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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
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3.6 Spinal cord injury
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3. Neuromuscular system
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Spinal cord injury

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Spinal cord injury (SCI) is a partial or complete disruption of the spinal cord resulting in paralysis, sensory loss, altered spinal reflexes, and altered autonomic function.

The causes of spinal cord injury can be falls, motor vehicle accidents, penetrating wounds, disc prolapse, or vascular compromise.

Pathophysiology

  • Primary injury: direct injury to the spinal cord or disruption of vascular supply
  • Secondary injury: edema, demyelination, or necrosis of axons
Definitions
Sacral sparing
Preserved sensory and/or motor function in the lowest sacral segments (S4-S5), tested around the anus. Its presence makes an injury incomplete, and it indicates a better prognosis for recovery.

American Spinal Injury Association (ASIA) levels of injury

  • A: complete
    • No motor or sensory function preserved below the level of injury
    • No motor or sensory function in sacral segments S4-S5 (no sacral sparing)
  • B: incomplete
    • Sensory but no motor below the level of injury
    • Sensory to sacral segments S4-S5, but no motor to these segments
  • C: incomplete
    • Motor function is preserved below the level of injury, and more than half of the key muscles below that level have a manual muscle test grade less than 3
  • D: incomplete
    • Motor function is preserved below the level of injury, and at least half of the key muscles below that level have a manual muscle test grade of 3 or greater
  • E: normal
    • Motor and sensory are normal

PTA scope of practice: The PTA collects objective data, such as ASIA classification findings and Modified Ashworth Scale scores, and reports changes to the supervising PT. The PTA does not reclassify the injury or alter the plan of care independently.

Classifications of incomplete spinal cord injuries

The four incomplete cord syndromes below are easiest to tell apart by tracking which of three tracts is affected: the corticospinal tract (motor), the spinothalamic tract (pain and temperature), and the dorsal columns (proprioception and vibration).

The following table compares four incomplete spinal cord syndromes by etiology and which tracts are affected.


Syndrome Etiology Motor (corticospinal) Pain/temperature (spinothalamic) Proprioception/vibration (dorsal columns)
Central cord Cervical hyperextension Bilateral loss, worse in the upper extremities Bilateral loss Intact
Anterior cord Cervical flexion or vascular compromise Bilateral loss below the level of injury Bilateral loss Intact
Posterior cord Posterior spinal artery ischemia (rarely, hyperextension trauma) Intact Intact Bilateral loss
Brown-Séquard Penetrating trauma (gunshot or stab wound) Ipsilateral loss Contralateral loss Ipsilateral loss

Example: identifying an incomplete spinal cord syndrome

After a hyperflexion injury to the cervical spine, a patient has bilateral loss of motor function and bilateral loss of pain and temperature sensation below the level of injury. Proprioception, vibration sense, and kinesthesia are intact. Which incomplete spinal cord syndrome does this presentation match?

Answer: Anterior cord syndrome - the corticospinal (motor) and spinothalamic (pain/temperature) tracts are affected, but the dorsal columns (proprioception, vibration, and kinesthesia) are spared.

Cauda equina injury is not a cord syndrome; it damages the lumbosacral nerve roots below the end of the cord:

  • Cauda equina injury (classified as lower motor neuron lesion)
    • Etiology: Trauma, herniated disk, spinal stenosis, or infection affecting the nerve roots below the L1-L2 vertebral level
    • Deficits:
      • Flaccid paralysis of bladder, bowel function (incontinence)
      • Impaired motor function - specifically lower extremities
      • Absent spinal reflexes
    • Intact: Variable dependent upon the severity of injury
    • Contrast with a spinal cord injury above the conus, which is an upper motor neuron lesion:
      • Tone: spastic (UMN) vs. flaccid (LMN)
      • Reflexes: hyperreflexive (UMN) vs. absent (LMN)
      • Bladder: reflexive, spastic bladder (UMN) vs. flaccid, areflexic bladder (LMN)

