Spinal cord compression and myelopathy

• Myelopathy is dysfunction of the spinal cord itself; it produces upper motor neurone signs and often a sensory level below the lesion.
• Malignant spinal cord compression is an oncological emergency that can present as back pain or weakness in a patient with cancer.
• Degenerative cervical myelopathy is the commonest progressive spinal cord disease of adults and is managed by watching mild disease or decompressing moderate or severe disease.
• Acute transverse myelitis is an inflammatory cord attack; urgent MRI and high-dose intravenous corticosteroids come first, with plasma exchange for severe or refractory disease.
• Subacute combined degeneration is caused by vitamin B12 deficiency; intramuscular B12 is mandatory once neurological signs appear.
• In a patient with weakness, a sensory level, and bladder or bowel dysfunction, jumping straight to treatment without imaging is unsafe.

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

1. Define myelopathy and separate it from radiculopathy and mechanical back pain.
2. Recognise the presentation of malignant cord compression and state the immediate imaging, corticosteroid, and radiotherapy steps from NICE NG234.
3. Classify degenerative cervical myelopathy with the modified Japanese Orthopaedic Association (mJOA) score and explain observation versus decompression.
4. Distinguish transverse myelitis from cord compression on MRI and outline urgent steroid treatment.
5. Explain the mechanism, tests, and parenteral treatment of subacute combined degeneration.
6. Explain why international guidelines differ in strength and how to act on that uncertainty.

The central clinical point is that damaged spinal cord tracts recover poorly, so the speed of recognition matters more than in most neurological disease.

This page groups myelopathy into four conditions that share a final common pathway:

• Malignant (metastatic) spinal cord compression (MSCC): compression of the cord or cauda equina by metastatic or haematological tumour or by direct malignant infiltration.
• Degenerative cervical myelopathy (DCM): a progressive spinal cord injury caused by narrowing of the cervical spinal canal.^[2]
• Transverse myelitis: an inflammatory attack producing transverse cord dysfunction; when it spans three or more vertebral segments it is called longitudinally extensive transverse myelitis (LETM).
• Subacute combined degeneration: a myelopathy of the posterior columns (and later lateral tracts) from vitamin B12 deficiency.

Other causes exist (trauma, epidural haematoma or abscess, vascular infarction, demyelination outside the inflammatory context), but these four are the ones a medical student must recognise and triage.

DCM is a common problem in spinal surgery practice and is the commonest cause of progressive spinal cord dysfunction in adults; presentation is often gradual, so recognition is delayed. This is why this topic is largely about reducing delay.

MSCC occurs in people with cancer involving bone. NICE NG234 is built around a service standard: a cancer alliance should have a designated MSCC service, a coordinator available 24 hours a day and 7 days a week, and local access to urgent MRI within 24 hours for people with neurological signs or symptoms of suspected MSCC.^[1]

NMOSD, an important cause of acute transverse myelitis, has a prevalence reported as 0.5 to 4 per 100 000 people, with geographical and racial variation and the highest mortality among African and Asian populations.^[4]

Subacute combined degeneration tracks vitamin B12 deficiency. Common routes include autoimmune gastritis with pernicious anaemia, gastrectomy or bariatric surgery, terminal ileal disease, metformin or long-term proton pump inhibitor use, vegan or vegetarian diet without supplementation, and recreational nitrous oxide. Severe deficiency can cause subacute combined degeneration of the spinal cord, which may not be fully reversible even after the deficiency is corrected.^[5]

The cord or cauda equina is compromised by vertebral collapse, an extradural soft-tissue mass, or direct infiltration. Common cancer primaries that spread to the spine in practice include breast, prostate, lung, kidney, and thyroid, with myeloma frequently producing spinal disease; any cancer can do it, including lymphoma.

Risk factors for dangerous delay rather than for the disease itself include known cancer, new severe unremitting back pain (which may be worse at night or provoked by coughing, sneezing, or straining), neurological symptoms (gait disturbance, limb weakness, sensory change), and bladder or bowel dysfunction. Pain suggesting spinal metastases in a patient with current or past cancer should lead to advice through the MSCC coordinator within 24 hours.^[1]

Age, cumulative degenerative change (spondylosis, disc herniation, posterior osteophytes, ligamentum flavum hypertrophy, ossification of the posterior longitudinal ligament), and a constitutionally narrow canal all act together. The process is slow and often progressive, and many people have imaging evidence of compression without symptoms.

