Interference pattern
Qualitative or quantitative description of the sequential appearance of MUAPs
It is the electrical activity recorded from a muscle during a maximum voluntary contraction, composed of recruitment + activation
Activation –> ability of a motor unit to fire faster to produce a greater contractile force & is controlled by a central process
Interference pattern can be decreased in CNS diseases, pain, & hysteria
If a patient is asked to generate a force & only a few MUAPs are seen while the frequency (Hz) continues to remain low, it can indicate decreased activation from poor patient cooperation & is not the result of abnormal recruitment
Interference patterns
Complete –> no individual MUAPS can be seen. A full screen represents 4-5 MUAPs
Reduced –> some MUAPs are identified on the screen during a full contraction
Discrete –> each MUAP can be identified on the screen with a full contraction
Single unit –> one MUAP is identified on the screen during a full contraction
Needle EMG for radiculopathy
The optimal number of muscles to screen for a cervical or lumbar radic is 6 (5 peripheral muscles & paraspinals)
If 1 of the 6 is abnormal, further muscles should be evaluated
Priority is placed on evaluating weak muscles
Classically, Fibs or PSWs should be found in 2 different muscles innervated by 2 different peripheral nerves originating from the same root (they may not be found if the lesion is a demyelinating neuropathy, pure sensory nerve injury, chronic nerve injury, or missed by random sampling
Cervical myotomes affected 2/2 a herniated nucleus pulposus
C3/4 (C2-3 + C3-4 HNP): clinical diagnosis. No discrete myotomal patterns. Innervates the posterior & lateral scalp. Patient may c/o HA. C2 & C3 become the greater & lesser occipital nerve, respecively
C5 (C4-5 HNP): Rhomboids, deltoid, biceps, supraspinatus, infraspinatus, brachialis, BR, supinator, paraspinals
C6 (C5-6 HNP): Deltoid, biceps, BR, supraspinatus, infraspinatus, supinator, PT, FCR, EDC, paraspinals
C7 (C6-7 HNP): PT, FCR, EDC, Triceps, paraspinals
C8 (C7-T1 HNP): triceps, FCU, FDP, ADM, FDI, PQ, APB, paraspinals
Lumbar myotomes affected 2/2 a herniated nucleus pulposus
L2/3/4 (L1-2, L2-3, L3-4 HNP): Iliopsoas, iliacus, gracilis, adductor longus, VMO, TA, paraspinals. It is difficult to distinguish radic & alternate lesions due to only 2 major peripheral nerves
L5 (Posterolateral L4-5 HNP): Glut max, glut med, TFL, TA, medial gastroc, medial hamstring, tibialis posterior, paraspinals
S1 (Posterolateral L5-S1 HNP): Glut max, glut med, TFL, medial gastroc, medial hamstring, tibialis posterior, paraspinals
S2/3/4 (Iatrogenic, CES, LSS): abductor hallucis, abductor digiti quinti, needle exam of the external anal sphincter. Other things to monitor: BCR, anal wink, external sphincter tone, bowel/bladder function
Muscles with dual peripheral innervation
Pec major: medial & lateral pectoral nerves
Brachialis: musculocutaneous & radial nerves
FDP: AIN (FDP 1, 2), ulnar nerve (FDP 3, 4)
Lumbricals: median & ulnar nerves
FPB: median (superficial head) & ulnar (deep) nerves
Pectineus: femoral & obturator nerves
Adductor magnus: sciatic (tibial portion) & obturator nerves
Biceps femoris: sciatic (tibial) & sciatic (peroneal) nerves
Chronology of EDX findings
Time 0: decreased recruitment, decreased recruitment interval, prolonged F wave, abnormal H-reflex (S1 radic)
4 days: decreased CMAP amplitude (about 50% compared to unaffected side) in severe cases
7 days: abnormal spontaneous activity occurs first in the paraspinals. They CAN be normal IF: they become re-innervated OR the posterior primary rami are spared. Paraspinal spontaneous activity can be the only abnormal finding 10-30% of the time
2 weeks: abnormal spontaneous activity beginning in limbs
3 weeks: abnormal activity present in both the paraspinals & limbs
5-6 weeks: re-innervation occurs
6 months-1 year: increased amplitude from re-innervated motor unit. Re-innervation complete
Every 3-4 months: serial EMG can be performed to monitor for reinnervation as clinically warranted
What is the main prognostic factor in a plexopathy?
Distal CMAP amplitude –> represents axonal loss in these conditions
Side to side comparison should be performed
Paraspinals will be normal in a plexopathy (will see abnormal activity in the peripheral muscles)
Why may you see preservation of SNAP is Klumpke palsy (C8-T1 root injury)?
Preservation of a SNAP may indicate a nerve root avulsion. Avulsions may be a/w this location of injury due to lack of protective support at these roots
In addition, MABC sensory will be absent or reduced
EDX findings in TOS
Decreased amplitudes for median CMAP, ulnar SNAP/CMAP, & MABC sensory. Median SNAP is spared
Abnormal spontaneous activity occurs in median & ulnar hand muscles (lower trunk) on EMG
Vascular is much more common than neurogenic (can test vascular etiology via Adson)
Hallmark of Parsonage Turner
Patchy or multifocal involvement (can be bilateral in 1/3 of patients). There is severe pain at first which then resolves after a week in the shoulder/peri-scapular region followed by weakness in patchy fashion
Muscles innervated by C5 & C6 are more commonly affected. Can present as mononeuropathy or plexopathy
Neoplastic vs radiation plexopathy
Tumor: lower trunk, a/w Horner’s syndrome, painful
Radiation: upper trunk, myokymia on EMG, painless
EDX findings of nerve root avulsion
Absent CMAPs with normal SNAPs
Needle EMG shows absent recruitment & abnormal spontaneous activity in a myotomal distribution of the avulsed nerve root, including the paraspinals
What does the AIN innervate (4 P’s)?
- FPL
- FDP 1
- FDP 2
- PQ
Median nerve entrapment at Ligament of Struthers
A 2-cm bone spur (supracondylar process) 3-6 cm proximal to the medial epicondyle exists & is connected to the epicondyle by this ligament in 1% of the population
Nerve becomes entrapped with the brachial artery under the ligament
Patient may have involvement of all median nerve-innervated muscles (including PT):
- Weakness in grip strength: FDS, FDP
- Weakness in wrist flexion: FCR
- Dull, achy sensation in distal forearm
- Active benediction sign from weakness in FDS, FDP
Brachial pulse may be diminished
Median nerve entrapment at bicipital aponeurosis (lacterus fibrosis)
Thickening of the antebrachial fascia attaching the biceps to the ulna. Overlies the median nerve in the proximal forearm
Nerve can be injured by entrapment or hematoma compression resulting from an ABG or venipuncture
Presentation & EDX same as Ligament of Struthers pathology
What muscle is usually first affected in AIN syndrome?
FPL (difficulty with OK sign or have difficulty forming fist because of inability to approximate the thumb & index finger due to FPL & FDP weakness)
More sensitive studies for CTS than routine NCS/EDX
Comparison studies:
- Identical distances between stimulator & recording electrodes for median & ulnar nerves are used
- These techniques create an ideal internal control in which several variables that are known to affect conduction time are held constant, including distance/temp/age/nerve size/muscle size
- Ideally, the only factor that varies in these paired median-versus-ulnar comparison studies is that the median nerve traverses the carpal tunnel & ulnar nerve does not
- Therefore, any slowing of median nerve compared with ulnar can be attributed to conduction slowing through the carpal tunnel
- Diagnostic yield goes from 75% to 95% when using comparison studies
- These sensitive studies are considered abnormal with very small differences between median & ulnar latencies (typically 0.4-0.5 ms)
Combined sensory index (Robinson index):
- Maximizes sensitivity for detecting CTS without reducing specificity using a single score derived from multiple sensory tests
- CSI is the sum of comparisons of sensory latencies collected with 3 established sensory tests for the study of CTS: CSI = ring diff + thumb diff + palm diff
- Ring diff is the peak latency difference of the median & ulnar antidromic sensory nerve conduction to the ring finger stimulating 14-cm proximally
- Thumb diff is the peak latency difference of the median & radial antidromic sensory nerve conduction to the thumb stimulating 10-cm proximally
- Palm diff is the trans-palmar peak latency difference of the median & ulnar orthodromic conduction using 8-cm
- Example: if latencies are 3.8 ms for median nerve conduction to ring finger & 3.4 ms for ulnar nerve conduction to the ring finger, then the ring diff is 0.4. If it was reversed, it would be -0.4. Using negative numbers helps to cancel random errors such as distance measurement –> consider ulnar or radial neuropathy if present
- Upper limit of normal is 0.9. Generally, a CSI of 1.0 ms or greater would be c/w CTS. Can also diagnose CTS if any of the following occur: >0.5 for Bactrian, >0.4 for ring, or >0.3 for palm
Last way to diagnose:
- Take 2 nerves of the same limb (of the same type). If latency >1.0 cm between them, the more prolonged nerve is the issue
- Example: median motor & ulnar motor- median is 4.0 & ulnar is 2.8 –> CTS
Prognosis for CTS
Poor outcome with conservative management may occur with:
- Symptoms >10 months in duration
- Constant paresthesia
- Positive Phalen test in <10 seconds
- Weakness, atrophy
- Marked prolonged latency on NCS
- Abnormal spontaneous activity on EMG
Martin Gruber anastamosis
- Most commonly encountered anomaly in the UE –> crossover of median-to-ulnar fibers. Involves only motor fibers; sensory fibers are spared (AIN)
- Crossover usually occurs in mid-forearm, either directly from the main trunk of the median nerve or from one of its branches, most commonly from the AIN
- Median fibers that have crossed over then run with the distal ulnar nerve to innervate any of the following ulnar muscles: hypothenar muscles (ADM), FDI, thenar muscles (adductor pollicis, FPB deep head), or combination
- Occurs in 15-30% of population
- May be unilateral or bilateral
MGA appearing on routine ulnar conduction study: pseudo-conduction block between wrist & below elbow sites
If the anastamotic fibers innervate the ADM:
- Drop in ulnar CMAP amplitude between wrist & below-elbow stim
- With stim at the wrist, the CMAP reflects all motor fibers innervating the hypothenar muscles, including those that have crossed over from the median nerve
- Stim at the below-elbow site activates fewer fibers, however, as a portion of the fibers innervating the ADM originate from the median nerve & crossover in the forearm & therefore do not contribute to the CMAP
- Whenever there is a >10% drop in amplitude between wrist & below-elbow sites on routine ulnar motor studies (up to 10% is considered normal 2/2 temporal dispersion), median nerve stim should be performed at the wrist & antecubital fossa while recording the hypothenar muscles. If no MGA present, there will be a small positive deflection at both sites, reflecting volume-conducted potential from median muscles. If MGA present, small positive volume-conducted potential will be present with median nerve stim at the wrist, however median nerve stim at the antecubital fossa will evoke a small CMAP over the ADM
Major danger in not recognizing MGA in this situation is mistakenly interpreting findings as a conduction block in the forearm, which is an unequivocal sign of demyelination. This error is serious because presence of a conduction block at a non-entrapment site usually signifies an acquired demyelinating peripheral neuropathy
MGA appearing on ulnar nerve conduction study recording FDI: pseudo-conduction block between wrist & below-elbow sites
Most common MGA occurs with crossing of median to ulnar fibers supplying the FDI. However, it usually isn’t picked up because we use ADM
The FDI is commonly recorded in 2 situations:
- Looking for a lesion of the deep palmarmotor branch of the ulnar nerve (ulnar neuropathy at wrist)
- When evaluating a suspected ulnar neuropathy at the elbow
Similar pattern as if anastamotic fibers innervate the ADM with drop in amplitude >10% between wrist & below-elbow sites. However, it is more complicated to prove an MGA to FDI than it is to ADM because a CMAP is normally provoked when stimulating the median nerve at the wrist or at the antecubital fossa, recording the FDI. This is a normal finding due to volume conduction from nearby median-innervated muscles, specifically the APB, OP, & superficial head of FPB. Thus, to prove MGA to FDI, median nerve must be stimulated at the wrist & antecubital fossa while recording at FDI, looking for higher amplitude CMAP with antecubital fossa stim than with wrist stim
MGA appearing on routine median study: increased CMAP amplitude proximally
Situation where median-to-ulnar crossover innervates one of the ulnar-innervated thenar muscles (adductor pollicis or deep head of the FPB)
With this, recording the ADM is normal when recording routine ulnar motor studies. However, during routine median studies, CMAP amplitude is higher stimulating at the antecubital fossa than at the wrist
To demonstrate that an MGA is present, must stim ulnar nerve at wrist & below-elbow while recording thenar muscles. Normally, while recording thenar muscles, ulnar stim at wrist evokes a thenar CMAP, usually with an initial positive deflection- reflects normal ulnar-innervated muscles in the thenar eminence. If no MGA present, subsequent stim of ulnar nerve at below-elbow site will evoke a CMAP potential with the same amplitude. If an MGA is present, CMAP amplitude will be substantially lower at below-elbow site than at wrist. The difference in amplitude between these two potentials approximates the contribution of the cross-over fibers
MGA with co-existing CTS: positive proximal dip & factitiously fast CV
Will see positive deflection with median nerve stim at antecubital fossa recording thenar muscles & surprising fast CV in median nerve in forearm
Distal median motor latency is prolonged when stimulating at wrist. However, when the median nerve is stimulated at the antecubital fossa, most fibers travel down the arm & through the carpal tunnel as usual, but some median nerve fibers bypass the carpal tunnel by traveling through the anastamosis innervating ulnar muscles
Because these fibers bypass the carpal tunnel, they arrive in the hand much sooner than the median nerve fibers that are delayed through the carpal tunnel. When they depolarize their ulnar-innervated muscles, a positive deflection is seen at the thenar electrodes, indicating that a depolarization has occurred at a distance from the recording electrode
Because the median fibers from the distal stim are delayed from slowing at the carpal tunnel, whereas anastamotic fibers from the proximal median stimulation arrive much sooner than expected –> time difference is artificially shortened, & the calculated CV in the forearm is surprisingly fast (>70-75 m/s)
In some severe cases of CTS, the median fibers traveling through the MGA with antecubital fossa stim arrive at the thenar eminence before the fibers stimulated at the wrist because of the marked delay that occurs with wrist stim. In such cases, proximal median latency is actually shorter than distal median latency (a very unusually occurrence)
Proximal MGA & pseudo-conduction block between above & below elbow sites on routine ulnar motor conduction studies
In patients with ulnar neuropathy at the elbow, one of the classic EP findings is conduction block across the elbow, whereby a drop in CMAP amplitude is seen between below & above elbow sites during routine ulnar motor studies
Very rarely, the crossover fibers of the MGA are very proximal
In these cases where the below-elbow stim might happen BELOW the MGA, MGA might result in mistaken diagnosis of ulnar neuropathy
Take home point: always look for an MGA in any patient that is diagnosed with ulnar neuropathy by conduction block across the elbow without any other supporting abnormalities
Accessory peroneal nerve
Most common anomalous innervation in LE
Involves innervation of EDB. This is the muscle usually recorded during routine peroneal motor conduction studies & normally innervated only by deep peroneal nerve
Patients with this anomaly to EDB display medial portion of EDB supplied by deep peroneal as usual, but lateral portion is supplied by an anomalous motor branch originating from the superficial peroneal nerve
Recognized during routine peroneal motor studies. If an anastamosis is present, CMAP amplitude recording EDB is higher when stimulating at below-fibular neck & lateral pop foss sites than at ankle
If present, APN originates from the distal aspect of the superficial peroneal nerve & travels down the lateral calf, posterior to the lateral mal. If stim is performed posterior to the lateral mal while recording EDB, a small CMAP will be evoked if an APN is present; otherwise, no potential would be seen
What is Riche-Cannieu (all ulnar hand) protective against?