Associated disorders with spinal cord injury

  • Spinal shock
    • A temporary period of absent reflexes and flaccidity below the level of injury caused by sudden loss of descending input to the cord
    • Timeframe can vary from 24 hours to 12 weeks
      • Difficult to get an accurate ASIA assessment due to spinal shock and changes in the level of injury
      • The return of reflexes, such as the bulbocavernosus reflex, signals that spinal shock is ending
  • Autonomic dysreflexia
    • Medical emergency for individuals with T6 or above injury
    • Caused by a noxious stimulus below the level of injury, which triggers a reflex sympathetic surge and widespread vasoconstriction below the lesion. Descending inhibitory signals from the brain can’t pass the lesion to calm this response, so blood pressure rises sharply. Baroreceptors then trigger a vagal (parasympathetic) response above the lesion, causing bradycardia and flushing above the level of injury.
      • Noxious stimuli can be constipation, catheter malfunction, pressure injuries, tight clothes, or sitting on a sharp object
    • Symptoms: headache, increased blood pressure, bradycardia, flushing and diaphoresis above the level of injury, pallor and piloerection (cool skin) below the level of injury, seizures. If left untreated, it can lead to death.
    • Medical management: stop the activity and sit the patient upright with legs lowered; loosen tight clothing or an abdominal binder; check the catheter, bladder, and bowel for the noxious stimulus; monitor blood pressure every few minutes; notify nursing and the supervising PT
  • Spasticity
    • A velocity-dependent increase in resistance to passive stretch (hyperactive stretch reflexes) in the extremities or trunk; leads to range of motion deficits and functional impairment
    • Will only be seen in upper motor neuron lesions
    • Occurs most often in incomplete lesions
    • Utilize the Modified Ashworth Scale to assess
  • Heterotopic ossification
    • Abnormal bone growth in the muscle
    • Symptoms: pain with palpation or muscle stretch, warmth, swelling, decreased range of motion
    • Typically occurs around large joints below the level of injury, most commonly the hips, followed by the knees
  • Deep vein thrombosis
    • Requires urgent medical attention; can lead to a life-threatening pulmonary embolism
    • Development due to immobility of extremities, which places individuals at increased risk for blood clot development
    • Warning signs: unilateral calf swelling, warmth, redness, or pain
    • If suspected: hold exercise and mobilization and notify the PT/medical team immediately
    • Prevention: graduated compression socks, anti-coagulation medication
  • Orthostatic hypotension
    • Defined as a drop of at least 20 mmHg systolic or 10 mmHg diastolic on moving upright; in SCI it results from loss of sympathetic vasomotor tone, with venous pooling in the legs and abdomen
    • Warning signs: dizziness, lightheadedness, or blurred vision on sitting or standing
    • If symptoms occur: recline the patient, elevate the legs, monitor blood pressure, and report to the PT
    • Treatment option: graduated compression stockings, abdominal binder, tilt table, or medication
  • Syringomyelia
    • A fluid-filled cavity (syrinx) in the spinal cord that commonly begins in the cervical area and causes a capelike loss of pain and temperature sensation over the shoulders, arms, and back, while light touch and position and vibration sensation are not affected

Distinguishing autonomic dysreflexia from orthostatic hypotension: both cause headache or lightheadedness tied to position or activity in SCI, but the blood pressure change and the correct response are opposite.

Feature Autonomic dysreflexia Orthostatic hypotension
Blood pressure Sharply increased Decreased
Heart rate Bradycardia Usually increased
Key symptoms Pounding headache, flushing and sweating above the lesion, pale skin below the lesion Dizziness, lightheadedness, blurred vision
Correct position Sit the patient upright, legs down Recline the patient, legs elevated

