Spinal Cord Injury — Causes, Classification, Complications & Rehabilitation — Symptoms, Causes & Treatment | MyMedicPlus

Spinal cord injury (SCI) is damage to the spinal cord — from trauma, vascular event, infection, malignancy, or degenerative disease — resulting in loss of motor function (voluntary movement), sensory function (sensation of touch, pain, temperature, proprioception), and autonomic function (bladder, bowel, cardiovascular, sexual, and thermoregulatory control) below the level of injury. SCI is classified as complete (no preserved motor or sensory function below the injury level — ASIA Impairment Scale grade A) or incomplete (some preserved function — grades B through D), and by the vertebral level of injury: cervical (C1-C8) — causing tetraplegia/quadriplegia (all four limbs and trunk affected); thoracic (T1-T12) — causing paraplegia (legs and trunk below injury level affected; arms generally spared); lumbar and sacral — causing lower limb weakness and loss of bladder/bowel control. Traumatic SCI is caused by road traffic accidents (the leading cause in high-income countries — accounting for 38-39% of cases), falls (the leading cause in elderly patients — 31%), sports injuries (diving, rugby, horse-riding), and violence (the leading cause in some low-income countries). Non-traumatic SCI (NTSCI) is increasingly prevalent — caused by malignant spinal cord compression (metastatic — the most common non-traumatic cause in the UK; breast, lung, prostate, myeloma, and lymphoma primary tumours), cervical myelopathy from degenerative disc disease (the most common non-traumatic cause globally), transverse myelitis (inflammatory — MS, NMO, post-infectious), spinal cord ischaemia, and abscess. Early specialist care at a designated spinal cord injury centre significantly improves outcomes — the evidence base for primary transfer to SCI centres from the scene of injury is compelling.

Traumatic causes: Road traffic accidents: the single largest cause of traumatic SCI in high-income countries (approximately 38% in the UK); motor vehicle accidents, motorcycle accidents, and pedestrian injuries; cervical SCI predominates from sudden high-velocity flexion-extension or axial loading. Falls: the leading cause in elderly patients above 65 years (reflecting the combination of osteoporosis, balance impairment, and fall risk — accounting for 31% of traumatic SCI); often associated with pre-existing cervical spondylosis which narrows the spinal canal (SCIWORA — spinal cord injury without radiological abnormality — in elderly patients with spondylotic myelopathy). Sports and recreation: diving into shallow water (cervical fracture-dislocation); rugby (dangerous tackles and scrums — front row players at particular risk); horse-riding, gymnastics, trampolining, and skiing. Violence: low-velocity gunshot wounds and stabbings causing penetrating SCI — higher proportion in low-income countries and urban environments. Non-traumatic causes: Malignant spinal cord compression (MSCC): metastatic disease causing vertebral collapse or direct cord compression — a medical emergency (NICE quality standard); primary cancers most commonly causing MSCC: prostate (17%), lung (15%), breast (12%), myeloma (10%), lymphoma, and kidney; presents with back pain (95% — the most common presenting feature), limb weakness, sensory change, and bladder/bowel dysfunction. Cervical myelopathy: progressive spinal cord compression from degenerative cervical spondylosis (disc prolapse, hypertrophied ligamentum flavum, osteophyte formation); the most common non-traumatic SCI globally; presents insidiously in adults above 50 with gait disturbance, hand clumsiness, and upper motor neurone signs. Transverse myelitis: acute inflammation across the transverse diameter of the spinal cord — idiopathic, MS-associated (20-30% of cases), neuromyelitis optica spectrum disorder (NMOSD — anti-AQP4 antibody positive — more severe, more likely to be complete, recurrent; anti-MOG antibody also identified), post-infectious (GBS-like, post-vaccination). Spinal cord ischaemia/infarction: anterior spinal artery syndrome (loss of motor and pain/temperature with preserved proprioception) — from aortic surgery (cross-clamping), aortic dissection, embolism, vasculitis, cocaine use. Spinal abscess: haematogenous seeding from IV drug use, post-spinal surgery, or contiguous infection; Staphylococcus aureus most common; requires emergency surgical decompression and prolonged IV antibiotics.

