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Introduction
1. Cardiovascular system
2. Pulmonary system
3. Neuromuscular system
3.1 Central nervous system
3.2 Anatomy and function of spinal cord
3.3 Peripheral nervous system
3.4 Stroke deficits and recovery
3.5 Traumatic brain injury
3.6 Spinal cord injury
3.7 Neurodegenerative disorders and epilepsy
3.8 Peripheral nervous system conditions
3.9 Other neurological conditions
3.10 Interventions for neurological conditions
3.11 Vestibular system
4. Pediatrics
5. Musculoskeletal system
6. Other systems
7. Non-systems
Wrapping up
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3.8 Peripheral nervous system conditions
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3. Neuromuscular system
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Peripheral nervous system conditions

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Peripheral nerve injuries

Injuries to the peripheral nerves due to trauma, chronic traction, compression, or shear.

Definitions
Wallerian degeneration
Degeneration of the axon and myelin sheath distal to the site of an axonal interruption.
Neuropathy
Degenerative changes in peripheral nerves that produce loss of motor and sensory function; caused by diabetes, nutritional deficits, or alcohol use.
Mononeuropathy
Degeneration of a single nerve.
Polyneuropathy
Bilateral, symmetrical involvement of peripheral nerves, typically in stocking/glove distribution. Diabetic peripheral neuropathy begins in the longest nerves of the body, affecting the feet first and later the hands in a stocking-glove pattern.
Entrapment syndrome
Pressure on a nerve where it passes through an opening or over a bony prominence.

Peripheral nerve injuries range in severity from a temporary compression injury to complete severance:

Type Cause Recovery
Neuropraxia Compression injury Reverses rapidly or persists for weeks; no surgery needed
Axonotmesis Crush injury; axon interrupted, causing distal degeneration Possible, with or without surgical intervention
Neurotmesis Complete severance of the nerve Fails without surgical intervention

Example: identifying a nerve injury type

A patient’s ulnar nerve is crushed but not severed. Motor and sensory function are absent distal to the injury, and the nerve is expected to regenerate over months without further surgery. Which type of injury is this?

Answer: Axonotmesis - the axon is interrupted and degenerates distally (a crush injury), but it can regenerate without surgery, unlike neurotmesis.

Interventions for peripheral nerve injuries and neuropathy

  • Protect insensate areas: teach daily skin and foot inspection, especially for stocking/glove polyneuropathy from diabetes, along with properly fitted footwear
  • Splint or position denervated muscles to prevent overstretching and contracture
  • Progress from ROM to strengthening as reinnervation occurs
  • Sensory re-education as protective sensation returns

Impaired sensation: superficial heat is contraindicated over an area the patient cannot feel, because the patient’s report of warmth is what prevents a burn. For cold, ultrasound and electrical stimulation, reduced sensation is a precaution: monitor closely and use lower intensities.

Nerve complications of interventions for other conditions

Treatment aimed at another body system can injure or stress the nervous system. Stop and report new neurological signs to the supervising PT:

  • Compression of a superficial nerve: a tight cast, splint, or compression wrap, prolonged bed rest, unpadded positioning, or habitual leg crossing can compress the common fibular (peroneal) nerve where it passes the fibular head. New numbness over the lateral leg or top of the foot, or new weakness of ankle dorsiflexion and eversion (foot drop), is reported right away so the device or position can be checked. Pad the fibular head when positioning.
  • Hypoglycemia during exercise: in a patient with diabetes, a low blood glucose can cause confusion, weakness, unusual behavior, focal deficits, or seizures; hypoglycemia is one of the most common stroke mimics. Check glucose and treat it as taught in Endocrine and metabolic systems.
  • Cervical manual therapy and exercise: treatment of the neck carries a rare risk of cerebral ischemia from the cervical arteries. Dizziness, diplopia, dysarthria, dysphagia, drop attacks, nystagmus, nausea, or numbness means stop and notify the PT (see the vertebral artery test in Cervical spine tests).

Myasthenia gravis

Definitions
Myasthenia gravis
An autoimmune disorder leading to decreased acetylcholine receptors at the neuromuscular junction, and thus a decrease in muscular contraction with repetition.