Intervention considerations

  • Follow a pressure-relief schedule (weight shifts every 15-30 minutes) during wheelchair use to prevent pressure injuries
  • Avoid stretching the fingers and wrist into extension at the same time in patients with C6-C7 tetraplegia relying on tenodesis grasp, since tenodesis depends on wrist extension creating passive finger flexion
  • Use gentle, pain-free range of motion around joints affected by heterotopic ossification; forceful stretching can worsen bone formation
  • Progress upright tolerance gradually (for example, with a tilt table) and monitor blood pressure frequently to manage orthostatic hypotension
  • Support breathing in patients with tetraplegia using assisted (quad) cough, diaphragmatic breathing or inspiratory muscle training, and an abdominal binder

Wheelchair wheelies

A wheelie is balancing a manual wheelchair on its rear wheels with the casters off the ground. It is the foundation for community skills such as going down a high curb: in a wheelie the rear wheels land first, so the foot supports do not catch the street and pitch the user forward. Going up a curb starts with a caster pop, a brief partial wheelie that lifts the casters onto the curb. Users with full upper extremity strength, such as at a low thoracic level, can learn independent wheelies and curbs.

  • The main risk is a backward tip, so the spotter stands behind the chair holding a spotter strap
  • Training starts with the rear wheels blocked and on a soft surface, then progresses to free balance and then to curbs
  • Rear anti-tip devices may need adjusting for wheelie training, which raises the risk of a backward tip
  • Users also learn to recover from a backward tip by flexing the neck and trunk and pulling back on the hand-rims

Levels of independence (for complete injuries)

Key preserved muscles drive these levels: C5 elbow flexors (biceps), C6 wrist extensors, which allow tenodesis grasp, and C7 triceps, which allow push-up depression transfers.

  • Transfers
    • C1-C5: dependent transfers
    • C6: independent with sliding board transfers on level surfaces
      • For a sliding board transfer, one side of the board is placed under the upper thigh or buttock, and the board must be firmly placed on both surfaces
    • C7 and beyond: independent with transfers without a sliding board on level surfaces; at C7-C8, uneven-surface transfers may still need some assistance
  • Wheelchair use
    • C1-C5: power wheelchair use with head control, mouth control, or joystick
    • C6: manual wheelchair on level surfaces with use of wheel projections and large knobby wheels - independent status
    • C7-C8: manual wheelchair with modified rims, independent indoors and on level outdoor terrain, with some assistance on uneven terrain; T1 and below: independent on all surfaces
  • Respiration
    • C1-C3: usually ventilator-dependent, since the phrenic nerve (C3-C5) innervating the diaphragm is lost
    • C4 and below: diaphragm function is typically preserved, but reduced vital capacity and a weak, ineffective cough remain common due to paralyzed abdominal and intercostal muscles

Gait (ambulation potential decreases, and orthosis and energy demands increase, as the level of injury rises):

The following table shows expected ambulation status, orthosis, and wheelchair use by neurological level for complete spinal cord injuries affecting gait.


Level Ambulation Orthosis Wheelchair use
T12 Exercise or limited household ambulation (high energy cost) Bilateral KAFOs with forearm crutches or a walker Manual wheelchair primary
L1-L2 Household ambulation only (high energy cost) KAFO, locked in extension for gait and unlocked for sitting Manual wheelchair primary
L3 Household ambulation KAFO or AFO (knee control) Manual wheelchair for community mobility
L4 and below Community ambulation AFO for ankle control Manual wheelchair as needed
Definitions
Reciprocating gait orthosis
A series of interconnected braces aiding in ambulation by a lever system attached to the torso; unweighting of the extremity is performed by lateral movement of the torso, causing the swing leg to move forward while the stance leg is pushed backward.

Spinal Cord Injury Overview

  • SCI: partial/complete cord disruption → paralysis, sensory loss, altered reflexes/autonomic function
  • Causes: falls, MVAs, penetrating wounds, disc prolapse, vascular compromise
  • Primary injury (direct/vascular damage) vs. secondary injury (edema, demyelination, necrosis)
  • Sacral sparing (preserved S4-S5 function) = incomplete injury, better prognosis

