Spinal cord injury

• A spinal cord injury is damage to the cord or its blood supply that produces motor, sensory or autonomic deficits below the level of the lesion. Most are traumatic, from road traffic crashes, falls and sport.
• Severity is graded with the ASIA Impairment Scale (AIS) from A (complete, no function at S4 to S5) to E (normal). Sacral sparing decides whether the injury is complete or incomplete.
• The classic incomplete syndromes are central cord, anterior cord (anterior spinal artery) and Brown-Sequard; each maps to the tracts that are damaged.
• Spinal shock is the transient flaccid, areflexic state below the lesion; neurogenic shock is a circulatory problem with vasodilatation, hypotension and bradycardia, usually with injuries at T6 or above.
• Cervical spine clearance in stable, alert adults uses the Canadian C-spine rule or NEXUS; when imaging is needed, CT is first line for bone and MRI for the cord.
• High-dose corticosteroids are no longer routine: NICE NG41 advises against methylprednisolone, nimodipine and naloxone in acute traumatic cord injury, while the AO Spine/Praxis 2024 guideline recommends surgical decompression within 24 hours when indicated and feasible.
• ATLS, NICE NG41, the 2024 AO Spine/Praxis guidelines and the 2020 autonomic dysreflexia guideline of the Consortium for Spinal Cord Medicine informed this page.

By the end of this page you should be able to:

1. Describe the spinal cord deficits produced by injuries at different levels, including why a high cervical lesion threatens breathing.
2. Grade a spinal cord injury with ISNCSCI/ASIA, and distinguish complete from incomplete injury using sacral sparing.
3. Recognise central cord, anterior cord and Brown-Sequard syndromes from their patterns of motor and sensory loss.
4. Distinguish spinal shock from neurogenic shock, and manage each.
5. Apply the Canadian C-spine rule and the NEXUS criteria, and choose CT, MRI and clinical observation appropriately.
6. Explain why corticosteroids are no longer routine, and state current evidence on surgical timing and on blood pressure targets.
7. Recognise, prevent and treat autonomic dysreflexia and the main long-term complications of spinal cord injury.
8. Combine head and spinal injury management in the first minutes after trauma.

A spinal cord injury (SCI) is damage to the spinal cord or to its blood supply that produces a deficit in motor, sensory or autonomic function below the level of the lesion. ^[1] Trauma is the usual cause: road traffic crashes, falls, sport and violence. Non-traumatic causes exist too - tumours, infections such as tuberculous (Pott) disease, degeneration and vascular malformations - but this page centres on the traumatic form, which is what first presents in emergency care. ^[1]

SCI is uncommon but devastating. Worldwide, 250,000 to 500,000 people sustain a spinal cord injury each year, and almost all of these are preventable. ^[1] In the United States alone about 17,000 new cases occur annually, roughly 55 per million population, and about 282,000 people are living with the injury; motor vehicle crashes account for about 38% of new cases, falls for about 30%, violence for 13%, sport for 9% and medical or surgical complications for about 5%. ^[1] Three-quarters of patients are injured before the age of 30. ^[1] Men dominate, particularly in sport-related injury.

The central organising idea of modern care is that the cord is injured twice. The first injury is the immediate mechanical damage at the moment of trauma; it is irreversible. The second is the biological cascade of ischaemia, inflammation, oedema and excitotoxicity that begins within minutes and continues for weeks, and it is the target of everything we do after the event. ^[5] Airway, breathing, circulation, spinal motion restriction, decompression, perfusion and avoidance of secondary insults are all aimed at this second injury. ^[5]

Head injury and spinal injury travel together. A patient with one may have the other, because the same acceleration-deceleration force injures both. Every traumatised patient is presumed to have a spinal injury until it is excluded; every suspected spine patient has their head surveyed. This cross-check runs through the whole of this page and through the parallel head-injury topic. ^[2]

The spinal cord is a column of nervous tissue running from the foramen magnum to about the L1 to L2 level, where it ends as the conus medullaris. Below that, the cauda equina carries nerve roots. Fibre tracts inside the cord carry motor commands downwards (the corticospinal tract) and sensory information upwards (the spinothalamic tract for pain and temperature, the dorsal columns for proprioception, vibration and fine touch). Damage at a given level disconnects everything below it.