CTS
Dorsal ulnar cutaneous nerve (DUC)
Branch of the ulnar nerve that does now travel through Guyon’s canal (arising 5-8-cm proximally) & is normal in a distal ulnar neuropathy at the wrist but abnormal in more proximal compressions
Ulnar neuropathy at guyon’s canal
Entrapment at the wrist can take on several patterns:
- Pure motor affecting only the deep palmar motor branch
- Pure motor affecting the deep palmar & hypothenar motor branches
- Motor & sensory (proximal canal lesion)
- Pure sensory involving only the sensory fibers to the volar 4th & 5th fingers (rare)
Shea’s classification:
Type 1: involvement of the deep ulnar branch, hypothenar, & sensory
Type 2: involvement of the deep ulnar motor branches
Type 3: involvement of the superficial ulnar sensory branch
Muscles innervated by radial nerve BELOW spiral groove
BR, ECRL, posterior cutaneous nerve of forearm
What does radial nerve split into & where?
At the lateral epicondyle, it splits into a motor (PIN) & sensory (superficial radial nerve) branch
PIN-innervated muscles
ECRB, supinator, EDC, EDM, ECU, APL, EPL, EPB, EIP
Monteggia fracture
Can cause PIN syndrome at arcade of frohse/supinator
Fracture of the proximal 1/3 of the ulna & dislocation of the radial head. Typically occurs from a FOOSH with forearm locked in pronation
Anatomy of the suprascapular nerve
Passes through the posterior triangle of the neck & runs beneath the trap to the superior margin of the scapula
Runs through the suprascapular notch, which is covered by the transverse scapular ligament & branches to innervate the spinoglenoid notch to innervate the infraspinatus
Suprascapular neuropathy
Only peripheral nerve injury at the trunk level
Most commonly involved nerve in neuralgic amyotrophy
Can be injured from trauma, including forced scapular protraction, penetrating wounds, traction from a massive RTC tear, stinger/Erb’s palsy, compression from spinoglenoid ganglions, hematoma, suprascapular or spinoglenoid notch entrapment, or paralabral cyst
Activities involving exaggerated shoulder movements, including sports with repetitive overhead throwing/hitting such as volleyball, baseball, & lacrosse may also injure the nerve. Volleyball more commonly injures branches to the infraspinatus muscle
Injury to the nerve at the suprascapular notch results in weakness in both supraspinatus & infraspinatus muscles. Nerve injury at the spinoglenoid notch will result in weakness only in the infraspinatus muscle
Patient may p/w weakness in abduction (SSp) and/or ER (infraspinatus) of the GHJ
NCS: SNAP not available, CMAP abnormal
EMG: abnormal activity in the infraspiantus only if entrapment is at the spinglenoid notch or both SSp & IS muscles if nerve entrapment is at the suprascapular notch
Does medial or scapular winging result in increased winging with shoulder abduction?
Lateral scapular winging (trap injury via spinal accessory)
Medial scapular winging (serratus via long thoracic) results in decreased winging with shoulder abduction
Treatment for scapular winging
Treatment of serratus anterior/injury to long thoracic nerve (SALT): acute stage- pain reduction & ROM exercise; intermediate stage- passive stretching of the rhomboids, levator scap, & pec minor; late stage- strengthening exercise of all shoulder girdle muscles, including trap
Treatment of trap palsy/injury to spinal accessory nerve: involves PT to adequately strengthen adjacent muscle groups, including rhomboids & levator scap
Surgical repair with a dynamic muscle transfer recommended if patient fails conservative treatment
Diabetic amyotrophy
Most common cause of femoral neuropathy. Proximal diabetic neuropathy is distinct from other types of distal diabetic peripheral neuropathies
AKA lumbosacral radiculoplexus neuropathy, as it can involve the plexus & nerve roots, as well as peripheral nerves. Predominantly affects the lumobsacral plexus
Believed to result from a multifocal immune-mediated microvasculitis. Nerve is believed to be injured from an abnormality of the vaso-nervorum due to DM
Nerve biopsy shows multifocal nerve fiber loss suggesting ischemic injury & perivascular infiltrate
Noted to occur after marked weight loss
Typically affects an older group of diabetics, more frequently males, usually >50 years. Most patients have T2DM
Begins with severe unilateral pain in the lumbar region or proximal LE, which commonly spreads to the contralateral side within weeks to months. Patients then develop weakness & atrophy of the proximal > distal LE musculature
Patient may c/o assymetric thigh pain, knee extension weakness (quadriceps), & atrophy. Loss of the patellar reflex may also occur
Self-limited condition, but the recovery process is gradual & occurs over a period of months. There are some patients who are left with residual LE weakness
Sciatic nerve anatomy
Exits the pelvis through the greater sciatic foramen between the lesser trochanter & ischial tuberosity
Sciatic nerve is comprised of a tibial (medial portion of the nerve) & peroneal (lateral portion). Travels as one unit up to the pop fossa where it splits into peroneal & tibial division
Sciatic nerve muscle innervation in the thigh:
- Peroneal division innervates the short head of the biceps femoris
- Tibial division innervates long head of the biceps femoris, semiten, semimem, adductor magnus (also innervated by obturator)
NCS findings in acquired vs hereditary neuropathies
Acquired: conduction block present, focal slowing present, increased temporal dispersion
Hereditary: no conduction block, diffuse slowing, normal temporal dispersion
Norepinephrine synthesis & release
Norepinephrine is the primary neurotransmitter for post-ganglionic sympathetic adrenergic nerves. It is synthesized inside the nerve axon, stored within vesicles, then released by the nerve when an AP travels down the nerve. Details:
- AA Tyrosine is transported into the sympathetic nerve axon
- Tyrosine is converted to DOPA by tyrosine hydroxylase
- DOPA is converted to dopamine by DOPA decarboxylase
- Dopamine is transported into vesicles then converted to norepinephrine by dopamine b-hydroxylase
- An AP traveling down the axon depolarizes the membrane & causes Ca to enter the axon
- Increased intracellular Ca causes the vesicles to migrate to the axonal membrane & fuse with the membrane, which permits the norepinephrine to diffuse out of the vesicle into the extracellular space
- Norepinephrine binds to the post-junctional receptor & stimulates the effector organ response
Sympathetic skin response
Means of evaluating the unmyelinated, sympathetic nerve fibers of the PNS
For median nerve testing using standard electrodes, E1 can be placed on the palm & E2 on the dorsum of the hand. The median nerve is stimulated at the wrist & elbow at the usual locations. Stimulation occurs over several minutes, & irregular stim intervals are required to prevent nerve habituation
Stimulus sources are electrical, coughing, noises, breathing, or tactile
Current: 10-20 mA with a pulse width of 0.1 ms
Sweep speed: 500 ms/cm
LFF: 0.5 Hz
HFF: 2000 Hz
UE CV: 1.6 m/s
LE CV: 1.0 m/s
Anal sphincter activity in healthy individuals
EMG recording of the external anal sphincter has continuous activity at rest
There is a brief contraction in response to rapid rectal distention, & a preserved or increased activity during a prolonged substantial rectal distention during defecation
What is considered an abnormality on repetitive nerve stimulation (RNS)?
> 10% decrease in amplitude from the 1st to 5th waveform
These are studies in which a repeated supramaximal stimulation of a motor nerve is performed
Progress from ADM/APB –> deltoid –> trap –> orbicularis oculi
Post-activation facilitation vs post-activation exhaustion vs pseudofacilitation
Post-activation facilitation: after a decrement is noted with low-rate repetitive stimulation, a 30- to 60-second isometric contraction or tetany-producing stimulation (50 Hz) should be performed. PAF demonstrates a repair in CMAP amplitude with an immediate follow-up low-rate repetitive stim because of an improvement in NM transmission
Post-activation exhaustion: this response is seen as a CMAP amplitude decreases. It occurs with a low-rate repetitive stimulation performed every minute for 5 minutes after an initial 30- to 60-second isometric contraction. The greatest drop-off is between 2 & 4 minutes. This test should be used if a decrement does not p/w the initial low-rate repetitive stimulation, but a diagnosis of a NMJ disorder is suspected
Pseudofacilitation: this is a normal reaction & demonstrates a progressive increase in CMAP amplitude with high-rate repetitive stimulation or voluntary muscle contraction. It represents a decrease in temporal dispersion due to increased synchronicity of muscle fiber contraction. The waveforms produced maintain a constant area under the curve though the amplitude appears increased because the duration is decreased
Difference among NMJ disorders in relation to RNS
MG: normal or reduced CMAP amplitude. RNS- >10% decrement noted between first and 4th-5th stimulation. 20-50% improvement with PAF. PAE observed 2-4 minutes after maximal voluntary contraction
LEMS: decreased CMAP amplitude. RNS- >10% decrement in amplitude. >100% improvement with PAF. A train of 5 stimuli every 5 minutes to monitor for decrease should be done for PAE
Botulism: decreased CMAP amplitude. >10% decrement in amplitude, or variable changes. >40% improvement with PAF. Absent PAE
Single fiber EMG
Monitors the parameters of single muscle fiber AP’s
Useful if repetitive stimulation of at least 3 muscles is normal & an abnormal diagnosis is still suspected
Most sensitive test for NMJ disorders, but has low specificity
Abnormalities can be a/w NMJ disorders, MND, & peripheral neuropathies
Parameters: fiber density, jitter, & blocking
SFEMG: fiber density
Represents the number of single fibers belonging to the same motor unit within the recording radius of the electrode
Determined by dividing the number of single muscle AP’s at 20 sites by 20
FD of 1.5 is normal. Anything higher than this represents a denervation & reinnervation process
SFEMG: jitter
During voluntary contraction, a small variation exists between the inter-potential discharges of two muscle fibers belonging to the same motor unit. This variation is normally 10-60 microseconds. Considered abnormal if longer than this
Disorders of NM transmission affect the safety factor & cause a delay in the time for an EPP to reach threshold for a muscle fiber AP, which increases the jitter between 2 neighboring muscle fibers. Reinnervation through collateral sprouting after a nerve injury can also cause a delay. The immature NMJs have poor activation, resulting in increase jitter in the first month
Seen in conditions including ALS, NMJ disorders, axonal neuropathies, & myopathies
SFEMG: blocking
Abnormality that occurs when a single muscle fiber AP fails to appear. Occurs if the jitter becomes >100 microseconds
Typically resolves in 1-3 months, after reinnervation has completed. However, increased jitter may take approximately 6 months to resolve
Difference between paramyotonia & myotonia
Paramyotonia: muscle stiffness brought on by repeated muscle contraction or exercise
Myotonia: warm-up period of repeated muscle contraction alleviates the muscle stiffness
Conditions seen in Type I vs Type II fiber atrophy
Type I fiber atrophy: myotonic dystrophy, nemaline rod myopathy, fiber type disproportion
Type II fiber atrophy: steroid myopathy, MG, deconditioning
Kennedy disease
Spinal & bulbar muscular atrophy
A/w tongue scalloping
Expanded CAG repeat on first exon of androgen receptor gene
X-linked disorder
Various endocrine abnormalities (DM, testicular atrophy, gynecomastia, oligospermia, ED)
Incidence & prevalence of SCI in US
Incidence: 54 cases per 1 million (17,700 cases a year)
Prevalence: 300K
What is the average age of injury for SCI?