ASIA Classification

  • A: complete, no motor/sensory below injury, no sacral sparing
  • B: sensory only below injury (incl. S4-S5)
  • C: motor preserved, >half key muscles below injury MMT <3
  • D: motor preserved, ≥half key muscles MMT ≥3
  • E: normal function
  • PTA collects data (ASIA, Modified Ashworth) and reports to PT; cannot reclassify or alter plan of care

Incomplete Cord Syndromes & Cauda Equina

  • Distinguished by tract: corticospinal (motor), spinothalamic (pain/temp), dorsal columns (proprioception/vibration)
  • Central cord (hyperextension): bilateral motor/sensory loss, worse in UEs; dorsal columns intact
  • Anterior cord (flexion/vascular): bilateral motor + pain/temp loss; dorsal columns intact
  • Posterior cord (posterior spinal artery ischemia; rarely hyperextension trauma): only dorsal column loss
  • Brown-Séquard (penetrating trauma): ipsilateral motor + proprioception loss, contralateral pain/temp loss
  • Cauda equina (LMN lesion, below L1-L2): flaccid paralysis, absent reflexes, incontinence
    • UMN = spastic tone/hyperreflexia/spastic bladder vs. LMN = flaccid tone/absent reflexes/flaccid bladder

Associated Disorders

  • Spinal shock: temporary areflexia/flaccidity below injury (24h–12wks); bulbocavernosus reflex return signals resolution
  • Autonomic dysreflexia (T6 or above): noxious stimulus → BP spike, bradycardia, flushing/pallor; manage by sitting upright, legs down, loosening clothing, checking catheter/bowel, monitoring BP
  • Spasticity: velocity-dependent stretch resistance, only UMN lesions; measured via Modified Ashworth Scale
  • Heterotopic ossification: abnormal bone growth near joints (hips most common); pain/warmth/swelling/decreased ROM
  • DVT: unilateral calf swelling/warmth/redness; hold exercise, notify team; prevent with compression socks/anticoagulants
  • Orthostatic hypotension: BP drop ≥20/10 mmHg with position change; recline, elevate legs, monitor BP
  • Key distinction: dysreflexia = BP up + bradycardia + sit upright; hypotension = BP down + recline

Intervention Considerations

  • Pressure relief every 15-30 min in wheelchair
  • Avoid simultaneous wrist/finger extension in C6-C7 tetraplegia (preserve tenodesis grasp)
  • Gentle pain-free ROM with heterotopic ossification; avoid forceful stretch
  • Gradual upright tolerance progression (tilt table) with frequent BP checks
  • Support respiration in tetraplegia: assisted cough, diaphragmatic breathing, abdominal binder

Wheelchair Wheelies

  • Balance on rear wheels, casters raised; foundation for curb skills
  • Down curb: rear wheels land first to avoid pitching forward; up curb starts with caster pop
  • Main risk: backward tip; spotter uses strap; progress from blocked wheels/soft surface to free balance to curbs
  • Users learn fall recovery: flex neck/trunk, pull back on hand-rims

Levels of Independence

  • Key muscles: C5 elbow flexors, C6 wrist extensors (tenodesis), C7 triceps (push-up transfers)
  • Transfers: C1-C5 dependent; C6 independent w/ sliding board; C7+ independent w/o board (uneven surfaces may need help at C7-C8)
  • Wheelchair: C1-C5 power w/ head/mouth/joystick; C6 manual w/ projections; C7-C8 manual w/ modified rims (indoor/level outdoor); T1+ independent all surfaces
  • Respiration: C1-C3 often ventilator-dependent (phrenic nerve C3-C5 lost); C4+ diaphragm preserved but weak cough/reduced vital capacity common

Gait by Level

  • Ambulation potential decreases, orthosis/energy demands increase as injury level rises
  • T12: household/exercise ambulation, bilateral KAFOs + crutches/walker, manual wheelchair primary
  • L1-L2: household ambulation, KAFO locked for gait, manual wheelchair primary
  • L3: household ambulation, KAFO/AFO, wheelchair for community
  • L4+: community ambulation, AFO only, wheelchair as needed
  • Reciprocating gait orthosis: interconnected braces with lever system; torso lateral movement drives reciprocal leg swing

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Spinal cord injury

Spinal cord injury (SCI) is a partial or complete disruption of the spinal cord resulting in paralysis, sensory loss, altered spinal reflexes, and altered autonomic function.