Causes group by mechanism:

• Demyelinating and autoimmune: multiple sclerosis, NMOSD, myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), systemic lupus erythematosus, Sjögren syndrome, sarcoidosis.
• Post-infectious or parainfectious: after viral, bacterial, or more rarely parasitic infection.
• Paraneoplastic and drug-related: including immune-mediated injury from cancer immunotherapy.
• Vascular: anterior spinal artery infarction can mimic acute myelitis clinically and on imaging.
• Idiopathic when work-up is extensive and unrevealing.

B12 deficiency causes functional deficiency of methionine synthase and methylmalonyl-CoA mutase, disrupting myelin maintenance. The posterior columns (and later lateral corticospinal tracts) are affected first. Causes include pernicious anaemia (autoimmune gastritis with antibodies against intrinsic factor), bariatric surgery or gastrectomy, terminal ileal resection or Crohn disease, coeliac disease, proton pump inhibitor or metformin use, a vegan or vegetarian diet without supplementation, and recreational nitrous oxide, which inactivates the vitamin B12 molecule and can produce normal serum B12 concentrations despite tissue deficiency.^[5]

An extradural tumour or collapsed vertebra narrows the canal and raises pressure in the epidural venous plexus. Cord ischaemia begins before structural crushing, and once a critical level of oedema or infarction is reached, function is lost quickly and may not recover. This is the basis for the modern urgent-management approach.

Chronic, low-grade compression plus repetitive injury to the cord from neck movement gradually damages myelin and axons. Corticospinal and posterior column function suffers first, so gait and fine hand use are the early currency of the disease rather than raw power.

Inflammation across a transverse section of cord damages myelin and axons and disrupts the blood-brain barrier enough to produce gadolinium leakage on MRI. Lesion length is read as a clue to cause: short (one or two segments) lesions lean toward multiple sclerosis; lesions of three or more vertebral segments (LETM) are characteristic of NMOSD and other connective-tissue causes.^[4]

Vitamin B12 is a cofactor in methylation and odd-chain fatty acid metabolism. Without it, methylmalonic acid and homocysteine accumulate and abnormal fatty acids are incorporated into myelin. The cord develops symmetric T2 hyperintensity in the dorsal columns (an inverted V). The first symptoms are paraesthesia and loss of vibration sense in the feet; later the gait becomes ataxic and upper motor neurone signs appear in the legs, with cognitive or psychiatric change when deficiency is severe.

Malignant or cauda equina compression. Severe, unremitting back pain is the commonest first symptom; it may be mechanical, worse at night, or provoked by coughing, sneezing, or straining. Radicular pain, numbness, paraesthesia, difficulty walking, and bladder or bowel dysfunction follow. NICE NG234 lists the pain and neurological features that should raise suspicion of spinal metastases or MSCC.^[1]

Degenerative cervical myelopathy. Burning or paraesthesia in the arms, clumsy hands with loss of dexterity, weakness of grip, neck stiffness, and an unsteady, broad-based gait, often without much pain. Later, bladder urgency or hesitancy may appear. Because the change is insidious and the patient is older, families often describe it more clearly than the patient does.

Acute transverse myelitis. Abrupt or subacute bilateral leg weakness, often after infection or in the setting of demyelinating disease, with a demarcated sensory level and bladder or bowel disturbance. Back pain or radicular pain may precede it; progression is rapid, reaching the worst over hours to days.

Subacute combined degeneration. Pins and needles in the feet, sometimes with hand (glove and stocking) paraesthesia, gait unsteadiness, and in advanced cases weakness, confusion, or memory loss. The onset is truly subacute, over weeks.

Malignant compression: motor power, reflexes, sensory level, plantar responses, sphincter and perineal sensation, and gentle spinal palpation. Repeat documentation frequently because change drives decisions.

DCM: upper motor neurone signs in all four limbs with a sensory level in the upper thoracic or lower cervical region; impaired finger opposition and rapid alternating movements; Hoffmann reflex (flick the terminal phalanx downward and watch the thumb and index flex); Babinski sign, hyperreflexia, ankle clonus. Gait is broad-based with reduced stride; Romberg is positive when proprioception is impaired.

