מבחן ריאשון Flashcards
1
Q
Negative Sign
A
which reveal a disorder. This is the absence of what should be present in a normal examination
Absence of what you normally expect to see
a. Non reactive pupils, atrophy, lack of ability to move, absent reflex
b. Parkinsons lose equilibrium reaction for maintaining head, lack normal posturing
2
Q
Positive Sign:
A
which reveal a disorder. This is a finding that should nor be normally present.
- Presence of what you do not normally expect to see
a. Clonus, babinski, dilated pupils, increase DTR reflex, spasticity, rigidity, abnormal posture,
b. TBI muscles firing and not do anything: posturing (not spasticity or rigidity but increased motor output secondary to severe head injury)
3
Q
History: Try to find the Primary Focus of the Problem (8)
A
A. Onset: slow vs. rapid [the time frame, is it related to trauma or a slow progressive onset]
B. Duration: constant vs. intermittent [does it go away at certain times, find out what relieves pain/positional]
C. Course: static or progressive [is it slowly getting better/worse or the constant no matter what]
D. Symptoms: as stated by patient [pain, weakness, muscle spasms]
E. Results of Test: [MRI, Xray, findings of other professionals]
F. What does the patient think is the cause:
G. Past Medical History: [one may cause the other]
H. Related Family History: [genetics]
4
Q
Mental Status:
A
assess during the history taking: evaluates association areas of the cerebral cortex, keep in mind the education level and cultural differences [you must take their SES and education level into account]
A. Orientation
B. Memory
C. Attention, Thought Processes
D. Calculation ability [count back by 7 from 100]
5
Q
Language/Speech:
A
assess during the taking of history
A. Follows and understands: Fluent and non-fluent aphasias
B. Reads, comprehends, names objects
C. Expressive (motor) aphasia (Frontal Lobe)
D. Receptive (sensory) aphasia (Temporal Lobe)
6
Q
Motor Function:
A
Root Distributions (know peripheral nerve and root distributions—be able to differentiate peripheral nerve involvement and a root compression)
7
Q
C5
A
deltoid
biceps
8
Q
C6
A
wrist extension
9
Q
C7
A
triceps
10
Q
C8
A
finger flexion
11
Q
T1
A
intrinsics
12
Q
L1,2,3
A
illiopsoas
13
Q
L2,3,4
A
quadriceps
14
Q
L4,5
A
anterior tibialis
15
Q
L5-S1
A
peroneus longus and brevis
EHL
16
Q
S1
A
gastroc
Soleus
17
Q
Muscle Fasciculation:
what are they
when are they seen
causes
A
- Involuntary muscle twitches of random muscles
- Can be seen normally in everyone (fatigue, nervous
- Positive sign when occur with other positive or negative signs and symptoms
- Can be caused by: Nerve irritation, electrolyte imbalance (nerve will randomly discharge)
(v. s. ALS occurs in many muscles)
sometimes people have random sensory complaints of this nature which can be sensory nerve irritation or electrolyte imbalance
18
Q
Deep Tendon Reflexes:
- 0 =
- 1+ =
- 2+ =
- 3+ =
- 4+ =
what makes the number lower?
what makes the number higher?
Where to test DTR? What NR? • Biceps: • Brachioradialis: • Triceps: • Quads: • Gastrocnemius:
A
know the root distributions and peripheral nerves:
root compression or peripheral makes the numbers lower,
CNS involvement makes the numbers go higher
- 0 = absent
- 1+ = diminished
- 2+ = Normal
- 3+ = Increased
- 4+ = Hyperactive
- Biceps: C5, C6
- Brachioradialis: C5, C6
- Triceps: C7, C8
- Quads: L2-L4
- Gastrocnemius: S1
19
Q
Where to test DTR? What NR? • Biceps: • Brachioradialis: • Triceps: • Quads: • Gastrocnemius:
A
- Biceps: C5, C6
- Brachioradialis: C5, C6
- Triceps: C7, C8
- Quads: L2-L4
- Gastrocnemius: S1
20
Q
Peripheral nerve distribution:
A
peripheral sensations tests peripheral nerves and does not need to be interpreted by the CNS
21
Q
Cortical Sensations:
A
need to be interpreted in the CNS, secondary areas of cerebral cortex of parietal lobe
22
Q
What are the peripheral sensations test?
A
peripheral sensations tests peripheral nerves and does not need to be interpreted by the CNS
a. Light touch
b. Pain and temperature
c. Proprioceptive
d. Vibrations
Test the good side first, and then test the involved side in order to be sure the person understands the testing and the response should be normal
Monofilament sensory testing is calibrated to discriminate between levels of sensation
23
Q
What are the Cortical Sensation tests?
A
need to be interpreted in the CNS, secondary areas of cerebral cortex of parietal lobe
a. Two Point Discrimination
b. Stereognosis (shape held)
c. Graphesthesia (drawn)
d. Bilateral Simultaneous
e. Localization
Test the good side first, and then test the involved side in order to be sure the person understands the testing and the response should be normal
Monofilament sensory testing is calibrated to discriminate between levels of sensation
24
Q
Abnormal Adult Tone and Reflexes:
A
Clasp knife: spasticity: corticospinal tracts
- Resistance and then resistance melts away
- Such as when opening up a pocket knife, or stretching silly putty
Lead pipe: rigidity: Basal Ganglia (ie Parkinson’s)
- Constant resistance throughout the range
- Such as a lead piece
Clonus: Corticospinal
- Can be sustained (continuous beats as long as maintain stretch after the quick movement) or un-sustained (3 beats)
- Both abnormal but different severities
Babinski: (CNS) Corticospinal tracts
Grasp Reflex: Frontal Lobe
1. Stimulation in the palm of hand cause closure of hand
25
Clasp knife:
spasticity: corticospinal tracts
1. Resistance and then resistance melts away
2. Such as when opening up a pocket knife, or stretching silly putty
26
Lead pipe rigidity:
Basal Ganglia (ie Parkinson’s)
1. Constant resistance throughout the range
2. Such as a lead piece
27
Clonus:
Corticospinal
1. Can be sustained (continuous beats as long as maintain stretch after the quick movement) or un-sustained (3 beats)
2. Both abnormal but different severities
28
Babinski:
(CNS) Corticospinal tracts
29
Grasp Reflex:
Frontal Lobe
| 1. Stimulation in the palm of hand cause closure of hand
30
Interpretation of Results and Clinical Implications:
A. Symmetrical distribution is WNL’s
B. Hypoactive Response:
C. Hyperactive Response:
D. Key:
A. Symmetrical distribution is WNL’s
B. Hypoactive Response: decreased responses (peripheral)
C. Hyperactive Response: exaggerated responses (CNS, but immediate stage we see flaccid in spinal shock for SCI when cannot reach threshold)
D. Key: finding a pattern of abnormalities fitting one or more distributions, then fitting this in with the subjective information
31
```
• SEE FLOW CHART: pick one thing and follow through the flow chart and see if it makes sense
o Myopathy (muscular dystrophy ie Duchene’s, Steroid cause muscle weakness)→
```
Weakness→ Motor Complaint (Sensory would be normal)
o Peripheral Nerve or Branch → Anatomic Distribution → Sensory Complaint
o LMN or Peripheral Nerve → Weakness → Motor Complaint
32
Gait
* Scissoring
* Peripheral in severe weakness
* Ataxic gait
* Parkinsons
* Scissoring goes with CNS, high tone of adductors
* Peripheral in severe weakness (not high tone, not narrow base of support—do sensory testing and look at impairments in tibial sural, peroneal/superficial tibial nerve, test sensation, for absent reflexes, no babinski, 0 DTR. Absence of CNS findings)
* Ataxic gait is about placement: if it is cerebellar: reflexes intact, muscle testing intact, sensory intact, all peripheral intact. Do Frankel’s, placing foot on target to practice better control
* Parkinsons: face, hand tremor,
33
Recovery of Function:
A. Effect of Age:
B. Type of Lesion:
C. Prior Experience:
A. Effect of Age: infants and children recover very well to some CNS injuries. Brain plasticity is very real but varies with type of injury.
B. Type of Lesion: small lesions have a better chance of recovery as long as the functional area is not totally lost. Slowly developing lesions allow for a better recovery. (location and size) (a slow growing lesion will allow more ability for brain to slowly accommodate to the changing size and pressure)
C. Prior Experience: greatly enhances recovery. Enhanced environment facilitates better recovery. (someone who had a more challenge to their brain before will recover better. Prior high level learning)
34
Motor System and Motor Control:
Sherrington Reflex Model
Is sensation needed for movement?
Sherrington—Reflex Model (he was a neurophysiologist, grandfather, thought movement to be sensory driven, not always the case but it is an effective tool to help the patient)
1. Sensory stimuli drive movements. Motor output predetermined by a specific type of sensory input.
2. However: Sensation not required for movement
3. Deafferented monkeys function almost normally
a. The study where importance of sensation was looked at, deafferented monkey on one side and with that loss of sensation the monkey didn’t use that side, but in bilateral deafferentation the monkey still used both sides
35
Hierarchical Model:
Movement organized from LOWEST levels in the spinal cord to INTERMEDIATE levels to HIGHER
levels in the cortex control is TOP-DOWN.
