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Introduction
1. Cardiopulmonary 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 system
7. Non systems
Wrapping up
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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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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

Severity of injury

  • Complete: no sensory or motor below the level of injury; no sacral sparing
  • Incomplete: inconsistent sensory or motor below the level of injury; sacral sparing present
Definitions
Sacral sparing
Sensory and/or motor innervation to the anus; its presence 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 segment S4-S5 (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

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 (classified as lower motor neuron lesion)
    • Etiology: Trauma, herniated disk, spinal stenosis, infections below the L1 nerve root
    • 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

Associated disorders with spinal cord injury

  • Spinal shock
    • Immediately after injury a time of absent reflexes and flaccidity due to the body working to protect itself after injury
    • 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
  • Autonomic dysreflexia
    • Medical emergency for individuals with T6 or above injury
    • Caused by noxious stimuli in individuals with spinal cord injury who are unable to regulate sympathetic responses below the level of injury.
      • Noxious stimulus causes activation of the sympathetic nervous system, and due to the spinal cord injury, the parasympathetic nervous system is unable to be activated below the level of injury (activation of the parasympathetic system would normally cancel out the effects of the sympathetic nervous system).
        • 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: sit the patient up and assess for noxious stimulus
  • Spasticity
    • Increased tone to extremities or trunk due to consistent contraction; 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: firmness at the muscle site, pain with palpation, pain with muscle stretch or palpation
    • Typically occurs around large joints below the level of injury, most commonly the hips, followed by the knees
  • Deep vein thrombosis
    • Medical emergency
    • Development due to immobility of extremities, which places individuals at increased risk for blood clot development
    • Treatment option: graduated compression socks, anti-coagulation medication
  • Orthostatic hypotension
    • Development due to a change in blood pressure: a systolic drop of 20 mmHg or a diastolic drop of 10 mmHg
    • Treatment option: graduated compression stockings, abdominal binder, tilt table, or medication

Levels of independence (for complete injuries)

  • Transfers
    • C1-C5: dependent transfers
    • C6: independent with sliding board transfers on level surfaces
    • C7 and beyond: independent with transfers without a sliding board on uneven surfaces
  • 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 and beyond: manual wheelchair usage without adaptations on all surfaces - independent status

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 ambulation only (high energy cost) HKAFO with the hip locked in extension, or an RGO 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 AFO for 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

  • Partial/complete disruption of spinal cord → paralysis, sensory loss, altered reflexes, altered autonomic function
  • Causes: falls, MVAs, penetrating wounds, disc prolapse, vascular compromise

Pathophysiology

  • Primary injury: direct trauma or vascular disruption to cord
  • Secondary injury: edema, demyelination, axon necrosis

Severity of injury

  • Complete: no sensory/motor below injury level; no sacral sparing
  • Incomplete: inconsistent sensory/motor below injury level; sacral sparing present
  • Sacral sparing = sensory/motor to anus; presence = better prognosis

ASIA levels of injury

  • A (complete): no motor/sensory below level, no S4-S5 function
  • B (incomplete): sensory only below level, sensory (no motor) at S4-S5
  • C (incomplete): motor preserved, >half key muscles below level MMT <3
  • D (incomplete): motor preserved, ≥half key muscles below level MMT ≥3
  • E (normal): motor and sensory normal

Incomplete spinal cord syndromes

  • Distinguished by tract involvement: corticospinal (motor), spinothalamic (pain/temp), dorsal columns (proprioception/vibration)
  • Central cord: cervical hyperextension; bilateral motor loss (worse in UE), bilateral pain/temp loss, dorsal columns intact
  • Anterior cord: cervical flexion/vascular compromise; bilateral motor + pain/temp loss below level, dorsal columns intact
  • Posterior cord: posterior spinal artery ischemia; motor/pain-temp intact, bilateral proprioception/vibration loss
  • Brown-Séquard: penetrating trauma; ipsilateral motor + proprioception loss, contralateral pain/temp loss
  • Cauda equina (LMN lesion): trauma/herniated disk/stenosis below L1
    • Flaccid bowel/bladder incontinence, impaired LE motor function, absent reflexes
    • Variable sparing depending on severity

