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.
- Definition: acute loss or depression of spinal cord function; (loss of all sensorimotor functions below the level of injury) and reflexes following a spinal cord injury
- Flaccid areflexic paralysis
- Anesthesia: below the level of the lesion
- Autonomic dysfunction
- Diagnostics and treatment: See ”“ below.
- Symptoms are usually reversible but during the acute phase the outcome (e.g., remaining disabilities) is difficult to predict.
- Prognosis is poor if transition to occurs (see below).
- Prognosis is better if transition to occurs.
Complete spinal cord syndrome
- Definition: damage to the spinal cord resulting in complete bilateral loss of communication between the nerve fibers above and below the lesion
- Epidemiology: ∼ 33% of annual spinal cord injuries in the US 
- Symptoms classically occur 6–8 weeks after spinal shock has worn off
Bilaterally absent sensory and motor function below the lesion (including lowest sacral segments S4–S5)
- Impaired sensation (i.e., to pain, position, etc.)
- Muscle hypertonia with
- Pathological reflexes, e.g., positive
- Neurogenic bladder: involuntary urination caused by contractions
- Neurogenic bowel: constipation/bowel impaction, bowel incontinence, diarrhea
- In men: erectile dysfunction can occur
- in spinal cord injuries at T6 or above (see section below)
- Stabilizing patient
- Examine for neurological damage (e.g., determine motor and sensory function, examine bulbocavernosus reflex)
- Determine level of injury
- Determine extent of injury (complete or incomplete)
- Exclude associated injuries
- Complete spinal imaging (cervical, thoracic, lumbar): plain x-rays or CT if available
- MRI: can provide further information on the extent of ligamentous/disc injuries, spinal cord pathology, or epidural hematoma
- Acute management
- Definitive management
- Rehabilitation (multidisciplinary care)
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!
Etiology: autonomic hyperreflexia develops in individuals with spinal cord injury who are exposed to stimuli affecting the body below the level of injury 
Spinal cord injury
- Usually at the level of T6 or higher
- Causes predisposition for episodes of life-threatening autonomic dysfunction
- Episode provoking stimulus: can initiate a cascade of imbalanced autonomic reflexes and is located below the level of the lesion
- Spinal cord injury
- Development of the predisposition: damage to descending spinal cord fibers → loss of modulating signaling from the brain → lack of inhibition of spinal cord reflexes → excessive sympathetic reflex response to stimuli below the lesion → life-threatening overactivation of the autonomic nervous system (sympathetic and parasympathetic)
- Development of a hypertensive emergency: stimulus (below the lesion) → uninhibited sympathetic activation → hypertension (through vasoconstriction and tachycardia) → parasympathetic activation (by carotid sinus baroreceptor) → vasodilation in the area above the lesion; and decrease in heart rate → bradycardia, heart block, and hypertensive emergency
Clinical features 
- Throbbing headache
- Dilated pupils
- Guttmann sign: a clinical feature in high spinal cord lesions that manifests with nasal congestion due to sympathetic overactivity
- Flushing (above the lesion)
- Paleness (below the lesion)
- Bradycardia (and AV block) or tachycardia
- Prevention of hypertensive episodes
- Bladder voiding
- Monitor frequency of defecation
- Assess for distension, bowel sounds, and masses
- Release stool impaction (e.g., enema, manual disimpaction)
- Regular skin assessment
- Frequent position changes
- Avoid localized pressure (e.g., from clothing or bedding)
- Detection and treatment of hypertensive episodes
- Prevention of hypertensive episodes
- Complications 
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).