1. Movement from higher up in CNS
2. reflex from bottom, control from top from motor cortex, lets get muscles moving an activate primary motor cortex
3. when someone has injury in CNS, lower systems take over because loss of higher inhibitory control (one model says spasticity and clonus when lose inhibition over spinal reflex and reflexes become more exaggerated)
Motor programs drive movement. Reflexes dominate with CNS injuries.
Prevent primitive reflex patterns
Types of reflexes elicited help identify general location of injury
Sophisticated movements at spinal cord level
Motor development is more sensory feedback oriented, not just hierarchical
36
Motor Programming Theories:
engrams
handwriting
apraxia
other factors that influence movement
A. Motor engrams exist and become wired with practice [new movement done slowly and purposefully with trial and error and hardwire a movement pattern to do automatically]
B. Handwriting on paper is similar to writing on a whiteboard [environment changes, task carryover, ie sit to stand and vary height of the chair]
C. Apraxia is loss of ability to execute a movement [lose the ability to tap into the engram and need to relearn]
D. Many other factors influence movement (environment, position, gravity)
37
Systems Model-Bernstein:
A. Are movements are not peripherally or centrally driven?
B. How is finer coordination achieved?
Systems Model-Bernstein: (he came up with degrees of freedom)
A. Movements are not peripherally or centrally driven but an INTEGERATION on many systems in the CNS, PNS, the musculoskeletal system, and the environment
B. Movement involves few or many degrees of freedom. Finer coordination exists as more degrees of freedom are achieved.
(complex movements multiple degrees of freedom, incorporating environment/person etc for how they perform an activity)
38
What is the Motor Homunculus?
1. what areas hive highest areas in the motor humunculus. Can it vary?
2. what has the lowest threshold for activation? what is activated first?
3. what requires more stimulation, primary motor cortec or pre-motor cortex or supplemental motor cortex requires?
1. Areas for highest dexterity have highest area in the motor homunculus, vary based upon individuals use. the same applies in the sensory
2. The primary motor cortex has lowest threshold for activation
- --with use and practice that is the area that gets activated first because it has the lowest threshold
Betz Cells
1 to 1 correspondence between cells and individual AHC’s
3. stimulation of pre-motor cortex or supplemental motor cortex requires more stimulation and produces more complex movements
39
Corticospinal Tract:
1. where does stroke commonly occur, what
2. what determines extremity affected
3. what is recovery based on
Corticobulbar and Corticospinal Tracts:
Stroke commonly internal capsule where Corticospinal Tract fibers go through, if lesion in the INTERNAL CAPSULE
extremity will be affected dependent on WHERE and AMOUNT, there is REDUNDANCY in the motor system, some is outside the internal capsule,
recovery is based on this redundancy and where the stroke was
B. 40-50% of corticospinal tract fibers originate in the primary motor cortex. The majority come from the premotor, supplementary motor areas and the parietal lobe
***Corticospinal Tract: Produce discrete movements and modify indirect motor centers in the Brain Stem
40
___% of corticospinal tract fibers originate in the primary motor cortex
B. 40-50% of corticospinal tract fibers originate in the primary motor cortex. The majority come from the premotor, supplementary motor areas and the parietal lobe
41
Corticospinal Tract:
what it does
***Corticospinal Tract: Produce discrete movements and modify indirect motor centers in the Brain Stem
42
Lesions of the Corticospinal Tracts
what it causes
????
A. Loss of distal extremity strength and dexterity [do not appear flaccid]
B. Babinski Signs
C. Loss of control over Brain Stem Control Centers [loss of high inhibition]
1. Increased Tone—does he want this or spasticity??? [spasticity is velocity dependent increased stretch reflex because not able to inhibit that from the higher centers, and tone is when one muscle is firing and another firing co-activation, cannot selectively recruit prime mover, happens after stroke]
2. Hyperreflexia
3. Clasp-knife phenomenon [increased response to stretch]
43
Lesion Primary motor cortex:
1. weakness or paralysis.
| 2. Hypotonia (decreased tone) and chronic change in tone.
44
Lesion Sensory Cortex:
1. loss of sensation,
2. loss of perception,
3. loss of proprioception,
4. problems with motor control. 5. Loss of dexterity.
(in deficits with sensory may not be aware of sensation, may be impaired, may not be able to interpret sensation)
45
Lesion Premotor Cortex:
1. weakness from disuse,
2. difficulty with planning motor tasks,
3. apraxia.
Anticipating motor needs based upon sensory information. [not pure flaccidity]
46
Lesion Supplemental Motor Region:
1. weakness from disuse,
2. difficulty with complex motor tasks.
3. difficulty with programming and planning movements.
4. Motor apraxia.
47
Lesion Basal Ganglia:
absence of movement, weakness from disuse, abnormal movements (chorea, tremor), or abnormal tone (rigidity) [not the primary motor system, ie Parkinson’s]
48
Lesion Cerebellum
1. incoordination
2. weakness from disuse
3. balance problems
4. changes in tone
49
Spinal Cord Injury:
1. UMN signs below the injury
2. LMN signs at the level of injury
3. Therefore: LMNL signs locate the level of the SCI
4. Above level of injury things will be normal, below level present with upper motor neuron signs because loss connection between higher motor area and the muscles so everything occurs on a spinal reflex level. At level of injury may have flaccid weakness if anterior horn cell problem (cell body of motor neuron [like in ALS and polio). Weakness or paralysis.
5. Sensation will be intact since this is a motor problem and dorsal root ganglia is fine sensory system is fine.
50
Lesion Alpha Motor Neuron:
(My famous AHC): weakness or atrophy
51
Lesion Muscle
weakness or flaccid: directly affected (muscular dystrophy, myopathy…). The nerve going to it is intact.
52
Afferent Sensory Input:
1. loss of sensory awareness
2. uncoordinated movement
3. balance problems
53
Receptors:
A. distribution is according to function. Consist of free nerve endings or highly specialized receptors.
B. Ex Meissner’s Corpuscles (respond to rapidly moving touch, low vibration) decrease in density in the hand from 40-50/mm^2 to 10/mm^2 by age 50. Decrease responsiveness not necessarily due to peripheral neuropathy.
also density of receptors on the back is less than on the hand
54
Dorsal Columns:
largest, rapid conducting
1. High degree of spatial orientation, Cortical Sensations
2. Lesion results in decreased proprioception, tactile discrimination, balance and coordination deficits, and general function of extremity is decreased. Graphesthesia.
55
Anterior and Lateral System:
pinothalamic. Slow conducting, low spatial orientation. Pain, temperature, crude touch.
1. Redundancy between these two systems is probably responsible for functional recovery after SCI. (dorsal and anterolateral)
56
Sensory Homunculus-
primary and secondary areas (close to 1:1 relationship with density of receptors, importance of sensory info, to area of the sensory cortex of brain—more in face and hands compared to leg or back—loss of interpretation in cortical tests)
A. Spomato-topic orientation in postcentral gyrus
B. The size of each body part representation is proportional to the number of receptors
C. Lesion produces inability to localize different sensations
D. Cannot judge critical degrees of pressure on the body. Unable to judge weights, shapes, texture. [be aware of this for safety]
57
Deficits with Lesions in the Somatosensory Area I:
A. Unable to localize sensations in the different body parts
B. Cannot judge critical degrees of pressure
C. Unable to judge exactly the weights of objects being held (not judge the change, difference)
D. Unable to judge shapes—Asterognosis
E. Unable to judge textures
F. Poor localization of pain and temperature (may think it is more proximal)
58
Peripheral Nerve Lesion:
loss of all sensations in the nerve distribution
59
Peripheral Polyneuropathy:
loss of all sensations in distributions. Distal stocking and glove loss. “Stocking and Glove Distribution” LE gets involved before UE, lower before upper –nerves along it more susceptible to injury (longer nerves)
60
Sensory Root Lesion:
sensory abnormalities in distribution (ex. Root compression in herniated/bulging disc)
61
Posterior Column Lesion:
loss of position sense, vibration sense, stereognosis and 2 point discrimination
62
Complete Spinal Cord Lesion:
loss of all sensation below the level (Aisa)
63
Thalamic Lesion:
loss or decrease all sensations and pain, on entire body on opposite side of lesion (in thalamic stroke where thalamus effected which is relay station for sensation, a stroke there will cause thalamic pain due to lesion in thalamus which is very hard to treat)
64
Sensory Cortex Lesion:
loss of discriminative sensations on entire body on opposite side of lesion
65
what is the motor unit made up of
The motor unit: made up of
1. anterior horn cell which is located in the spinal cord. **Therefore anterior horn cell body is LMN (UMN is anything proximal to the anterior horn cell). Severe involvement will not cause spasticity. .
2. nerve root
3. plexus
4. axon
5. NMJ
6. Muscle it innervates
66
Is anterior horn cell body UMN or LMN?
**it is part of the motor unit, anterior horn cell body is LMN
(UMN is anything proximal to the anterior horn cell).
Severe involvement will not cause spasticity. .