Injuries are classified by:

• Level - the lowest segment with normal motor and sensory function, named by the neurological level of injury (cervical C1 to C8, thoracic T1 to T12, lumbar L1 to L5, sacral S1 to S5).
• Completeness - complete (no motor or sensory function, including at S4 to S5) or incomplete (some preserved function below the lesion).
• Syndrome - whether one of the recognised incomplete patterns is present.
• Severity - the ASIA Impairment Scale grade, A to E.

A tetraplegic (quadriplegic) patient has cervical injury with loss of function in all four limbs; a paraplegic patient has thoracic or lumbar injury with preserved arm function. ^[1]

• C1 to C3: total loss of inspiratory muscle function, mainly diaphragm and external intercostals; these patients need continuous, permanent ventilatory support. ^[5]
• C3 to C5: ventilation is required in the first days or weeks, with reduced lung volumes and limited pulmonary reserve. ^[5]
• C6 to C8: diaphragmatic innervation is intact and spontaneous breathing is compatible, but abdominal muscles no longer aid the inspiratory phase; these patients remain at risk of respiratory failure and pneumonia from poor secretion control. ^[5]
• High spinal injuries above C5 also cause respiratory compromise through loss of diaphragm innervation, and injuries at any high level can produce neurogenic shock. ^[1]
• T1 to T12: diaphragmatic function is intact; cough effectiveness depends on how high the thoracic lesion is. ^[5]

The segmental map matters for bedside assessment: cervical nerves C1 to C8 supply the neck, shoulders, arms and hands; thoracic T1 to T12 the trunk and abdominal muscles; lumbar L1 to L5 the lower back and legs; sacral S1 to S5 the pelvic organs, genitals and lower limbs. ^[1]

Three facts explain almost everything below:

• The corticospinal tract fibres to the upper limbs lie near the centre of the cord, fibres to the lower limbs more peripherally. Injury to the centre (central cord syndrome) therefore weakens the arms more than the legs. ^[1]
• The spinothalamic tract (pain and temperature) decussates in the cord, so hemisection (Brown-Sequard) causes contralateral loss of pain and temperature.
• The dorsal columns (proprioception, vibration) do not cross in the cord, so hemisection causes ipsilateral loss of proprioception and vibration.

These patterns are why a careful bedside motor and sensory examination localises the lesion even before imaging.

SCI can occur at any age, but the pattern differs. Historically it affected young men; now, partly because populations are older and better protected in vehicles, an increasing proportion is older adults whose cords are injured by falls on an osteoporotic or spondylotic spine. The commonest level is cervical (16% to 75%), then thoracic (16% to 36%) and lumbar (9% to 17%). ^[5]

Non-traumatic SCI also matters and is seen more often in older adults: tumours, infections such as epidural abscess, degenerative spinal stenosis and spondylosis, which narrow the canal so that even minor trauma damages the cord. ^[1]

• Mechanism. Direct trauma to the cord (compression by fracture or dislocation, penetration, distraction), transient compression from hyperextension of a stenotic canal, and ischaemia from arterial injury.
• Modifiable risks. Alcohol, failure to use seat belts or helmets, unsafe diving, unprotected falls.
• Non-modifiable or contextual risks. Older age (osteoporosis, cervical spondylosis), ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, pre-existing canal stenosis.
• Male sex is strongly associated, especially in sport. ^[1]

The primary injury is the mechanical insult itself - compression, contusion, laceration or transection - and it is irreversible. ^[5] Within minutes a secondary cascade begins: vascular damage, ionic dysregulation, free-radical generation, glutamate-mediated excitotoxicity, inflammation and blood-brain (blood-cord) barrier disruption, proceeding through the acute (2 hours to 2 weeks), subacute (days to 2 weeks), intermediate (weeks to 6 months) and chronic phases. ^[1] It is in this secondary phase that early stabilisation and perfusion can limit the final deficit. ^[5]

• C1 to C3 produces complete loss of inspiratory function and inevitable ventilator dependence. ^[5]
• Above C5 damages the phrenic outflow and threatens ventilation.
• At or above T6 the sympathetic outflow is disrupted. Two very different clinical pictures result: spinal shock and neurogenic shock, discussed immediately below.

