Spinal Shock Physiology
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Direct answer
Within seconds to minutes of an acute spinal cord transection, everything below the lesion shuts down: flaccid paralysis, complete anaesthesia, abolished reflexes, atonic bladder with urinary retention, gut ileus, and loss of sympathetic vasomotor tone — the phase called spinal shock, lasting hours to six weeks or more in humans (minutes in dogs, days in monkeys — duration lengthens up the phylogenetic scale). A lesion above T6 additionally produces neurogenic shock: hypotension with bradycardia from the loss of cardiac sympathetic acceleration, distinguishable from haemorrhagic shock by warm, dry extremities. Recovery is heralded by the bulbocavernosus reflex (S2-S4) returning first, followed by cutaneous and then pathological reflexes; reflexes eventually become hyperactive, and in lesions above T6 the mass reflex of autonomic dysreflexia appears — paroxysmal hypertension 50 mmHg or more above baseline with reflex bradycardia and sweating above the lesion.
What you must remember
- Definition: sudden loss of all cord function below an acute lesion — reflex, motor, sensory and autonomic — from interruption of tonic descending facilitation, not from the structural cut alone.
- Duration gradient: dogs minutes to hours, monkeys days, humans weeks (commonly 1-6 weeks) — the classic comparative-physiology line for vivas.
- First reflex back: bulbocavernosus (S2-S4), then anal wink, cremasteric, and finally Babinski and clonus appear as denervation supersensitivity renders segments hyperreflexic.
- Bladder behaviour: initial atonic retention with overflow incontinence, evolving over weeks into automatic (reflex) bladder emptying triggered by any cutaneous or visceral stimulus below the lesion.
- Neurogenic versus spinal shock: neurogenic shock is the cardiovascular state (hypotension plus bradycardia from sympathetic loss); spinal shock is the reflex state — they coexist after cervical injury but are not synonyms.
- Autonomic dysreflexia: lesions above T6; distension of bladder or bowel fires a massive reflex sympathetic discharge — systolic pressures can exceed 200 mmHg with pounding headache, flushing and sweating above the level, reflex bradycardia below the brain's baroreflex attempt; relieve the trigger first, then nifedipine or nitrates.
- Onset clue: priapism in the early hours of cord injury is a classical sign of the spinal shock phase and frequently appears as a one-mark question.
- Contrast with cerebral shock: an upper motor neuron lesion after stroke also passes through a flaccid stage before spasticity develops — the same loss-then-supersensitivity logic above and below the foramen magnum.
A worked case from injury to dysreflexia
A 24-year-old man sustains a C5 transection in a road accident. On arrival he is hypotensive at 85/50 with a heart rate of 50 — the sympathetic outflow to vasculature and heart is disconnected while vagal tone survives. The skin is warm: no compensation, no tachycardia, the signature that separates neurogenic from haemorrhagic shock and prevents the fatal error of over-infusing crystalloid. Below the neck he is flaccid and areflexic; the bladder distends silently.
Six weeks later the picture inverts: reflexes are hyperactive, plantars are extensor, and an overdistended bladder sets off autonomic dysreflexia — blood pressure shoots to 210/110, his head pounds, he sweats over the face and neck while the baroreceptors brake the heart to 45. The emergency manoeuvre is physiological: sit him up, catheterise or relieve the obstructed tube, and only then use antihypertensives. Every caregiver of a T6-plus patient is taught this algorithm because a full bladder in a disconnected cord is a hypertensive emergency.
Where students slip
The commonest confusion is between spinal shock and neurogenic shock, and the viva probe is direct: which has bradycardia? Neurogenic — because sympathetic cardiac accelerator fibres (T1-T4) are lost while the vagus, travelling extraspinally, keeps firing. The second slip is expecting hyperreflexia immediately; early flaccidity with absent reflexes is the expected stage, so a Babinski on day one should prompt a search for a second lesion. Third, students forget why reflexes return hyperactive: isolated segments develop denervation supersensitivity to excitatory transmitters, so recovery means exaggeration — the same reason the atonic bladder later becomes spastic.
Frequently asked questions
What defines the spinal shock phase?
Abrupt total loss of reflex, motor, sensory and autonomic function below an acute cord lesion — flaccid areflexia, anaesthesia, atonic bladder — from withdrawal of tonic descending facilitation.
Which reflex returns first as spinal shock resolves?
The bulbocavernosus reflex at S2-S4; its reappearance is the classical bedside marker that spinal shock has ended, after which reflexes return progressively and eventually become exaggerated.
How does neurogenic shock differ from haemorrhagic shock?
Neurogenic shock combines hypotension with bradycardia and warm dry peripheries from sympathetic denervation, whereas haemorrhagic shock produces compensatory tachycardia with cold, vasoconstricted extremities.
What triggers autonomic dysreflexia and at which lesion level?
Noxious stimuli below the lesion — classically bladder catheter blockage or faecal impaction — in patients with lesions above T6, provoking reflex hypertension with headache, sweating above the level and reflex bradycardia.
Why does priapism occur at the onset of spinal shock?
Loss of sympathetic vasoconstrictive tone in the acute phase allows parasympathetic-dominated pelvic vasodilatation, producing transient penile engorgement that is a recognised early sign of cord injury.