67
Peripheral Neuropathies and Neuromuscular Transmission Deficits
where can they occur?
a. Peripheral Nerve:
b. The motor unit: (anterior horn cell, nerve root, plexus, axon, NMJ, Muscle it innervates)
c. Schwann Cells:
d. The NMJ:
68
Schwann Cells:
what is Wallerian Degeneration
Axon-Schwann Cell becoming a myelinated nerve fiber:
Wallerian Degeneration is breakdown of myelin sheath composed of multiple layers of Schwann Cells
---Myelin sheath around the axon
---Multiple layers of connected sheath that insulates the nerve and helps the AP travel down the nerve
---The AP travels along the node of ranvier (less than 1mm)
69
The NMJ:
what is it
what is collateral nerve sprouting
the end of the motor axon, where myelin sheath ends, last segment not myelinated
--Collateral nerve sprouting when nerve axon sends out new branches to innervate adjacent muscle fibers that became de-innervated
70
Peripheral rediculopathy affects the _____, plexopathy affects the ____
Peripheral rediculopathy affects the nerve root, plexopathy in the plexus
71
Symptoms of Peripheral Neuropathy:
1. Motor: (Weakness, DTR absent, Atrophy, Fibrillations, Fasiculations)
2. Sensory: (numbness, decreased sensation: hypoesthesia, Pins and needles, tingling-paresthesia (large fiber involvement), Burning: dysesthesia (small fiber involvement) [unmyelinated small fibers], Increased Sensitivity: hyperesthesia [sign of nerve coming back], Severe Deficits )
c. Sympathetic: if localized within a limb, then usually neuropathic (Altered sweating, blood flow, temperature (change in autonomic system), Trophic changes—texture, color, smoothness, Hair loss, edema, hyperesthesia (hair loss can also be vascular), Cardiac, GI, GU symptoms )
72
Motor Sx
| Peripheral Neuropathy
1. Weakness,
2. DTR absent (could still be in normal range or decreased)
3. Atrophy (muscle atrophy can be mild, moderate, severe)
4. Fibrillations: muscle fibers: diagnostic EMG will show it, the muscle is discharging randomly by itself without any voluntary effort. Mainly when the muscle gets irritated.
5. Fasiculations: entire motor units randomly discharge, often associated with peripheral neuropathy but can be totally normal
73
Sensory Sx
| Peripheral Neuropathy
1. numbness, decreased sensation: hypoesthesia
2. Pins and needles, tingling-paresthesia (large fiber involvement)
- ---when it re-awakens get the tingling
- ---Tinel’s Sign: a way to detect irritated nerves by tapping over the nerve to elicit pins and needles – see when nerve is re-awaken, nerve regeneration when this occurs
3. Burning: dysesthesia (small fiber involvement) [unmyelinated small fibers]
4. Increased Sensitivity: hyperesthesia [sign of nerve coming back]
5. Severe Deficits: decreased joint position sense and sensory ataxia
- ---Ataxic gait can be related to sensory impairment—test sensation. If it is UE and LE more likely to be cerebellar, especially post stroke, but can have a sensory ataxia. Sensory neuropathy affects proprioception.
74
Sympathetic Sx:
| Peripheral Neuropathy
if localized within a limb, then usually neuropathic
1. Altered sweating, blood flow, temperature (change in autonomic system)
2. Trophic changes—texture, color, smoothness
3. Hair loss, edema, hyperesthesia (hair loss can also be vascular)
4. Cardiac, GI, GU symptoms
75
In peripheral neuropathy get ______sx before _____ sx because those nerves are more sensitive
In peripheral neuropathy get sensory before motor because those nerves are more sensitive
76
Reflex Sympathetic Dystrophy: CRPS Type I (Complex Regional Pain Syndrome I)
etiology
treatment
ETIOLOGY: light splint or cast, localized trauma or surgery, improper use of a sling, not elevating a limb to reduce edema, failure to use the limb after minor episode
1. A small involvement or injury
2. Redness, edema, swelling, pain—disuse—cycle of more painful
TREATMENT for CRPS Type I:
1. use the limb!—try to reverse the overly protective response, desensitize with stimulation that is continuous but low intensity at first , get them to be able to deal with light sensations and not interpret it as pain and slowly increase it over time (they have hypersensitivity or pain on non-painful stimuli), use and get muscles working, try to reverse the whole sequence
2. Reduce edema: get rid of swelling, we do not want stasis of edema and we don’t want the condition to worsen
3. Progressive, intense, multidisciplinary therapy
77
Neurogenic Neuropathy:
(Neurological)
1. Skin dry: peripheral nerve denervation of sweat glands
2. Localized Trophic Changes (shiny skin)
3. Edema can cause nerve compression
- ----General swelling puts pressure on all structures including nerves and they are susceptible to nerve compression, ie if wearing a cast and swelling occurs
78
Vascular Neuropathy:
1. If majority of the limb presents with hair loss, shiny skin, cold
2. Blue skin-venous insufficiency
3. Pale skin—arterial insufficiency
***We can use a doppler to check pulse
79
Neurapraxia:
what is it
what causes it
when recover
mechanism
how to treat
local conduction block
1. Usually mechanical compression:
- --Mild compression, usually intermittent compression.
- --Not systemic
- --Common nerve compression: herniated disc, carpal tunnel syndrome
2.. Mechanism:
---First:
compression cause vein collapses-->
poor vascularity to area of nerve= hypoxia nerve--->
nerve less functional sensory complaints first
---Second:
the capillary walls breakdown and fluid leaks in--->more pressure (increase pressure like mini compartmental syndrome)
---Third: Intraneural fibrosis, secondary fibroblast proliferation and resultant NEUROPRAXIA --more breakdown of the nerve itself
3.. Recovery starts in less than 1 minute. After release:
As a PT try to recognize this, we want to get rid of the cause of the compression.
***Removal of compression, nerve re-waken within a minute
80
Mechanism: Neurapraxia:
---First:
due to the compression the vein collapses,
poor vascularity to that area of the nerve due to localized mechanical compression causes hypoxia to the nerve
which will lead to the nerve becoming less functional, sensory nerve first affected, sensory complaints
---Second:
the capillary walls breakdown and fluid leaks in,
get more pressure on the nerve like a mini compartmental syndrome, increased pressure like mini compartment syndrome
---Third:
Intraneural fibrosis, secondary fibroblast proliferation and resultant neuropraxia --more breakdown of the nerve itself
81
Axonotomesis:
damage to axon with Wallerian Degeneration
1. Demyelination with axonal degeneration
2. >6 hours of continuous compression—this is due to the compression lasting continuously more than 6 hours or it could also be due to compression of higher intensity of less duration
3. true anatomical changes to the nerve as each single nerve axon goes through wallerian degeneration due to prolonged compression and prolonged anoxia
4. sensory more here too
5. axons may take weeks or months to heal if remove the compression source
82
Axonotomesis:
damage to axon with Wallerian Degeneration
Demyelination + axonal degeneration
1. CAUSE:
>6 hours of continuous compression
or compression of higher intensity of less duration
2. wallerian degeneration due to prolonged compression and prolonged anoxia :
anatomical changes to the nerve
sensory more here too
5. axons may take WEEKS or MONTHS to heal if remove the compression source
83
Neurotmesis
damage to axon and one or more protective sheaths
***Poor prognosis for recovery
Damage to nerve axon and surrounding sheaths that surround each axon
More derangement to internal architecture of peripheral nerve, more internal sheaths start to break down, and in the healing process when connective tissue is healing, get more scar tissue
Levels of Neurotmeseis severity based on which sheaths around axons or fascicles of nerve are involved
84
Neurotmesis
mechanism
damage to axon and one or more protective sheaths
1. External sheath contains fascicles or bundles of axons with an external sheath and each axon has a sheath around it as well—well insulated and compartmentalized
2. Compression cause localized conduction block nothing happens to sheaths, but if the perinurium breaks down the axons are all over the place and some individual axons and their external sheaths will break down:
more attempt to heal but more scar tissue development.
If get peripheral nerve injury, trauma to nerve, especially if need to surgically re-attach the two ends of the nerve, that is where biggest prob for recovery will the proximal nerve axons find their way to the distal tube or sheath to regenerate it.
It is hard for a surgeon to attach the proximal perfectly to the distal—avoid surgery unless very necessary.
85
Diagnosis of Peripheral Neuropathies:
1. Motor: peripheral nerve distribution vs. root distribution vs. plexus distribution
- --ulnar vs nerve root C7,8
- --MMT to see pattern of weakness
2. Sensory: in what distribution are the sensory complaints?
3. Nerve conduction studies:
4. EMG: more sensitive looking at the electric activity of MU of muscle at rest and contraction –see if innervated and if normal ie myopathy vs neuropathy, and if neuropathy, where is the nerve affected
86
Manifestations of Peripheral Neuropathies:
sensory vs motor
prox vs distal
1. Sensory greater than motor (sensory is more common and earlier on)
2. Distal greater than proximal –due to loss of axoplasmic flow: degeneration starts distally, proceeds proximally. “Dying back phenomena”
1. LE affected before UE affected because LE nerves are longer
2. Distal segment of nerve affected because the axoplasmic flow from anterior horn cell is affected, since flow proximal to distal, the distal segment is affected first. (can see a backup of axoplasmic flow if compress nerve). Need axoplasmic flow. Affects nerve and muscle.
3. Dying back phenomena: becoming more severe
87
Is sensory or motor more in peripheral neuropathy?
Sensory greater than motor (sensory is more common and earlier on)
88
Is distal or proximal more affected in peripheral neuropathy?