Transverse myelitis: initially reduced tone and power, later spasticity; a sensory level with impaired pinprick, temperature, joint position, and vibration sense; bladder and bowel dysfunction.

Subacute combined degeneration: loss of joint position and vibration sense with an ataxic, Romberg-positive gait and only mildly impaired strength; reduced or absent ankle reflexes early, then brisk reflexes; Lhermitte sign can occur.

Two questions arise: could this be a compressive emergency, and if not, what inflammatory, vascular, or metabolic cause fits?

• Whole-spine MRI is the test for suspected malignant compression. NICE NG234 recommends sagittal T1 and/or STIR sequences to identify metastases, sagittal T2-weighted sequences to show the level and degree of compression, and supplementary axial imaging through any significant abnormality.^[1]
• Suspected MSCC: MRI as soon as possible and always within 24 hours. Offer overnight MRI only when urgent diagnosis is needed to start treatment immediately.^[1]
• Suspected spinal metastases without cord compression: MRI within one week at the local hospital.^[1]
• If MRI is contraindicated, perform CT; plain X-ray of the spine should not be used to diagnose or rule out spinal metastases or MSCC. Myelography is reserved for rare cases at neuroscience centres.^[1]
• DCM: MRI of the cervical spine with sagittal and axial T2 and T1 sequences, assessing stenosis, compression, and intramedullary signal; flexion-extension films if instability is suspected.
• Transverse myelitis: MRI of the whole spinal cord with sagittal and axial T2 and post-gadolinium T1 sequences; the aim is to show an intrinsic, often enhancing lesion over a specific number of segments and to exclude compression or abscess. Add brain and optic nerve MRI when multiple sclerosis, NMOSD, or MOGAD is suspected.
• Subacute combined degeneration: MRI of the cervical and thoracic cord may show dorsal column T2 hyperintensity, but diagnosis is biochemical and clinical.

• B12 replacement: severe symptomatic deficiency with neurological involvement or subacute combined degeneration is treated with intramuscular hydroxocobalamin 1000 micrograms on alternate days until no further improvement, then 1000 micrograms every 3 months lifelong.^[5]
• B12 thresholds: serum B12 less than 133 pmol/L makes deficiency likely, 133 to 258 pmol/L is indeterminate, and greater than 258 pmol/L makes it unlikely; active B12 less than 25 pmol/L is likely deficient, 25 to 70 pmol/L indeterminate, and greater than 70 pmol/L unlikely.^[5]
• Functional tests: methylmalonic acid and homocysteine when B12 results are indeterminate (both may be elevated in other conditions, including chronic kidney disease).
• Transverse myelitis work-up: CSF examination, AQP4 and MOG antibodies, autoantibody screening, brain and optic nerve MRI.
• MSCC work-up: tissue diagnosis when the primary is unknown, site-appropriate staging, and assessment of spinal stability and prognosis using validated tools alongside full clinical assessment.^[1]

DCM is graded with an 18-point scale (the mJOA, based on the Benzel modification; 18 is normal). Severity is defined as: ^[2]

• mild: 15 to 17,
• moderate: 12 to 14,
• severe: 11 or lower.^[2]

These cut-offs are conditionally recommended by an AO Spine 2026 review that summarises the derivation work (740 patients, receiver operating characteristic analysis using a Nurick score anchor).^[2]

NICE NG234 recommends considering validated tools such as the Spinal Instability Neoplastic Score (SINS) and a prognostic scoring system such as the revised Tokuhashi score, alongside full clinical assessment and imaging. A scoring system should support, not substitute for, clinical judgement.^[1]

Inflammatory myelitis spanning three or more contiguous vertebral segments on sagittal T2 MRI is LETM.^[4] It is highly suggestive of NMOSD, although the term is also used in other connective-tissue and parainfectious causes.

