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# Spinal shock and the isolated cord

- Mechanism
- Exam priority: medium

When the spinal cord is cut, everything below goes silent for a while; later the cord's own reflexes return, sometimes too strongly.

Updated Nov 13, 2026

Also called: Mass reflex, Autonomic dysreflexia

**See it in 3D:** [Spinal cord](https://durgical.com/en/anatomy/spinal-cord/) · [Grey matter of the cord](https://durgical.com/en/anatomy/grey-matter-of-spinal-cord/) · [Sympathetic trunk](https://durgical.com/en/anatomy/sympathetic-trunk/)

## Key points

- Spinal shock = loss of reflexes and tone below the lesion (a neurological state); neurogenic shock = hypotension with bradycardia from lost sympathetic outflow (a hemodynamic state).
- Cause: sudden loss of tonic descending facilitation (reticulospinal, vestibulospinal, corticospinal), not damage to the cord below the lesion.
- Reflexes return over days to weeks; the bulbocavernosus reflex is often one of the first to reappear; later hyperreflexia and spasticity develop.
- Mass reflex: in a chronic isolated cord, one strong stimulus below the lesion triggers widespread flexor spasm, bladder and bowel emptying, sweating and a rise in blood pressure.
- Autonomic dysreflexia (lesions at or above about T6): a stimulus below the lesion causes a sympathetic surge with severe hypertension; reflex bradycardia and flushing appear above the lesion.

## What it is

Spinal shock is the temporary loss of all cord function below an acute transection: reflexes, muscle tone and autonomic reflexes. It happens because cord neurons lose the constant excitatory drive they get from the brain. Over days to weeks the isolated cord regains its own reflexes, which may then become exaggerated and can trigger dangerous autonomic surges.

## How it works, step by step

- Cord neurons below the lesion normally sit close to threshold thanks to steady excitatory input from brainstem and cortex.
- Transection removes that input at once, so motor and autonomic neurons are hyperpolarized and reflexes fail (areflexia, flaccid limbs).
- Sympathetic preganglionic neurons (T1–L2) lose their drive; vascular tone and, with high lesions, cardiac sympathetic drive fall.
- Blood pressure falls sharply; with lesions above the cardiac outflow, unopposed vagal tone slows the heart.
- Over days to weeks, cord neurons become more excitable (receptor up-regulation, sprouting of remaining synapses), and reflexes return.
- Without descending inhibition, reflexes overshoot: brisk tendon reflexes, clonus, spasms and a Babinski sign.
- Autonomic reflexes inside the cord also return, so bladder distension can drive a large, unchecked sympathetic discharge below the lesion.

## Spinal shock vs neurogenic shock

| Feature | Spinal shock | Neurogenic shock |
| --- | --- | --- |
| What it is | Loss of reflexes and tone below the lesion | Distributive shock from loss of sympathetic tone |
| Key signs | Flaccid paralysis, areflexia, atonic bladder | Hypotension, bradycardia, warm dry skin |
| Level | Any cord level | Usually cervical or high thoracic (above about T6) |
| Course | Reflexes return over days to weeks | Improves as vascular tone recovers |

## Clinical notes

- A cord-injured patient who is hypotensive and bradycardic with warm skin fits neurogenic shock; a tachycardic, cold patient suggests bleeding instead.
- Autonomic dysreflexia is often triggered by a full bladder, a blocked catheter or constipation; removing the stimulus is the first step.
- During spinal shock the bladder is atonic and retains urine; later a reflex (spastic) bladder empties without voluntary control.

## Memory aid

Cut the cable, the cord goes quiet; given time it talks again, but now with no one to tell it to calm down.

## Test yourself

Think of the answer, then tap the question to see it.

## What is the main reason reflexes disappear below an acute spinal cord transection?

Cord neurons suddenly lose the tonic excitatory input from brainstem and cortex, so they fall far below threshold; the reflex circuits themselves are intact.

## A patient with a C6 cord injury has BP 80/50 mmHg, heart rate 48/min and warm skin. What is the likely cause?

Neurogenic shock: loss of sympathetic vascular tone causes vasodilation, and loss of cardiac sympathetic drive leaves vagal tone unopposed, causing bradycardia.

## Why does a patient with a T4 lesion and a blocked catheter develop severe hypertension with bradycardia?

Bladder distension triggers a cord sympathetic reflex below the lesion that the brain cannot inhibit; baroreceptors sense the hypertension and slow the heart through the intact vagus.

## What is the mass reflex?

In a chronic isolated cord, a strong stimulus below the lesion spreads through cord circuits to cause widespread flexor spasm, bladder and bowel emptying, sweating and raised blood pressure.

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## Connections

## See it in 3D 3

The structures of Durgical's 3D anatomy where it happens.

- [Spinal cord](https://durgical.com/en/anatomy/spinal-cord/)
- [Grey matter of the cord](https://durgical.com/en/anatomy/grey-matter-of-spinal-cord/)
- [Sympathetic trunk](https://durgical.com/en/anatomy/sympathetic-trunk/)

## Related topics 6

- [Spinal cord reflexes](https://durgical.com/en/physiology/spinal-cord-reflexes/)
- [Upper versus lower motor neuron lesions](https://durgical.com/en/physiology/upper-versus-lower-motor-neuron-lesions/)
- [Micturition and the bladder reflex](https://durgical.com/en/physiology/micturition-and-the-bladder-reflex/)
- [The autonomic nervous system: organization](https://durgical.com/en/physiology/the-autonomic-nervous-system-organization/)
- [Nervous control of the circulation and the CNS ischemic response](https://durgical.com/en/physiology/nervous-control-of-the-circulation-and-the-cns-ischemic-response/)
- [Shock physiology](https://durgical.com/en/physiology/shock-physiology/)

## Related conditions 2

- [Spinal cord injury](https://durgical.com/en/conditions/spinal-cord-injury/)
- [Autonomic dysreflexia](https://durgical.com/en/conditions/autonomic-dysreflexia/)

[← All of physiology](https://durgical.com/en/physiology/)

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: [Spinal Cord Injuries](https://www.ncbi.nlm.nih.gov/books/NBK560721/) (StatPearls (NCBI Bookshelf), 2025); [Neuroanatomy, Spinal Cord](https://www.ncbi.nlm.nih.gov/books/NBK559056/) (StatPearls (NCBI Bookshelf), 2025); [Spinal Cord Injury | MedlinePlus](https://medlineplus.gov/spinalcordinjuries.html) (MedlinePlus, US National Library of Medicine, 2025).

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Representative model, for educational purposes only.

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/spinal-shock-and-the-isolated-cord/