Spinal cord compression

Overview

Spinal cord compression (SCC) is a neurological emergency - compression disrupts ascending sensory and descending motor tracts, causing irreversible injury without prompt treatment. Metastatic disease is the most common cause in the UK.

Presentation

Classic sequence: back pain → motor/sensory symptoms → bladder/bowel dysfunction (late, indicates significant cord damage).

•Back pain - severe, progressive, unremitting; worse with straining (coughing, sneezing); night pain disturbing sleep; percussion tenderness over spine

•Bilateral leg weakness - progressive, usually symmetrical; corticospinal tract compression

•Sensory level - dermatomal boundary below which sensation is reduced; localises compression

•Bladder and bowel dysfunction - urinary retention/incontinence, constipation; late features demanding immediate action

•Radicular pain - shooting, dermatomal, at the level of compression

•Neurogenic shock (high cervical/upper thoracic injury) - hypotension, bradycardia, warm dry peripheries, priapism; loss of sympathetic tone

💡

In ~25% of patients, MSCC is the first presentation of an undiagnosed malignancy - always search for an occult primary. Breast, prostate, and lung cancers are the most common causes; thoracic spine is most commonly affected.

Investigations

🏆 Gold standard

•MRI whole spine - images cord, disc spaces, vertebrae, epidural mass; whole spine must be imaged (multiple levels possible); within 24 hours of onset (immediately if rapidly deteriorating or unable to walk)

•First-line alternative: CT spine - if MRI contraindicated (pacemaker, severe claustrophobia); excellent bony detail, inferior soft tissue resolution

•Bloods: FBC, CRP, ESR (infection/malignancy), U&Es, blood cultures if infective cause suspected

🥈 Second-line

•CT chest/abdomen/pelvis - identify primary tumour if MSCC is first presentation; staging

🚨

Do not delay MRI waiting for analgesia or senior review. A patient ambulant at treatment has ~80% chance of remaining so; non-ambulant at diagnosis has only ~30% chance of regaining ambulation.

Differential diagnosis

•Cauda equina syndrome - compression below L1; LMN signs, saddle anaesthesia, urinary retention; urgent MRI and surgical decompression

•Transverse myelitis - inflammatory; clinically identical to SCC; MRI distinguishes (intrinsic cord signal change vs structural compression)

•Spinal cord infarction - sudden onset, often painless; bilateral weakness with dissociated sensory loss (pain/temperature lost, dorsal columns preserved)

•Guillain-Barré syndrome - ascending flaccid weakness, areflexia, no sensory level; CSF albuminocytological dissociation

Management

Management is a medical emergency - proceed in parallel with imaging. Goal: relieve compression, minimise further injury, preserve neurological function.

•Immediate: dexamethasone 16 mg IV - reduces cord oedema in MSCC

•Urinary catheterisation - if retention present

•Urgent referral - neurosurgical and oncological MDT

•Surgical decompression - for structural compression where patient is fit; followed by radiotherapy in MSCC

•Radiotherapy - for radiosensitive tumours or patients unfit for surgery

Complications

•Autonomic dysreflexia - cord injury at or above T6; triggered by noxious stimulus below injury (e.g. bladder distension, faecal impaction); acute severe hypertension, pounding headache, bradycardia, sweating/flushing above lesion, pallor below; remove precipitant first (check catheter/bowel) before antihypertensives

•Respiratory failure - high cervical lesions (C3-5) compromise diaphragm; may require mechanical ventilation

•VTE - immobility markedly increases DVT/PE risk; thromboprophylaxis mandatory

•Neurogenic bladder - recurrent UTIs, hydronephrosis, renal failure if unmanaged

•Chronic neuropathic pain - managed with gabapentin or amitriptyline

🚨

Autonomic dysreflexia mimics hypertensive emergency and occurs at T6 and above. The priority is identifying and removing the precipitant (most commonly a blocked catheter or faecal impaction) before reaching for antihypertensives.

Prognosis

•Ambulant at time of treatment → ~80% chance of remaining ambulant

•Non-ambulant at diagnosis → only ~30% regain ambulation

•MSCC prognosis also driven by cancer type, radiosensitivity, and systemic disease extent - early palliative care involvement appropriate

Anatomy - the L1 watershed

•Spinal cord runs C1 to ~L1 (conus medullaris); below L1 = cauda equina (peripheral nerve roots only)

•Compression above L1 = cord injury → UMN signs

•Compression at or below L1 = cauda equina injury → LMN signs

UMN vs LMN signs in SCC

Feature	UMN (above L1)	LMN (below L1 / cauda equina)
Tone	Hypertonia / spasticity	Flaccidity
Reflexes	Hyperreflexia, clonus	Hyporeflexia / areflexia
Plantar response	Upgoing (Babinski +ve)	Downgoing

⚠️

Reflexes may be transiently absent even with UMN lesions immediately after acute injury (spinal shock) - UMN signs emerge over days to weeks.