43 years
Most common cause of SCI
MVC
*Although falls is most common after 45 years
What type of SCI is most common?
C5 overall most common
T12 overall most common cause of paraplegia
Incomplete tetraplegia –> incomplete para –> complete para –> complete tetra
Return to work post SCI
1 year: 12-18%
5 years: 25%
10 years: 35%
Causes of death in SCI population
- Acute phase: respiratory disorders are the leading cause, with PNA being most common. Heart disease ranks 2nd, followed by septicemia (usually a/w pressure injuries, urinary tract, or respiratory infections) & CA
GU diseases (like renal failure) were the leading cause of death >40 years ago, but this has declined dramatically, most likely due to advances in urology
Suicide risk: rate is 3x higher than for non-injured. Risk is highest in first 6 years after injury, for people with paraplegia, if AIS A-C, & for non-Hispanic whites
Spinal cord anatomy
Located in upper 2/3 of the vertebral column
Terminal portion –> conus medullaris, which becomes cauda at the L1-2 vertebral levels
Spinal cord has white matter surrounding an inner core of gray matter. The white matter consists of nerve fibers, neuroglia, & blood vessels. The nerve fibers form spinal tracts, which are divided into ascending, descending, & inter-segmental tracts
Long tracts of the spinal cord
Lateral corticospinal: pyramidal, deep lateral column
- Motor: theorized to have motor fibers running medial (cervical, thoracic) to lateral (sacral)
- Descending pathway
Anterior corticospinal: medial ventral column
- Motor: neck & trunk movements
- Descending pathway
Lateral spinothalamic: ventrolateral column
- Pain & thermal sensation
- Ascending pathway
Ventral spinothalamic: ventral column
- Tactile sensation of crude touch & pressure
- Ascending pathway
Spinocerebellar: superficial lateral column
- Muscular position & tone, unconscious proprioception
- Ascending pathway
Dorsal columns: fasciculus gracilis (medial dorsal column), fasciculus cuneatus (lateral dorsal column)
- FG: proprioception from the leg- light touch, vibration
- FC: proprioception from the arm- light touch, vibration
- Ascending pathway
Lateral corticospinal tract (descending pathway)
Main motor tracts for controlling voluntary muscle activity
Origin is the pre-central gyrus of the frontal lobe of the brain. Axons descend through the internal capsule to the medulla
80-90% of axons cross-over (decussate) to contralateral side at the pyrimidal decussation in the medulla. Nerve fibers then descend in the lateral white columns of the SC (lateral corticospinal tracts). At each level of the SC, the axons from the lateral tract peel off & enter the gray matter of the ventral horn to synapse with secondary neurons
The remaining 10-20% of axons that do not decussate/travel in the anterior (ventral) corticospinal tracts. The axons of the ventral tract then crossover at the corresponding level of muscles that they innervate
Both tracts travel from the pre-central gyrus to the ventral horn as uninterrupted neurons & are terms UMN, while the secondary neurons that they synapse on are termed LMN
Spinocerebellar tracts (ascending pathway)
Transmit unconscious proprioception (muscle proprioceptive, stretch, tension fibers) from the IPSILATERAL side of the body to the brain
Lateral spinothalamic tracts (ascending pathway)
Transmit pain & temp from the CONTRALATERAL side of the body to the brain
Pain & temp sensory fibers enter the SC & synapse in the dorsal horn of the gray matter. The fibers cross-over to the contralateral side of the SC within 1-3 vertebral segments, ascend in the lateral spinothalamic tracts to the contralateral thalamus, & then ascend in the internal capsule to the post-central gyrus of the cerebral cortex
A lesion of the lateral spinothalamic tract will result in loss of pain-temperature sensation CONTRALATERALLY below the level of the lesion
Dorsal (posterior) columns
Transmit proprioception, fine touch, & vibration sense from the IPSILATERAL side of the body to the brain
These sensory fibers synapse at the DRG & immediately ascend into the ipsilateral dorsal white columns
They travel up the medulla, at which point they decussate. Fasciculus gracilis & cuneatus synapse in the medulla & form a bundle called the medial lemniscus, which ascends to the post-central gyrus
A lesion of the posterior columns –> loss of proprioception & vibration ipsilaterally below the level of the lesion
Artery of Adamkiewicz
Provides the major blood supply to the lumbar & sacral cord. Generally arises from the left intercostal or lumbar artery at the levels of T9-L3 & provides the major blood supply to the lower two-thirds of the SC
Lower thoracic region of SC
Referred to as watershed area because there are fewer radicular arteries that supply the mid-thoracic region of the SC
This area (T4-6) is most affected when there is low blood flow to the SC (like clamping aorta intra-op)
Cervical flexion/extension injuries
Flexion/axial loading (burst/compression fracture)
- Stable if ligaments remain intact
- Compression fracture with fragmentation of VB & projection of bony spicules into canal
- Most common level: C5
Flexion/rotation injury (unilateral facet dislocation):
- Unstable if PLL disrupted
- VB <50% anteriorly displaced on XR
- Likely to be incomplete SCI if SC is compromised
- Most common level: C5-6
Flexion (bilateral facet dislocation)
- Unstable if PLL is disrupted
- VB displaced >50% anteriorly on XR
- Anterior dislocation of C-spine with SC compression/compromise
- More likely to result in complete SCI
- Most common level: C5-6
Hyper-extension (central cord):
- Stable; ALL may be disrupted
- Hyper-extension of C-spine, UE weaker than LE
- Likely to be incomplete injury
- Most common level: C4-5
NMO (Neuromyelitis optica) AKA Devic’s disease
Fairly uncommon disease of CNS that affects optic nerves & SC, causing a combination of optic neuritis & transverse myelitis
Marked female predominance
Often mimics MS, also immune-mediated
Clinically, the myelopathy is more severe in NMO than in MS, & on MRI the lesions tend to be more longitudinal (>3 spinal segments). These lesions can lead to weakness or complete paralysis, painful spasms, sensory loss, & bowel/bladder dysfunction. Optic neuritis can cause blindness in one or both eyes
Most of these lesions cause permanent deficits, although some flare-ups can be reversible
Treatment: IV glucocorticoids followed by plasmapheresis if not responsive to steroids. IVIg also can be considered
Long-term immunosuppression has become standard –> Rituximab, mycophenylate, mofetil, or azathioprine
Extradural spinal tumors
Largely comprised of spinal mets & primary bony tumors. Extradural mets account for up to 95% of spinal lesions
Highest incidence between 40-65 years
Majority of cases involve T-spine, followed by L-spine & then C-spine
Most common primary malignancies with spinal mets are lung, breast, & prostate as well as lymphoma
Major presenting symptoms are non-specific & include local or radicular pain with or without motor weakness, sensory changes, as well as loss of sphincter control. Radicular pain is usually unilateral in the C- & L-spines but bilateral with thoracic lesion
Pain is worse with movement & worse at night
Completeness of injury based on radiological findings
Complete: bilateral cervical facet dislocations, TL flexion-rotation injuries, trans-canal GSW
Incomplete: cervical spondylosis with a fall, unilateral facet joint dislocation, non-canal penetrating GSW/stab injury
Hangman fracture (C2 burst)
Usually bilateral from an abrupt deceleration injury (MVC with head hitting windshield)
Most often stable with only transient neuro findings
Treatment: external orthosis (Halo is first-line). Unstable fracture will require surgery
Chance fracture
Transverse fracture of the T- or L-spine from posterior to anterior through the SP, pedicles, & VB
Usually affects T12, L1, or L2
Lap belt injury, a/w falls/crush injury with acute hyper-flexion of the thorax
Tend to be stable & seldom a/w neuro compromise unless significant amount of translation occurs
How many key sensory dermatomes are there on AISA?
28 on each side
How many key myotomes are there on AISA?
10 on each side
What is the NLI?
Most caudal segment of the SC with both normal sensory & motor function >/= 3/5 with cephalad segments graded 5/5 on both sides of the body
Motor & sensory levels are the same in <50% of complete injuries
In cases where there is no key muscle available (cervical levels at & above C4, T2-L1, & sacral levels below S2), the NLI is that which corresponds to the sensory level, if testable motor function above that level is also normal
Sacral sparing
Presence represents at least partial structural continuity of the white matter long tracts
There is better prognosis for motor & sensory return the level of injury as well as the possibility of return of bowel/bladder function in a person with sacral sparing relative to persons without sacral sparing
AIS Impairment scale
A: no motor or sensory is preserved in S4-5
B: Sensory but not motor function is preserved below the NLI & at the most caudal sacral segments S4-5 (light touch or pinprick at S4-5 or DAP) AND no motor function is preserved >3 levels below the motor level on either side of the body
C: Motor function is preserved at the most caudal sacral segments (S4-5) on VAC OR the patient meets criteria for secondary incomplete status with sparing of motor function >3 levels below the ipsilateral motor level on either side of the body. This includes key or non-key muscle functions >3 levels below the motor level to determine motor incomplete status. For AIC C –> <50% of key muscle functions below NLI has a muscle grade of 3 or more
D: Motor incomplete status as defined previously, with 50% or more of key muscle functions below the NLI having a muscle grade of 3 or more
Central cord syndrome
Most common incomplete SCI syndrome
Motor weakness in UE > LE with variable loss of sensation, bowel, & bladder function
Predominantly a white matter lesion
May occur at any age but is more common in older patients with cervical spondylosis who sustain a cervical hyper-extension injury, usually from a fall
Recovery: LE’s recover first & to a greater extent –> bladder recovery –> proximal UE recovery –> intrinsic hand function
Age <50 is a favorable prognostic indicator
Brown Sequard syndrome
Results from a lesion that causes a relative hemi-section of the SC
Rare injury (2-4% of all traumatic SCI)
A/w with stabbing but can occur from other causes (like MVC)
At level of lesion:
- Ipsilateral flaccid paralysis (anterior horn cells)
- Ipsilateral loss of all sensory modalities
Below level of lesion:
- Ipsilateral paralysis (corticospinal tract)
- Ipsilateral loss of light touch & proprioception (dorsal columns)
- Contralateral loss of pain & temp (spinothalamic)
Overall –> ipsilateral motor & proprioceptive loss & contralateral loss of pain & temp
Anterior cord syndrome
Lesion affecting the anterior 2/3 of the SC while preserving the posterior columns
Can occur from flexion injuries, direct injury to the anterior SC from bone fragments or disc herniation, or anterior spinal artery lesions
Results in:
- Variable loss of motor function (corticospinal tract)
- Variable loss of pain, temp, & pinprick sensation (spinothalamic tract)
- Preservation of proprioception, light touch, & deep pressure sensation (dorsal columns)
Motor recovery is poor compared to other incomplete syndromes
CES
Injuries below L1-2 vertebral levels affecting the cauda equina (nerve rootlets), which innervate the lumbar & sacral segments
Cauda is comprised of spinal nerve rootlets, which are peripheral nerves, & would result in LMN signs & symptoms
Results in motor weakness & atrophy of the LE’s (L2-S2) with neurogenic bowel & bladder (S2-4), sexual dysfunction, & areflexia below level of lesion (including absence of anal wink/BCR)
Has a better prognosis relative to UMN injuries for recovery, most likely due to fact that the nerve roots (peripheral nerves) are more resilient to injury & are more likely to regenerate
Functional outcomes after SCI
Most important factors in determining functional outcome are the motor level & AIS classification
Highest level that can live independently without the aid of an attendant is a C6 complete tetra (extremely motivated)
C7 is the usual level for achieving independence
Levels to remember in SCI
T6 and above –> at risk for BP dysregulation –> orthostatic hypotension & AD
T8 & above –> temp8ture –> cannot regulate & maintain normal body temp. Central temp regulation in the brain is located in the hypothalamus
Orthostatic hypotension in SCI
Transient reflex depression caused by a lack of sympathetic outflow & triggered by tilting the patient upright to >60 degrees
Mechanism:
- Upright position causes decrease in BO
- Aortic & carotid baroreceptors sense decrease in BO (would usually increase sympathetic outflow in neurologically intact individual); however, efferent pathway interrupted following SCI
- Brainstem unable to send message through SC to cause sympathetic outflow & vasoconstriction of splanchnic bed to increase BP
- Orthostasis lessens with time due to development of spinal postural reflexes which allow for vasoconstriction due to improved autoregulation of cerebrovascular circulation in the presence of perfusion pressure
Management:
- Reposition: Trendelenberg/recliner WC
- Elastic stocking/abdominal binder
- Accommodation (use of tilt table)
- Increase fluid intake
- Pharm: salt tab 1g QID, Midrodrine (alpha-1 agonist) 2.5-10 mg TID, Florinef 0.05-1.0 mg qD, Droxidopa 100 mg TID (careful because once orthostasis improves, at risk for AD)
Autonomic dysreflexia
Syndrome of massive imbalanced reflex sympathetic discharge in patients with SCI above the splanchnic outflow (T5-L2). Secondary to the loss of descending central sympathetic control & hypersensitivity of receptors below the level of the lesion
Noxious stimulus increases sympathetic reflex spinal release –> regional vasoconstriction causes a marked rise in arterial BP –> increases PVR, increases CO, increases BP –> aortic & carotid baroreceptors respond to increased BP & relay impulses to vasomotor center in brainstem –> impulses via vagus nerve that can lead to bradycardia (not effective in combatting the increased BP) (bradycardia not always seen & may actually see tachycardia/tachy-arrhythmias)
Brainstem is unable to send messages through the injured SC to decrease sympathetic outflow & allow vasodilation of splanchnic bed to decrease BP
Onset occurs after spinal shock & may appear within 2-4 weeks post-injury. If it is going to occur, usually occurs within first year of injury for first time
More commonly occurs in complete injuries
Most common causes:
- Bladder (#1)
- Bowel: fecal impaction
- Abdominal emergency, etc
Elevated BP –> systolic BP >20 mmHg above baseline
Spinal anesthesia is recommended during delivery with SCI at T6 or above
Predisposes the patient to cardiac dysrhythmias (like AF) by altering the normal pattern of repolarization of the atria, making the heart susceptible to re-entrant type arrhythmias
Does the bladder wall have baroreceptors?