Distal greater than proximal –due to loss of axoplasmic flow: degeneration starts distally, proceeds proximally. “Dying back phenomena”
1. LE affected before UE affected because LE nerves are longer
2. Distal segment of nerve affected because the axoplasmic flow from anterior horn cell is affected when the nerve is affected and don’t have the axoplasmic flow flowing down the nerve axon when damage to anterior horn cell. Since flow proximal to distal, the distal segment is affected first. (can see a backup of axoplasmic flow if compress nerve). Need axoplasmic flow. Affects nerve and muscle.
3. Dying back phenomena: becoming more severe
89
Mononeuropathy:
compression, traction, vascular origin ->one nerve is affected due to compression or localized injury (mechanical or vascular, usually mechanical)
Ie carpal tunnel, thoracic outlet, root compression, tarsal tunner
90
Mononeuropathy multiplex:
multiple mononeuropathies
1. This implies discrete lesions of several individual peripheral nerves
2. Often vascular disorders affecting blood supply to peripheral nerves
3. There is one mononeuropathy but then later see the patient and hx of involvement of a nerve and then another nerve that isnt bilateral and symmetrical, they seem to be random: it seems random, but it is due to vascular disorder affecting blood supply to theses specific nerves. Notify the doctor about this.
91
Polyneuropathies:
it may be motor, sensory, sensorimotor, or autonomic
1. Multiple nerves affected, can be symmetrical or bilateral
2. Affect first LE but if etiology progresses it is eventually all four extremities
3. Start as sensory in the LE and then a little more severe going up to knees and then the UE is the classic finding in a systemic disorder of polyneuropathy.
4. Some causes: (see chart) systemic: Diabetes, alcoholism, gulliam barre (polyrediculopathy), toxins
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Plexopathy:
plexus (tumor, trauma)
1. They do not have hx trauma, have more than one nerve affected in the arm, check for thoracic outlet syndrome, look at imaging for tumor putting pressure in brachial plexus
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Radiculopathy:
root (disc, tumor): root compression: can be motor or sensory or both
Dorsal root: herpes zoster = shingles (an example)
Caused by herpes simplex virus / chicken pox that is reactivated
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Common Causes of Neuropathies
1. Metabolic causes: see CIBA, plate #5:
2. Diabetes: most common
3. Drugs: oncology drugs: toxic to the body – may need to change dose, switch medication, notify doctor
4. Alcoholic: alcohol is neurotoxic (alcoholic is CNS inhibitor and stop breathing, don’t have balanced diet)
5. Uremic: dialysis patients. Restless leg syndrome—creeping sensation in legs at night, due to increased concentration of metabolites. This is a sign dialysis is not adequate and getting buildup of toxins which are causing depolarizations of the nerves.
6. Infectious processes:
AIDS (destroys myelin sheath in CNS or PNS. MS type symptoms; weakness, sensory loss)
Herpes Zoster: (shingles): peripheral neuropathy, most common neurotopic viral infection. Affects the posterior root ganglia causing pain and vesicular skin eruption in sensory distribution of the affected nerve. Occasionally affects AHC (5%). Produces severe burning pain.
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Most common cause of neuropathy
diabetes
96
how can drugs cause neuropathy
oncology drugs: toxic to the body – may need to change dose, switch medication, notify doctor
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how can alcohol cause neuropathy
alcohol is neurotoxic (alcoholic is CNS inhibitor and stop breathing, don’t have balanced diet)
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how can dialysis patients get neuropathy
Uremic: dialysis patients.
Restless leg syndrome—creeping sensation in legs at night, due to increased concentration of metabolites.
This is a sign dialysis is not adequate and getting buildup of toxins which are causing depolarizations of the nerves.
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How can AIDS cause neuropathy?
destroys myelin sheath in CNS or PNS. MS type symptoms; weakness, sensory loss
1. CNS presents like MS!
2. PNS presents like peripheral neuropathy
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how can Herpes Zoster cause neuropathy?
Herpes Zoster: (shingles): peripheral neuropathy, most common neurotopic viral infection. Affects the posterior root ganglia causing pain and vesicular skin eruption in sensory distribution of the affected nerve. Occasionally affects AHC (5%). Produces severe burning pain.
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Herpes Zoster
what is the sign
sx
tx
Shingles is a peripheral neuropathy maybe at the root level.
Sign
1. first finding is skin eruptions in distribution of sensory root where the virus has become active again. (rash is contagious)
2. Skin eruptions in the distribution of the root distributions
Sx
3. Ie skin eruptions in distribution of C5. Sensory complaints if motor, ie deltoid. Cannot abduct with deltoid and using upper trap, cannot flex shoulder with deltoid and elbow flex instead.
Eval
4. PT eval: test sensation of whole arm, scattered MMT: if only deltoid maybe axillary nerve, PT indicated for disuse atrophy, tight shoulder almost frozen so maybe painful on movement, check range in shoulder and in whole arm.
Tx
5. Stretch shoulder with Codmans for increase ROM to 90-110 degrees passively forward and back, side to side (upper body supported, use trunk movements to get arm to swing).
Teach self range in supine for gravity to help on 90-180 degrees prolonged stretch. Reps: prolonged stretch less reps. As recover can hold with other arm letting go, bring it up then do eccentric to bring the arm down. As nerve recovers start to work on strengthening again. Then eventually work on all the other shoulder muscles.
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What is the the most common cause of neuropathy in developed countries?
Diabetic Neuropathy
. Its prevalence is as high as 50%.
Can be very painful.
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Types of Diabetic Neuropathy
1. SYMMETRICAL, mainly *sensory* (stocking and glove), some progress to be motor too
2. PROXIMAL, asymmetric predominantly *motor* neuropathy (ex. Femoral):
- -start in DISTAL SEGMENT of nerve of a PROXIMAL NERVE that is affected first and in its most distal muscles first: ie femoral nerve –quadriceps weakness.
3. Can be an ISOLATED or MULTIPLE MONONEUROPATHY:
- --Generally start as a mononeuropathy and then can progress to polyneuropathy
4. An AUTOMATIC neuropathy: sx such as GI because of the nerves innervating the organs
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most common diabetic neuropathy:
Sensory polyneuropathy
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Sensory polyneuropathy
the most common diabetic neuropathy:
1. onset
2. early sign
3. sx
1. Insidious onset
2. Early signs: loss of ankle reflex and decreased vibratory sense in the feet
3. Decreased vibration, decrease DTR, Sensory complaints of tingling, burning, etc.
[may or may not have weakness since sensory more than motor.]
* *The clinical features reflect, to some extent, the fiber type affected:
- -if small myelinated and some unmyelenated nerve fibers are damaged, distal pain and parasthesia are prominent symptoms
FOOT
---Pain and temperature loss lead to persistent foot ulceration and inadvertent foot injury can lead to fractures or neuropathic joints
(—don’t have good sensory feedback from feet, need foot care, good shoes, feet inspections, look for deformities, patient education)
---Neuropathic ulcerations have good vascularity and present as “beefy red”
1. Just pressure can cause skin breakdown and they wont feel it
2. Charcot joint when joints become unstable
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Autonomic neuropathy (5)
affect internal organs and/or the heart:
1. Loss of sexual response or impotence
2. Hypotonic bladder with recurrent infection and incontinance
3. Disturbance of blood pressure and heart rate control (symptom of orthostatic hypotension)
4. GI dysfunction, bloating, nausea, diarrhea, constipation, difficulty swallowing
5. Diffuse or absent sweat responses
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Diabetic Focal Neuropathy:
can occur sensory/motor proximally or distally or viscera
1. Appears suddenly, affecting specific nerves
2. Tends to improve in weeks or a few months without chronic damage
3. examples: femoral, pelvic pain, chest or abdominal pains, pain behind eyes or blurred vision, or other CN symptoms
4. Carpal tunnel syndrome and other compression syndromes occur more commonly in this population
----Double crush syndrome: more susceptible to cervical root compression if have carpal tunnel and visa versa
5. Important to monitor feet and blood sugar
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What causes the diabetic neuropathy?
Diabetes: blood sugar levels cause nerves to break down
In hyperglycemia the neurotoxic sorbitol is released into the blood stream
need to monitor blood glucose levels to maintain at optimal levels to prevent peripheral neuropathy.
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Treatment of Diabetic Neuropathy:
1. Relieve discomfort and prevent further damage. First priority—control blood glucose level
Reinforce diet, exercise, monitoring
2. Special care of feet
- --Skin care, proper shoes ie custom made to protect feet
- --Foot/toe deformities. Curling toes need high box shoes to prevent callouses, can then open and get infected.
3. Medication for pain:
4. Do not use heat modalities for cold feet:
- --they will not realize it is hot and may burn themselves
5. Blood pressure regulation and elastic stockings
- --monitor blood pressure
- --if susceptible to dependent edema, get support stockings
6. exercise to promote ideal body weight, improve insulin uptake and general conditioning
- --general conditioning to help glucose uptake
- --help QOL
- --maintain a healthy weight
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Alcoholic Neuropathy:
cause
presentation
Vitamin B deficiency assoc. w development of PN secondary to alcoholism
2. Presentation:
weakness, parasthesia and pain ( ie painful light touch )
---Mainly LE
3. intense burning parasthesia in the soles of the feet
4. proximal weakness in these patients may be neuropathic
5. Autonomic fiber involvement leads to segmental loss of sweating
6. Pathology:AXONAL DEGENERATION
(lose motor and sensory axons: do nerve conduction studies for diagnosis)
- --mild reduction of motor and sensory conduction velocities
- --Severely decreased amplitude of sensory action potentials
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Guillain Barre’ Syndrome:
***Greatest concern: progressive weakness resulting in quadriplegia and respiratory failure (25%)
after peak of severity, slow reversal of symptoms. Dependent upon extent of demylenation and axonal damage, recovery in 2-3 months up to 5 years. Long recovery.
