Incomplete Spinal Cord Syndromes

An incomplete cord injury is defined by preservation of some sensory or motor function below the neurological level, including the lowest sacral segments (sacral sparing at S4 to S5). On the American Spinal Injury Association impairment scale, grades B, C and D are incomplete, while grade A is complete and grade E is normal.

Patterned syndromes result from selective tract involvement

• Central cord syndrome: the commonest incomplete syndrome. It follows cervical hyperextension injury in older adults with pre-existing spondylosis or canal stenosis, often without fracture. The central grey matter and adjacent corticospinal tracts are damaged.
• Anterior cord syndrome: from flexion injuries, vertebral burst fractures, disc herniation, or infarction of the anterior spinal artery (aortic dissection, aortic surgery, hypotension). It has the worst prognosis for motor recovery.
• Brown-Séquard syndrome: hemisection of the cord from penetrating trauma, lateral mass fracture, tumour, demyelination or disc herniation. It has the best prognosis.
• Posterior cord syndrome: rare. Causes include trauma, vitamin B12 deficiency, tabes dorsalis and copper deficiency.
• Conus medullaris syndrome: injury at the T12 to L2 vertebral level, with a mix of upper and lower motor neuron signs.
• Cauda equina syndrome: injury to lumbosacral roots below L1 to L2, with lower motor neuron signs.

Non-traumatic causes include epidural haematoma or abscess, tumour, disc herniation, spinal cord infarction, transverse myelitis, multiple sclerosis, neuromyelitis optica spectrum disorder, dural arteriovenous fistula and radiation myelopathy.

Spinal shock (areflexic flaccid paralysis lasting 24 to 72 hours, and sometimes weeks) follows acute injury and ends with return of the bulbocavernosus reflex. Neurogenic shock (hypotension with bradycardia) occurs in injuries above T6 and reflects loss of sympathetic outflow.

Central cord syndrome

• Motor loss greater in the arms than the legs, with the hands most severely affected.
• Variable sensory loss below the lesion, burning dysaesthesias in the hands, and bladder retention.
• Recovery is typically lower limbs first, then bladder, then proximal arms, with the hands last.

Anterior cord syndrome

• Complete or near complete motor paralysis and loss of pain and temperature sensation below the level.
• Preserved dorsal column function (light touch, vibration, proprioception).

Brown-Séquard syndrome

• Ipsilateral weakness and ipsilateral loss of proprioception, vibration and fine touch below the lesion.
• Contralateral loss of pain and temperature beginning one to two segments below the lesion, because spinothalamic fibres cross.
• Ipsilateral segmental lower motor neuron signs and a band of anaesthesia at the lesion level.

Posterior cord syndrome

• Loss of proprioception and vibration, sensory ataxia and a positive Romberg sign, with preserved power.

Conus medullaris syndrome

• Early and prominent bladder, bowel and sexual dysfunction, saddle anaesthesia, symmetrical sensory loss, minor leg weakness, and perianal sensory loss.

Cauda equina syndrome

• Asymmetric radicular pain, lower motor neuron weakness, areflexia, saddle anaesthesia and sphincter dysfunction.

Autonomic features of injuries at T6 and above include hypotension, bradycardia, poikilothermia and autonomic dysreflexia, with paroxysmal hypertension, pounding headache and sweating above the lesion triggered by bladder distension or bowel impaction. Respiratory compromise follows high cervical injuries.

Red flags are progressive neurological deficit, urinary retention, priapism, and a rising sensory level.

Trauma assessment follows resuscitation principles with spinal immobilisation. Neurological examination uses the standardised International Standards for Neurological Classification of Spinal Cord Injury:

• Strength grading of key muscles (C5 to T1 and L2 to S1), light touch and pinprick across 28 dermatomes, anal sensation and voluntary anal contraction.
• Determination of motor and sensory levels and of the impairment grade.
• Rectal examination and bulbocavernosus reflex to define spinal shock.