The causes of spinal cord injury can be falls, motor vehicle accidents, penetrating wounds, disc prolapse, or vascular compromise.

Pathophysiology

  • Primary injury: direct injury to the spinal cord or disruption of vascular supply
  • Secondary injury: edema, demyelination, or necrosis of axons
Definitions
Sacral sparing
Preserved sensory and/or motor function in the lowest sacral segments (S4-S5), tested around the anus. Its presence makes an injury incomplete, and it indicates a better prognosis for recovery.

American Spinal Injury Association (ASIA) levels of injury

  • A: complete
    • No motor or sensory function preserved below the level of injury
    • No motor or sensory function in sacral segments S4-S5 (no sacral sparing)
  • B: incomplete
    • Sensory but no motor below the level of injury
    • Sensory to sacral segments S4-S5, but no motor to these segments
  • C: incomplete
    • Motor function is preserved below the level of injury, and more than half of the key muscles below that level have a manual muscle test grade less than 3
  • D: incomplete
    • Motor function is preserved below the level of injury, and at least half of the key muscles below that level have a manual muscle test grade of 3 or greater
  • E: normal
    • Motor and sensory are normal

PTA scope of practice: The PTA collects objective data, such as ASIA classification findings and Modified Ashworth Scale scores, and reports changes to the supervising PT. The PTA does not reclassify the injury or alter the plan of care independently.

Classifications of incomplete spinal cord injuries

The four incomplete cord syndromes below are easiest to tell apart by tracking which of three tracts is affected: the corticospinal tract (motor), the spinothalamic tract (pain and temperature), and the dorsal columns (proprioception and vibration).

The following table compares four incomplete spinal cord syndromes by etiology and which tracts are affected.


Syndrome Etiology Motor (corticospinal) Pain/temperature (spinothalamic) Proprioception/vibration (dorsal columns)
Central cord Cervical hyperextension Bilateral loss, worse in the upper extremities Bilateral loss Intact
Anterior cord Cervical flexion or vascular compromise Bilateral loss below the level of injury Bilateral loss Intact
Posterior cord Posterior spinal artery ischemia (rarely, hyperextension trauma) Intact Intact Bilateral loss
Brown-Séquard Penetrating trauma (gunshot or stab wound) Ipsilateral loss Contralateral loss Ipsilateral loss

Example: identifying an incomplete spinal cord syndrome

After a hyperflexion injury to the cervical spine, a patient has bilateral loss of motor function and bilateral loss of pain and temperature sensation below the level of injury. Proprioception, vibration sense, and kinesthesia are intact. Which incomplete spinal cord syndrome does this presentation match?

Answer: Anterior cord syndrome - the corticospinal (motor) and spinothalamic (pain/temperature) tracts are affected, but the dorsal columns (proprioception, vibration, and kinesthesia) are spared.

Cauda equina injury is not a cord syndrome; it damages the lumbosacral nerve roots below the end of the cord:

  • Cauda equina injury (classified as lower motor neuron lesion)
    • Etiology: Trauma, herniated disk, spinal stenosis, or infection affecting the nerve roots below the L1-L2 vertebral level
    • Deficits:
      • Flaccid paralysis of bladder, bowel function (incontinence)
      • Impaired motor function - specifically lower extremities
      • Absent spinal reflexes
    • Intact: Variable dependent upon the severity of injury
    • Contrast with a spinal cord injury above the conus, which is an upper motor neuron lesion:
      • Tone: spastic (UMN) vs. flaccid (LMN)
      • Reflexes: hyperreflexive (UMN) vs. absent (LMN)
      • Bladder: reflexive, spastic bladder (UMN) vs. flaccid, areflexic bladder (LMN)