No!
What does bladder activation of A1 adrenergic receptors produce?
Contraction of the internal sphincter at the base of the bladder & prostatic urethra, preventing leakage –> promotes storage
What does bladder activation of B3 adrenergic receptors produce?
Relaxation of body of bladder to allow expansion –> promotes storage
Post-SCI urologic function & management
Acutely, patients in spinal shock p/w an areflexic bladder, which retains urine. This can last from 1 week to many months, but most cases resolve in 2-12 weeks
Indwelling catheter, especially while IVF are administered
IC program can begin once patients no longer receiving IVF, UOP has stabilized (<100 mL/hr), & ~2-3 L/day fluid restriction can be maintained. Best started q4h with goal volume <500 mL
What is spinal shock?
Temporary loss or depression of all spinal reflex activity below the level of the lesion, although this may not occur in all patients
Detrusor-sphincter dyssynergia
Up to 85% of SCI patients develop this
Occurs via neurologic injury between pontine micturition centers & sacral (S2-4) centers –> lack of coordinated regulation of bladder function
Can lead to above normal bladder pressures determined on urodynamics & should be treated to minimize renal dysfunction
Result: small, overactive, spastic bladder (detrusor hyperreflexia), tight, spastic internal sphincter (sphincter hyperactivity), failure to empty & high voiding pressures if able to empty any
If not treated –> vesicoureteral reflux, increased volumes, colonized infected stagnant urine, high-pressure voiding against a closed sphincter with risk of VUR
Treatment: anti-cholinergic meds to prevent long-term complication of VUR & quiet bladder wall contractions, IC, botox to detrusor wall, alpha-blockers to open bladder neck, sphincterotomy
Abnormal bladder anatomy
Bladder wall hypertrophy causes the course of the distal ureter to become progressively perpendicular to the inner surface of the bladder. The vesicoureteral junction then becomes incompetent, permitting reflux of urine
During relaxation of the bladder, the ureter pumps urine into the bladder like normal
The valve cannot close during bladder contraction given the perpendicular orientation of the distal ureter to the inner surface of the bladder. As such, urine is forced up the ureter to the kidney & hydronephrosis can result
Reflux can be further complicated by acute or chronic pyelo with progressive renal failure
Congenital abnormalities of the ureters, including posterior placed ureteral orifices & severe trabeculation disrupting the posterior bladder wall, have been a/w VUR after SCI
Asymptomatic UTIs in SCI
When managed with IC or indwelling foley, not treated. Exceptions: patients undergoing invasive procedures, presence of VUR, or growth of urease-producing organisms (Proteus, Pseudomonas, Klebsiella, Providentia, E. coli, staph epidermidis
Urea-splitting organisms produce struvite calculi made of ammonium & mag phosphate
Prevention of UTIs
Use of ppx abx to prevent UTIs after SCI is not supported
Some complications can be prevented by adequately draining the bladder at pressures <40 cm H20, either by IC (in conjunction with the use of anti-cholinergic meds) or by timely surgical relief of outflow obstructions that would not otherwise respond to meds
Vit C supplementation & methenamine salts can be used as acidifying agents to discourage bacterial growth
Most common urinary tract complication in neurogenic bladder
Earliest changes –> irregular, thickened bladder wall & small diverticuli
Rate of ejaculation after SCI
Varies depending on the location & nature of the neurological injury
5-15% of men with complete UMN lesions & 18% with complete LMN lesions have ejaculations
%’s are higher with incomplete injuries
Electroejaculation
Sperm retrieval for those unable to ejaculate
Performed if penile vibratory stimulation (done at home) is unsuccessful
Medical supervision is required. May lead to AD
Why do men have poor semen quality after SCI?
- Stasis of prostatic fluid
- Testicular hyperthermia
- Recurrent UTI’s
- Abnormal testicular histology
- Changes in hypothalamic-pituitary-testicular axis
- Possible sperm antibodies
- Type of bladder management
- Long-term use of various medications
What causes afferent signals to travel via the pudendal nerve into S2-4 segments in women during sex?
Stimulation of the genital region, including clitoris, labia majora & minora
Is the likelihood of pregnancy changed after SCI in women?
No! Fertility is unimpaired (although may have amenorrhea in first 6-12 months after injury, but this goes away)
What may be the only clinical manifestation of labor?
Autonomic dysreflexia
What is treatment of choice for AD during pregnancy?
Epidural anesthesia extending to T10 level
Epidural should continue for at least 12 hours after delivery or until AD resolves
Colonic dysfunction in SCI patient
In an UMN lesion such as an SCI, the GI system can be affected by loss of sympathetic & parasympathetic input at the transverse & descending colon, resulting in decreased fecal movement
Fecal impaction & constipation are the most common complications during recovery
Gastrocolic reflex
Contraction of the colon occurring with gastric distention
When feasible, SCI patients should be instructed to perform their bowel programs 20-30 minutes after a meal
Increased colonic activity occurs in the first 30-60 minutes after a meal (usually within 15 mins)
Rectocolic reflex
Occurs when rectal contents stretch the bowel wall reflexively, relaxing the internal anal sphincter & leading to left colonic contraction
Suppositories & digital stimulation cause the bowel wall to stretch & take advantage of the reflex
Reflex can be manipulated by digital stimulation of the rectum
Digital stim –> gently inserting a gloved, lubricated finger into the rectum & slowly rotating finger clockwise in a circular motion until relaxation of the bowel wall is felt or stool/flatus passes (approximately 1 minute)
Most common cause of emergency abdominal surgery in chronic SCI patients
Cholecystitis
When does pancreatitis typically occur in the SCI patient?
Most commonly within 1 month from injury
Metabolic complications in SCI
Hypercalciuria
Hypercalcemia
Osteoporosis
Fractures
CV Disease
Hyperglycemia & metabolic syndrome
Metabolic complications in SCI: hypercalciuria
Immobilization & reduced body weight bearing result in uncoupling of normal mechanism responsible for maintaining bone, promoting bone resorption, & hyeprcalciuria
Vit D & PTH are NOT involved
Metabolic complications in SCI: hypercalcemia
Treat both sx & asx as prolonged hypercalcemia can cause nephrocalcinosis
Restriction of dietary Ca is unnecessary; 1,25-dihydroxy Vit D levels already are low, suppressing intestinal absorption of Ca
Restriction of Vit C may be a good idea
Give IVF to help pee out Ca
Pamidronate can be used to inhibit osteoclast-mediated resorption & reduces osteoclast viability. The drug is administered as a single IV infusion & rapidly lowers serum Ca within 3 days. Serum Ca then falls to nadir within 1 week & may remain normal for several weeks or longer. Can repeat if needed. IVF can be discontinued 2-3 days after Pamidronate is completed
Other meds: Didronel (Etidronic acid), calcitonin
Metabolic complications in SCI: osteoporosis
Rapidbone loss occurs below level of injury & primarily at load-bearing sites
FES may help
Metabolic complications in SCI: fractures
Knee (distal femur & proximal tibia) is the most common site
Risk factors: prior fragility fracture, family history of fracture, female gender, age (bimodal: </= 16 years old & increasing age), time post-injury (>10 years), BMI <19, paraplegia, motor complete SCI, alcohol intake >5 servings per day
Fractures are usually non-op with soft padded splints (well-padded knee immobilizer for femoral supracondylar, femoral shaft, & proximal tibial fractures; well-padded ankle immobilizer for distal tibial fractures)
With non-op management, patient can sit within a few days. Callus formation –> 3-4 weeks. ROM is initiated at 6-8 weeks, with WB delayed for a longer period
Metabolic complications in SCI: CV disease
Low HDL, high LDL, high CRP
Tetras & complete injuries have higher risk
Higher prevalence of insulin resistance, DM, metabolic syndrome
Metabolic complications in SCI: hyperglycemia & metabolic syndrome
Both FES & arm ergometry (high-intensity target HR 70-80% of max HR predicted) have increased glucose tolerance & reduced lipid profile in SCI
Most frequent complications in SCI
PNA, atelectasis, vent failure. Most common in first year following injury but persist throughout life. Within first 15 years, respiratory illnesses comprise 20-25% of all deaths
Diaphragm (innervated by C3-5) is major muscle of inspiration contributing 65% of VC
Primary muscles of expiration to help clear secretions: rectus, transversus abdominus, internal & external obliques (T4-L2), & intercostal muscles of the lower rib cage (T6-12)
For persons with neurologically complete injuries with high cervical injuries, reported rates of successful weaning from MV:
- 0% at C1
- 0-30% C2
- 25-50% C3
- 77-83% C4
What is the leading cause of death among chronic SCI patients?
PNA
What type of lung disease do tetraplegics develop?
Restrictive
All volumes shrink, except residual volume
If VC <1L –> consider MV
Once VC 15-20 mL/kg, can usually wean off vent
When to MV SCI patient
- VC <1L
- ABG shows increasing PCO2 (>50 mmHg) or decreasing PO2 (<50 mmHg)
- Severe atelectasis
Weaning from ventilator in SCI
Useful indices:
- Maximum inspiratory pressure -20 cm H2O or more negative
- VC >10-15 mL/kg ideal weight (can use larger TV target but must keep plateau pressures <30 cm H2O to prevent atelectasis) & patient must not have ARDS
Method for highest success rates for weaning off MV: progressive free breathing, with or without the use of PEEP 5 cm H2O or less
Potential benefits of pacing for ventilation compared to MV
Improved quality of life, engagement of patient’s own breathing muscles, improved level of comfort, improved speech, restoration of olfactory sensation, increased mobility, reduced anxiety & embarrassment, elimination of vent noise, & reduced overall costs
Signs of pacemaker failure for ventilation
Sharp chest pain, SOB, absence of breath, erratic pacing
Most common joints to experience HO in SCI
Hip (anteromedial aspect)»_space; knee/shoulder/elbow
Onset of HO in SCI
1-3 months s/p injury is most common; peaks at 2 months
Can still present after 6 months. When it occurs after 1 year, usually a/w an acute fracture, DVT, or pressure injury (usually with benign course)
Gold standard for DVT diagnosis in SCI
LE venogram
What is the leading cause of death in acute SCI?