Cancer alliances should ensure MRI and radiotherapy capacity for these timelines, with 7-day availability.^[1]

Red flag recognition: think about the possibility of spinal metastases or MSCC in people with any recognised risk factors; if a person with current or past cancer presents with symptoms or signs of cord compression, immediately contact the MSCC coordinator and treat as an oncological emergency.^[1]

Corticosteroids: 16 mg oral dexamethasone, or equivalent parenteral dose, as soon as possible; continued at 16 mg daily while awaiting surgery or radiotherapy; tapered after surgery or from the start of radiotherapy.^[1] If dexamethasone is given before imaging and MSCC is excluded, stop it. Corticosteroids are not routine in people without neurological symptoms or signs unless severe pain or haematological malignancy is present.^[1] For confirmed haematological malignancy with spinal metastases, NICE recommends the same 16 mg initial dose, then further corticosteroid treatment in discussion with the haematology multidisciplinary team.^[1]

Monitoring and pain: during corticosteroid treatment, monitor blood glucose and provide proton pump inhibitor acid suppression.^[1] Analgesia should be given promptly while awaiting investigation or treatment, and non-mechanical spinal metastasis pain may be treated with 8 Gy in a single fraction (or stereotactic ablative body radiotherapy where prognosis is good or only a few metastases are present). Bisphosphonates reduce pain and risk of vertebral collapse in myeloma or breast cancer spinal involvement; they are not routinely used for other tumours or to prevent MSCC. Denosumab follows the relevant technology appraisal guidance for bone metastases from breast and solid tumours other than prostate.^[1]

There is no drug that reverses DCM; management is watchful waiting in mild disease or surgical decompression. Older recommendations strongly supported surgery for moderate and severe disease, with a weaker basis for mild disease, and an AO Spine 2026 review on mild disease adds nuance.^[2]

Observation is reasonable in stable mild disease (mJOA 15 to 17), particularly with low pain and good function. Conditional, low-quality evidence suggests surgery benefits mild DCM patients with high baseline neck pain and Neck Disability Index scores, improving neck disability and bodily pain at one year even when composite mJOA change is modest. Conditional evidence also suggests surgery for progressive mild disease can help pre-operative symptoms, but upper-extremity sensory deficits frequently persist; angular-edged spinal cord deformity on axial MRI is a risk factor for residual post-operative upper-extremity sensory impairment and should be discussed before consenting.^[2]

Surgical decompression is standard for moderate and severe DCM, or mild disease with progression, significant disability, or pain. Approach (anterior, posterior, or combined) depends on levels, alignment, and morphology; stabilisation and fusion are added when needed. The goal is to stop progression and improve quality of life; some recovery is expected, but residual deficit is common, especially sensory.

Important limitations to carry into practice:

• MRI compression alone does not predict future neurological deterioration. Severe compression at two disc levels in an otherwise normal spinal canal carried higher risk, whereas the compression pattern is less relevant when the spinal canal diameter is 14.5 mm or less or more than 15.75 mm. Routine use of these MRI parameters to guide timing of surgery in mild DCM is not currently recommended.^[2]
• Composite scores such as mJOA have a ceiling effect and are relatively insensitive to pain and upper-limb sensory symptoms. Clinical examination and patient-reported function should be integrated with the score, not replaced by it.^[2]

This is a medical-neurological emergency even though treatment is pharmacological rather than surgical.

1. Confirm and define: urgent MRI of the whole spinal cord with post-gadolinium sequences to show an intrinsic lesion, classify its length, and crucially exclude compression, epidural abscess, or tumour.
2. High-dose IV corticosteroids first: in NMOSD-associated myelitis, high-dose IV methylprednisolone 1 g per day for 5 consecutive days is used, followed by oral prednisolone 1 mg/kg/day tapered gradually, with long-term immunosuppression where appropriate. In an incompletely responsive case, a 2 g IV methylprednisolone pulse can be considered. For myelitis generally, high-dose IV methylprednisolone is the standard first-line acute treatment in most centres, with plasmapheresis or immunoadsorption reserved for steroid-unresponsive or severe disease.^[4]
3. Plasma exchange is added for poor response; the exact regimen and decisions belong to the responsible neurology service.
4. Aetiology work-up in parallel: brain and optic nerve MRI, CSF examination, AQP4 and MOG antibodies, autoantibody screening, and post-infectious serology. NMOSD specifically is distinguished from multiple sclerosis by its clinical picture, MRI features, and AQP4 antibody, and it tends to cause attack-related disability that demands treatment of each attack.^[4]
5. Rehabilitation: sphincter management, neuropathic pain control, spasticity care, and physiotherapy.

The most useful clinical habit is to remember that when MRI shows cord compression, it is not transverse myelitis, and steroids alone are not the plan.