These almost always arrive together after a spinal cord injury, but they are not the same thing, and understanding the difference drives management. ^[4][5][10]

• Spinal shock is a neurologic state, not a circulatory one. Its danger is that it masks an incomplete injury: a patient with apparently complete A-grade injury may turn out to have sacral sparing once spinal shock resolves. Repeat the ISNCSCI examination after spinal shock passes. ^[4][5][10]
• Neurogenic shock is a circulatory emergency. It needs vasopressors and perfusion; it is the reason a high cord injury produces a warm, dry, hypotensive patient with a slow pulse. ^[1][5][10]
• Spinal shock should also be distinguished from a second cause of hypotension in trauma: haemorrhagic shock from other injuries. A spinal patient who is shocked and tachycardic is bleeding, not neurogenic. ^[2]

After trauma, ask about:

• Neck or back pain, and whether it is midline.
• Numbness or tingling in the hands or feet, "glove and stocking" sensory loss, or loss of sensation in the saddle area.
• Weakness in the arms, legs or trunk, and whether it came on immediately or after a delay.
• Ability to move the fingers, toes, wrists and ankles.
• Bladder or bowel symptoms: retention, incontinence, priapism.
• Respiratory symptoms: breathlessness, weak cough, difficulty clearing secretions.

An incomplete injury can produce an evolving picture over hours, so repeated examination matters more than a single assessment. ^[1][5]

1. Cervical spine control first. Keep the neck still while assessing. A complete spinal injury produces flaccid paralysis, absent reflexes and absent anal tone below the lesion in the first hours. ^[1][10]
2. Motor strength in the key muscles from C5 to S1, scored 0 (none) to 5 (normal): shoulder abduction (C5), elbow flexion (C6), wrist extension (C7), finger flexion (C8), knee extension (L3), ankle dorsiflexion (L4), great-toe extension (L5), ankle plantarflexion (S1). A maximum score of 100 across both sides.
3. Sensation at dermatomes C2 to S5 for light touch and pinprick, scored 0 to 2, and sacral sparing: any sensation at S4 to S5, or voluntary anal contraction. Sacral sparing is what separates complete from incomplete. ^[1][5]
4. Reflexes: the bulbocavernosus reflex (anal contraction on squeezing the glans or clitoris, or tugging a catheter) returns within the first days and marks the end of spinal shock. ^[5][10]
5. Autonomic signs: hypotension, bradycardia, warm dry skin and temperature dysregulation with injuries at T6 or above; priapism in an unconscious or exposed male. ^[2][10]
6. Respiratory capacity: vital capacity, ability to cough strongly - both are documented in the ASIA chart. ^[2]

The examination is only reliable if the patient can cooperate, is not intoxicated or sedated, and has no distracting injury. ^[2]

• High cervical (above C5) - ventilation threatened; neurogenic shock likely; greatest disability.
• Low cervical - tetraplegia with variable hand and diaphragm function.
• Thoracic - paraplegia with variable trunk control; respiratory and cardiovascular effects depend on height.
• Lumbar/conus/cauda equina - lumbosacral and pelvic dysfunction; lower-extremity patterns vary.

Always ask whether the injury is anatomically stable: unstable injuries can worsen with movement, which is why spinal motion restriction applies until imaging. ^[5]

Spinal cord injury must be separated from:

• Other causes of acute weakness after trauma: intracranial (stroke, traumatic brain injury), peripheral nerve injury, brachial or lumbosacral plexus injury, entrapment.
• Cord compression from non-traumatic causes: epidural haematoma or abscess, metastatic disease, cervical spondylosis (degenerative cervical myelopathy, a "slow-motion" spinal cord injury), transverse myelitis.
• Guillain-Barré syndrome, tick paralysis, botulism and organophosphate toxicity, which can mimic a spinal syndrome with flaccid weakness.
• Conversion or functional weakness.
• Cord contusion (myelopathy) without fracture - spinal cord injury without radiographic abnormality (SCIWORA), seen mainly in children, in whom MRI is essential. ^[2][7]