Symptoms

  • Muscle weakness, especially in the eyes, face, throat, and limbs
  • Double vision
  • Drooping eyelids
  • Difficulty swallowing or speaking
  • Weakness that worsens with activity and improves with rest
Definitions
Myasthenic crisis
Occurs when the exacerbation of symptoms progresses to the respiratory system, leading to life-threatening weakness.

Tests and measures: manual muscle testing before and after repetition documents MG’s fatigue pattern; monitor respiratory and swallowing status for signs of crisis.

Pyridostigmine, an oral medication that increases acetylcholine, may improve muscle strength in myasthenia gravis. Its effect builds within about 30 minutes of a dose and peaks over the next 1 to 3 hours, so schedule exercise and demanding activities for that window, not for just before the next dose is due.

Interventions for myasthenia gravis

  • Prioritize energy conservation techniques
    • Avoid exercising to fatigue, because weakness worsens with repeated activity; when the disease is stable, low- to moderate-intensity strengthening and aerobic exercise with rest breaks is safe and can improve strength
  • Attempt to conduct therapy sessions in the morning to decrease fatigue
  • Heat is a precaution, not a contraindication: raising body or muscle temperature can temporarily worsen fatigable weakness, so use superficial heat cautiously over limited areas, avoid whole-body heating such as a hot whirlpool, and monitor for increased weakness

PTA role: if fatigue increases with repetition, or signs of myasthenic crisis appear (sudden weakness, new difficulty breathing or swallowing), stop and report to the supervising PT rather than progressing the plan of care.

Bell’s palsy

Definitions
Bell’s palsy
A lower motor neuron lesion involving cranial nerve VII (facial nerve), causing unilateral facial paralysis due to acute inflammation of unknown etiology, resulting in compression of the nerve in the temporal bone.

Symptoms peak within the first few hours or days and typically last for several weeks to months.

Symptoms

  • Facial droop and weakness of the whole half of the face, forehead included: the patient may be unable to raise the eyebrow or fully close the eye on that side. A cortical stroke (an upper motor neuron lesion) usually spares the forehead, because the forehead receives input from both sides of the brain
  • Drooling from one side
  • Loss of taste to the anterior 2/3 of the tongue
  • Changes in saliva and tear production
  • Ear pain
  • Sensory to face remains intact

Tests and measures: grade facial muscle function with a standardized scale (e.g., House-Brackmann) to track recovery.

Interventions for Bell’s palsy

  • Spontaneous recovery can occur
  • Medical management: corticosteroids, prescribed by the physician, to reduce inflammation
  • Electrical stimulation: used selectively and only as the plan of care directs, since evidence of benefit is limited and incorrect parameters can worsen abnormal reinnervation (synkinesis)
  • Exercises for facial muscles
  • Taping of the eyelid to prevent dry eye due to the inability to close the eyelid

Ramsay Hunt syndrome is caused by reactivation of the varicella-zoster virus along the facial nerve, with a triad of ipsilateral facial paralysis, ear pain, and vesicles near the ear; hearing loss, tinnitus, and vertigo can occur with vestibulocochlear nerve involvement.

Guillain-Barré syndrome (GBS)

Definitions
Guillain-Barré syndrome (GBS)
An acute autoimmune disorder in which the myelin sheath of peripheral nerves is damaged. It typically occurs days to weeks after a respiratory or gastrointestinal infection (viral or bacterial, most commonly Campylobacter jejuni), causing demyelination of both cranial and peripheral nerves.

Symptoms

  • Causes motor and mild sensory loss distal to proximal in a symmetrical pattern
  • Usually begins in the legs and will ascend towards the trunk and upper extremities (UE)
  • Worse prognosis if the disease involves the respiratory muscles, requiring mechanical ventilation
  • Motor/sensory loss progressively worsens over a 4-week period and then stabilizes

Tests and measures: MMT and functional mobility measures track weakness progression; monitor vital capacity during the ascending phase.

