Spinal shock
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spinal shock definition clinical features reflexes phase management MSD Manual
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https://www.ncbi.nlm.nih.gov/books/NBK448163
Spinal shock
Spinal shock is the transient suppression of all spinal cord functions below an acute spinal cord injury. It is a physiologic state, not proof that the cord has been anatomically transected.
Clinical features below the lesion
- Flaccid paralysis with hypotonia
- Loss of deep tendon and superficial reflexes, or areflexia
- Loss of sensation
- Loss of bowel and bladder reflex activity:
- Atonic bladder with urinary retention or overflow dribbling
- Reduced anal tone
- Loss of autonomic reflexes
It can make a severe but incomplete injury initially appear to be a complete spinal cord lesion. A definitive assessment of completeness should therefore be deferred until spinal shock has resolved.
Mechanism
Sudden interruption of descending supraspinal facilitation causes hyperpolarization and reduced excitability of spinal neurons and reflex arcs. With time, receptor upregulation and synaptic reorganization allow reflexes to return, often followed by hyperreflexia and spasticity.
Course and phases
The duration varies, commonly 24-72 hours, but some reflex and autonomic changes can evolve for weeks or longer.
| Phase | Typical timing | Findings |
|---|---|---|
| 1. Areflexia/hyporeflexia | 0-24/48 h | Flaccidity and absent reflexes |
| 2. Initial reflex return | Day 1-3 | Delayed plantar and cutaneous reflexes return; bulbocavernosus reflex often returns early |
| 3. Early hyperreflexia | Days 4 to 1 month | Deep tendon reflexes return, increasingly brisk |
| 4. Spasticity/hyperreflexia | 1-12 months | Hypertonia, exaggerated reflexes, possible spasms |
A common bedside convention is that return of the bulbocavernosus reflex (BCR) marks the end of spinal shock. The BCR is contraction of the anal sphincter after squeezing the glans penis or clitoris, or gently tugging an indwelling urinary catheter. However, not every clinician uses the same endpoint, and reflex recovery differs across patients. Miller's Review of Orthopaedics, p. 793.
Spinal shock versus neurogenic shock
| Feature | Spinal shock | Neurogenic shock |
|---|---|---|
| Primary issue | Neurologic/reflex dysfunction below SCI | Hemodynamic loss of sympathetic tone |
| Motor/reflexes | Flaccid paralysis, areflexia | May coexist with spinal shock |
| Blood pressure | May be normal or low | Hypotension |
| Heart rate | Variable | Bradycardia |
| Skin | Not defining | Often warm, dry, vasodilated |
They can occur together after a high cervical or upper thoracic injury. Neurogenic shock is treated as a circulatory emergency with airway support, cautious fluids, and vasopressors as indicated, while also excluding hemorrhage and other causes of hypotension.
Key point
Spinal shock is not the same as permanent paralysis. It is an early, temporary phase after acute spinal cord injury; later emergence of hyperreflexia and spasticity reflects an upper motor neuron pattern below the injury.
The textbook description notes that the BCR is commonly an early returning reflex and that its return signals resolution, though injuries involving the conus or cauda equina can permanently abolish it. Miller's Review of Orthopaedics, p. 793. A current NCBI clinical review similarly distinguishes spinal shock from neurogenic shock and describes the typical sequence of reflex return.
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