Spinal Cord Compression Syndromes
Written 10th June 2020 - Last Update 28th August 2026
Spinal Cord Compression Syndromes
Three related syndromes of spinal cord/canal compromise, from the acute surgical emergency (cauda equina syndrome) through progressive cord compression (myelopathy) to intermittent canal narrowing on exertion (spinal claudication).
Cauda equina syndrome
Rare but potentially devastating — dysfunction of multiple lumbosacral nerve roots in the vertebral canal. Caused by large central disc herniation (most commonly L4/5 or L5/S1), space-occupying lesion (neoplasm, abscess), or fracture.
Low back pain with radiculopathy is one of the most frequent GP presentations — but true CES accounts for only ~0.08% of these presentations. Because of the disproportionate medico-legal risk of a missed diagnosis, referral thresholds are appropriately low — but <10% of “suspected CES” referrals to neurosurgery result in intervention, and most of those are for “threatened”/“impending”/“incomplete” CES rather than frank cauda equina compression. Rather than treating CES as a fixed checklist, think of it as a spectrum of severe lumbosacral radiculopathy — the goal is identifying nerve root injury causing motor, continence or sexual dysfunction, or bilateral symptoms at risk of progressing.
Presentation
May be acute (low back pain as the initial symptom, then evolving neurological signs) or chronic (chronic back pain with slow progression to numbness and urinary symptoms).
- Saddle anaesthesia/paraesthesia — assess with pinprick/light touch over the “saddle” region (genital/perineal area in contact with a bike seat) — this is preferred over anal tone assessment (see below), and also allows testing the anal wink reflex.
- Urinary symptoms — incomplete CES: loss of desire to void, poor stream, reduced sensation. Complete CES: urinary retention/overflow incontinence. Urinary retention is a cardinal sign of significant lower sacral root dysfunction and generally warrants emergent investigation even in the presence of severe pain (an alternative explanation for retention).
- Anal sphincter disturbance — faecal incontinence or constipation.
- Bilaterally absent ankle jerk reflexes — highly specific for CES (~95% in one series), since direct assessment of lower sacral root reflexes is difficult but the adjacent S1 root/ankle jerk is easily tested.
On digital rectal examination / anal tone
International consensus now recommends against performing a rectal exam to assess anal tone in primary care — it is invasive, and its sensitivity and specificity for CES are each only ~50% (essentially non-contributory to triage). Perianal saddle-region sensory testing (pinprick/light touch) is preferred as a less invasive alternative with better discriminatory value.
Investigation
No investigation needed in primary care — refer to the emergency department for urgent assessment and MRI. MRI is preferred over CT — guidelines and expert consensus recommend MRI for suspected cauda equina compression, and obtaining a community CT scan first is not required and may even delay care (despite one study finding modern CT has 98% sensitivity/86% specificity for excluding significant central canal compression).
Triage — indications for referral
Emergency referral:
- Bilateral pain or altered sensation extending below the knee (including saddle/genital region).
- Bilateral weakness.
- Bilaterally absent ankle jerks in the setting of radicular pain.
- Unilateral weakness with power 3/5 or worse.
- Any concern for urinary retention.
- Any other red flag for serious non-CES spinal pathology — UMN signs, unexplained weight loss, night sweats, fevers, IV drug use, history of metastatic malignancy.
Urgent referral (within 24 hours/rapid assessment clinic):
- Bilateral pain or altered sensation extending below the knee, without saddle/genital involvement or the other red flags above.
- Single nerve root territory weakness with power ≥4/5.
- Severe radicular pain refractory to oral analgesia.
Document examination findings — reflexes, pinprick and light touch over the saddle area — whenever CES is being considered.
Management
Refer to ED for urgent assessment and MRI, then urgent surgical decompression if confirmed.
Myelopathy
Myelopathy is any neurological deficit related to compression of the spinal cord. The classic pattern: LMN signs at the level of the lesion, UMN signs below the level of the lesion.
Causes
- Degenerative cervical spondylotic myelopathy — the most common cause: osteophyte formation in the cervical spine progressively compresses the cord.
- Congenital canal stenosis
- Epidural abscess
- Trauma
- Bony metastases / sarcoma
- Disc herniation
- Thoracic degenerative osteophytes (less common)
Clinical features — cervical spondylotic myelopathy
- Neck pain and stiffness
- Arms — LMN signs (at the level of the lesion):
- Arm pain, numbness and weakness
- Muscle wasting
- Reduced tendon reflexes
- Symptoms provoked by neck movement
- Legs — UMN signs (below the level of the lesion):
- Spasticity
- Hyperreflexia
- Ataxia
- Sphincter involvement
- Weakness less prominent than the spasticity
Differential diagnosis
- Multiple sclerosis — see Multiple Sclerosis
- Amyotrophic lateral sclerosis / MND — see Motor Neuron Disease
- Hereditary spastic paraparesis
- Spinal cord tumour
Investigations
- MRI — first-line; can be ordered in general practice for suspected cervical radiculopathy
- Nerve conduction studies
- B12/folate — to exclude peripheral neuropathy as a mimic
Spinal claudication
A syndrome, not a diagnosis: back pain radiating down the legs with ambulation, improving with lumbar spinal flexion.
Cause
Lumbar spinal canal stenosis — walking (lumbar extension) narrows the canal and puts pressure on the cauda equina; flexion opens it up again.
- “Shopping cart sign” — no pain when pushing a shopping trolley, because the patient can flex forward while pushing.
- Distinguish from vascular claudication: spinal claudication is posture-dependent (relieved by flexion/sitting, not just by stopping), whereas vascular claudication is relieved by rest in any position and is associated with absent pulses.
Investigation
- Imaging — CT or MRI of the lumbar spine
Treatment
- Physical therapy ± bracing, ± epidural steroid injections
- Surgical decompression if refractory to conservative management