The safest habit is: if a neurological deficit below a level is present, treat as spinal cord injury until proven otherwise, and image the whole cord. ^[2]

The first minutes follow ATLS, 11th edition (2025): a systematic, structured primary survey of airway with in-line spinal immobilisation, breathing, circulation, disability and exposure, with resuscitation started at once. ^[11][2]

NICE NG41 adds the catastrophic-bleeding-first ABCDE structure and the key point that the cervical spine is protected manually in line, particularly during any airway intervention, while the remainder of the spine is not moved. ^[2]

Imaging strategy balances urgency, what needs to be seen and radiation. ^[2][1]

• CT is the primary study for bone in adults: it detects fractures far better than plain radiographs and approaches 100% sensitivity for cervical and thoracolumbar injuries; NICE NG41 recommends CT for adults when cervical injury is suspected by the Canadian C-spine rule, and MRI after CT when a neurological abnormality could be due to cord injury, whether or not it shows on CT. ^[1][2]
• MRI is the best study for the cord itself: cord contusion, oedema, compression, ligament and disc injury, epidural haematoma. In adults it is suggested during the acute phase, pre- or post-operatively, to enhance prognostication. ^[1][2]
• Plain radiographs are less sensitive and are not recommended for initial screening in adults; they still have a role in children and in low-resource settings.
• CT angiography is added when fracture or subluxation suggests vertebral artery injury. ^[3]
• Whole-body CT is used in major blunt trauma; imaging of the cord is completed with sagittal and coronal reformats of the thoracic and lumbosacral spine. ^[2]

Slice thickness of 3 mm or smaller in the cervical spine and 5 mm or smaller in the thoracolumbar spine improves accuracy. ^[1]

• For anyone over 4 years, complete an ASIA chart (ISNCSCI) as soon as possible in the emergency department. ^[2]
• In suspected SCI, do a full motor and sensory examination, vital capacity and ability to cough, and record trend, not single measurements. ^[2]

The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), developed by the American Spinal Injury Association (ASIA) with ISCoS, provide the standardised motor and sensory examination. ^[1][5] Motor testing covers key muscles C5 to S1 (maximum 100); sensory testing covers dermatomes C2 to S5 for light touch and pinprick; sacral sparing is tested with deep anal pressure and voluntary anal contraction. ^[1] Injuries are then graded: ^[1]

An injury is therefore complete only when S4 to S5 are empty; sacral sparing converts a complete-looking picture into an incomplete one, usually with a better prognosis. ^[1][5]

Neuroprognosis: AIS conversion (improvement of at least one grade) varies by initial grade: 19% from A, 73% from B, 87% from C and 46% from D. ^[1] Cervical recovery rates lie below thoracic and lumbar rates, and penetrating injuries recover less well than blunt. ^[1]

Incomplete injury means some motor or sensory function is preserved below the lesion, including at S4 to S5. The pattern of loss identifies the syndrome. ^[1]

• Central cord syndrome - the commonest incomplete syndrome. Hyperextension of the neck in a stenotic, spondylotic canal compresses the centre of the cord. It produces more weakness in the upper limbs than the lower, often with bladder dysfunction but preserved sacral sensation. Loss of pain and temperature may occur below the lesion. The arm-heavy pattern follows from the central placement of upper-limb fibres in the corticospinal tract. ^[1]
• Anterior cord (anterior spinal artery) syndrome - compromise of the anterior spinal artery, from cord compression, hypotension or aortic pathology. There is bilateral loss of motor function and of pain and temperature below the lesion, with preserved vibration, proprioception and some touch (the dorsal columns are spared). ^[1]
• Brown-Sequard syndrome - hemisection of the cord, most often from penetrating trauma. Ipsilateral loss of motor function, proprioception, vibration and (some) touch; contralateral loss of pain and temperature. It accounts for 1% to 4% of traumatic spinal cord injuries and has the best prognosis for walking, with up to 90% of people walking without aids after rehabilitation. ^[9]
• Posterior cord syndrome - rare in trauma, more often from infection, toxins or metabolic causes. Loss of proprioception and vibration, with motor and pain-temperature functions spared. ^[1]
• Conus medullaris syndrome - injury to the terminal cord at L1 to L2, with sacral dysfunction: loss of the Achilles reflex, and bladder, bowel and sexual dysfunction. ^[1]
• Cauda equina syndrome - technically nerve-root injury below the conus, with patchy deficits and radicular pain; surgical decompression is urgent.
• Complete transection - bilateral loss of motor, pain, temperature, proprioception, vibration and touch below the lesion; high cervical lesions compromise respiration by denervating the diaphragm. ^[1]

