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