The treatment of choice is B12 replacement; route and loading depend on cause and severity.^[5]

• Severe symptomatic deficiency with neurological involvement or subacute combined degeneration: intramuscular hydroxocobalamin is mandatory. Loading is aggressive (1000 micrograms intramuscularly on alternate days until no further improvement, often at least 2 to 3 weeks); maintenance is 1000 micrograms intramuscularly every 3 months lifelong. Rapid parenteral therapy is needed to prevent irreversible neurological damage, and MRI and symptoms often improve within days to weeks.^[5]
• Irreversible malabsorption (autoimmune gastritis, pernicious anaemia, total gastrectomy, terminal ileal resection): intramuscular loading, then 1000 micrograms intramuscularly every 3 months lifelong.
• Reversible or potentially reversible malabsorption: the same loading regimen, then maintenance parenterally or, if correction is proven, high-dose oral cyanocobalamin at least 1 mg daily. ^[5]
• Dietary deficiency: high-dose oral cyanocobalamin (1 mg daily), with long-term maintenance of 1 mg daily or 1 to 2 mg weekly. ^[5]
• Drug-induced deficiency: treat while the offending drug is reviewed; re-test 3 to 6 months after stopping it. ^[5]
• Nitrous oxide exposure: intramuscular replacement (one suggested regimen is 1000 micrograms daily for 1 week, then weekly for 4 weeks, then monthly to recovery, up to 3 months) followed by review. ^[5]

Safety points:

• Loading can unmask folate deficiency, cause iron deficiency, or precipitate hypokalaemia; check folate and iron and re-check haemoglobin.^[5]
• Neurological symptoms improve gradually over 6 to 12 weeks; bone marrow recovery begins within 3 to 5 days (reticulocytosis); haemoglobin usually normalises within 4 to 8 weeks.^[5]
• Oral B12 is unreliable when absorption is impaired; parenteral replacement is mandatory in neurological disease.^[5]
• If symptoms do not improve, reconsider the diagnosis, drug exposure (including nitrous oxide and metformin), copper deficiency, or an irreversible cord lesion.

• MSCC: paralysis, loss of sphincter control, neuropathic pain, pathological fracture, and late permanent dependency. Outcome tracks the degree of neurological deficit at the start of treatment, which is the whole case for speed.
• DCM: residual gait and hand impairment, neck and neuropathic arm pain, progressive deformity, and diagnostic confusion with polyneuropathy.
• Transverse myelitis: residual weakness, spasticity, sensory loss, bladder and bowel dysfunction, neuropathic pain, and (in paediatric NMOSD) developmental sequelae.
• Subacute combined degeneration: if replacement is delayed, cord damage can become irreversible even though peripheral blood counts recover; removing the cause (especially nitrous oxide) is essential.

MSCC threatens independent mobility; the best outcomes belong to patients treated while still ambulatory. Many details of 30-day mortality or long-term survival are tumour- and patient-specific and are best assessed case by case by the multidisciplinary team.

DCM, when treated at moderate or severe stage, usually halts progression; meaningful recovery depends on duration and severity of pre-operative symptoms. Transverse myelitis can end in full, partial, or poor recovery; poor recovery is more likely with long lesions, severe presentation, delayed treatment, and NMOSD. SCD recovery is good when replacement is early and often incomplete when delayed, especially for dorsal column and cognitive features.

• MSCC: not fully preventable, but early recognition is. Patients with cancer should be told what changes to look out for (new back pain characteristics, neurological change, bladder or bowel disturbance) and whom to contact urgently.^[1]
• DCM: no primary prevention beyond general spinal care, good bone health, and avoidance of smoking.
• Transverse myelitis: not preventable; reducing triggers (for example, continuing appropriate NMOSD immunosuppression) reduces relapse.
• SCD: B12 should be checked in patients with risk factors (gastrectomy, pernicious anaemia, terminal ileal disease, metformin or long-term proton pump inhibitor use, vegan diet, nitrous oxide use, cognitive change). Vegetarians, vegans, and older adults may need supplementation.^[5]

• Pregnancy: MRI without gadolinium is preferred when possible; high-dose corticosteroids and plasma exchange are used for acute myelitis or NMOSD when clinically necessary; B12 deficiency needs prompt parenteral treatment because of fetal neurological risk. Management should be multidisciplinary.
• Children: transverse myelitis occurs in children, and NMOSD or MOGAD may present with LETM. DCM is uncommon in children and usually genetic or metabolic, requiring paediatric spinal referral.
• Older adults: both DCM and B12 deficiency (from atrophic gastritis or medication) are common; cognitive change can dominate the presentation of B12 deficiency and be mistaken for dementia.
• Immunocompromised and post-transplant: new myelitis raises infection (including viral myelitis and tuberculosis), paraneoplastic, and drug-related causes.
• Frailty: weigh major spinal surgery against life expectancy and function in advanced cancer or frail older adults; palliative radiotherapy and best supportive care remain standard options.