The presenting features depend on the level and completeness of injury. Above the injury level: function is typically intact. At and below the injury level: motor paralysis — upper motor neurone signs initially flaccid (spinal shock phase — 24-72 hours post-injury), then evolving to spasticity, hyperreflexia, clonus, and extensor plantar responses (Babinski sign) from cortical disinhibition; sensory loss — complete loss of pain, temperature, light touch, and proprioception below the lesion level (complete SCI); or partial, dissociated, or asymmetric loss (incomplete SCI — depends on which spinal cord tracts are involved); autonomic dysfunction — neurogenic bladder (urinary retention is universal immediately post-SCI; detrusor overactivity or detrusor-sphincter dyssynergia develops later), neurogenic bowel (constipation and faecal incontinence from loss of cortical control and reflex bowel activity), sexual dysfunction (loss of erection, ejaculation, and sensation; altered female sexual response), thermoregulatory failure (inability to sweat below injury level — risk of hyperthermia). Spinal cord injury syndromes (incomplete SCI): Central cord syndrome (the most common incomplete SCI syndrome — bilateral motor weakness greater in arms than legs; bladder dysfunction; occurs in hyperextension injuries in elderly patients with cervical spondylosis; the best prognosis of incomplete syndromes). Anterior cord syndrome: paraplegia and bilateral loss of pain and temperature with preserved proprioception and vibration (posterior column intact — from anterior spinal artery ischaemia). Brown-Séquard syndrome (hemisection — often from penetrating injury): ipsilateral motor loss and proprioception loss; contralateral pain and temperature loss (decussation of spinothalamic tract). Cauda equina syndrome: compression of lumbar and sacral nerve roots (below conus medullaris — L1/L2); lower motor neurone flaccid weakness and areflexia in legs; saddle anaesthesia (perineum, inner thighs); urinary retention with overflow incontinence and faecal incontinence — surgical decompression within 24-48 hours is critical. Neurogenic shock: in cervical or high thoracic SCI — hypotension (from loss of sympathetic tone) with bradycardia (paradoxical — distinguishes from haemorrhagic shock which causes tachycardia); requires vasopressors (noradrenaline preferred) rather than excessive fluid resuscitation.

ASIA Impairment Scale (AIS — American Spinal Injury Association): the standard classification tool — grades A (complete — no motor or sensory function below level) to E (normal function); B (sensory but no motor below); C (some motor below — most key muscles below graded less than 3/5); D (most key muscles grade 3/5 or more); E (normal). The neurological level of injury (NLI) is the most caudal spinal cord level with normal motor and sensory function bilaterally. Imaging: Plain X-rays (AP and lateral) of the suspected injured spinal segments — adequate initial assessment in conscious cooperative patients; identifies fractures, alignment, and disc space changes. CT spine (the investigation of choice in the emergency setting): highly sensitive for bony injury — identifies fractures, subluxation, and canal compromise; CT angiography if vascular injury suspected (cervical SCI after trauma). MRI spine (essential): defines soft tissue injury — cord signal change (haemorrhage on T2-weighted imaging — haematomyelia — indicates severe injury; oedema — better prognosis), disc herniation, epidural haematoma, ligamentous injury, spinal cord contusion, and cord compression extent; MRI is mandatory for surgical planning and for non-traumatic SCI diagnosis. Electrophysiology: somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) — used intraoperatively to monitor cord function during spinal surgery and decompression; can provide prognostic information about completeness of injury. Neurological assessment: ASIA motor key muscles (0-5/5) graded at 10 specific myotomes bilaterally; ASIA light touch and pin-prick scored at 28 key sensory points bilaterally; rectal examination for sacral sparing (voluntary anal contraction, perineal sensation, bulbocavernosus reflex — key to determining completeness). Urodynamics: formal urodynamic assessment 6-12 weeks after injury when spinal shock has resolved — defines neurogenic bladder type (detrusor overactivity, detrusor-sphincter dyssynergia, low compliance) to guide long-term bladder management. Investigations for non-traumatic SCI: MRI spine with contrast (gadolinium enhancement in inflammatory/malignant causes); CT chest, abdomen, pelvis (primary malignancy staging); serum anti-AQP4 and anti-MOG antibodies (NMOSD); CSF analysis (oligoclonal bands — MS; cytology — malignant meningitis); blood tests (ESR, CRP, WBC for infection; LDH, protein electrophoresis for haematological malignancy).