Interventions for Guillain-Barré syndrome (GBS)

  • Sessions focus on compensatory strategies to assist with gait and mobility
  • Avoidance of overstretching and overuse during acute phases of diagnosis
  • Strength training is performed once stabilization of the disease process occurs, with progression from isometric to concentric to eccentric activities

PTA role: if weakness or fatigue worsens with activity, ascending weakness reaches respiratory muscles, or signs of autonomic instability appear (orthostatic hypotension, marked blood pressure or heart-rate swings, arrhythmia), stop and report to the supervising PT rather than progressing the plan of care. Monitor vital signs before, during, and after upright activity.

Comparing myasthenia gravis, Bell’s palsy, and GBS

These three conditions overlap in that each produces weakness, but they differ in the pattern of that weakness and, critically, in how therapy is progressed. Lining them up side by side keeps the management distinctions from blurring together.

The following table compares myasthenia gravis, Bell’s palsy, and Guillain-Barré syndrome by presentation pattern and physical therapy approach.


Condition Presentation pattern Therapy approach
Myasthenia gravis Fatigable weakness that worsens with repetition and improves with rest Energy conservation, low- to moderate-intensity exercise with rest (never to fatigue), morning sessions
Bell’s palsy Lower motor neuron CN VII lesion; unilateral facial paralysis Often spontaneous recovery; facial exercises, e-stim, eyelid taping
Guillain-Barré syndrome Symmetrical weakness ascending from the legs (distal to proximal), progressing over ~4 weeks then stabilizing Phase-specific: compensatory strategies acutely, then strength training (isometric → concentric → eccentric) after stabilization

Peripheral nerve injuries

  • Wallerian degeneration: axon/myelin breakdown distal to injury site
  • Severity spectrum: neuropraxia (compression, reversible, no surgery) → axonotmesis (crush, axon degenerates, may recover ± surgery) → neurotmesis (full severance, needs surgery)
  • Neuropathy: mononeuropathy (single nerve) vs. polyneuropathy (bilateral, stocking/glove; e.g., diabetes)
  • Interventions: protect insensate skin/feet, splint denervated muscles, progress ROM→strengthening with reinnervation
  • Caution: superficial heat contraindicated with impaired sensation (burn risk); lower intensity + monitor with cold/US/e-stim
  • Complications of other interventions: tight casts, wraps, or positioning can compress the fibular nerve at the fibular head (foot drop); exercise-induced hypoglycemia can mimic a stroke; cervical manual therapy can provoke vertebrobasilar signs; stop and report

Myasthenia gravis

  • Autoimmune loss of ACh receptors at NMJ → fatigable weakness, worse with repetition, better with rest
  • Signs: ptosis, diplopia, dysphagia, facial/limb weakness; myasthenic crisis = respiratory involvement (life-threatening)
  • MMT pre/post repetition shows fatigue pattern; monitor respiratory/swallow status
  • Treatment: energy conservation, low-moderate exercise with rest (never to fatigue), morning sessions, avoid whole-body heat (hot whirlpool) and use superficial heat cautiously
  • Stop/report if fatigue worsens with repetition or crisis signs emerge

Bell’s palsy

  • LMN lesion of CN VII → unilateral facial paralysis from inflammation/compression in temporal bone
  • Signs: facial droop with the whole half of the face weak, forehead included (a cortical stroke spares the forehead), drooling, loss of anterior 2/3 tongue taste, altered tears/saliva, ear pain; facial sensation intact
  • Often resolves spontaneously; House-Brackmann tracks recovery
  • Treatment: corticosteroids (MD-prescribed), facial exercises, cautious e-stim (synkinesis risk), eyelid taping for dry eye

Guillain-Barré syndrome (GBS)

  • Autoimmune demyelination of peripheral/cranial nerves, often post-infection (e.g., Campylobacter jejuni)
  • Symmetrical motor/mild sensory loss ascending distal→proximal (legs first); worsens ~4 weeks then stabilizes
  • Worse prognosis with respiratory involvement (possible ventilation)
  • Therapy: compensatory strategies acutely; strengthening (isometric→concentric→eccentric) only after stabilization; avoid overstretching/overuse early
  • Monitor vitals; stop/report if weakness ascends to respiratory muscles or autonomic instability occurs

Comparing the three conditions

  • All cause weakness but differ in pattern: MG = fatigable w/ repetition; Bell’s palsy = unilateral facial (CN VII); GBS = ascending symmetrical, phase-dependent
  • Therapy matches pattern: MG avoids fatigue; Bell’s palsy allows spontaneous recovery + facial exercises; GBS compensates early, strengthens only after stabilization

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Peripheral nervous system conditions

Peripheral nerve injuries

Injuries to the peripheral nerves due to trauma, chronic traction, compression, or shear.