1. Young adults to middle age
2. Acute onset *unlike the other neuropathies*
progressive,
symmetrical polyradiculopathy (polyradiculopathy because it affects the root)
3. Primarily affects weakness (motor). Can also be sensory.
Pathologically, presents as an inflammatory cell attack on the myelin sheaths with myelin breakdown and often axonal degeneration.
- --Ascending paralysis progression to cranial nerves
- --Almost like an ascending SCI
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Three Main Types
| GBS
progression depends on case by case basis (EMG, nerve biopsy)
1. Acute inflammatory demylinating polyradiculoneuropathy is the most common.
2. Acute motor axonal neuropathy—axonal destruction, severe with slow recovery
3. Acute motor and sensory neuropathy—rarest, with poor prognosis for recovery
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Acute inflammatory demylinating polyradiculoneuropathy
GBS, most common. Affects motor and sensory
a. Most common
b. This is motor and sensory
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Acute motor axonal neuropathy
GBS, axonal destruction, severe with slow recovery
a. Axonal degeneration, affect anterior horn cell breaking down
b. Sensation is intact so it is different
c. More severe involvement with much longer progression
d. Slow recovery
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Acute motor and sensory neuropathy
GBS, rarest, with poor prognosis for recovery
a. Axonal
b. Motor and sensory
c. Present like a patient with SCI, treat patient like patient with SCI
d. poor prognosis for recovery
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GBS: Greatest concern:
progressive weakness resulting in quadriplegia and respiratory failure (25%)
**Respiratory monitoring, blood gases: this person may go into respiratory arrest, must monitor patient, do not send patient home
work on respiratory function: incentive spirometer
after peak of severity, slow reversal of symptoms. Dependent upon extent of demylenation and axonal damage, recovery in 2-3 months up to 5 years. Long recovery.
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Why does a GBS patient need respiratory monitoring?
**Respiratory monitoring, blood gases: this person may go into respiratory arrest, must monitor patient, do not send patient home
work on respiratory function: incentive spirometer
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Reversal of symptoms in GBS
after peak of severity, slow reversal of symptoms. Dependent upon extent of demylenation and axonal damage, recovery in 2-3 months up to 5 years. Long recovery.
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GBS Acute stage
1. prevent contractures
2. manage pain
3. respiratory management and blood gas levels (pulse-ox)
4. protect for potential skin breakdown (bony prominence, positioning, check their skin)
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GBS Subacute stage
1. ROM--> PROM to AAROM to AROM
2. ADL: bed mobility, sitting balance, transfers, gait
3. Muscle strengthening—low rep, less than 5 reps
4. don’t over-fatigue (we do not want to over-stress the healing PNS)
5. respiratory management continued
6. orthostatic hypotension precaution
- --manage with support stockings to replace venous tone they lost in their legs
- --do it slowly and let them stabilize at each transition point
- --when they can have them do ankle pumps to help with blood flow
- --some patients have abdominal binder for stability/support and to help respiratory status
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GBS Long term rehab:
1. strengthening, ROM and stretching as needed
- --lower reps with more resistance for strengthening and not for endurance
2. increase endurance and aerobic conditioning
- --eventually work for endurance
- --need to do endurance conditioning for any patient that has been inactive
3. independent in ADL-transfers, progressive ambulation and/or wheelchair management
- --functional hierarchy: what can they do and what can they do to get to the next level of independence/function (curb then stairs)
4. always avoid undue fatigue
5. pain management—modalities (TENS, heat, cold, soft tissue work, stretch and ROM for pain)
6. skin care as necessary (important)
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What is Charcot-Marie Tooth Disease:
genetic motor and sensory peripheral neuropathy (I and II)
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How is CMT Dx?
1. Patient history
2. Family history: since the condition is genetic
3. Physical examination: ROM, tone (decreased), sensation
- --Peripheral neuropathy are LMN
- --You can check the reflexes of UMN but only as a rule out
4. Nerve conduction studies
5. Nerve biopsy—look at a branch of a nerve with specific findings on changes in the nerves
6. Genetic testing—if they want counseling, and also can help with the diagnosis
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What is Hereditary Motor and Sensory Neuropathy (HMSN)
= Charcot-Marie Tooth Disease
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3. CMT: Differential Diagnosis—Rule Out Other Etiologies of Peripheral Neuropathy
1. Rule out:
a. Alcoholism, Vitamin B12 deficiency, Thyroid disease, DM, HIV infection, Vasculitis, Neurosyphilis, Occult Malignancy, Heavy-metal toxicity, Chronic inflammatory demyelinating polyneuropathy (CIDP), Hereditary ataxis with neuropathy (eg Friedreich ataxia)
2. Blindness, seizures, dementia, and mental retardation are not part of the CMT syndrome
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Types of CMT/HMSN: (hereditary motor sensory neuropathy)
1. CMT: Demyelination-Type 1 (myelin sheath break down, axons intact)
2. Axonal-Type II: lose the axons so more severe weakness and sensory impairment
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CMT: Demyelination-Type 1 (myelin sheath break down, axons intact)
1. Proliferation of Schwann Cells
2. Repeated cycles of demyelination and re-myelination
- ---Have some periods of remission if re-myelination
----Biopsy shows thickening of nerves, changes in myelin sheath, sometimes able to palpate the larger diameter because scarred myelin sheath which is not good for conduction
3. Thickened/abnormal myelin around axons
4. “onion building”
5. mutation of peripheral myelin protein (PMP) gene
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CMT: Axonal-Type II:
lose the axons so more severe weakness and sensory impairment
**Direct axonal death
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CMT
Clinical presentation:
1. Prevalence: 1/2,500 population in the US
2. Inheritance is autosomal dominant (70%) but many variations exist
3. Positive family history
4. Symptoms by age 20—motor and sensory (more motor)
5. Characterized by slowly progressive weakness and atrophy beginning in the distal limb muscles --> goes DISTAL TO PROXIMAL
6. Progressions vary widely with some patients becoming wheelchair bound early and others fully ambulatory to the age of 60
7. “high-stepping” gait due to foot drop: for high steppage gait need standard posterior leaf spring AFO: ankle foot orthosis
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CMT
Gait
1 weakness of anterior tibialis
2 other compensation: circumduction is possible
3 may hear a foot slap when they land on heel typically
4 tend to have contractures of longitudinal arch-- high arch: teach stretching, maintain plantar fascia tightness
5 clawing of the toes : need high toe box shoe
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signs to recognize CMT
1. “inverted champagne bottles” appearance of the limbs: hypertrophy of calf and narrow ankle—more DISTAL ATROPHY
2 PES CAVUS due to intrinsic foot muscle weakness and wasting
3 AREFLEXIA: sensory loss
4 diminished VIBRATION and PROPRIOCEPTION LOSS
5 GAIT ATAXIA, positive Rhomberg test: they do not know their foot placement unless they are visually watching
6 difficulty walking (ankle sprains, tipping due to foot and distal leg weakness): need orthotics--ORTHOTIC
7 HAND WEAKNESS (poor finger control, clumsiness with manipulating small objects): hand stretching, OT stuff that we should do
8 MUSCLE CRAMPS:
9 although sensory nerves are also affected, patients do not complain of numbness as they never had normal sensation and do not perceive their lack of sensation
10 spinal deformities-thoracic SCOLIOSIS 37-50%
11 essential TREMOR 30-50%
12 HEARING loss
13 enlarged and PALPABLE PERIPHERAL NERVES
14 PHRENIC nerve involvement with diaphragmatic weakness
15 CARDIAC CONDUCTION ABNORMALITIES
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CMT: Clinical Presentation
a. Spinal deformities—thoracic scoliosis 37-50%
b. Essential tremor 30-50%--during movement see a tremor which stops when they stop doing movement, probably due to peripheral neuropathy and asynchrinization of motor units
- --Opposite from cerebellar tremor
- --Parkinsons have tremor at rest
- --Vs intention tremor
c. Hearing loss.
d. Enlarged and palpable peripheral nerves—demylination and remyelination, scar tissue forms around the nerves, more palpable
e. Phrenic nerve involvement with diaphragmatic weakness
f. Cardiac conduction abnormalities
i. Different presentations in genetic diseases?