The goals are to prevent secondary injury and transfer to the right place.:

1. Scene safety, primary survey. ATLS 11th edition (2025) structures the approach: one safe, reliable, systematic method for assessing and initially managing the trauma patient. ^[11]
2. Spinal motion restriction, not "immobilisation": the American College of Surgeons/Trauma Quality Programs now prefer this term, because complete immobilisation is unattainable. ^[1]
3. Spinal motion restriction is applied when there is altered consciousness, midline spinal pain, focal neurological deficit, spinal deformity, or a distracting injury that prevents reliable assessment. ^[1]
4. Airway with manual in-line stabilisation of the cervical spine; avoidance of movement of the rest of the spine; avoidance of hypoxia and hypotension; keeping the head neutral in line. ^[2]
5. Cervical spine clearance and imaging as below.
6. Transport to the right destination. Anyone with suspected acute traumatic spinal cord injury (with or without column injury) goes to a major trauma centre, with full in-line spinal immobilisation, regardless of transfer time, unless an immediate life-saving intervention is needed first. ^[2]
7. Recognition of concurrent injuries - a spinal patient in trauma has a high prevalence of associated brain, chest and abdominal injuries. ^[5]

Imaging can be deferred in a fully alert, sober patient with no distracting injury, no neurologic deficit, no midline cervical tenderness and no intoxication. Two validated instruments guide this decision in stable adults. ^[3][4][2]

NEXUS (Hoffman et al., 2000). A patient has a low probability of significant cervical injury only if all five criteria are met: ^[3]

• No midline cervical tenderness.
• No focal neurologic deficit.
• Normal alertness (GCS 15).
• No intoxication.
• No painful distracting injury.

In the validation cohort of 34,069 patients, the rule had 99.0% sensitivity for any cervical spine injury and 99.6% for a clinically significant injury; applying it could have avoided imaging in 12.6% of cases. ^[3]

The Canadian C-spine rule (Stiell et al., 2001) is a three-step algorithm for alert adults with GCS 15: ^[4]

1. Any high-risk factor (age 65 or more, dangerous mechanism such as a fall from greater than 1 metre or 5 steps, axial load such as diving, high-speed collision, rollover, ejection, motorised recreational vehicle or horse-riding accident, bicycle collision, or paraesthesia in the limbs) -> image.
2. If none, any low-risk factor (simple rear-end collision, sitting in the emergency department, ambulatory at any time, delayed onset of neck pain, no midline tenderness) -> if present, proceed to step 3; if absent -> image.
3. Active neck rotation of 45 degrees left and right. If the patient cannot do this -> image.

By cross-validation the rule had 100% sensitivity (95% CI 98 to 100%) and 42.5% specificity for 151 clinically important injuries. ^[4] NICE NG41 recommends the Canadian C-spine rule by name for assessment of suspected cervical injury. ^[2] (NEXUS is simpler; the Canadian rule is more sensitive and more selective, but needs range-of-motion testing.)

A patient with spinal trauma is often a head-injury patient too, and vice versa. The cross-check includes: ^[2]

• If the mechanism is severe, both head and cervical spine are imaged.
• A severe head injury with impaired consciousness or reliable examination: treat as spinal until proven otherwise.
• Head injury protocol is followed for the brain (NICE CG176 and local trauma protocol); cervical imaging is governed by NEXUS or the Canadian rule.
• Children under 16: radiation risk matters, so NICE recommends MRI for suspected cervical cord or column injury in children, with X-ray only if suspicion remains after reassessment. ^[2]

Decompression and stabilisation have a clear, evidence-based timetable. ^[1][6][5]