Definitions
Wallerian degeneration
Degeneration of the axon and myelin sheath distal to the site of an axonal interruption.
Neuropathy
Degenerative changes in peripheral nerves that produce loss of motor and sensory function; caused by diabetes, nutritional deficits, or alcohol use.
Mononeuropathy
Degeneration of a single nerve.
Polyneuropathy
Bilateral, symmetrical involvement of peripheral nerves, typically in stocking/glove distribution. Diabetic peripheral neuropathy begins in the longest nerves of the body, affecting the feet first and later the hands in a stocking-glove pattern.
Entrapment syndrome
Pressure on a nerve where it passes through an opening or over a bony prominence.

Peripheral nerve injuries range in severity from a temporary compression injury to complete severance:

Type Cause Recovery
Neuropraxia Compression injury Reverses rapidly or persists for weeks; no surgery needed
Axonotmesis Crush injury; axon interrupted, causing distal degeneration Possible, with or without surgical intervention
Neurotmesis Complete severance of the nerve Fails without surgical intervention

Example: identifying a nerve injury type

A patient’s ulnar nerve is crushed but not severed. Motor and sensory function are absent distal to the injury, and the nerve is expected to regenerate over months without further surgery. Which type of injury is this?

Answer: Axonotmesis - the axon is interrupted and degenerates distally (a crush injury), but it can regenerate without surgery, unlike neurotmesis.

Interventions for peripheral nerve injuries and neuropathy

  • Protect insensate areas: teach daily skin and foot inspection, especially for stocking/glove polyneuropathy from diabetes, along with properly fitted footwear
  • Splint or position denervated muscles to prevent overstretching and contracture
  • Progress from ROM to strengthening as reinnervation occurs
  • Sensory re-education as protective sensation returns

Impaired sensation: superficial heat is contraindicated over an area the patient cannot feel, because the patient’s report of warmth is what prevents a burn. For cold, ultrasound and electrical stimulation, reduced sensation is a precaution: monitor closely and use lower intensities.

Nerve complications of interventions for other conditions

Treatment aimed at another body system can injure or stress the nervous system. Stop and report new neurological signs to the supervising PT:

  • Compression of a superficial nerve: a tight cast, splint, or compression wrap, prolonged bed rest, unpadded positioning, or habitual leg crossing can compress the common fibular (peroneal) nerve where it passes the fibular head. New numbness over the lateral leg or top of the foot, or new weakness of ankle dorsiflexion and eversion (foot drop), is reported right away so the device or position can be checked. Pad the fibular head when positioning.
  • Hypoglycemia during exercise: in a patient with diabetes, a low blood glucose can cause confusion, weakness, unusual behavior, focal deficits, or seizures; hypoglycemia is one of the most common stroke mimics. Check glucose and treat it as taught in Endocrine and metabolic systems.
  • Cervical manual therapy and exercise: treatment of the neck carries a rare risk of cerebral ischemia from the cervical arteries. Dizziness, diplopia, dysarthria, dysphagia, drop attacks, nystagmus, nausea, or numbness means stop and notify the PT (see the vertebral artery test in Cervical spine tests).

Myasthenia gravis

Definitions
Myasthenia gravis
An autoimmune disorder leading to decreased acetylcholine receptors at the neuromuscular junction, and thus a decrease in muscular contraction with repetition.

Symptoms

  • Muscle weakness, especially in the eyes, face, throat, and limbs
  • Double vision
  • Drooping eyelids
  • Difficulty swallowing or speaking
  • Weakness that worsens with activity and improves with rest
Definitions
Myasthenic crisis
Occurs when the exacerbation of symptoms progresses to the respiratory system, leading to life-threatening weakness.

Tests and measures: manual muscle testing before and after repetition documents MG’s fatigue pattern; monitor respiratory and swallowing status for signs of crisis.