Associated disorders with spinal cord injury

  • Spinal shock
    • A temporary period of absent reflexes and flaccidity below the level of injury caused by sudden loss of descending input to the cord
    • Timeframe can vary from 24 hours to 12 weeks
      • Difficult to get an accurate ASIA assessment due to spinal shock and changes in the level of injury
      • The return of reflexes, such as the bulbocavernosus reflex, signals that spinal shock is ending
  • Autonomic dysreflexia
    • Medical emergency for individuals with T6 or above injury
    • Caused by a noxious stimulus below the level of injury, which triggers a reflex sympathetic surge and widespread vasoconstriction below the lesion. Descending inhibitory signals from the brain can’t pass the lesion to calm this response, so blood pressure rises sharply. Baroreceptors then trigger a vagal (parasympathetic) response above the lesion, causing bradycardia and flushing above the level of injury.
      • Noxious stimuli can be constipation, catheter malfunction, pressure injuries, tight clothes, or sitting on a sharp object
    • Symptoms: headache, increased blood pressure, bradycardia, flushing and diaphoresis above the level of injury, pallor and piloerection (cool skin) below the level of injury, seizures. If left untreated, it can lead to death.
    • Medical management: stop the activity and sit the patient upright with legs lowered; loosen tight clothing or an abdominal binder; check the catheter, bladder, and bowel for the noxious stimulus; monitor blood pressure every few minutes; notify nursing and the supervising PT
  • Spasticity
    • A velocity-dependent increase in resistance to passive stretch (hyperactive stretch reflexes) in the extremities or trunk; leads to range of motion deficits and functional impairment
    • Will only be seen in upper motor neuron lesions
    • Occurs most often in incomplete lesions
    • Utilize the Modified Ashworth Scale to assess
  • Heterotopic ossification
    • Abnormal bone growth in the muscle
    • Symptoms: pain with palpation or muscle stretch, warmth, swelling, decreased range of motion
    • Typically occurs around large joints below the level of injury, most commonly the hips, followed by the knees
  • Deep vein thrombosis
    • Requires urgent medical attention; can lead to a life-threatening pulmonary embolism
    • Development due to immobility of extremities, which places individuals at increased risk for blood clot development
    • Warning signs: unilateral calf swelling, warmth, redness, or pain
    • If suspected: hold exercise and mobilization and notify the PT/medical team immediately
    • Prevention: graduated compression socks, anti-coagulation medication
  • Orthostatic hypotension
    • Defined as a drop of at least 20 mmHg systolic or 10 mmHg diastolic on moving upright; in SCI it results from loss of sympathetic vasomotor tone, with venous pooling in the legs and abdomen
    • Warning signs: dizziness, lightheadedness, or blurred vision on sitting or standing
    • If symptoms occur: recline the patient, elevate the legs, monitor blood pressure, and report to the PT
    • Treatment option: graduated compression stockings, abdominal binder, tilt table, or medication
  • Syringomyelia
    • A fluid-filled cavity (syrinx) in the spinal cord that commonly begins in the cervical area and causes a capelike loss of pain and temperature sensation over the shoulders, arms, and back, while light touch and position and vibration sensation are not affected

Distinguishing autonomic dysreflexia from orthostatic hypotension: both cause headache or lightheadedness tied to position or activity in SCI, but the blood pressure change and the correct response are opposite.

Feature Autonomic dysreflexia Orthostatic hypotension
Blood pressure Sharply increased Decreased
Heart rate Bradycardia Usually increased
Key symptoms Pounding headache, flushing and sweating above the lesion, pale skin below the lesion Dizziness, lightheadedness, blurred vision
Correct position Sit the patient upright, legs down Recline the patient, legs elevated

Intervention considerations

  • Follow a pressure-relief schedule (weight shifts every 15-30 minutes) during wheelchair use to prevent pressure injuries
  • Avoid stretching the fingers and wrist into extension at the same time in patients with C6-C7 tetraplegia relying on tenodesis grasp, since tenodesis depends on wrist extension creating passive finger flexion
  • Use gentle, pain-free range of motion around joints affected by heterotopic ossification; forceful stretching can worsen bone formation
  • Progress upright tolerance gradually (for example, with a tilt table) and monitor blood pressure frequently to manage orthostatic hypotension
  • Support breathing in patients with tetraplegia using assisted (quad) cough, diaphragmatic breathing or inspiratory muscle training, and an abdominal binder