• Surgical decompression is recommended within 24 hours when indicated and feasible, regardless of level, with moderate evidence that patients are more likely (RR 2.76 at 6 months, 95% CI 1.60 to 4.98; RR 1.95 at 12 months, 95% CI 1.26 to 3.18) to recover by at least two AIS grades if treated early, and improve by an additional 4.50 points in motor score. ^[6]
• Ultra-early surgery (within roughly 8 to 12 hours) could not be recommended on current evidence because of small samples and inconsistent definitions. ^[6]
• Closed reduction of cervical facet dislocation may be attempted early, as an emergency, before definitive surgery, where expertise allows. ^[2]
• Surgery also stabilises the spine, relieves pain, limits deformity and removes compressing material (disc, clot, foreign body), and allows early mobilisation. ^[1]
• Expansile duraplasty, timing in elderly or frail patients, and the effect in milder (AIS D) central cord injury remain knowledge gaps. ^[6]

The cord's autoregulation fails within 30 minutes of injury, so blood pressure becomes spinal cord perfusion pressure. ^[5][7]

• Avoid hypotension (systolic below 90 mm Hg), which worsens secondary injury. ^[5]
• The 2024 AO Spine/Praxis hemodynamic guideline suggests augmenting MAP to a lower limit of 75 to 80 mm Hg and an upper limit of 90 to 95 mm Hg, for 3 to 7 days, recognising that the evidence is very low quality and the recommendation weak. ^[1][7]
• Older guidance (AANS/CNS 2013) suggested MAP 85 to 90 mm Hg for 7 days. Both sets of figures exist and local neurocritical care protocols should be followed. ^[5]
• Spinal cord perfusion pressure (MAP minus intrathecal or intraspinal pressure) is of growing interest where invasive monitoring is available. ^[5]
• Vasopressors. Norepinephrine is preferred in several studies over dopamine, with fewer arrhythmias and better cord perfusion; dopamine is an alternative. ^[5]
• Fluids. Maintain normovolaemia with goal-directed therapy; avoid excessive fluid. ^[5]
• Ventilation. Normoxia and normocapnia; avoid both hypoxia and hypercapnia. Tracheostomy if mechanical ventilation beyond 2 weeks is likely; early intubation with injuries above C5, complete paralysis, low lung volumes or chest-wall injury. ^[1][5]
• Temperature, glucose, pain and anxiety control, and avoidance of early hyperthermia where possible, in the neurocritical care bundle. ^[5]
• Intensive care in a neurological critical care unit is better than general ward management. ^[1]

The evidence on steroids has shifted strongly against routine use. ^[2][5][9]

• NICE NG41 (2016, updated May 2021) say do not use methylprednisolone, nimodipine or naloxone in the acute stage after traumatic spinal cord injury. ^[2]
• The 2017-era literature (as summarised in StatPearls) still considers a 24-hour high-dose methylprednisolone infusion within 8 hours of injury; NASCIS and subsequent studies have not shown consistent advantage, and methodological quality is widely questioned. ^[1][5]
• Valdez-Resendiz 2025 (and the 2013 AANS/CNS position and GRADE reviews it cites) conclude that no level I or II evidence supports high-dose methylprednisolone, while level I to III evidence links it with possible harm. ^[5]
• Different sources therefore disagree, and practice varies by centre. Pragmatically most UK/NICE-based systems avoid steroids; honest counselling to students is that the evidence is uncertain and local policy decides. ^[2][5]

• Neurogenic shock - treated with oxygen, fluids, vasopressors and temperature control (see the table). ^[5]
• Spinal shock - supportive; the injury is stabilised and reflexes monitored; the bulbocavernosus reflex marks resolution. ^[5][10]
• Respiratory failure - high cervical (C1 to C3) injuries need permanent ventilatory support; C3 to C5 need ventilation in the first days to weeks; C6 to C8 need intensive respiratory therapy. ^[5]
• Autonomic dysreflexia - see the section below.
• Deep vein thrombosis - the Neurocritical Care Society advises starting prophylaxis as soon as possible, and no later than 72 hours after the injury; enoxaparin is superior to unfractionated heparin for preventing pulmonary embolism. ^[1]
• Pressure injury, pneumonia, sepsis, neurogenic bowel and bladder, spasticity and chronic pain - anticipated and prevented, not waited for. ^[1]
• Succinylcholine avoidance. Succinylcholine is contraindicated from 72 hours after acute injury and for 6 months in the chronic patient, because of hyperkalaemia and arrhythmia risk. ^[5]

