Central cord syndrome

Summary

Central cord syndrome (CCS) is the most common form of incomplete spinal cord injury. It is classically characterised by disproportionate motor impairment of the upper limbs compared to the lower limbs, bladder dysfunction, and variable sensory loss below the level of the lesion. It typically occurs due to hyperextension injury in patients with pre-existing cervical spondylosis.

Pathophysiology and anatomy

Mechanism

The injury involves the central grey matter and the medial aspect of the corticospinal tracts.

Hyperextension injury: Most common mechanism. Often involves an elderly patient with pre-existing cervical spondylosis or congenital stenosis falling forward and striking their chin.
Pincer mechanism: The cord is compressed anteriorly by osteophytes/disc material and posteriorly by buckling of the ligamentum flavum.
Haemorrhagic necrosis: Selective destruction of central grey matter.

Anatomical basis

The somatotopic organisation of the lateral corticospinal tract explains the clinical presentation:

Medial fibres: Innervate cervical segments (upper extremities).
Lateral fibres: Innervate sacral/lumbar segments (lower extremities).
Result: Central cord damage disproportionately affects the medially located cervical fibres, sparing the lateral sacral fibres.

Clinical features

Motor: Weakness is more profound in the upper extremities than the lower extremities (UE > LE). Distal weakness (hands) is often worse than proximal weakness ("Man in a barrel" syndrome).
Sensory: Variable. Often dissociated sensory loss (pain and temperature loss due to spinothalamic tract involvement, with preserved proprioception/vibration). A "cape-like" distribution may be present.
Autonomic: Urinary retention is common.

Imaging findings

CT cervical spine

Role: Assess bony architecture, alignment, and canal diameter.
Findings:
- Multi-level degenerative changes (osteophytes).
- Congenital or acquired canal stenosis (AP diameter < 10–13 mm).
- Ossification of the posterior longitudinal ligament (OPLL).
- Acute fractures (less common in pure CCS).

MRI cervical spine

Gold standard for assessment of cord signal and ligamentous injury. NICE guidelines (NG23) recommend MRI within 1 hour for patients with abnormal neurological signs.

T2/STIR:
- Focal area of high signal intensity within the central spinal cord (typically C3–C4 or C4–C5 levels).
- Represents cord oedema or contusion.
- May demonstrate pre-existing myelomalacia.
T1: Usually isointense; may be hypointense in severe necrosis.
T2 GRE / SWI:*
- Crucial for detecting intramedullary haemorrhage.
- Prognostic value: Presence of haemorrhage correlates with a poorer neurological outcome (Type II injury).
DWI/ADC: Restricted diffusion may indicate acute cytotoxic oedema (spinal cord infarction).

Differential diagnosis

Condition	Distinguishing features
Anterior cord syndrome	Loss of motor function and pain/temp; preserved dorsal columns (proprioception/vibration). Associated with flexion injuries/anterior spinal artery ischaemia.
Brown-Séquard syndrome	Hemisection of the cord. Ipsilateral motor/proprioception loss; contralateral pain/temp loss.
Posterior cord syndrome	Rare. Loss of proprioception/vibration only.
Cruciate paralysis of Bell	Rare injury to the decussation of pyramids. Bilateral arm paralysis with leg sparing (cruciate fibres damage). Localises to cervicomedullary junction.
Syringomyelia	Chronic, cystic cavity. Cape-like sensory loss is classic, but history is non-traumatic or remote trauma.

Management and prognosis

Management

Initial: Immobilisation and haemodynamic support (maintain MAP > 85 mmHg to ensure cord perfusion).
Surgical vs Conservative:
- Historically conservative.
- Current consensus trend favours early surgical decompression (< 24 hours) if there is persistent compression or progressive neurological deficit, citing the STASCIS trial data.
- RCR/NICE: Emphasise urgent specialist referral. Decompression is indicated for stable patients with progressive deficit or gross compression.

Prognosis

Generally favourable compared to other cord syndromes.
Poor prognostic factors:
- Advanced age (> 50–70 years).
- Intramedullary haemorrhage on MRI.
- High-energy mechanism.
Recovery pattern: Lower extremities $\to$ Bladder $\to$ Proximal upper extremities $\to$ Hand function (fine motor skills are often the last to return and may remain permanently impaired).