Pyridostigmine, an oral medication that increases acetylcholine, may improve muscle strength in myasthenia gravis. Its effect builds within about 30 minutes of a dose and peaks over the next 1 to 3 hours, so schedule exercise and demanding activities for that window, not for just before the next dose is due.

Interventions for myasthenia gravis

  • Prioritize energy conservation techniques
    • Avoid exercising to fatigue, because weakness worsens with repeated activity; when the disease is stable, low- to moderate-intensity strengthening and aerobic exercise with rest breaks is safe and can improve strength
  • Attempt to conduct therapy sessions in the morning to decrease fatigue
  • Heat is a precaution, not a contraindication: raising body or muscle temperature can temporarily worsen fatigable weakness, so use superficial heat cautiously over limited areas, avoid whole-body heating such as a hot whirlpool, and monitor for increased weakness

PTA role: if fatigue increases with repetition, or signs of myasthenic crisis appear (sudden weakness, new difficulty breathing or swallowing), stop and report to the supervising PT rather than progressing the plan of care.

Bell’s palsy

Definitions
Bell’s palsy
A lower motor neuron lesion involving cranial nerve VII (facial nerve), causing unilateral facial paralysis due to acute inflammation of unknown etiology, resulting in compression of the nerve in the temporal bone.

Symptoms peak within the first few hours or days and typically last for several weeks to months.

Symptoms

  • Facial droop and weakness of the whole half of the face, forehead included: the patient may be unable to raise the eyebrow or fully close the eye on that side. A cortical stroke (an upper motor neuron lesion) usually spares the forehead, because the forehead receives input from both sides of the brain
  • Drooling from one side
  • Loss of taste to the anterior 2/3 of the tongue
  • Changes in saliva and tear production
  • Ear pain
  • Sensory to face remains intact

Tests and measures: grade facial muscle function with a standardized scale (e.g., House-Brackmann) to track recovery.

Interventions for Bell’s palsy

  • Spontaneous recovery can occur
  • Medical management: corticosteroids, prescribed by the physician, to reduce inflammation
  • Electrical stimulation: used selectively and only as the plan of care directs, since evidence of benefit is limited and incorrect parameters can worsen abnormal reinnervation (synkinesis)
  • Exercises for facial muscles
  • Taping of the eyelid to prevent dry eye due to the inability to close the eyelid

Ramsay Hunt syndrome is caused by reactivation of the varicella-zoster virus along the facial nerve, with a triad of ipsilateral facial paralysis, ear pain, and vesicles near the ear; hearing loss, tinnitus, and vertigo can occur with vestibulocochlear nerve involvement.

Guillain-Barré syndrome (GBS)

Definitions
Guillain-Barré syndrome (GBS)
An acute autoimmune disorder in which the myelin sheath of peripheral nerves is damaged. It typically occurs days to weeks after a respiratory or gastrointestinal infection (viral or bacterial, most commonly Campylobacter jejuni), causing demyelination of both cranial and peripheral nerves.

Symptoms

  • Causes motor and mild sensory loss distal to proximal in a symmetrical pattern
  • Usually begins in the legs and will ascend towards the trunk and upper extremities (UE)
  • Worse prognosis if the disease involves the respiratory muscles, requiring mechanical ventilation
  • Motor/sensory loss progressively worsens over a 4-week period and then stabilizes

Tests and measures: MMT and functional mobility measures track weakness progression; monitor vital capacity during the ascending phase.

Interventions for Guillain-Barré syndrome (GBS)

  • Sessions focus on compensatory strategies to assist with gait and mobility
  • Avoidance of overstretching and overuse during acute phases of diagnosis
  • Strength training is performed once stabilization of the disease process occurs, with progression from isometric to concentric to eccentric activities

PTA role: if weakness or fatigue worsens with activity, ascending weakness reaches respiratory muscles, or signs of autonomic instability appear (orthostatic hypotension, marked blood pressure or heart-rate swings, arrhythmia), stop and report to the supervising PT rather than progressing the plan of care. Monitor vital signs before, during, and after upright activity.

