Complete spinal cord injury

Last updated: February 7, 2022

Summarytoggle arrow icon

Complete spinal cord injury is the complete sensory and motor loss below the site of spinal cord injury following acute or chronic destruction, compression, or ischemia of the spinal cord. Initially, this may manifest as spinal shock, which is an acute physiological loss or depression of spinal cord function. It manifests as a flaccid areflexic paralysis below the level of the injury with autonomic features (e.g., hypotension, bradycardia). After some days to weeks the spinal shock wears off and a complete spinal cord injury may remain which manifests with spastic paresis, hyperreflexia, and continued sensory loss. Acute stabilization, a thorough neurological examination, and imaging is required for adequate diagnosis. Treatment involves acute care (e.g., analgesia, urinary catheterization) and definitive treatment (bracing or surgery). Symptomatic treatment, assistant devices, and physical therapy can improve mobility and quality of daily life. Less than five percent of cases fully recover after complete spinal cord injury. Autonomic dysreflexia is a long-term complication from thoracic spinal cord injury, leading to life-threatening episodes with cardiovascular instability.

Spinal shocktoggle arrow icon


Complete spinal cord syndrometoggle arrow icon

Symptoms of complete spinal cord injury classically occur 6–8 weeks after acute spinal cord injury (spinal shock) and include spastic paralysis, hyperreflexia, and presence of pathological reflexes (e.g., plantar reflex) below the site of injury.

If spinal injury is suspected (e.g., previous trauma to the neck or back), the patient's spine should be stabilized and the patient should be moved with extreme caution to avoid further damage to the spine!

A complete spinal cord injury above C4 represents a life-threatening situation due to the risk of diaphragmatic paralysis.


Autonomic dysreflexiatoggle arrow icon

Autonomic dysreflexia is a medical emergency!

Patients with spinal cord injuries at T6 or above are at the highest risk for autonomic dysreflexia.

The most common stimuli for autonomic dysreflexia are bladder irritation (e.g., distended bladder, UTI), bowel irritation (bowel obstruction, constipation), and breakdown of skin (e.g., cutaneous lesions).

Referencestoggle arrow icon

  1. Neurogenic Bladder. Updated: September 1, 2016. Accessed: February 22, 2017.
  2. SPINAL CORD INJURY STATISTICS. Updated: January 1, 2021. Accessed: September 3, 2021.
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  4. Bycroft J. Autonomic dysreflexia: a medical emergency. Postgrad Med J. 2005; 81 (954): p.232-235.doi: 10.1136/pgmj.2004.024463 . | Open in Read by QxMD
  5. Eltorai I, Kim R, Vulpe M, Kasravi H, Ho W. Fatal cerebral hemorrhage due to autonomic dysreflexia in a tetraplegic patient: case report and review. Paraplegia. 1992; 30 (5): p.355-360.doi: 10.1038/sc.1992.82 . | Open in Read by QxMD
  6. Vaidyanathan S, Soni BM, Sett P, Watt JW, Oo T, Bingley J. Pathophysiology of autonomic dysreflexia: long-term treatment with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysreflexic episodes.. Spinal cord. 1998; 36 (11): p.761-70.doi: 10.1038/ . | Open in Read by QxMD

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