Autonomic dysreflexia is a hypertensive emergency in people with injury at or above T6. It is a sudden, severe rise in blood pressure from an unopposed sympathetic discharge below the lesion, triggered by a noxious or distending stimulus. ^[8]

Recognition:

• Elevated blood pressure: more than 20 mm Hg above baseline systolic in adults and more than 15 mm Hg in children, often with bradycardia or tachycardia. ^[8]
• Adults with high lesions normally run a systolic pressure of 90 to 110 mm Hg, so 20 to 40 mm Hg above baseline is alarming. ^[8]
• Sudden severe headache, flushing and sweating above the lesion, piloerection, nasal congestion, blurred vision, anxiety. ^[8]
• It is much more common in chronic than in acute injury, often between months 3 and 6. ^[5]

The trigger is almost always below the level of the lesion:

1. Bladder distension or blocked catheter (the commonest).
2. Bowel distension or faecal impaction.
3. Skin pressure or ulcer, ingrowing toenail, fracture or dislocation.
4. Uterine contractions in pregnancy, deep vein thrombosis, even tight clothing. ^[8]

Acute management (2020 Consortium for Spinal Cord Medicine guideline, web-accessed at PMC8152175): ^[8]

1. Sit the patient up and lower the legs; remove tight clothing or devices.
2. Monitor pulse and blood pressure every 1 to 2 minutes until stable. ^[8]
3. Check for a urinary trigger first: catheterise if none is in place; if the patient is already catheterised, check for kinking or blockage and replace if needed. Instil lidocaine jelly into the urethra before insertion. ^[8]
4. If systolic pressure is at or above 150 mm Hg before catheterisation, use a rapid-onset, short-duration antihypertensive such as nitropaste, nifedipine, hydralazine or sublingual clonidine. ^[8]
5. Never use nitropaste if the patient has taken a phosphodiesterase-5 inhibitor (sildenafil, tadalafil, vardenafil): this is a contraindication. ^[8]
6. Check for faecal impaction once the bladder is dealt with, using topical lidocaine, and evacuate gently. ^[8]
7. If the cause is not found and pressure remains high, admit for monitoring and further investigation. ^[8]
8. Monitor for 2 hours afterwards for recurrence; educate the patient to seek help if symptoms return. ^[8]
9. Document baseline pressures and all interventions. ^[8]

A rise of 20% above baseline systolic pressure should be treated as AD even without symptoms. ^[5]

• Prognosis is guarded and depends on cause, level and completeness. The disability tracks the level: higher lesions, greater disability, greater complication burden. ^[1]
• Complications are the long-term killers and disabled: neurogenic bladder, bowel dysfunction, urinary tract infection, pressure injury, venous thromboembolism, autonomic dysreflexia, blood pressure instability, spasticity, chronic pain, impaired thermoregulation, psychological distress. ^[1]
• Respiratory vulnerability in high lesions: pneumonia is a leading cause of death. ^[1]
• Thromboembolism risk in the first 3 months is approximately 85%, falling thereafter, when routine prophylaxis is stopped; the muscle pump returns as spasticity develops. ^[5]
• Temperature dysregulation is common, especially above T6, because sweating and sympathetic vascular tone are disrupted below the lesion. ^[5]
• Spasticity and contractures complicate positioning; succinylcholine is contraindicated from 48 hours to 6 months after injury because of hyperkalaemia from denervation. ^[5]
• Bowel, bladder and sexual function require structured rehabilitation and continuation in the community. ^[5]
• Life expectancy varies from 1.5 years in mechanically ventilated older adults to 50 years in 20-year-olds with preserved motor function; cardiovascular and respiratory disease dominate in older survivors. ^[5]
• Early rehabilitation with physiatry, physical and occupational therapy improves outcomes, and should be integrated during acute admission. ^[1]
• A dedicated life-long model of care guided by a spinal cord injury centre is the standard. ^[2]