Wheelchair wheelies

A wheelie is balancing a manual wheelchair on its rear wheels with the casters off the ground. It is the foundation for community skills such as going down a high curb: in a wheelie the rear wheels land first, so the foot supports do not catch the street and pitch the user forward. Going up a curb starts with a caster pop, a brief partial wheelie that lifts the casters onto the curb. Users with full upper extremity strength, such as at a low thoracic level, can learn independent wheelies and curbs.

  • The main risk is a backward tip, so the spotter stands behind the chair holding a spotter strap
  • Training starts with the rear wheels blocked and on a soft surface, then progresses to free balance and then to curbs
  • Rear anti-tip devices may need adjusting for wheelie training, which raises the risk of a backward tip
  • Users also learn to recover from a backward tip by flexing the neck and trunk and pulling back on the hand-rims

Levels of independence (for complete injuries)

Key preserved muscles drive these levels: C5 elbow flexors (biceps), C6 wrist extensors, which allow tenodesis grasp, and C7 triceps, which allow push-up depression transfers.

  • Transfers
    • C1-C5: dependent transfers
    • C6: independent with sliding board transfers on level surfaces
      • For a sliding board transfer, one side of the board is placed under the upper thigh or buttock, and the board must be firmly placed on both surfaces
    • C7 and beyond: independent with transfers without a sliding board on level surfaces; at C7-C8, uneven-surface transfers may still need some assistance
  • Wheelchair use
    • C1-C5: power wheelchair use with head control, mouth control, or joystick
    • C6: manual wheelchair on level surfaces with use of wheel projections and large knobby wheels - independent status
    • C7-C8: manual wheelchair with modified rims, independent indoors and on level outdoor terrain, with some assistance on uneven terrain; T1 and below: independent on all surfaces
  • Respiration
    • C1-C3: usually ventilator-dependent, since the phrenic nerve (C3-C5) innervating the diaphragm is lost
    • C4 and below: diaphragm function is typically preserved, but reduced vital capacity and a weak, ineffective cough remain common due to paralyzed abdominal and intercostal muscles

Gait (ambulation potential decreases, and orthosis and energy demands increase, as the level of injury rises):

The following table shows expected ambulation status, orthosis, and wheelchair use by neurological level for complete spinal cord injuries affecting gait.


Level Ambulation Orthosis Wheelchair use
T12 Exercise or limited household ambulation (high energy cost) Bilateral KAFOs with forearm crutches or a walker Manual wheelchair primary
L1-L2 Household ambulation only (high energy cost) KAFO, locked in extension for gait and unlocked for sitting Manual wheelchair primary
L3 Household ambulation KAFO or AFO (knee control) Manual wheelchair for community mobility
L4 and below Community ambulation AFO for ankle control Manual wheelchair as needed
Definitions
Reciprocating gait orthosis
A series of interconnected braces aiding in ambulation by a lever system attached to the torso; unweighting of the extremity is performed by lateral movement of the torso, causing the swing leg to move forward while the stance leg is pushed backward.
Key points

Spinal Cord Injury Overview

  • SCI: partial/complete cord disruption → paralysis, sensory loss, altered reflexes/autonomic function
  • Causes: falls, MVAs, penetrating wounds, disc prolapse, vascular compromise
  • Primary injury (direct/vascular damage) vs. secondary injury (edema, demyelination, necrosis)
  • Sacral sparing (preserved S4-S5 function) = incomplete injury, better prognosis

ASIA Classification

  • A: complete, no motor/sensory below injury, no sacral sparing
  • B: sensory only below injury (incl. S4-S5)
  • C: motor preserved, >half key muscles below injury MMT <3
  • D: motor preserved, ≥half key muscles MMT ≥3
  • E: normal function
  • PTA collects data (ASIA, Modified Ashworth) and reports to PT; cannot reclassify or alter plan of care