Acute management: Spinal immobilisation: rigid cervical collar and log-roll technique for all suspected cervical or thoracic SCI from the point of rescue — maintained until imaging confirms stability or injury is excluded. Haemodynamic stability: maintain mean arterial pressure (MAP) above 85-90 mmHg for the first 7 days post-injury (cord perfusion pressure optimisation — current ATLS/ASIA guideline recommendation) — noradrenaline is preferred vasopressor for neurogenic shock; avoid excessive fluid (can worsen cord oedema). Respiratory support: cervical SCI (C3-C5 injuries) — phrenic nerve involvement causes respiratory failure requiring mechanical ventilation; C5 and below — may have preserved diaphragmatic function but reduced accessory muscle and cough efficacy — non-invasive ventilation (NIV) or assisted cough techniques. Methylprednisolone (high-dose IV): controversial — the NASCIS II and III trials suggested modest neurological benefit if given within 8 hours of injury; however, subsequent evidence challenged this, and side effects (pneumonia, GI bleeding, immunosuppression) are significant; current guidelines (ATLS) do not strongly recommend routine use — shared decision-making with patient and family. Surgical decompression and stabilisation: the most important acute intervention — decompression within 24 hours of traumatic SCI is associated with improved neurological outcomes (AO Spine evidence) vs. delayed surgery; surgical stabilisation (fixation) allows early mobilisation and rehabilitation. Non-traumatic SCI — MSCC: dexamethasone 16 mg daily (reduces cord oedema); emergency radiotherapy or surgery (decompressive laminectomy) within 24 hours of developing paralysis — timing is critical for neurological recovery. Rehabilitation: Inpatient multidisciplinary rehabilitation (specialist SCI centre): physiotherapy (wheelchair skills, transfer training, standing and walking with assistive devices for incomplete injuries, upper limb function in tetraplegia); occupational therapy (activities of daily living, environmental adaptations, splinting, assistive technology); neuropsychology; social work; specialist nursing (pressure area care, bowel and bladder management). Neurogenic bladder management: intermittent self-catheterisation (ISC) every 4-6 hours — the gold standard for neurogenic bladder in SCI; anticholinergics (oxybutynin, solifenacin) for detrusor overactivity; botulinum toxin A intradetrusor injection (200 units — effective for refractory detrusor overactivity); suprapubic catheter for those unable to perform ISC; urological follow-up including annual renal ultrasonography and urodynamics. Neurogenic bowel management: high-fibre diet; regular planned bowel care programme (digital rectal stimulation, suppositories or enemas — bisacodyl or glycerol suppositories; transanal irrigation systems — Peristeen, Navina — for inadequately managed neurogenic bowel). Spasticity: physiotherapy (stretching, positioning, splinting); oral baclofen (5-20 mg three times daily — GABA-B agonist — dose limited by sedation); intrathecal baclofen pump (ITB) for severe spasticity unresponsive to oral treatment; botulinum toxin A for focal spasticity. Neuropathic pain: pregabalin (NICE-approved for neuropathic pain — start 75 mg BD, titrate to 300-600 mg daily); amitriptyline (10-75 mg at night); gabapentin; duloxetine. Autonomic dysreflexia (see complications): treat immediately — sit upright, identify and remove trigger, nifedipine 10 mg sublingual or glyceryl trinitrate spray for persistent hypertension. Sexuality and fertility: specialist counselling, phosphodiesterase-5 inhibitors (sildenafil, tadalafil) for erectile dysfunction in men with SCI; vibrostimulation and electroejaculation for male infertility; fertility counselling and assisted reproduction for women.

Autonomic dysreflexia (AD): a life-threatening emergency in patients with SCI above T6 — sudden severe hypertension (systolic above 200 mmHg) triggered by a noxious stimulus below the injury level (the most common triggers: blocked urinary catheter or distended bladder — the most common cause; constipated bowel/rectal impaction; pressure ulcer; tight clothing; urinary tract infection; ingrown toenail; sexual activity); symptoms: pounding headache, profuse sweating above the injury level, blotchy flushing, nasal congestion, bradycardia; can cause stroke, hypertensive encephalopathy, myocardial infarction, and death if untreated; management: immediately sit patient upright (reduces blood pressure by gravity), identify and remove trigger (drain bladder, disimpact bowel with lubricant — use topical lidocaine gel before any procedure as stimulation can worsen AD), apply GTN spray or nifedipine 10 mg sublingual for persistent hypertension. Pressure ulcers: the most common complication — affecting 30-40% of SCI patients during lifetime; most common sites: ischial tuberosities (sitting), sacrum and heels (lying); can progress to full-thickness skin and tissue destruction, osteomyelitis, and sepsis; prevention is paramount — regular 30-minute weight shifts in wheelchair, appropriate pressure-relieving mattresses/cushions, regular skin inspection, adequate nutrition. Urinary tract infections (UTIs) and urosepsis: universal in catheter-using SCI patients — most common cause of hospitalisation after SCI; prevention: ISC technique and hygiene, adequate hydration (above 1.5 litres daily), avoid prophylactic antibiotics (resistance risk); cranberry extract (evidence inconsistent). Deep vein thrombosis (DVT) and pulmonary embolism (PE): the leading cause of death in the first year after SCI — impaired venous return from paralysed lower limbs; prophylaxis: low molecular weight heparin (LMWH — enoxaparin 40 mg daily or 20 mg BD) for the first 3 months minimum; graduated compression stockings; sequential pneumatic compression devices. Pneumonia and respiratory failure: particularly in cervical SCI with respiratory muscle weakness — atelectasis, aspiration pneumonia; physiotherapy-assisted cough (manual, mechanical in-exsufflator), chest physiotherapy, vaccination (influenza, pneumococcal), and NIV during respiratory infections are essential. Chronic neuropathic pain: affects 70-80% of SCI patients; complex pain syndrome requiring multidisciplinary management (physiotherapy, psychology, pharmacology). Psychological sequelae: depression affects approximately 30% of SCI patients; post-traumatic stress disorder; adjustment disorder; specialist neuropsychological support should be integrated from the outset of rehabilitation.