Imaging

• CT of the whole spine for fractures and alignment.
• MRI within 24 to 72 hours, earlier if there is progressive deficit or surgical planning. T2 and STIR sequences show cord oedema, haemorrhage, compression, disc rupture and ligamentous injury.
• Anterior spinal artery infarct shows a pencil like anterior T2 hyperintensity and owl's eyes on axial images.
• CT angiography of the neck when vertebral artery injury is suspected.

Non-traumatic evaluation

• MRI with gadolinium of the cord and brain, CSF analysis (cells, protein, oligoclonal bands, cytology).
• Vitamin B12, copper, HIV, syphilis serology, aquaporin-4 IgG and MOG IgG, ACE, ANA, and inflammatory markers.
• Spinal angiography for suspected dural arteriovenous fistula.

Bladder assessment by post void residual (bladder scan) and urodynamics.

Acute traumatic management

• Spinal immobilisation, airway and ventilatory support, and avoidance of hypoxia and hypotension.
• Maintain mean arterial pressure at 85 to 90 mmHg for 5 to 7 days in a monitored setting. Use norepinephrine at 0.05 to 0.5 mcg/kg/min if fluids are insufficient.
• Neurogenic shock: judicious fluids, atropine 0.5 to 1 mg IV for symptomatic bradycardia, and vasopressors.
• Early surgical decompression within 24 hours is reasonable, particularly for incomplete injuries with persistent compression, instability or progressive deficit.
• In central cord syndrome, surgical decompression is considered early for ongoing compression, severe deficits or instability. Neurologically stable patients without instability can be managed conservatively with close observation.
• High dose methylprednisolone is not recommended routinely because of infection and metabolic complications and limited benefit.

Prevention of complications

• Thromboprophylaxis: enoxaparin 40 mg SC daily (or 30 mg twice daily) started within 72 hours once bleeding risk is acceptable, plus mechanical compression, continued for 8 to 12 weeks in motor complete injuries.
• Gastric protection with a proton pump inhibitor in the acute phase.
• Pressure area care with turning every 2 hours, nutrition, and early mobilisation.
• Bladder management with intermittent catheterisation every 4 to 6 hours, and a structured bowel programme.
• Heterotopic ossification prophylaxis with early range of motion and consideration of NSAIDs.

Autonomic dysreflexia (injuries at T6 and above)

• Sit the patient upright, loosen tight clothing, check and relieve bladder and bowel.
• If systolic pressure stays above 150 mmHg, give nifedipine 10 mg (bite and swallow), glyceryl trinitrate 0.4 mg sublingually, or captopril 25 mg.

Spasticity and pain

• Baclofen 5 mg three times daily titrated to a maximum of 80 mg/day, tizanidine 2 mg at night titrated to 36 mg/day, dantrolene 25 mg daily increased to 100 mg four times daily, botulinum toxin for focal spasticity, and intrathecal baclofen for refractory cases.
• Neuropathic pain with gabapentin, pregabalin, duloxetine or amitriptyline.

Non-traumatic causes

• Multiple sclerosis relapse: methylprednisolone 1 g IV daily for 3 to 5 days.
• Neuromyelitis optica spectrum disorder: high dose steroids and plasma exchange.
• Vitamin B12 deficiency: hydroxocobalamin 1 mg IM on alternate days until no further improvement, then every 2 months.
• Neurosyphilis: aqueous benzylpenicillin 18 to 24 million units per day IV for 10 to 14 days.
• Epidural abscess: drainage and prolonged antibiotics. Epidural haematoma: reverse coagulopathy and evacuate.
• Cord compression by tumour: dexamethasone 10 mg IV then 4 mg every 6 hours, with radiotherapy or surgery.
• Anterior spinal artery infarct: aspirin 75 to 300 mg daily, treat the cause, maintain blood pressure, and use CSF drainage with lumbar drain during aortic surgery to keep CSF pressure under about 10 mmHg.

Rehabilitation

• Multidisciplinary spinal rehabilitation from the earliest safe point, gait training, hand function therapy, bone health, psychological support and vocational planning.

Prognosis varies by syndrome

• Central cord syndrome: most patients regain walking, with 75 to 85% reaching ambulation, and younger patients do better.
• Brown-Séquard syndrome: over 90% regain walking.
• Anterior cord syndrome: useful motor recovery is uncommon.