• Injury prevention - road safety, fall prevention in older adults, safe diving and sport practice, in particular no diving into shallow water.
• Secondary prevention after survival: DVT, pressure injury, infection and autonomic dysreflexia are all preventable events with structured care. ^[1]
• Patient and family education on recognising autonomic dysreflexia and on bowel and bladder management reduces re-admission. ^[8]

• Children. Assessment is difficult: their developmental stage matters, and the Canadian C-spine rule does not transfer cleanly. CT is used less willingly because of radiation; MRI is preferred for suspected cervical cord or column injury. Children are also more prone to SCIWORA. ^[2]
• Older adults. Falls dominate; cervical injuries are more common in spondylotic spines; presentation can be delayed; functional reserve is lower; mortality rises steeply over 60. ^[1][5]
• Pregnancy. Autonomic dysreflexia in the third trimester is an obstetric emergency; obstetric and spinal teams co-manage it. ^[8]
• People with continuous positive airway pressure or obstructive sleep apnoea carry a high prevalence of sleep-disordered breathing after SCI. ^[5]

• Spinal motion restriction using a tree trunk as a stretcher, a rolled blanket for blocks and tape is better than no restriction. ^[2]
• Imaging. Where CT is not available, CT unavailable, use repeated clinical assessment; plain X-ray can screen; if suspicion persists or the patient is high risk, refer to a trauma or spinal centre. ^[2]
• Stabilisation and transfer. Transfer to a major trauma or spinal unit rather than managing locally; limit time at the scene to life-saving interventions. ^[2]
• Blood pressure and oxygenation targets, with the cheapest vasopressor available, and meticulous avoidance of hypoxia and hypotension. ^[5]
• Pressure injury and bowel-bladder care cost very little and save lives. A turning schedule, clean intermittent catheterisation and nutrition are the backbone. ^[1]
• Autonomic dysreflexia emergency care can be done with a manual blood pressure cuff and simple measures: sit up, remove triggers, catheterise. ^[8]
• Rehabilitation depends on physiotherapy and community teams rather than high technology. ^[1]

Trauma primary survey and the trauma patient; traumatic brain injury; increased intracranial pressure and brain herniation; skull base fracture and concussion; spinal imaging; shock (haemorrhagic and distributive); autonomic dysreflexia as a separate neurological topic; pressure injury; neurogenic bladder and bowel; deep vein thrombosis prevention; pneumonia and respiratory failure; cervical spine surgery.

• Spinal cord injury is complete only when there is no function, including at S4 to S5; sacral sparing changes everything.
• The level determines the disability, the respiratory risk (high cervical), and whether neurogenic shock will occur (at or above T6).
• Central cord syndrome is the commonest incomplete injury; it weakens the arms more than the legs. Anterior cord syndrome spares vibration and proprioception. Brown-Sequard syndrome spares half the cord.
• Spinal shock is the flaccid, areflexic, transient state; neurogenic shock is the circulatory collapse from loss of sympathetic tone. Treat neurogenic shock with oxygen, fluids and vasopressors.
• Cervical clearance: NEXUS needs all five no-danger criteria; the Canadian C-spine rule proceeds by high-risk, low-risk and active rotation. When in doubt, image - CT for bone, MRI for the cord.
• High-dose corticosteroids are no longer routine: NICE NG41 advises against methylprednisolone; guideline summaries still cite the old 24-hour infusion within 8 hours approach, and practice varies honestly.
• Surgery for decompression and stabilisation is recommended within 24 hours when feasible; ultra-early surgery is not supported by current evidence.
• Blood pressure matters: keep MAP roughly 75 to 95 mm Hg and avoid systolic below 90; older advice was 85 to 90 mm Hg for 7 days, and local protocols differ.
• Prophylaxis for venous thromboembolism should start as soon as possible, and no later than 72 hours.
• Autonomic dysreflexia is a hypertensive emergency at T6 or above: sit up, monitor every 1 to 2 minutes, fix the bladder or bowel trigger, and use rapid antihypertensives when systolic is at or above 150 mm Hg.
• Long-term complications (pressure injury, urinary infection, spasticity, pain, dysreflexia) are the killers; they must be anticipated and prevented.
• Head and spinal injury commonly coexist; every traumatised patient is presumed to have a spinal injury and has their head surveyed concurrently.