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HMS Neuropathy Type I
things to note physically
a. Stocking and glove distribution .
b. Significant atrophy distally .
c. Bilateral pes cavus: tight plantar fascia, intrinsics are more involved than extrinsic: muscle imbalance: high arches –stretching to maintain flexibility, high toe box shoes to accommodate them, last resort surgical correction
d. Inverted champaign bottle appearance of lower leg: calf looks big—imbalance, not symmetrical, can have atrophy as on the right and on the left in the champaigne bottle, may have weakness but less atrophy (vs pseudohypertrophy in duchennes where it is fat and connective tissue)
e. Distal wasting and weakness in the upper limbs follow:
- --Many peripheral neuropathy have DISTAL involvement in the HANDS
- --if they have a HIGH STEPPAGE GAIT gait, look at their hands and notice atrophy in hands. This will indicate neurapothy
---look at the first DI to know if there is atrophy (note that first DI is last innervation of the ulnar nerve)
---Muscle imbalance: have CLAW HAND—have the wrist extensor (ED) not the hood mechanism intrinsics for full extension of fingers (long finger extensors vs extensor hood mechanism)
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Where to look for atrophy in CMT?
---look at the first DI to know if there is atrophy (note that first DI is last innervation of the ulnar nerve)
135
Why Bilateral pes cavus in CMT?
tight plantar fascia, intrinsics are more involved than extrinsic: muscle imbalance: high arches –stretching to maintain flexibility, high toe box shoes to accommodate them, last resort surgical correction
136
Why Inverted champaign bottle appearance of lower leg in CMT?
Inverted champaign bottle appearance of lower leg: calf looks big—imbalance, not symmetrical, can have atrophy as on the right and on the left in the champaigne bottle, may have weakness but less atrophy (vs pseudohypertrophy in duchennes where it is fat and connective tissue)
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CMT: assess: Distal wasting and weakness in the upper limbs follow:
i. Many peripheral neuropathy have distal involvement in the hands
ii. if they have a high step-page gait, look at their hands and notice atrophy in hands. This will indicate neurapothy
iii. look at the first DI to know if there is atrophy (note that first DI is last innervation of the ulnar nerve)
iv. Muscle imbalance: have clawing of the hand—have the wrist extensor (ED) not the hood mechanism intrinsics for full extension of fingers (long finger extensors vs extensor hood mechanism)
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Thoracic Outlet Syndrome:
refers to compression neuropathies or vascular involvement of brachial plexus or subclavian vessels (nerve or vessel or both vascular and neurological)
a. Vascular symptoms could be arterial or venous (1.5% of etiologies)—vascular and or neurological
b. Neurogenic in any distribution including autonomic nervous system (98% of etioloies)
- -Most common to be neurological
- -Can be in any distribution
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Neurogenic TOS:
TOS has characteristic sign, called the Gilliatt-Sumner-Hand, in which there is severe wasting in the base of the thumb—affect the median nerve. There may be numbness along underside of hand and forearm, or dull aching pain in the neck, shoulder, and armpit.
140
Gilliatt-Sumner-Hand
, in which there is severe wasting in the base of the thumb—affect the median nerve.
see in Neurogenic TOS
141
Vascular TOS
sx
what to do to know
what can cause
TOS features pallor, a weak or absent pulse in the affected arm, with also may be cool to touch and appear paler than the unaffected arm.
Symptoms nay include numbness, tingling, aching, and heaviness, temperature complaints in the hand.
i. Take pulse in different positions and see if obliterates pulse palpation
ii. Can be anatomical cervical rib, posture being poor
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Causes of TOS
1) Cervical rib: compressing neurovascular structure
2) Anterior scalene syndrome: (Adson’s Test)
(puts pressure on outlet and check radial pulse changes)
3) Pectoralis Minor Syndrome:
4) Costoclavicular syndrome:
143
4 Most common causes of TOS: things people do (4)
1. Acute neck trauma plus an anatomical predisposition—trauma, muscle imbalance, predisposition
2. Repetitive stress and poor posture—correct this
3. Occupational-secondary to poor posture
4. Heavy backpacks (uncommon) –can even damage long thoracic nerve and get winging scapula
144
TOS: Cervical rib:
compressing neurovascular structure-diagnose with xray
| 1. They may treat with resect the rib
145
TOS: Anterior scalene syndrome:
(Adson’s Test)
1. Adson’s Test: test for this: Turn head to involved side, extend head and neck, abduct arm and have person deeply inhale: puts pressure on outlet and check radial pulse changes and or replication of symptoms
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TOS: Pec Minor Syndrome
Pectoralis Minor Syndrome: between muscle and rib with elevation and abduction above head –this is a postural problem: prtotracted shoulder, FHP, closing down anterior thoracic area (also could be hypertrophy of the muscle as well causing pec minor tightness)
147
TOS: Costoclavicular syndrome:
--narrowing between clavicle and 1st rib space –test with depression and retraction to close the space more and see if causes more symptoms
148
Costoclavicular maneuvers:
see how sx are influenced by closing and opening the space
retraction, depression, elevation, protraction: closing and opening the space
TOS: Costoclavicular syndrome:
149
Progressive Postural Decompensation with neuromuscular compression
how to tx
tx: –stretch to open anterior chest wall, arm on mezuza (progress by prolonged stretch)
1. Normal resting posture
2. Shoulder protraction beginning; sternomastoid muscles are shortening, drawing head anteriorly and inferiorly
3. Advanced deformity with adaptive shortening of scalene and pectoralis minor muscles
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TOS
| Role of PT: Early on PT better than surgery (unless problem is anatomical)
1. Determine probable etiology
2. Patient education
3. What if vascular—not much we can do if vascular, maybe work to fix posture
4. what if neurogenic—would nerve mobilization help
5. when refer to doctor—when it is beyond our scope and we arent helping
6. when to use conservative intervention
7. what are examples of PT
interventions
---postural ---stretch---ergonomic assess---work environment---what do they do most of the day, replicate it
8. if muscle atrophy, may indicate for surgery, if not try non surgical PT
9. neurotension testing, treatment, mobilization—stretch nerves through their anatomical path and how to elongate them through their entire pathway ie median nerve anterior to elbow so extend elbow and extend wrist –see if nerve and not muscle
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neurotension testing
treatment, mobilization—stretch nerves through their anatomical path, elongate them through their entire pathway –see if nerve is bound down/tight somwhere
ie median nerve anterior to elbow so extend elbow and extend wrist
(ie feel when stretch median nerve when wrist extension--see if nerve is bound down somehwere)
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Carpal tunnel syndrome
what is it
5 causes
most common compression syndrome
1. repetitive motions
2. tendon hypertrophy
3. edema
4. anatomical changes
5. metabolic conditions (Diabetes: make more susceptible)
153
causes of CARPAL TUNNEL SYNDROME
1. Repetitive motion
2. Tendon hypertrophy
- --Long finger flexors go through the carpal tunnel too
- --The carpal tunnel getting narrowed or this causing less space will create less space for the nerve
3. Edema
- --Takes up space---Tx the edema—ie happens in last trimester of pregnancy
4. Anatomical Changes
- --Arthritic changes produce more bone growth in the tunnel
5. Metabolic Conditions-diabetes
- --They are in general more susceptible to other peripheral neuropathies
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CTS: Differential diagnosis
1. Distribution of weakness
2. Distribution of sensory changes
3. Phalen’s Test:
4. Tinel’s sign-less reliable
5. Carpal Compression Test: good reliability
6. EMG/NCV’s
7. Double Crush Syndrome
If they have root compression then findings wont just be after wrist
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Double Crush Syndrome
someone with carpal tunnel and cervical root compression (ie C6, C7)
more frequent in diabetic where nerves more susceptible so mild compression will cause more compression and symptoms than in a regular person
156
Carpal Tunnel
Distribution of weakness
NOT ALL OF THE MEDIAN NERVE distribution: forearm,
finger flexors and
wrist flexors
*** it has to be distal to the site of the compression:
so the root compresion can be anywhere in arm, but if carpal tunnel, it is more distal muscles which is the
THENAR EMINANCE—median innervation below the wrist (bc the rest is ulnar)
157
Carpal Tunnel
Distribution of sensory changes
Median nerve palmar side of thumb, until ½ of the ring finger (after that is ulnar)
158
CTS: Phalen’s Test: good sensitivity
Closes down the carpal tunnel more, put more pressure there, if feel tingling and numbness in the median distribution is a positive phalen’s test
90 degree shoulder flexion, 90 degree elbow flexion, wrist flexion, dorsum of hands touching---do you feel numbing?