PE
Gold standard for PE diagnosis in SCI
Pulmonary arteriogram
Duration of DVT ppx in SCI
Incomplete SCI & ambulating injured patients: can continue until discharge, but can be continued if soon after injury or other co-morbidities present
Complete SCI: 8 weeks post-injury if uncomplicated
Complete, complicated SCI: 12 weeks post-injury or until discharge from rehab (if >12 weeks). Complicated: LE fracture, history of thrombosis, CA, HF, obesity, >70 years old
General uses for e-stim or FES in SCI
- As exercise to avoid complications of muscle inactivity
- As a means of producing extremity motion for functional activities
- FES can be used to provide a CV conditioning program
- Increase muscle bulk, strength, & endurance
- Produce motion for UE activity, bladder function, standing, & ambulation
Pain in the SCI patient
There are NO consistent associations between presence of pain & SCI characteristics
Nociceptive –> from bone, ligaments, muscle, skin, other organs
Neuropathic –> from peripheral or central neural tissue damage
Shoulder is most commonly affected joint (nociceptive)
Incidence of CTS in SCI patients
Between 20-65% with persons with paraplegia, who are more affected than tetras
Due to recurrent stress from transfers, WC propulsion, & pressure relief. Padded glove use may decrease the trauma of WC propulsion
25% of people have bilateral UE involvement
Post-traumatic syringomyelia/cystic myelopathy
Lesion progresses in a cephalad & caudad direction. As the lesion progresses & compromises more nerve fibers, symptoms may become more apparent
Most common presenting symptom is pain –> aching or burning, often worse with coughing, sneezing, straining, & usually in sitting (rather than supine) position
Earliest sign is ascending loss of DTRs
Ascending sensory loss is also common. Dissociated sensory loss (impaired pain & temp sensation but intact touch, etc)
Weakness occurs but rarely in isolation
Diagnosis: MRI with gad is gold standard
Tendon transfer by spinal level
C5: BR –> ECRB: restores wrist extension; deltoid –> triceps: provides elbow extension
C6: Moberg “key grip” procedure: restores lateral or “key” grip to improve grooming, eating, writing, desktop skills; BR (or other active muscles) –> FPL (or other finger flexors) to restore lateral pinch (FPL) or grasp (finger flexors), which provides better function & preferable to Moberg procedure; posterior deltoid –> triceps- recommended prior to hand reconstruction (or simultaneously); re-routing of biceps around radial neck- correct supination contracture of forearm that may occur in C5 & C6 motor injuries
C7: BR –> FPL to restore thumb function; ECRL or FCU –> FDP to restore finger flexion
C8: intrinsic minus or “claw hand” may be addressed with lumbrical bar, preventing hyper-extension of MCPs to improve function; this surgery is rarely indicated
Incidence of dual diagnosis
Between 25-75%
Incidence of depression in SCI
Occurs in 20-45% of those injured & usually occurs within first month
Suicide rate for injured people is 3-5x the age- & sex-specific rate in the US
Leading cause of death in individuals with SCI in the youngest age groups
Pressure injuries
Most common location in SCI within first 2 years is the sacrum, followed by ischium, heels, & trochanters
In children, the occiput is the most frequent site
NPUAP staging of pressure injuries
Stage I: intact skin with localized area of non-blanchable erythema, which may appear differently in darkly pigmented skin. Blanchable erythema or changes in sensation, temp, or firmness may precede visual changes. Color changes do NOT include purple or maroon discoloration
Stage II: partial-thickness loss of skin with EXPOSED DERMIS. Wound bed is viable, pink/red, moist, & may also present as an intact or ruptured serum-filled blister. Adipose & deeper tissues are NOT visible. Granulation tissue, slough, & eschar are NOT present
Stage III: Full-thickness loss of skin, in which ADIPOSE is visible in the ulcer & GRANULATION TISSUE & EPIBOLE (rounded wound edges) are often present. SLOUGH and/or ESCHAR may be visible, but will not obscure extent of tissue loss. Depth varies; areas of significant adiposity can develop deep wounds. UNDERMINING & TUNNELING may occur. Fascia, muscle, tendon, ligament, cartilage, and/or bone are NOT exposed
Stage IV: Full-thickness skin & tissue loss with EXPOSED or DIRECTLY PALPABLE FASCIA, MUSCLE, TENDON, LIGAMENT, CARTILAGE, or BONE in the ulcer. SLOUGH & ESCHAR may be visible. EPIBOLE, UNDERMINING, and TUNNELING often occur
Unstageable: Full-thickness skin & tissue loss in which extent of tissue damage within the ulcer is obscured by slough or eschar. A stable eschar (dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be softened or removed
Risk factors for developing pressure injuries
Persistent pressure & shear forces
Mechanisms of developing a pressure injury
Local soft tissue ischemia results due to prolonged pressure over bony prominences that exceed supra-capillary pressure
Ischemia: a/w hyperemia in surrounding tissue, increased local O2 consumption occurs
Pressure: prolonged pressure over bony prominences, exceeding supra-capillary pressure continuously for 2 or more hours, resulting in occlusion of the microvessels of the dermis with subsequent tissue ischemia. Muscle is more susceptible to pressure ischemia than skin
Friction (shearing): removes corpus striatum of skin
Prevention of pressure injuries
Decrease duration of pressure forces –> patient should initially be turned & positioned q2h
Pressure relief (weight shifting) & repositioning should be done for >2 minutes at a time, every 15-30 mins when sitting
What has been shown to significantly increase tendon extensibility?
Combined heat & stretching
Contraindications to heat therapy
Ischemia (arterial insufficiency) –> metabolic requirement of the limbs is increased with the use of heat; for every 10 degrees F increase in skin temp, there is a 100% increase in metabolic demand
Scar tissue –> elevation of temp increases tissue’s metabolic demand. Scar tissue has inadequate vascular supply & is unable to provide an adequate vascular response when heated, which can lead to ischemic necrosis
Which conversion technique is the only to produce superficial heat?
Radiant heat (infrared lamps)
Light energy (non-thermal) is absorbed through the skin & converted to superficial heat
Distance from the lamp to skin is usually 45-60 cm (18-24 inches). Most lamps work as heat sources, & their heating effectiveness decreases with the square of their distance from the body (1/r2)
Used in patients who cannot tolerate the weight of hot packs
Precautions: general heat precautions, light sensitivity (dermal photo-aging), & skin drying. Use with photosensitizing meds
Where is absorption greatest when using U/s as a deep heating modality?
At the bone-muscle soft tissue interface
U/s indications for deep heating modality
Bursitis, tendinitis (calcific), MSK pain, degenerative arthritis & contracture (adhesive capsulitis, shoulder peri-arthritis, hip contracture) to maintain a prolonged stretch & increase ROM; when used to address small joints like fingers/toes, must be done underwater but only if water is degassed, subacute trauma.
Less established: scar tissue (keloids), post-herpetic neuralgic pain, plantar warts
U/s contraindications for deep heating modality
General heat contraindications, near brain/cervical ganglia/spine, laminectomy sites (can cause SC heating), near the heart or reproductive organs, near pacemakers (may cause thermal or mechanical injury to the pacemaker), near tumors, gravid or menstruating uterus, at infection sites, on contact lenses/eyes (fluid-filled cavity with risk of cavitation & heat damage), skeletal immaturity (open epiphysis can be affected with decreased growth due to thermal injury, THA or TKA with PMMA or high-density polyetyhlene (high coefficient of absorption- more than soft tissue; prosthesis may loosen due to unstable cavitation in the cement), arthroplasties
U/s prescription for deep heat modality
Frequency: 0.8-1.1 MHz
Intensity: 0.5-2.0 W/cm2 (max should be 3.0)
For tendinitis/bursitis, average intensity used is 1.2-1.8 W/cm2, which generates temperatures up to 115F in deep tissues
Shortwave diathermy for deep heat modality
Produces deep heating through the conversion of radio wave electromagnetic energy to thermal energy
Most commonly used frequency is 27.12 MHz (11 m wavelength)
Provides heat over a larger area as well as deep heat to 4-5 cm depth. Preferentially heats low impedance tissues –> skeletal muscle, blood, synovial fluid, so good choice if deep muscle heating is primary goal
Inductive coil method: produces high temps in water-rich tissues (superficial muscles, skin) via a coiled magnetic field (induction coil); body acts as a receiver & eddy currents are induced in tissues in its field; applicators are in the form of cables or a drum. Indicated when heat to more superficial muscles or joints with minimal superficial tissue is desired; muscle tends to become warmer than fatty tissue
Condensor method: produces high temps in water-poor tissues (fat, bone) with low conductivity via rapid oscillation of an electrical field. Treatment area is placed between 2 capacitor plates to which the shortwave output is applied. Body acts as an insulator in a series circuit. Indicated for subq adipose tissue & superficial muscle, more effect in deep joints (like the hip)
Microwave diathermy for deep heat modality
Conversion of microwave electromagnetic energy to thermal energy
Frequencies: 915 MHz (33 cm wavelength) - 2,456 MHz (12 cm)
Do not penetrate tissues as deeply as U/s or SWD
Preferentially heats fluid-filled cavities
Summary of deep heating modalities (diathermy)
Options: U/s, SWD, microwave diathermy. All are conversion
U/s: sound waves, frequency 0.8-1.1. MHz, heats at 8-cm depth (deepest penetration)
SWD: radio waves, freq 27.12 MHz, heats at 4-5 cm depth. Indications: chronic prostatitis, refractory PID, myalgia, back spasms
Microwave: micro waves, freq 915-2,456 MHz, superficial heat: 1-4 cm depth. Indications: superficial heat for muscles & joints, speed resolution of a hematoma
Therapeutic cold techniques
Decrease spasticity due to:
- Decreased muscle spindle activity: decreased firing rates of Ia & II afferent fibers
- Decreased golgi tendon organ activity: decreased firing rates of Ib afferent fibers
Evaporation: vapocoolant sprays used for spray & stretch techniques to treat myofascial & MSK pain
Ultraviolet radiation for therapeutic modality
Wavelength of 2000-4000 A. Bactericidal wavelength is 2,537 A
Produces a non-thermal photochemical reaction with resultant alteration of DNA & cell proteins
Physiologic effects: bactericidal on motile bacteria, increased vascularization of wound margins, hyperplasia & exfoliation, increased Vit D production, excitation of Ca metabolism, tanning
Precaution: scar, atrophic skin
Dosage: prescribed as the minimal exposure time required to cause erythema on the volar surface of the forearm –> measured in minimal erythema dosage (MED). The MED subsides in 24 hours. Usual initial prescription is in the dose of 1-2 MED & kept <5
2.5 MED: exposure produces a second-degree erythema in 4-6 hours with pain & subsides in 2-4 days followed by desquamation
5 MED: 3rd degree erythema in 2-4 hours with local edema, pain, & followed by local desquamation
10 MED: 4th degree erythema with superficial blister
Treatment can be given 2-3x/week
Goeckerman’s technique
Psoriasis treatment –> coal-tar ointment is applied to the skin prior to UV treatment
How does TENS provide pain control?