Comparing myasthenia gravis, Bell’s palsy, and GBS

These three conditions overlap in that each produces weakness, but they differ in the pattern of that weakness and, critically, in how therapy is progressed. Lining them up side by side keeps the management distinctions from blurring together.

The following table compares myasthenia gravis, Bell’s palsy, and Guillain-Barré syndrome by presentation pattern and physical therapy approach.


Condition Presentation pattern Therapy approach
Myasthenia gravis Fatigable weakness that worsens with repetition and improves with rest Energy conservation, low- to moderate-intensity exercise with rest (never to fatigue), morning sessions
Bell’s palsy Lower motor neuron CN VII lesion; unilateral facial paralysis Often spontaneous recovery; facial exercises, e-stim, eyelid taping
Guillain-Barré syndrome Symmetrical weakness ascending from the legs (distal to proximal), progressing over ~4 weeks then stabilizing Phase-specific: compensatory strategies acutely, then strength training (isometric → concentric → eccentric) after stabilization
Key points

Peripheral nerve injuries

  • Wallerian degeneration: axon/myelin breakdown distal to injury site
  • Severity spectrum: neuropraxia (compression, reversible, no surgery) → axonotmesis (crush, axon degenerates, may recover ± surgery) → neurotmesis (full severance, needs surgery)
  • Neuropathy: mononeuropathy (single nerve) vs. polyneuropathy (bilateral, stocking/glove; e.g., diabetes)
  • Interventions: protect insensate skin/feet, splint denervated muscles, progress ROM→strengthening with reinnervation
  • Caution: superficial heat contraindicated with impaired sensation (burn risk); lower intensity + monitor with cold/US/e-stim
  • Complications of other interventions: tight casts, wraps, or positioning can compress the fibular nerve at the fibular head (foot drop); exercise-induced hypoglycemia can mimic a stroke; cervical manual therapy can provoke vertebrobasilar signs; stop and report

Myasthenia gravis

  • Autoimmune loss of ACh receptors at NMJ → fatigable weakness, worse with repetition, better with rest
  • Signs: ptosis, diplopia, dysphagia, facial/limb weakness; myasthenic crisis = respiratory involvement (life-threatening)
  • MMT pre/post repetition shows fatigue pattern; monitor respiratory/swallow status
  • Treatment: energy conservation, low-moderate exercise with rest (never to fatigue), morning sessions, avoid whole-body heat (hot whirlpool) and use superficial heat cautiously
  • Stop/report if fatigue worsens with repetition or crisis signs emerge

Bell’s palsy

  • LMN lesion of CN VII → unilateral facial paralysis from inflammation/compression in temporal bone
  • Signs: facial droop with the whole half of the face weak, forehead included (a cortical stroke spares the forehead), drooling, loss of anterior 2/3 tongue taste, altered tears/saliva, ear pain; facial sensation intact
  • Often resolves spontaneously; House-Brackmann tracks recovery
  • Treatment: corticosteroids (MD-prescribed), facial exercises, cautious e-stim (synkinesis risk), eyelid taping for dry eye

Guillain-Barré syndrome (GBS)

  • Autoimmune demyelination of peripheral/cranial nerves, often post-infection (e.g., Campylobacter jejuni)
  • Symmetrical motor/mild sensory loss ascending distal→proximal (legs first); worsens ~4 weeks then stabilizes
  • Worse prognosis with respiratory involvement (possible ventilation)
  • Therapy: compensatory strategies acutely; strengthening (isometric→concentric→eccentric) only after stabilization; avoid overstretching/overuse early
  • Monitor vitals; stop/report if weakness ascends to respiratory muscles or autonomic instability occurs

Comparing the three conditions

  • All cause weakness but differ in pattern: MG = fatigable w/ repetition; Bell’s palsy = unilateral facial (CN VII); GBS = ascending symmetrical, phase-dependent
  • Therapy matches pattern: MG avoids fatigue; Bell’s palsy allows spontaneous recovery + facial exercises; GBS compensates early, strengthens only after stabilization

More from Neuromuscular system

  • Central nervous system
  • Anatomy and function of spinal cord
  • Stroke deficits and recovery
  • Traumatic brain injury
  • Spinal cord injury