• The two highest-value, cheapest actions are a fast systematic neurological examination looking for a sensory or motor level, and early transfer or referral when cord compression is suspected.
• When MRI is unavailable, CT can be used for suspected MSCC and CT myelography in selected cases at neuroscience centres, but treatment should not be delayed. Plain X-ray has no screening role for cord compression.
• Dexamethasone, intramuscular hydroxocobalamin, oral prednisolone, analgesia, and physiotherapy are inexpensive and should be used while arranging specialist care.
• NICE's 24-hour coordinator service is an aspiration for systems; the clinical clock (same-day suspicion, same-day steroids, imaging as soon as possible) is universal. Naming one responsible lead clinician for suspected cord compression captures most of what is needed.
• B12 levels, intrinsic factor antibodies, and AQP4 or MOG testing may be limited geographically; clinical recognition of B12-deficiency syndromes and NMOSD-type patterns then carries the diagnosis, and empiric replacement or immunosuppression may be justified when risk is high.

• Myelopathy is spinal cord dysfunction, not radiculopathy and not back pain.
• Malignant spinal cord compression is an oncological emergency. Suspect it in a patient with cancer and new back pain (especially nocturnal or straining-related), neurological change, gait disturbance, or bladder or bowel disturbance.
• Oral dexamethasone 16 mg is the acute corticosteroid regimen in NICE NG234, with an equivalent parenteral dose, continued at 16 mg daily while awaiting surgery or radiotherapy, then tapered.
• Suspected MSCC requires MRI as soon as possible and always within 24 hours; spinal metastases without cord compression can be imaged within a week.
• Radiotherapy for MSCC not managed surgically is 8 Gy in a single fraction given urgently (within 24 hours), except with complete tetraplegia or paraplegia of 2 weeks or longer with pain controlled, or poor overall prognosis.
• Plain X-ray does not diagnose or exclude spinal metastases or MSCC; MRI, or CT if MRI is contraindicated, is the test.
• Degenerative cervical myelopathy is a slow compressive myelopathy graded by mJOA: mild 15 to 17, moderate 12 to 14, severe 11 or lower. ^[2]
• Surgery is standard for moderate and severe DCM; mild DCM may be observed, with conditional evidence that surgery benefits patients with high baseline pain or disability, and with pre-operative counselling about persistent upper-extremity sensory deficits in some cases.
• Imaging compression alone does not predict deterioration; it was less relevant at canal diameters of 14.5 mm or less or more than 15.75 mm, whereas severe compression at two disc levels in an otherwise normal canal carried risk.
• Acute transverse myelitis is inflammatory: confirm MRI, exclude compression, give high-dose IV corticosteroids, and add plasma exchange or immunoadsorption for severe or refractory disease.
• LETM (three or more vertebral segments) points away from multiple sclerosis and toward NMOSD and connective-tissue causes.
• Subacute combined degeneration is reversible until it is not. Neurological involvement demands mandatory intramuscular hydroxocobalamin; severe disease is treated with 1000 micrograms on alternate days until no further improvement, then 1000 micrograms every 3 months lifelong.
• Nitrous oxide can produce tissue B12 deficiency with normal serum B12 concentrations.
• Evidence bases differ in strength (NICE strongest; AO Spine mild-DCM recommendations conditional and low to very-low quality; ESMO bone health offers broader oncology framing).^[3] State uncertainty plainly where guidelines differ.

Metastatic bone disease; multiple sclerosis; neuromyelitis optica spectrum disorder; myelin oligodendrocyte glycoprotein antibody-associated disease; vitamin B12 deficiency; peripheral neuropathy; anterior spinal artery infarction; spinal trauma; palliative radiotherapy; rehabilitation after neurological injury.