Placebo effect –> 30-35%
Gate Control Theory (Melzack & Wall)
- Attempts to account for mechanisms by which non-noxious stimuli can modulate pain sensation (how non-painful stimuli can suppress pain)
- TENS stimulates large Ia myelinated (delta) afferent nerve fibers –> stimulate substantia gelatinosa in the SC, closing the gate on pain transmission to Lissauer’s tract (posterior lateral tract of pain & temp), & ultimately to the thalamus. Pain signals can be blocked at the SC before they are transmitted to the brain
Conventional TENS
High frequency, low intensity stim –> most effective
Pain relief begins in 10-15 minutes & stops shortly after removing stimulation
Useful for neuropathic pain
Clinical use of NMES
Strengthens muscles & maintains muscle mass after immobilization
Benefits: has been shown to potentially increase muscle mass, stroke volume, & CO, as well as reduce venous pooling. Also shown to potentially improve cardiorespiratory fitness
Physiologic effects of therapeutic massage
Reflex vasodilation with improvement in circulation
Assist in venous blood return from periphery
Effleurage
Gliding, rhythmic strokes of the hand over the skin in a distal to proximal direction; performing gently & slowly results in muscle relaxation, whereas performing at a faster pace will increase stimulation
Deeper strokes result in more mechanical effects on circulatory & deep myofascial system: relieving pain, increasing lymphatic drainage, & reducing vascular congestion a/w specific conditions
Petrissage
Kneading technique in which the muscle tissue is pinched with the fingers & lifted from its underlying origin; increases circulation & tissue pliability, & reduces edema & adhesions. Other variations: wringing, rolling, or shaking techniques
Tapotement
Percussion
Helps with desensitization, allows clearing of secretions, & improves circulation. Used for chest physiotherapy in conjunction with postural drainage
Soft tissue mobilization
Forceful massage of the fascia muscle system. Massage is done with the fascia muscle in a stretched position rather than relaxed or shortened. Used for reduction of contractures
Physiologic effect of traction
Vertebral joint distraction –> elongation of the C-spine of 2-20 mm can be achieved with 25 lb or more of tractive force
Contraindications to C-spine traction
Cervical ligamentous instability (RA, Down syndrome, Marfan syndrome, achondroplasia, EDS), infectious process of the spine, cervical spinal stenosis with significant cord compromise, AA subluxation with SC compromise, vertebrobasilar insufficiency
Amount of spinal traction required
C-spine: distraction requires >25 lbs. Weights >50 lbs do not provide an advantage
L-spine: posterior vertebral distraction >50 lbs is needed; for anterior separation >100 lbs is needed
Effect of friction between treatment table & body should be counterbalanced before true traction of the spine is accomplished
A pull equal to about 1/2 weight of the body part treated is needed to overcome friction. For lower body, this is ~25% of the total body weight. Another option is using a split table, which eliminates the lower body segment friction
Regardless of the effect of friction, another 25% or more of body weight is needed to cause vertebral separation
Muscle physiology
Skeletal muscle fibers contain hundreds-thousands of myofibrils, each subdivided into units of contraction called sarcomeres
Sarcomere is composed of contractile proteins, actin & myosin, that lie parallel to the axis of the fiber. Muscle shortening is produced by coordinated movement of the thin (actin) & thick (myosin) filaments within the myofibrils
Actin filaments attach to the outer margins of the sarcomere (Z line) & the myosin filaments are located centrally
Sarcomere is measured from Z line to Z line
During muscle rest, the filaments overlap a little. The A band runs the length of the thick (myosin) filament), with continuous overlap except at the center (H zone). The I band is composed of thin (actin) filaments that remain bare throughout the outermost portion of the sarcomere
Thick & thin filaments are linked to each other via cross bridges that arise from the myosin molecule. During muscle contraction, an increasing amount of myosin overlap is observed. Contraction results in the Z lines approaching each other, shrinking the H zone & I band
Transient muscle fiber shortening takes place whenever an AP is generated & travels through the sarcolemma (muscle fiber cell membrane)
Relationship between force generation & velocity during eccentric, concentric, & isometric contractions
Greatest force is generated with:
Fast eccentric contractions > slow eccentric contractions > isometric contractions > slow concentric contractions
Fast concentric contractions generate the least force
Plyometric exercises
Training technique designed to increase muscular power & explosiveness (hopping, box jumps, forward hurdle hops)
Should be used as an advanced level of exercise in carefully selected patients such as athletes who want to return to high demand functional activities. Exercises are intended to mimic motions used in sports
Uses short, explosive movements that cause alternating eccentric & concentric muscle contractions. Increased elastic energy is stored in the eccentric phase, resulting in a more powerful concentric contraction
Increased risk of injury due to high-intensity load on muscles
Aquatic exercises
Pool-based therapy takes advantage of buoyancy & viscosity of water
Buoyancy: weight of a patient can be reduced in proportion to water depth. Being chest deep has a decreased WB load of 40% of total body weight
Viscosity: allows for increased resistance to movement equal to the force exerted by the patient. Resistance also decreases in proportion to the speed of movement
Improvements can last up to 2 years after participation
Biofeedback
Technique of using visual & audio equipment to reveal & translate normal & abnormal internal physiologic events in order to teach patient to manipulate otherwise involuntary events
Various types. Training requires potential for voluntary control & ability to follow commands
Clinical applications: CVA, SCI, TBI, chronic pain, urinary/fecal incontinence management, sports-related muscle strengthening. Also used in CP, MS, dystonia, dyskinesis, peripheral nerve denervation, & Raynaud’s
Types: EMG, pressure/force, position, temp/peripheral blood flow, BP, respiratory, sphincter control training
Although EMG biofeedback has been studied & is used extensively in CVA rehab, it has less efficacy when there are major sensory deficits, especially severe deficits in proprioception. Additionally, proprioceptive deficits, marked spasticity, & receptive aphasia correlate with lower functional improvements when using biofeedback. This is more evident in UE training than LE training
Effects of extended bedrest: muscle
Immobilization decreases strength by 1.0-1.5% daily. Strength can decrease as much as 20-30% during only 1 week of bedrest. 5 weeks of total inactivity costs 50% of the previous muscle strength. A plateau is reached at 25-40% of original strength. One contraction per day of max strength is enough to prevent this decrease
Percentage of muscle mass lost per week is ~5-10%
Effects of extended bedrest: bone & joints
Lack of stress & tension on the bone through WB & muscle pull on the bone cause osteopenia. Hypercalcemia develops. Calcium is excreted in urine & feces starting at 2-3 days after immobilization, peaking at 3-7 weeks. After activity is resumed, Ca levels remain high for 3 weeks, reaching normal values at 5-6 weeks
Effects of extended bedrest: cardiac
Reduction in blood & plasma volumes
Redistribution of body fluids leads to postural hypotension. Venous blood pooling occurs in the legs. In addition, beta-adrenergic sympathetic activity is increased
CV efficiency is decreased: patients develop an increased resting HR & decreased SV. HR increases 0.5 beats/minute/day, leading to immobilization tachycardia & abnormal HR with minimal or sub-max workloads. SV decrease may reach 15% within 2 weeks of bedrest due to blood volume changes & venous pooling in LE. Also a decrease in VO2 max that can occur as early as 3-5 days
Increased risk of thromboembolism due to decrease in blood volume & increased coagulability
FIM score
Documents severity of disability, measures activity limitations, & documents outcomes of rehab treatment as part of a uniform data system
Consists of 18 items organized under 6 categories (ordinal scale):
- Self-care (eating, grooming, bathing, UB dressing, LB dressing, toileting)
- Transfers
- Sphincter control
- Locomotion
- Communication
- Social cognition (interaction, problem-solving, memory)
Graded in each category on scale of 1 (total assistance required) to 7 (complete independence)
Physiologic effects of aging: cardiac
Progressive decline in max HR –> decreased chronotropic response to adrenergic stim
Increased LV end-systolic volume & decreased EF with exercise. When added to a decreased HR, CO during exercise is more dependent on an increased SV by with higher end diastolic volumes
CO decreases with aging
Rate of diastolic early filling is decreased. More dependent on late filling through atrial contraction. Patients are more susceptible to AF or atrial tachycardia as well as CHF
VO2 max decreases regardless of level of activity, but more physically active patients have smaller decreases than sedentary patients
Progressive, gradual increases in systolic & diastolic BP –> decreased arterial elasticity
Decreased baroreceptor sensitivity is a/w orthostatic hypotension. Diminished reflex tachycardia with position change, in a/w blunted plasma renin activity & reduced vasopressin & angiotensin II levels. Decreased baroreceptor sensitivity is also a/w cough & micturition syncope syndromes. Meds to monitor for causing orthostatic hypotension: anti-hypertensives, levodopa, phenothiazines, TCAs
Physiologic effects of aging: pulmonary
Decreased VC
Decreased PO2 –> linear decline a/w mild degree of impaired gas exchange
NO change in PCO2 or pH
Decreased FEV1. This decreases consistently at 30 mL/year
Decreased maximum minute ventilation –> stiffening of rib cage, weakening of intercostal muscles, small airway narrowing due to decreased elastic recoil
Increase in residual volume & functional reserve capacity related to loss of elastic recoil of the lung tissue
No change in total lung capacity
High incidence of PNA
Physiologic effects of aging: renal
Digitalis toxicity in the elderly is commonly 2/2 impaired renal function. Toxicity manifests with cardiac dysrhythmias, anorexia, n/v, abdominal pain, fatigue, depression, drowsiness, lethargy, HA, confusion, & ocular disturbances
NSAIDs can also cause injury to kidneys with most common finding being pre-renal azotemia. In settings where the renal blood flow is dependent on the activity of vasodilating prostaglandins, NSAIDs can precipitate ARF. In states of prostaglandin inhibition, patients develop hypo-reninemic hypo-aldosteronism
Physiologic effects of aging: GI
Dysphagia –> age-related changes in swallowing physiology & age-related diseases are pre-disposing factors for dysphagia in the elderly
Physiologic effects of aging: hearing
Presbyacusis –> loss of ability to perceive or discriminate sounds as one ages. Age of onset & pattern may vary
TCAs in elderly
Nortriptyline (Pamelor) is preferred due to fewer anticholinergic effects, decreased sedating effect, & causes less orthostatic hypotension (which is a result of alpha-1 blockade)
Amitryptiline (Elavil) should be used in agitation in elderly
Benefits of pulmonary rehab
- Improvement in exercise tolerance, symptom-limited O2 consumption, work output, & mechanical efficiency
- Exercise increases arterial venous O2 (AVO2) difference by increasing O2 extraction from arterial circulation
- Reduction in dyspnea & RR at rest & at various levels of activity
- Improvement in general QoL, decreased anxiety & depression, as well as improvement in the capacity to perform ADLs
- Improvement in ambulation capacity
- Decreased hospitalization rates/reduced healthcare resource utilization
- Focus on conditioning peripheral musculature to improve efficiency & reduce stress on heart & lungs
Who benefits the most from a pulmonary rehab program?