159
CTS: Tinel’s sign-less reliable
+: tap over wrist with reflex hammer, if they feel shock down hand in the distribution of the nerve ie thumb, index, middle and radial part of ring finger: positive
(means there was nerve damage, because the nerve was degenerated, and now regenerating)
1. Tap over nerve that was degenerated or injured as it regenerates the most distal part produces shock in distribution of nerve
2. Tap over wrist with reflex hammer and if they feel shocks down their hand it is a positive tinel sign—if regenerating it means at some point earlier they were degenerating
=Sign of nerve damage
3. Track a nerve regeneration—tap along course of the nerve and see where get the tinel sign along the course of the nerve after the injury
* online says pins and needles
**it needs to be regenerating to get the Tinel's sign
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CTS: Carpal Compression Test: good reliability
1. Put pressure over carpal tunnel with sphygmomanometer or compression with your hand
2. If this replicates the symptoms it is indicative of carpal tunnel syndrome when do it over median nerve
161
CTS: EMG/NCV’s
1. EMG and nerve conductions for diagnosis of carpal tunnel
2. Recording over sensory distribution of nerve and stimulate AP above the carpal tunnel, when zap it will go down nerve to finger and record amplitude and time and
compare to normal values –see is SLOWED or PARTIALLY BLOCKED
162
Double Crush Syndrome
1. Have carpal tunnel and cervical root compression
2. Occurs more in diabetic patients where nerves already precarious and mild compression has more affect in these patients who have diabetes
163
Diff Dx
carpal tunnel syndrome vs root compression
If they have root compression then findings wont just be after wrist
164
What is normal carpal tunnel pressures:
pressure in the wrist is normally 2.5mmHg
pt with carpal tunnel can have 10X the value, produces anoxia to the nerve at that site, nerve starts to break down because not getting its BF
165
Carpal Tunnel Pressures and Normal Pressures (we dont need to memorize)
1. Normal subject neutral wrist: 2.5mmHg
2. Neutral wrist, CTS pt = 32mmHg ---this is 10x the pressure –anoxia to the site, nerve not getting blood flow and starts breaking down
3. Normal subject, wrist flexed = 31mmHg---doing the philen’s test
4. Normal subject, MP flexion = 55mmHg: doing sustained grasp, working the flexors
5. 45 Pronated, MP flexion = 12mmHg
6. Max finger flexion = > 300mmHg –not good to do this
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PT management: Compartment Syndrome
CARPAL TUNNEL SYNDROME
1. SPLINTING INTO NEUTRAL --- 24 hrs or just at night--hold wrist and fingers in neutral position –ppl who sleep with flexed wake up with pins and needles –if answer is yes ask them which fingers are tingling—classic sign for carpal tunnel syndrome
2. PULSED ULTRASOUND—increase blood-flow to the area
3. NERVE GLIDING—neutral tension testing: nerve mobilization if nerve is being bound down
- --stretch long finger flexors wrist extension and finger extensors
4. TENDON GLIDING EXERCISES—mobilize the tendon that goes through the tunnel: see picture !!!
5. HAND STRENGTHENING –focus on intrinsics—power grip and not long finger flexors
there needs to be more research. there is limited and very low quality evidence of benefit for all of a diverse collection of exercises and mobilization interventions for CTS
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Can splinting help in carpal tunnel?
yes
SPLINTING INTO NEUTRAL --- 24 hrs or just at night--hold wrist and fingers in neutral position –ppl who sleep with flexed wake up with pins and needles –if answer is yes ask them which fingers are tingling—classic sign for carpal tunnel syndrome
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Carpal Tunnel Tx:
hand strengthening
which muscle?
which nerve?
hand strengthening –focus on intrinsics (not the long finger flexors)
—power grip (ulnar innervated muscles are needed in powergrip)
!!!! and not the median nerve long finger flexors!!!
169
Upper Limb Tension Test—Median Nerve:
6 places
1. GHJ abduction
2. Wrist extension
3. Supination
4. ER
5. EE
6. Neck lateral flexion
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Pronator Teres Syndrome:
who has it
diff dx
it can seem like carpal tunnel
- -KNOW THE DIFFERENCE
- -it is still median nerve but it is between the bellies of the pronator teres
1. Most common in females
- --Also common in people who use screw drivers: MEDIAN NERVE BETWEEN BELLIES OF PRONATOR TERES, if a narrowing where the nerve goes through it is more susceptible to compression
DIFF DX:
1. Anterior proximal forearm pain
2. Point tenderness over pronator teres [on palpation]
3. Positive TINEL's SIGN --OVER AREA OF PRONATOR TERES
4. RESISTED PRONATION: Test resisted pronation ---does it replicate symptoms [probably pronator teres syndrome]
5. Positive neutral tension test
6. Rule out philen test
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Pronator Teres Syndrome:
PT interventions:
1. Pain modulation: manage acute pain, swelling, and symptoms
2. Nerve gliding/ mobilization :
is nerve bound down and can we free it –maybe localized trauma and not hypertrophy
3. Pt education work modification:
what increases symptoms to avoid, give exercises and explain why it will help—it will free up the nerve
4. Splinting forearm into neutral, with elbow flexed (to put it on more rest)
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Can splinting help Pronator Teres Syndrome?
YES, last resort
Splinting forearm into neutral, with elbow flexed (to put it on more rest)
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Ulnar at the Elbow (Tardy Ulnar Palsy / Cubital Tunnel)
how does it happen
what sx
Ulnar Nerve: pain in medial forearm
- --sensory complaints, intrinsic weakness
- --due to traction, compression, friction, or trauma at the medial elbow
- --occurs with prolonged elbow flexion and/or subluxation of nerve from ulnar grooves
*determine whether it is root compression or peripheral ulnar nerve
Tardy Ulnar Palsy:
often 15-20 yrs post fx: medial epicondyle
Ulnar Nerve Frays: rougher surface from the healing and bending and extending elbow will move nerve up and down in the groove--ulnar weakness as the nerve breaks down
1. Cumulative trauma to nerve can result in ulnar sensory weakness in the hand
---------ask patient if they had injury at medial epicondyle
---------note increased carrying angle
a surgery would be to move it from that rough space
pain in forearm, sensory and weakness in ulnar hand distribution
2. Ulnar compression: can be localized compression, leaning on elbows. Patients that do a lot of mat work on elbows. (elbow pads are important)
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What can seem similar to Ulnar at the Elbow (Tardy Ulnar Palsy / Cubital Tunnel)?
Peripheral Ulnar Nerve vs. Nerve Root
3
1. CERVICAL REDICULOPATHY: seems similar (pinched nerve: causes pain, weakness, numbness radiates to arm, chest)
2. THORACIC OUTLET SYNDROME: ulnar usually affected in thoracic outlet syndrome bc it is in the lower brachial plexus
3. MEDIAL EPICONDYLITIS—not nerve issue but an inflammation causing pain at the elbow (find out what makes it worse and better)
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Tests for Cubital Tunnel: Ulnar Nerve:
1. Upper limb tension test:
check for cervical rediculopathy: puts stress on a nerve to look at peripheral nerve compression-- (if that is the case then we mobilize the entrapped nerve)
2. Full elbow flexion test
check for cubital tunnel syndrome: (put nerve on stretch and see if causes pain or tingling)
3. Tinels sign –tap nerve above/below elbow to get electric shock sensation in nerve distribution
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Cubital Tunnel PT Intervention
1. Avoid positions and compression
2. Nerve mobilization
3. Intrinsic muscle strengthening--because of weakness there
4. Elbow extension splint --if acute
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Ulnar compression at Guyon’s Canal in the wrist:
compression of ulnar nerve in the top of the palm where the nerve splits to deep palmar branch of ulnar nerve
—handball, cycling
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Compartmental syndromes
1) carpal tunnerl syndrome
2) pronator teres syndrome
3) cubital tunnel syndrome
4) guyon's canal
5) brachial plexus compression at axilla
6) mid-humeral radial nerve (sat night palsy)
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Brachial plexus compression at axilla:
1. Differentiate between this and TOS
2. What are some etiologies?
- --Traction injuries
1) Axillary crutches: COMPRESSION at axilla
2) Erb’s Palsey: TRACTION during birth causes brachial plexus injury
3) MVA: arm jammed and trunk moves forward create traction on brachial plexus
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Mid-Humeral Radial Nerve
patient presentation
etiology
what to look for
*****(Saturday night palsy)
PATIENT PRESENTATION:
* **WRIST DROP*** wrist extensors and finger extensors
* **(NO weakness of TRICEPS which branch comes off before mid humeral area)
ETIOLOGY:
1. Humeral fx: Radial nerve wraps around humerus – can get entrapped in callous formation of humeral healing –may not happen immediately but a delayed radial nerve impingement (weakness)--DELAYED RADIAL NERVE IMPINGEMENT FROM CALLOUS FORMATION OF A FX
2. Saturday night palsy: Someone leaning on a hard surface and radial nerve gets compressed under humerus, or arm around someone and compresses radial nerve
WHAT TO LOOK FOR:
1. Look for wrist drop
2. Pins and needles when nerve re-awakens and excites APs
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Compression on a nerve: the lasting effects:
what will happen if short or long time?
If there is compression for a short period of time then it is a
Neurapraxia, short time will be mild neuropraxia that will go away when you take away the pressure
if pressure stays long enough it progresses to Axonotomesis--this is nerve destruction and we want to avoid this
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UE and LE Neuropathies Secondary SCI
what 2 nerves
1. ULNAR NERVE frequently affected at elbow (WC), more than median nerve [median can be in carpal tunnel]
2. PERONEAL NERVE head of fibula because leg ER, pressure at head of fibula, potential for nerve damage
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UE and LE Neuropathies secondary CVA
what nerves affected
how to prevent
What peripheral nerve might be involved:
Brachial plexus –severe strokes flaccidity will have brachial plexus involvement because weight of arm doing traction on brachial plexus
prevent
Arm support: good slings and not bad slings, make sure arm is supported so that elbow is supported when they are sitting.