Incomplete Cord Syndromes & Cauda Equina

  • Distinguished by tract: corticospinal (motor), spinothalamic (pain/temp), dorsal columns (proprioception/vibration)
  • Central cord (hyperextension): bilateral motor/sensory loss, worse in UEs; dorsal columns intact
  • Anterior cord (flexion/vascular): bilateral motor + pain/temp loss; dorsal columns intact
  • Posterior cord (posterior spinal artery ischemia; rarely hyperextension trauma): only dorsal column loss
  • Brown-Séquard (penetrating trauma): ipsilateral motor + proprioception loss, contralateral pain/temp loss
  • Cauda equina (LMN lesion, below L1-L2): flaccid paralysis, absent reflexes, incontinence
    • UMN = spastic tone/hyperreflexia/spastic bladder vs. LMN = flaccid tone/absent reflexes/flaccid bladder

Associated Disorders

  • Spinal shock: temporary areflexia/flaccidity below injury (24h–12wks); bulbocavernosus reflex return signals resolution
  • Autonomic dysreflexia (T6 or above): noxious stimulus → BP spike, bradycardia, flushing/pallor; manage by sitting upright, legs down, loosening clothing, checking catheter/bowel, monitoring BP
  • Spasticity: velocity-dependent stretch resistance, only UMN lesions; measured via Modified Ashworth Scale
  • Heterotopic ossification: abnormal bone growth near joints (hips most common); pain/warmth/swelling/decreased ROM
  • DVT: unilateral calf swelling/warmth/redness; hold exercise, notify team; prevent with compression socks/anticoagulants
  • Orthostatic hypotension: BP drop ≥20/10 mmHg with position change; recline, elevate legs, monitor BP
  • Key distinction: dysreflexia = BP up + bradycardia + sit upright; hypotension = BP down + recline

Intervention Considerations

  • Pressure relief every 15-30 min in wheelchair
  • Avoid simultaneous wrist/finger extension in C6-C7 tetraplegia (preserve tenodesis grasp)
  • Gentle pain-free ROM with heterotopic ossification; avoid forceful stretch
  • Gradual upright tolerance progression (tilt table) with frequent BP checks
  • Support respiration in tetraplegia: assisted cough, diaphragmatic breathing, abdominal binder

Wheelchair Wheelies

  • Balance on rear wheels, casters raised; foundation for curb skills
  • Down curb: rear wheels land first to avoid pitching forward; up curb starts with caster pop
  • Main risk: backward tip; spotter uses strap; progress from blocked wheels/soft surface to free balance to curbs
  • Users learn fall recovery: flex neck/trunk, pull back on hand-rims

Levels of Independence

  • Key muscles: C5 elbow flexors, C6 wrist extensors (tenodesis), C7 triceps (push-up transfers)
  • Transfers: C1-C5 dependent; C6 independent w/ sliding board; C7+ independent w/o board (uneven surfaces may need help at C7-C8)
  • Wheelchair: C1-C5 power w/ head/mouth/joystick; C6 manual w/ projections; C7-C8 manual w/ modified rims (indoor/level outdoor); T1+ independent all surfaces
  • Respiration: C1-C3 often ventilator-dependent (phrenic nerve C3-C5 lost); C4+ diaphragm preserved but weak cough/reduced vital capacity common

Gait by Level

  • Ambulation potential decreases, orthosis/energy demands increase as injury level rises
  • T12: household/exercise ambulation, bilateral KAFOs + crutches/walker, manual wheelchair primary
  • L1-L2: household ambulation, KAFO locked for gait, manual wheelchair primary
  • L3: household ambulation, KAFO/AFO, wheelchair for community
  • L4+: community ambulation, AFO only, wheelchair as needed
  • Reciprocating gait orthosis: interconnected braces with lever system; torso lateral movement drives reciprocal leg swing

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