Respiratory limitation of exercise at 75% of predicted maximum O2 consumption
Obstructive airway disease with FEV1 <2000 mL or FEV1/FVC <60%
Restrictive lung disease or pulmonary vascular disease with carbon monoxide diffusion capacity <80% of predicted value
Classification of functional pulmonary disability: Moser classification
1 –> normal at rest, dyspnea on strenuous exertion
2 –> normal ADL performance, dyspnea on stairs/inclines
3 –> dyspnea with certain ADLs, able to walk 1 block at slow pace
4 –> dependent with some ADLs, dyspnea with minimal exertion
1-4 –> NO dyspnea at rest
5 –> housebound, dyspnea at rest, in need of assistance with most ADLs
Active muscle during inspiration
Diaphragm, innervated by phrenic nerve
Contraction of diaphragm increases the volume & decreases intra-thoracic pressure –> decrease in intra-thoracic pressure relative to atmospheric pressure –> inspiration
Lung voume definitions
Vital capacity (VC) –> greatest volume of air that can be exhaled from the lungs after maximum inspiration
Forced vital capacity (FVC) –> VC measured with the patient exhaling as rapidly as possible
Maximal mid-expiratory flow rate –> average flow rate, between 25-50% of FVC
Total lung capacity (TLC) –> amount of gas within the lungs at the end of maximal inspiration
Tidal volume (TV) –> amount of gas moved in normal resting inspiratory effort
Functional residual capacity (FRC) –> amount of gas in lungs at end of normal expiration
Residual volume (RV) –> amount of gas in the lungs at end of maximal expiration
Maximal voluntary ventilation –> max volume of air exhaled in a 12-second period in liters per second
Maximal static inspiratory pressure (PI max) –> static pressure measured near residual volume after maximum expiration
Maximal static expiratory pressure (PE max) –> static pressure measured near total lung capacity after maximal inspiration
Minute volume –> volume of gas inhaled or exhaled per minute
Maximal O2 consumptions
Expired gases during maximal exercise are collected & analyzed for O2 content
VO2 max: maximal volume of O2 that can be utilized in 1 minute during maximal or exhaustive exercise
VO2 max is measured in mL of O2 in 1 minute per kg of body weight
Fick equation:
VO2 max = (HR x SV) x AVO2 difference
So, increasing amount of O2 that gets extracted from arteries increases VO2 max
Individual VO2 max is dependent on body weight, age (peak is ~20 years), sex (values for females are 70% of males), & inherent genetics (the most important)
Training or the presence of pathological conditions can affect this potential
Endurance exercise training increases VO2 max, CO, & physical work capacity of untrained healthy individuals
COPD
C/b increased airway resistance due to bronchospasm, which may result in air trapping, low maximum mid-expiratory flow rate, & normal to increased compliance
Possible V/Q mismatching resulting in hypoxemia
Can be a/w increased airway resistance, impaired expiratory airflow, & respiratory muscle fatigue. Flattening of the diaphragm seen on CXR due to increased total & residual lung volumes
Types of COPD
Chronic bronchitis
Emphysema
CF
Asthma
COPD: emphysema
Distention of air spaces distal to the terminal non-respiratory bronchioles with destruction of alveolar walls, 2/2 unimpeded action of neutrophil-driven elastase
Destruction of the alveolar wall elasticity –> loss of lung recoil, leading to excessive airway collapse on exhalation & chronic airflow obstruction
Decreased gas exchange surface area of the lung (alveolar membranes in a/w V/Q mismatch causes hypoxemia)
Chronic increase in pulmonary vascular resistance in the presence of pulmonary tissue hypoxia can lead to severe pulmonary artery hypertension & RV heart failure
O2 is the only proven therapy that improves mortality in hypoxemic patients
COPD: CF
AR disease involving the chloride ion channels found in exocrine glands. Respiratory involvement is caused by failure to adequately remove secretions from the bronchioles, resulting in widespread bronchiolar obstruction & subsequent bronchiectasis, overinflation, & infection
Aerobic exercise for CF patients helps to increase sputum expectoration. Patients have increased ciliary beat with improved mucous transport
Aerobic exercise also improves exercise capacity & respiratory muscle endurance, & reduces airway resistance by facilitating expectoration of retained secretions
Chest PT can help to mobilize airway secretions
SMA syndrome
3rd part of the duodenum is intermittently compressed by overlying SMA –> GI obstruction
Predisposing factors:
- Rapid weight loss (decrease in protective fatty layer)
- Prolonged supine position, most common in tetraplegia
- Spinal orthosis
- Flaccid abdominal wall causes hyperextension of the back
Symptoms: post-prandial n/v, bloating, abdominal pain
Diagnosis: upper GI series demonstrates abrupt duodenal obstruction to barium
Treatment: typically conservative
- Eat small, frequent meals in upright position
- Lie in left lateral decubitus after eating
- Metocopramide (Reglan) to stimulate motility of upper GI tract (primarily stomach)
- Rarely requires surgery. If conservative treatment fails, surgical duodenojejunostomy should be performed
Any condition that decreases the normal distance between the SMA & aorta may result in compression of the duodenum –> nutcracker effect
General guidelines to assessing functional limitations of COPD patients based on PFTs
When the predicted FEV1 is close to 4L, the patient should NOT have a h/o significant exercise impairment
Impairment usually develops when FEV1 falls below 3L/second, but is variable
- FEV1 between 2-3L/second –> mild exercise limitation, able to walk long distances but not at high speed
- FEV1 between 1-2L/second –> moderate degree of exercise impairment, intermittent rest periods are required to walk significant distances or to climb stairs
- FEV1 <1L/second –> severe exercise impairment, very short-distance ambulation
Restrictive lung disease
Impaired lung ventilation due to loss of normal elastic recoil of the lungs or chest wall, can be a/w respiratory muscle dysfunction or stiffness of chest wall or lung tissue itself, thereby resulting in increased work to breathe
A/w variable levels of hypercapnia or hypoxia
Almost all lung volumes are decreased & flow rates are increased owing to loss of compliance
Causes of restrictive lung disease
Intrinsic lung disease (stiffness of lung tissue) –> can lead to pHTN, RV hypertrophy, & cor pulmonale; examples are sarcoid, asbestosis, silicosis, & IPF
Extrinsic lung disease (stiffness of chest wall)
NM diseases –> DMD, ALS, GBS, MG; weakness of respiratory muscles impairs the bellowing activity of the chest wall, limiting ventilatory capacity & causing hypoventilation
Thoracic deformities –> if scolitoic angle >90, patients have dyspnea; if >120, will have hypoventilation & may have cor pulmonale
Pleural disease
Ankylosing spondylitis –> limited expansion of chest wall
Cervical SCI
Obesity
Surgical removal of lung tissue
DMD pulmonary effects
X-linked recessive
Atelectasis 2/2 hypoventilation & PNA can occur
No clear guidelines have been established for determining the point at which vent support should be instituted in patients with DMD, but suggestions:
- Dyspnea at rest
- 45% predicted VC
- Maximal inspiratory pressure <30% of expected
- Hypercapnia
PFT volume changes
Normal changes noted with age: decreased VC, maximal voluntary ventilation, FEV1 (decreases at a rate of 30 mL/year, PO2. NO change in TLC or PCO2. Will see INCREASE in RV & FRC
Obstructive lung disease: air trapping occurs. Limitation in expiration before air is fully expired. Flattening of diaphragm is increased. Impaired gas exchange as a result of air trapping leads to respiratory muscle fatigue. Decreases in VC, FEV1 (decreases 45-75 mL/year), maximal voluntary ventilation, & FVC. INCREASE in RV, FRC, TLC
Restrictive lung disease: all volumes are decreased. Increased stiffness of lung & elastic work of breathing. Decreases in VC, TLC, RV (although this is increased in cervical SCI), FRC, FVC, maximal voluntary ventilation. FEV1 is NORMAL
What PFT should be followed in ALS?
FVC –> best prognostic indicator for non-invasive ventilation
Once below 50% of predicted –> risk of imminent respiratory failure & need for vent
If symptoms begin with limb weakness, the disorder may progress to respiratory failure in 2-5 years
Earliest changes noted are decreases in maximum inspiratory & expiratory muscle pressures, followed by reduced VC & maximum breathing cpacity
When VC falls to 25 mL/kg, the ability to cough is impaired
Pulmonary changes in C 5 tetra
Diaphragm remains intact & expiratory muscles are paralyzed
Patients retain approximately 60% of their inspiratory capacity & ventilate well, but have weak cough & difficulty clearing secretions during respiratory infections
All volumes are greatly reduced because of limited expansion of the chest wall (although with increased RV)
In SCI patients, the abdominal contents sag due to greater strength of the diaphragm relative to weakness of the abdominal wall muscles. This decreases diaphragmatic excursion & the VC in the sitting position. This improves with use of abdominal binder
One goal of pulmonary rehab for these patients is to increase VC
Rehab of the COPD patient: pharmacologic optimization prior to rehab program
For dyspnea & to decrease exacerbations of COPD:
- Inhaled anti-cholinergics (ipratropium, umeclidinium bromide, tiotropium) –> block muscarinic receptors
- Short-acting inhaled beta-2 agonists
Young patients with moderate asthma, who have tried B2 agonists during exercise as well as mast cell stabilizers or leukotriene inhibitors, may benefit from theophylline use for EIA/bronchospasm
Rehab of the COPD patient: supplemental O2 use
Recommended for patients who desat during exercise. Use if exercise-induced SaO2 falls below 90%
Benefit of home O2: reduction of polycythemia, improvement in pHTN, reduction of the perceived effort during exercise, prolongation of life expectancy, improvement in cognitive function, reduction in hospital needs, decreased BP & pulse in patients with COPD who have increased sympathetic activity & reduced baroreflex sensitivity
Rehab of the COPD patient: training in controlled breathing techniques
Used to reduce dyspnea, reduce work of breathing, & improve respiratory muscle function & pulmonary function parameters
Different types may be used in patients with obstructive pulmonary disease & restrictive disease
Diaphragmatic breathing benefits: increased TV, decreased FRC, & increase in maximum O2 uptake
Pursed lip breathing:
- Patient inhales through nose for a few seconds with mouth closed, then exhales slowly for 4-6 seconds through pursed lips. Expiration lasts 2-3x as long as inspiration
- By forming a wide, thin slit with the lips, the patient creates an obstruction to exhalation, slowing the velocity of exhalation & increasing mouth pressure
- Benefits: prevents air trapping due to small airway collapse during exhalation & promotes greater gas exchange in the alveoli. Increases TV & reduces dyspnea & work of breathing in COPD patients. When added to diaphragmatic breathing, it reduces the RR & can improve ABGs
Rehab of the COPD patient: secretion mobilization techniques (positions for postural drainage)
Commonly used position is Tberg (feet higher than head) in supine or prone
To drain upper lobes: patient is sitting up
- Exceptions: right anterior segment- place patient supine, lingular- place patient in lateral decubitus Tberg, both posterior segments- place patient prone
To drain the right middle & lower lobes: lateral decubitus Tberg
- Exceptions: superior segment of lower lobe- place patient prone with butt elevated, posterior lower segment- place patient prone Tberg with butt elevated, anterior segment- supine Tberg
Precautions: COPD patients can only tolerate up to 25 degree tilt
Avoid in: pulmonary edema, CHF, HTN, dyspnea, abdominal problems- hiatal hernia, obesity, recent food ingestion, abdominal distension
Side-lying contraindications: axillofemoral bypass graft, MSK pain (like rib fractures)
Postural changes in COPD
Not only help with secretion mobilization but also affect work of breathing by changing the mechanical load on respiratory muscles & O2 supply/consumption in these areas
Mechanical load: weight of the pulmonary tissue also contributes to overall pressure on the most dependent alveoli. The dependent alveoli expand in size when changing from sitting to supine, increasing ventilation at base of lung
Blood flow: difference in blood flow distribution is based on the pressure affecting the capillaries
Zone 1 (top): good ventilation, bad perfusion
Zone 2 (middle): ventilation & perfusion are fairly equal
Zone 3 (base): most-gravity dependent region of the lung where pulmonary artery pressure > pulmonary venous pressure > alveolar pressure –> perfusion > ventilation
When changing from sitting to supine, venous pressure increases in relation to arterial pressure in dependent areas of the lung
Rehab of the COPD patient: secretion mobilization techniques (chest therapy program peri-operatively)
Pre-op & post-op chest therapy program:
- Decreases incidence of PNA
- Reduces probability of developing post-op atelectasis following thoracic & abdominal surgery
Rehab of the COPD patient: instruction on reconditioning exercises
Aerobic exercise in patients with CF: exercises involving the trunk muscles (sit ups), swimming, jogging)
Patients with CF that participate in a structured running program show significant improvements in exercise capacity, respiratory muscle endurance, & a reduction in airway resistance. Also see increased sputum expectoration & an improvement in lung function after several weeks of strenuous regular aerobic exercise
Uses of glossopharyngeal breathing (controlled breathing technique for restrictive lung disease)
Enables patient to breathe without MV (up to 4 or more hours if the lungs are normal; if lungs are affected, may only tolerate minutes). This time off the ventilator can be used to transfer to different types of aids
Improves volume of voice & rhythm of speech, allowing patient to shout
Helps prevent micro-atelectasis
Allows patient to take deeper breaths for more effective cough
Improves or maintains pulmonary compliance
Use of non-invasive ventilation for restrictive lung disease: positive pressure body ventilator
Intermittent abdominal pressure ventilator (IAPV)
Examples: Pneumobelt (BachBelt), exsufflation belt
- Abdominal corset containing a battery-operated rubber air sac is cyclically inflated & deflated by a portable vent that delivers 2.5 L of air at a time. When the air sac inflates, it compresses the abdomen, causing the diaphragm to move upwards & assist with expiration
- With cessation of air flow, the sac empties & the diaphragm descends due to gravity, causing inhalation. Inhalation is mostly passive & dependent on gravity –> only useful in sitting or standing. A trunk angle of 30 degrees or more from horizontal is necessary for it to be effective, but 75 degrees is optimal
- Device is worn from the xiphoid to above pelvic arch. Cycles are 40% inspiration & 60% expiration. About 250-1,200 mL of TV can be provided
- This is the most useful mode of ventilation for wheelchair-bound patients with <1 hour of vent-free time during the day
- Benefits also include liberating the mouth & hands for other activities
- Contraindicated in severe scoliosis & severe obesity. Patient should have a mobile abdomen
- Not useful in patients with decreased pulmonary compliance or increased airway resistance
- Most beneficial when used during the day in addition to nocturnal non-invasive IPPV. Inspiration may be supplemented by the use of available inspiratory muscles and/or glossopharyngeal breathing
Use of non-invasive ventilation for restrictive lung disease: positive & negative pressure body ventilator
Rocking bed
- Rocks the patient along a vertical axis (15-30 degrees from the horizontal) utilizing gravity to assist ventilation
- When the head of the bed is up, inspiration is assisted by using gravity to pull the diaphragm down –> negative pressure
- With head down, exhalation assist is obtained. Cephalad movement of the abdominal contents pushes the diaphragm up with production of positive pressure
- Used for patients with diaphragm paralysis with some accessory muscle function
- Benefits: prevents venous stasis, improves clearance of bronchial secretions, weight-shifting prevents pressure ulcers, benefits bowel motility, easy to apply
- Disadvantages: heavy (not portable), not effective in patients with poor lung or chest wall compliance or in those with increased airway resistance
Fenestrated vs non-fenestrated tubes
Fenestrated:
- Good for patients who are able to speak & require only intermittent ventilatory assistance
Non-fenestrated:
- If patient wants to talk, a one-way talking valve may be used on the trach tube. These devices open on inhalation & close during exhalation to produce phonation
Talking trach tubes versus speaking valves
Speaking trach tubes –> Portex Talk tube, Bivona Fome-cuff with side-port airway connector, Communi-Trach
- Used in alert & motivated patients, who require an inflated cuff for ventilation & who have intact vocal cords & ability to mouth words
- Distinguishing characteristic of talking trach’s is that the cuff remains inflated at all times so patient is able to speak while maintaining a closed system for ventilation
- Talking tach’s contain a gas line with an external thumb port. When the thumb port is occluded, gas passes through the larynx via small holes above the inflated cuff, allowing patient to speak
- Quality of speech is altered (lower pitch, coarser, low whisper) & some patients may not be able to produce adequate voice even with practice. Patients need to speak short sentences (because constant flow through the vocal cords can cause the voice to fade away)
- Patient requires manual dexterity & some strength to occlude the external port
One-way speaking valves (Passy-Muir speaking valve, Olympic Trach Talk)
- PMV is the only valve that has a biased, closed position; opens only on inspiration
- All the other valves are open at all times until they are actively closed during expiration (when enough force is placed)
- Air is directed into the trachea & up through the vocal cords, creating speech as air passes through oral & nasal chamber
- Requires less work- opening & closing the valve is not needed
- Indications: patient awake/alert/attempting to communicate, medically stable & able to exhale efficiently & completely around the tracheostomy tube/upper airway, able to tolerate complete cuff deflation, able to tolerate speaking valve trial
- Contraindications: unconscious/comatose patients, vocal cord paralysis in adducted position, inflated trach tube cuff of any kind, foam-filled cuffed trach tubes (may cause airway obstruction), severe airway obstruction, laryngeal stenosis, or tracheal stenosis
Speaking valve trial
Cuff must be completely deflated when PMV is on. Failure to deflate can cause immediate respiratory distress. Uncuffed trach tube is recommended
Assess vitals –> monitor breathing sounds (should remain same after PMV placement); decreased breath sounds or prolonged expiratory phase indicate possible airway obstruction –> slowly deflate cuff & allow patient to adjust to this –> proceed with PMV placement
Trach suctioning complications
Bleeding, infection, atelectasis, hypoxemia, CV instability (dysrhythmias & in extreme cases cardiac arrest & death), elevated ICP, lesions to tracheal mucosa
Which phase of the cardiac rehab program is the convalescent stage following hospital discharge?
