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
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
- 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).
- 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 |