Associated disorders

  • Spinal shock: temporary areflexia/flaccidity post-injury; lasts 24 hrs–12 weeks; complicates accurate ASIA scoring
  • Autonomic dysreflexia: medical emergency for T6+ injuries
    • Triggered by noxious stimuli (constipation, catheter issues, pressure injury, tight clothing)
    • Symptoms: headache, hypertension, bradycardia, flushing/diaphoresis above level; pallor/piloerection below level; seizures possible
    • Management: sit patient upright, identify/remove noxious stimulus
  • Spasticity: increased tone from sustained contraction; seen only in UMN lesions, most common in incomplete injuries; assessed via Modified Ashworth Scale
  • Heterotopic ossification: abnormal bone growth in muscle; firmness/pain with palpation or stretch; most common at hips, then knees
  • Deep vein thrombosis: medical emergency from immobility; treat with compression socks, anticoagulants
  • Orthostatic hypotension: systolic drop ≥20 mmHg or diastolic drop ≥10 mmHg; treat with compression stockings, abdominal binder, tilt table, or medication

Levels of independence (complete injuries)

  • Transfers: C1-C5 dependent; C6 independent with sliding board (level surfaces); C7+ independent without board (uneven surfaces)
  • Wheelchair: C1-C5 power WC (head/mouth/joystick control); C6 manual WC independent on level surfaces w/ adaptations; C7+ manual WC independent on all surfaces without adaptations

Gait potential by level

  • Ambulation potential decreases, orthosis/energy demands increase as injury level rises
  • T12: exercise ambulation only; HKAFO (hip locked extension) or RGO; manual WC primary
  • L1-L2: household ambulation only; KAFO (locked for gait, unlocked for sitting); manual WC primary
  • L3: household ambulation; AFO for knee control; manual WC for community mobility
  • L4 and below: community ambulation; AFO for ankle control; manual WC as needed
  • Reciprocating gait orthosis (RGO): interconnected braces with lever system on torso; lateral torso movement swings leg forward while stance leg pushes back

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Spinal cord injury

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

Severity of injury

  • Complete: no sensory or motor below the level of injury; no sacral sparing
  • Incomplete: inconsistent sensory or motor below the level of injury; sacral sparing present
Definitions
Sacral sparing
Sensory and/or motor innervation to the anus; its presence 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 segment S4-S5 (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

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 (classified as lower motor neuron lesion)
    • Etiology: Trauma, herniated disk, spinal stenosis, infections below the L1 nerve root
    • 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

Associated disorders with spinal cord injury

  • Spinal shock
    • Immediately after injury a time of absent reflexes and flaccidity due to the body working to protect itself after injury
    • 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
  • Autonomic dysreflexia
    • Medical emergency for individuals with T6 or above injury
    • Caused by noxious stimuli in individuals with spinal cord injury who are unable to regulate sympathetic responses below the level of injury.
      • Noxious stimulus causes activation of the sympathetic nervous system, and due to the spinal cord injury, the parasympathetic nervous system is unable to be activated below the level of injury (activation of the parasympathetic system would normally cancel out the effects of the sympathetic nervous system).
        • 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: sit the patient up and assess for noxious stimulus
  • Spasticity
    • Increased tone to extremities or trunk due to consistent contraction; 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: firmness at the muscle site, pain with palpation, pain with muscle stretch or palpation
    • Typically occurs around large joints below the level of injury, most commonly the hips, followed by the knees
  • Deep vein thrombosis
    • Medical emergency
    • Development due to immobility of extremities, which places individuals at increased risk for blood clot development
    • Treatment option: graduated compression socks, anti-coagulation medication
  • Orthostatic hypotension
    • Development due to a change in blood pressure: a systolic drop of 20 mmHg or a diastolic drop of 10 mmHg
    • Treatment option: graduated compression stockings, abdominal binder, tilt table, or medication

Levels of independence (for complete injuries)

  • Transfers
    • C1-C5: dependent transfers
    • C6: independent with sliding board transfers on level surfaces
    • C7 and beyond: independent with transfers without a sliding board on uneven surfaces
  • 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 and beyond: manual wheelchair usage without adaptations on all surfaces - independent status