Phase II
This period is the most closely monitored phase of rehab
Exercise physiology
Total O2 consumption (VO2) –> O2 consumption of the whole body. Corresponds to work of the peripheral skeletal muscles rather than myocardial muscles
Aerobic capacity (VO2 max) –> maximum O2 consumption that an individual can achieve during exercise. As person increases exercise, VO2 increases in a linear fashion until it levels off & reaches a plateau despite further increases in the workload. This is the aerobic capacity of the individual. Usually expressed in mL of O2 consumed per kg of body weight per minute (mL O2/kg/min). Provides good measure of dynamic work capacity as well as CV fitness. Provides info regarding prognosis in patients with heart disease & can assist in evaluating work resumption after recovery. Treadmill or leg cycle ergometer testing is primarily used to estimate VO2 max
Myocardial O2 consumption (MVO2) –> actual O2 consumption of the heart (like myocardial workload). Can be measured directly with cardiac cath. In a clinical setting, can use rate pressure product (AKA double product) to estimate this value = SBP x HR
Fick equation: VO2 max = CO x AVO2 difference
Metabolic equivalent (MET) –> ratio of working metabolic rate to basal (resting) metabolic rate. 1 MET is 3.5 mL O2 consumed per kg of body weight per minute. 1 MET is the energy consumption while at basal metabolic rate (seated rest)
Outcomes of cardiac rehab services
Improvement in exercise tolerance
Improvement in symptoms
Improvement in blood lipid levels
Reduction of cigarette smoking
Improvement in psychosocial well-being & stress reduction
Reduction in mortality
Safety
Graded exercise testing
Assesses the patient’s ability to tolerate increased physical stress. Can be used for diagnostic, prognostic, & therapeutic application, with or without addition of radionuclide or echo
Cardiac rehab professions usually use these as functional rather than diagnostic tools
Can also provide useful info when applied to risk stratification models. Allow establishment of appropriate limits & guidelines for exercise therapy & the assessment of functional change over time
Sub-maximal graded exercise testing is recommended for inpatients & prior to outpatient cardiac rehab programs
These may be sub-maximal or maximal relative to patient effort in addition to common indications for stopping the exercise test. Endpoint criteria for sub-maximal testing may include HR limits, perceived exertion, & pre-determined MET levels
Most of the ADLs in the home environment require <4 METs
AHA suggests a HR limit of 130-140 bpm for patients not on BB agents, or a Borg Rating of Perceived Exertion of 13-15 as additional criteria for low level testing (serves as baseline for ambulatory exercise therapy). Frequency of the test should be relative to the patient’s clinical course rather than a fixed schedule
Exercise testing protocols
Can use treadmill, cycle, or arm ergometer
LE amputees can use arm ergometers
Treadmill testing provides a more common form of physiologic stress (like walking), in which subjects are more likely to attain a slightly higher VO2 max & peak HR
Cycle ergometer has the advantage of requiring less space & generally is less costly than the treadmill. Minimized movements of the arm & thorax facilitate better quality EKG recording & BP monitoring
To perform a stress test in an AKA, an upper extremity ergometer is used
Balke-Ware protocols that increase metabolic demands by 1 MET per stage are appropriate for high-risk patients with functional capacity <7 METs
Bruce protocol
Metabolic demands of >2 METs per stage may be appropriate for low-intermediate risk patients with functional capacity >7 METs
Bruce protocol allows 2-3 METs per stage with stable patients with functional capacities of 10 METs
Pharm stress testing in debilitated patients for whom exercise testing cannot be performed has been used to evaluate ischemia. The data from this CANNOT be used in exercise presumption
Physical activity program & associated METs
Slow walk –> 2-3 METs (2 mph)
Regular speed walk –> 3-4 METs (3 mph)
Very brisk walk –> 5-6 METs (4 mph)
Sex –> 3-4 METs (if reaching 5-6 METs on stress testing without ischemia or arrhythmias, can resume normal sexual activities without risk
Outdoor work (shovel snow, spade soil) –> 7 METs
Jog –> 9 METs (5 mph)
Sex after MI
Cleared after 2 weeks
Intercourse is as physically intense as climbing 2 flights of stairs
Intercourse with familiar partners in a known environment requires 4 METs
Target HR for exercise intensity
HR range based on the clearance HR. There are 3 main methods of measuring target HR:
1. Clearance HR method
2. Age-predicted method
3. Karvonen method
Target HR is 70-85% of the maximum HR
Clearance HR is the clinical maximum HR attained on stress test
- For the CARDIAC patient, max HR is obtained based on max HR achieved on exercise stress test (clearance HR) –> 70% of max HR attained on exercise stress test
- For HEALTHY patient, the max HR is gotten via age-predicted formula (220-age), but still using the 70-85% of that number; has the potential for over & underestimating the actual exercise intensity; can place patients with heart disease at risk for exercise-induced CV complications
Karvonen method uses the subject’s potential HR increase & assumes that the resting HR represents zero intensity
- Target HR = 0.70 to 0.85 (max HR - resting HR) + resting HR
- Useful for those on chronic BB or with abnormally high resting HR
Borg Scale of Ratings of Perceived Exertion
Linear scale of rating from 6-20. Valid indication of physical exertion & correlates linearly with HR, ventricular O2 consumption, & lactate levels
The new exerciser can proceed with exercise to level 13 (somewhat hard) provided they have been given clearance to do so from the exercise stress test
AHA suggests a HR limit of 130-140 bpm for patients not on BB, or Borg RPE of 13-15 as an additional point criteria for low-level testing
6: no exertion at all
9: very light
11: light
13: somewhat hard
15: hard (heavy)
17: very hard
19: extremely hard
20: max exertion
Duration & frequency of exercise
ACSM recommends that in order to develop & maintain comprehensive physical fitness, healthy adults need to engage in:
- Moderate cardio-respiratory exercise for 30 minutes or more for 5 or more days a week
- Vigorous cardio-respiratory exercise 20 minutes or more 5 or more days a week or combination of moderate-vigorous exercise to achieve a TEE of 500-1000 MET minutes per week
- Resistance & neuromotor exercise involving balance, agility, & coordination 2-3 days a week. Adults can benefit from exercising in amounts less than recommended
Cardio-respiratory aerobic exercise:
- Freq: >/= 5 days/week of moderate exercise or 3 or more days per week of vigorous exercise, or a combo on 3-5 days or more per week
- Intensity: moderate and/or vigorous intensity for most adults; light-to-moderate intensity exercise may be beneficial in de-conditioned patients
- Time: 30-60 minutes per day (150 minutes per week) of purposeful moderate exercise or 20-60 minutes per day (75 minutes per week) of vigorous exercise, or a combination
- Type: regular, purposeful exercise that involves major muscle groups & is continuous & rhythmic in nature
- Volume: increase steps to 2000 or more daily to reach 7000 or more per day
- Pattern: may be performed in one continuous session per day or broken up into 10 minutes or more to get to desired duration & volume. <10 minutes may be helpful in very de-conditioned people
- Progression
Resistance exercise: each major muscle group should be performed on 2-3 days per week
Flexibility: 2-3 days a week or more
Neuromotor exercise training: 2-3 days a week or more; balance, agility, coordination, & gait. Proprioceptive exercise training (tai chi, yoga)
ACSM recommends that exercise intensity be prescribed within a range of 70-85% of maximal HR, 50-85% of VO2 max, or 60-80% of maximal METs. Lower intensities elicit a favorable response in low-fit individuals, inpatients, & people with MSK pain
Orthotopic heart transplant
Consists of over 99% of all cardiac transplants
Orthotopic bicaval technique is the preferred method & makes up 75% of all OHT –> donor heart is excised with intact RA & a long segment of the SVC. Donor heart LA is sutured to the stump of the 4 pulmonary veins in the recipient. The superior & inferior vena cavae are sutured to the recipient atrial cuff & the great arteries are anastamosed
Heterotopic heart transplant
Less than 1% of all heart transplants
Recipient heart is left in place to assist the donor heart
Physiologic response after heart transplant
Transplanted hearts are denervated & lack vagal innervations & central regulation (parasympathetic tone) –> lack vagal inhibition to the SA node –> resting tachycardia of 100-110 bpm
Loss of sympathetic innervation results in circulating catecholamines acting on the chronotropic response –> delayed HR response to exercise. Peak HR is 20-25% lower than controls
Patients have HTN 2/2 renal effects of calcineurin inhibitors & prednisone from maintenance medication regimens. Diastolic dysfunction may be present in some patients
Altogether result in reduced work output & O2 by 1/3 compared to controls
Summary: catecholamine-induced inotropy is reported during peak dynamic exercise in denervated patients
- High resting HR due to parasympathetic denervation
- Lower peak exercise HR
- Resting HTN is common, caused in part by the renal effects of anti-rejection meds
- Slower return to resting HR post-exercise
- At maximum effort, the work capacity, CO, SBP, & VO2 are lower
After transplant, the 1-year survival is 90%. 5-year is 70%. 20-year is 20%
Accelerated atherosclerosis occurs following transplantation
Exercise prescription for heart transplant patient
Standard HR guidelines are NOT used
Intensity of exercise is based on the following:
- Borg RPE scale 11-14
- Percentage of VO2 max or maximum workload performed on stress test
- Anaerobic threshold
- Duration, frequency, & types of exercise follow the same principles as those with other types of cardiac problems
During exercise testing, heart transplant patients with cardiac ischemia do not present with typical symptoms of angina. Instead, EKG changes & other symptoms should be followed
How does exercise improve PAD & walking economy?
By increasing bio-mechanical & metabolic efficiency
How do amputees compensate for the increase in energy consumption with ambulation?
By using slower speeds to keep the rate of energy expenditure stable
Energy cost of ambulation for the amputee
Based on the % increase above the cost of normal ambulation at 3 METs
No prosthesis with crutches –> 50% increase –> 4.5 METs
Unilateral BKA with prosthesis –> 9-28% increase –> 3.3-3.8 METs
Unilateral AKA with prosthesis –> 40-65% increase –> 4.2-5.0 METs
Bilateral BKA with prosthesis –> 41-100% increase –> 4.2-6.0 METs
Unilateral BKA + contralateral AKA –> 75% increase –> 5.3 METs
Bilateral AKA with prosthesis –> 280% increase –> 11.4 METs
Unilateral hip disarticulation –> 82% increase –> 5.5 METs
Hemipelvectomy with prosthesis –> 125% increase –> 6.75 METs