Primary prevention of traumatic SCI: road traffic accident prevention — seatbelt laws (seatbelts reduce SCI by 60-80% in vehicle occupants); speeding enforcement; drink-driving campaigns; helmet use for motorcyclists and cyclists; safe sports participation guidelines — diving only into water of confirmed adequate depth (above 2 metres — diving into shallow water is the leading cause of cervical SCI in young adults in recreational settings); sports-specific equipment and coaching (spear tackling rules in rugby — strictly prohibited since the laws reduce cervical SCI rate). Fall prevention in elderly: hip protectors, home safety modifications, balance and strength training (Otago Exercise Programme — proven to reduce fall-related fractures), regular medication review for fall-risk drugs (sedatives, alpha-blockers, antihypertensives, polypharmacy), regular footwear and vision assessment. Non-traumatic SCI prevention: early diagnosis and treatment of malignant spinal cord compression (MSCC) — all cancer patients with new-onset back pain require urgent MRI spine within 24 hours per NICE guidelines (QS56); decompression before loss of ambulation preserves walking ability in 80% vs. 20% if paraplegic at time of surgery; cervical myelopathy — early surgical decompression in symptomatic patients prevents further neurological deterioration. Pressure ulcer prevention: regular 2-hourly repositioning (sitting patients — 30-minute weight-shift every 30 minutes); high-specification foam or dynamic air-fluidised mattresses; wheelchair with appropriately prescribed pressure-relieving cushion (gel or air); daily skin inspection; nutritional support (adequate protein, vitamins C and E, zinc); education for patient and carers; annual skin review by tissue viability nurse. Prevention of UTI in catheter users: strict ISC technique; adequate hydration; catheter change as per schedule; cranberry extract (uncertain benefit); treatment only for symptomatic UTI (avoid treating bacteriuria without symptoms — reduces antibiotic resistance).

Call 999 immediately for: any patient with neck or back pain, weakness, numbness, or loss of bladder/bowel control following a fall, road traffic accident, or sports injury — suspected acute SCI requires emergency attendance, spinal immobilisation, and immediate imaging; autonomic dysreflexia (a known SCI patient with sudden severe headache, extreme sweating, facial flushing, and high blood pressure) — this is a medical emergency requiring immediate trigger identification and blood pressure management; and any SCI patient with a urinary catheter who develops fever, confusion, or rigors — possible urosepsis. For known cancer patients: back pain is an oncological emergency — new or worsening back pain in a patient with known malignancy should be reported to the oncology team immediately (same day) for urgent MRI spine to exclude malignant cord compression. See a GP urgently for: progressive leg weakness, gait disturbance, or hand clumsiness in a patient above 50 — possible cervical myelopathy requiring MRI spine; new bladder or bowel dysfunction — urinary retention, difficulty initiating voiding, or urinary or faecal incontinence — in a patient with back or neck symptoms; and any symptom suggesting cauda equina syndrome (saddle anaesthesia, urinary retention, bilateral leg weakness) — emergency same-day assessment and MRI. Community nursing or SCI specialist contact: patients with known SCI should contact their specialist SCI nurse or community team early for any: suspected pressure ulcer (red, broken, or discoloured skin over pressure point); recurrent UTI; uncontrolled spasticity or new pain; and autonomic dysreflexia episodes (to identify and address the trigger).