When ambulating get arm-swing short term but if long term need to support the elbow we don’t want this traction
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LE compartmental compression syndromes
| 2
Fibular nerve at fibula head: significant external rotation
b. Tarsal Tunnel Syndrome: as nerve passes medially under flexor retinaculum TIBIAL NERVE THROUGH ANKLE :
1. Calcaneal –sensory only
2. Lateral plantar nerve—sensory and motor
3. Medial plantar nerve—sensory and motor
1. Do nerve conduction study EMG to see for sure
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Tarsal Tunnel Syndrome
what is sx
how to dx
Tarsal Tunnel Syndrome:
as nerve passes medially under flexor retinaculum
TIBIAL NERVE THROUGH ANKLE :
Sx depends on where the compression is:
1. Calcaneal –sensory only
2. Lateral plantar nerve—sensory and motor
3. Medial plantar nerve—sensory and motor
Do nerve conduction study and EMG to see for sure
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New Discoveries into Symptom Patterns of Peripheral Neuropathies and Neurogenic Pain
Neurovascular Patterns:
Neurovascular Patterns: if vascular involvement to blood vessels that feed nerves are affected it will produce a different sx pattern (seems like nerve but wrong pattern)
1. Pain patterns that do not fit into other well established sensory patterns
2. Circumferential pain a burning ring
(Note that herpes zoster also in a ring pattern)
3. Variations in sympathetic nerve activity to the arterioles of a limb may result in ischemic pain, numbness, or parasthesias that follow neurovscular rather than somatosensory patterns
4. Vasomoter mapping of periphery, vascular supply to nerve, symptoms are not same as peripheral somatosensory patterns ie femoral nerve vascular innervation is entire anterior thigh
complaints sounds like peripheral neuropathy but they have a vascular problem!!!
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Sural Nerve: if involved where will they have weakness
Long thoracic nerve:
Sural Nerve: IT IS ONLY SENSORY
long thoracic nerve nerve to serratus, only motor
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Sx Sequence of NEUROVASCULAR Involvement
New Discoveries into Symptom Patterns of Peripheral Neuropathies and Neurogenic Pain
EARLY
1. Fluctuating thermal sensations and patchy skin coloration
2. Parasthesia- patchy distribution –atypical, not the nerve root distribution and not peripheral nerve distribution, suspect this to be neurovascular
Mild-ischemia secondary to SNS irritation
1. Pain in a certain pattern
2. Color of skin may be blue--hint vascular
3. Increased sweat (in certain distribution)
4. Piloerection
LATE
-hyperemia-incr BF- secondary SNS fiber conduction block
-Warm/red and dry. May not be painful.
It is a different distribution
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Neurovascular: Implications for PT
---Knowledge pf vascular innervation patterns
---Identify a weird pattern as being vascular innervation
- --These can occur secondary
1) trauma
2) compression,
3) entrapment,
4) complex regional pain syndrome (reflex sympathetic dystrophy,
5) various neuropathies also affecting vascular supply
Avasculitis: inflammation of blood vessels present diff than neuromuscular normally does
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Bell's Palsy
CN involvement: infection, compression from tumor affecting facial nerve on one side
Recovery
tx
causes
70+% spontaneously recover within 1 year, without treatment
Treatment: with acyclovir (anti-viral) + prednisone
CAUSES
HERPES ZOSTER VIRUS main cause (antibiotics will not work)—unless you can rule out a tumor or something put them on ANTIVIRAL MEDICATION
1. IDIOPATHIC: 50%
2. Infection: 15%
3. Neurologic: 14%
4. Neoplastic: 14%: ACOUSTIC NEROMA: most common tumor that causes this –need to remove without damaging facial nerve (because next to facial nerve)
5. Trauma : 8%
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BELLS PALSY vs STROKE FACIAL PARALYSIS
FRONTALIS IS AFFECTED IN BELL’s PALSY:
Bells Palsy: peripheral cranial nerve, flaccidity/weakness in frontalis
it is not affected after stroke because dual innervation (facial paralysis)
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Grading system for severity of Bell’s Palsy:
House Brackmann Facial Nerve Grading System: level of dysfunction: facial nerve is motor
mild to severe involvement (total flaccidity in all branches)
Movements of corner of mouth and eyebrows
---points for ¼ cm of motion
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What gives face motor?
facial nerve
| -bells palsy
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What gives face sensory?
trigeminal
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BELL's PALSY
CN #7
UMN vs LMN:
UMN vs LMN: lesion in relation to cell body. 7th CN leaves the skull with Acoustic Nerve. Can get compression secondary to acoustic neuroma, inflammation
Peripheral Nerve, cranial nerve, CN 7: facial paralysis, Bell's palsy
NOT CNS
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BELL's PALSY
tx (8)
1. ANTIGRAVITY MASSAGE: gravity is pulling cheek down and slowly stretching the connective tissue making it worse - drooping more severe (mirror)
*****2. ARTIFICIAL TEARS: cannot close their own eyelid, susceptible to dry lens damage, need to lubricate eyes --protect the eye
3. Eyelid weight to help patient close eye—not an exercise, ie if sleeping, w eyedrop
4. BIOFEEDBACK: teach them light effort movement of specific muscles
–don’t do heavy effort movement, specific target to one muscle at a time movement even if a small excursion
--EMG is a way to show them that they have some ability
****5. AVOID ABNORMAL SYNERGY = SYNKINESIS:
Avoid synkinesis during active exercise: synkinesis is the abnormal synergy of the face that we do not want to get. A lot of effort they will recruit all muscles in face that have voluntary movement but then they will only do mass movements and lose individual face muscle motions. We don’t want synkinesis or abnormal facial muscle synnergy.
6. (waste of time: Electrical stimulation not really necessary or effective: they do it to prevent atrophy but 5x/day not going to help prevent atrophy)
7. CHART OF FACES: have them try to imitate the faces
8. LOOK FOR TUMOR: Facial nerve and acoustic nerve: sx come on SLOW IN HEARING LOSS so that isnt picked up right away
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NMJ Issues
Neuromuscular Transmission Defects
Myasthenia Gravis
Botulism
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Myasthenia Gravis is it central or peripheral?
PNS--because NMJ is peripheral
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Myasthenia Gravis
4 sx
PT intevention
Initially:
1. extra-ocular muscle weakness, PTOSIS, and/or DIPLOPIA
* ***PTOSIS: eyelid droop on one side: because the skeletal muscle to lift the eye: the levator palpabre superior is a skeletal muscle working all the time and in the day starts to fatigue and eyelid droops, ptosis is early sign of myasthenia gravis
2. May see other WEAKNESS and FATIGUE as day progresses
Weakness with abnormal fatigue, especially proximal muscles. UE’s, neck, trunk and hip flexors also affected
especially antigravity muscles
3. BULBAR manifestations: DYSPHAGIA (swallow), DYSPHONIA (nasal or horse sounding speech)
- --difficulty speech and swallow
4. Includes FACIAL WEAKNESS, difficulty chewing, and RESPIRATORY WEAKNESS
PT interventions: energy conservation
1. ADL easier: raised toilet seat,
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Pathophysiology: Myasthenia Gravis:
tx
acetylcholine not getting to the muscle
1) decreased ACH packets of nerve at NMJ
2) decreased # of receptor sites on the muscle side of NMJ,
also have blockage of some receptor sites so they stop functioning
Severe onset of bulbar and or respiratory weakness, myasthenic crisis and is a medical emergency.
Triggers can include pregnancy, stress, infections, or new medications
TX:
1) Responds to ANTIcholinesterase drugs
- --Block the breakdown of ACH by acytelcholinesterase
2) PT intervention: energy conservation, low impact aerobic exercise helps!
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Myasthenia Gravis: To Who
Autoimmune disorder linked to the thymus gland
*Occurs in about 15-20/1,000
* women after age 30, men after age 50,
- ---More in females, and earlier
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Myasthenia Gravis: TX (3)
TX:
1) Responds to ANTIcholinesterase drugs
- --Block the breakdown of ACH by acytelcholinesterase
2) PT intervention: ENERGY CONSERVATION:
LOW IMPACT AEROBIC EXERCISE HELPS!!! condition them
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Myasthenia Gravis: Emergencies
Myasthenic crisis is a medical emergency:
| Severe onset of bulbar and or respiratory weakness,
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Myasthenia Gravis: Triggers (4)
Triggers can include
1) pregnancy
2) stress
3) infections
4) new medications
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Botulism
1. blocks the release of Ach
2. DESCENDING PARALYSIS with dyspnea within 12 hours of initial symptoms
3. symptoms 18-36 hours after eating infected foods
* ***cans that are getting expanding from bacteria
* **HONEY: children <12mo no honey
CN involvement
- Swallowing difficulty
- Speech problems
4. Can be very serious and descending paralysis!!!
5. Botox to reduce spasticity : used to manage high tone by knocking out NMJ temporarily--decreasing the higher tone towards a lower level
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Phenol Blocks
neurotoxic injected into motor nerve instead of botox (cheaper than botox)
```
Disadvantages: non selective for motor vs sensory nerves,
painful recovery (can get into sensory nerve)
```
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Summary-PT interventions for patients with peripheral neuropathy
1. AD, orthotics, protective, supportive devices
2. Biofeedback, neuromuscular electrical stimulation (NMES, TENS)
3. Therex: ROM Positioning, sensory re-education
4. Manual therapy: nerve gliding
We can increase strength****there is inadequate evidence to determine effect of exercise on functional ability in patients with peripheral neuropathies—can increase strength but NOT SURE IF IT WILL HAVE FUNCTIONAL IMPLICATIONS
***Strengthening, PREs may improve strength in affected ms (musculoskeletal)***Not early on, don't want to strain it, wait until more chronic to improve strength to hopefully improve function