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 ambulation only (high energy cost) HKAFO with the hip locked in extension, or an RGO 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 AFO for 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

  • Partial/complete disruption of spinal cord → paralysis, sensory loss, altered reflexes, altered autonomic function
  • Causes: falls, MVAs, penetrating wounds, disc prolapse, vascular compromise

Pathophysiology

  • Primary injury: direct trauma or vascular disruption to cord
  • Secondary injury: edema, demyelination, axon necrosis

Severity of injury

  • Complete: no sensory/motor below injury level; no sacral sparing
  • Incomplete: inconsistent sensory/motor below injury level; sacral sparing present
  • Sacral sparing = sensory/motor to anus; presence = better prognosis

ASIA levels of injury

  • A (complete): no motor/sensory below level, no S4-S5 function
  • B (incomplete): sensory only below level, sensory (no motor) at S4-S5
  • C (incomplete): motor preserved, >half key muscles below level MMT <3
  • D (incomplete): motor preserved, ≥half key muscles below level MMT ≥3
  • E (normal): motor and sensory normal

Incomplete spinal cord syndromes

  • Distinguished by tract involvement: corticospinal (motor), spinothalamic (pain/temp), dorsal columns (proprioception/vibration)
  • Central cord: cervical hyperextension; bilateral motor loss (worse in UE), bilateral pain/temp loss, dorsal columns intact
  • Anterior cord: cervical flexion/vascular compromise; bilateral motor + pain/temp loss below level, dorsal columns intact
  • Posterior cord: posterior spinal artery ischemia; motor/pain-temp intact, bilateral proprioception/vibration loss
  • Brown-Séquard: penetrating trauma; ipsilateral motor + proprioception loss, contralateral pain/temp loss
  • Cauda equina (LMN lesion): trauma/herniated disk/stenosis below L1
    • Flaccid bowel/bladder incontinence, impaired LE motor function, absent reflexes
    • Variable sparing depending on severity

Associated disorders

  • Spinal shock: temporary areflexia/flaccidity post-injury; lasts 24 hrs–12 weeks; complicates accurate ASIA scoring
  • Autonomic dysreflexia: medical emergency for T6+ injuries
    • Triggered by noxious stimuli (constipation, catheter issues, pressure injury, tight clothing)
    • Symptoms: headache, hypertension, bradycardia, flushing/diaphoresis above level; pallor/piloerection below level; seizures possible
    • Management: sit patient upright, identify/remove noxious stimulus
  • Spasticity: increased tone from sustained contraction; seen only in UMN lesions, most common in incomplete injuries; assessed via Modified Ashworth Scale
  • Heterotopic ossification: abnormal bone growth in muscle; firmness/pain with palpation or stretch; most common at hips, then knees
  • Deep vein thrombosis: medical emergency from immobility; treat with compression socks, anticoagulants
  • Orthostatic hypotension: systolic drop ≥20 mmHg or diastolic drop ≥10 mmHg; treat with compression stockings, abdominal binder, tilt table, or medication

Levels of independence (complete injuries)

  • Transfers: C1-C5 dependent; C6 independent with sliding board (level surfaces); C7+ independent without board (uneven surfaces)
  • Wheelchair: C1-C5 power WC (head/mouth/joystick control); C6 manual WC independent on level surfaces w/ adaptations; C7+ manual WC independent on all surfaces without adaptations

Gait potential by level

  • Ambulation potential decreases, orthosis/energy demands increase as injury level rises
  • T12: exercise ambulation only; HKAFO (hip locked extension) or RGO; manual WC primary
  • L1-L2: household ambulation only; KAFO (locked for gait, unlocked for sitting); manual WC primary
  • L3: household ambulation; AFO for knee control; manual WC for community mobility
  • L4 and below: community ambulation; AFO for ankle control; manual WC as needed
  • Reciprocating gait orthosis (RGO): interconnected braces with lever system on torso; lateral torso movement swings leg forward while stance leg pushes back

More from Neuromuscular system

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