Brown-Séquard syndrome
Description
- Hemisection (or hemi-injury) of the spinal cord -> a dissociated syndrome that reflects where each tract decussates
- *Pure Brown-Sequard is rare. Brown-Sequard PLUS is common* - most lesions are incomplete and asymmetric rather than a clean hemisection
The anatomy that generates the signs
| Tract | Decussates | Consequence |
|---|---|---|
| Corticospinal | In the medulla (above the cord) | Ipsilateral weakness below the lesion |
| Dorsal columns | In the medulla (above the cord) | Ipsilateral loss of vibration and proprioception |
| Spinothalamic | In the cord, within 1-2 segments of entry | CONTRALATERAL loss of pain and temperature, beginning 1-2 levels BELOW the lesion |
- *The one tract that crosses in the cord is the one that produces contralateral signs. Everything else stays on the same side*
Epidemiology
- Rare - ~1-4% of traumatic spinal cord injuries
- Trauma: M>F ~4:1, peak 15-40 yrs (penetrating injury, road trauma)
- Non-traumatic causes predominate in older patients and in specialist neurology practice
- Cervical > thoracic location in most series
Aetiopathogenesis
Common causes
- Multiple sclerosis - the commonest non-traumatic cause; a partial, asymmetric transverse myelitis
- Vascular malformation - AVM, dural arteriovenous fistula, cavernoma
- Glioma and other intramedullary tumours; extramedullary compression (meningioma, schwannoma, metastasis)
- Trauma - penetrating (stab, gunshot) is the classic; also facet dislocation, fracture, disc herniation
- Myelitis - infective (HSV, VZV, HIV, HTLV-1, syphilis, TB, schistosomiasis), post-infectious, NMOSD/MOGAD
- Post-radiation myelopathy
Also consider
- Epidural haematoma or abscess; spinal cord infarction (usually anterior spinal artery, so more often a different syndrome)
- Cervical spondylotic myelopathy with asymmetric compression
- Decompression sickness; hyperextension injury in a stenotic canal
- Sarcoidosis, Behcet, vasculitis, neurosyphilis
Diagnosis
Motor features
- Ipsilateral UPPER motor neurone signs BELOW the level - weakness, spasticity, hyperreflexia, extensor plantar response
- Ipsilateral LOWER motor neurone signs AT the level - segmental weakness, wasting, absent reflex (anterior horn cell and root involvement)
- Spinal shock may make everything flaccid and areflexic acutely - the UMN pattern emerges over days to weeks
Sensory features
- Contralateral loss of pain and temperature, beginning 1-2 segments below the lesion
- Ipsilateral loss of vibration and proprioception below the lesion
- Light touch is generally preserved (carried in both the dorsal columns and the anterolateral system - the redundancy protects it)
- Sometimes an ipsilateral band of complete sensory loss at the level of the lesion (dorsal root involvement)
Other
- Ipsilateral Horner syndrome if the lesion is at or above T1
- Bladder, bowel and sexual dysfunction are less prominent than in a complete cord lesion - often the clue that the lesion is a hemisection
- Ipsilateral vasodilatation and anhidrosis below the lesion
Localise the level
- The sensory level from the contralateral pain and temperature loss is 1-2 segments BELOW the true lesion - image above the apparent level
- Landmarks: nipple T4, xiphisternum T6, umbilicus T10, inguinal ligament L1
- Segmental LMN signs give the most accurate level
Investigations
- URGENT MRI whole spine with gadolinium - the only adequate test; identifies compression, cord signal change, enhancement, syrinx, vascular flow voids
- Whole spine, not just the presumed level
- CT if trauma (fracture, dislocation) or MRI contraindicated; CT myelogram
- If no compressive lesion: CSF (cells, protein, oligoclonal bands, cytology, PCR panel), AQP4 and MOG antibodies, B12, copper, HIV, syphilis, HTLV-1, ACE, ANA/ENA, ANCA
- MRI brain - looking for demyelinating lesions
- Spinal angiography if a vascular malformation is suspected
Differential of a myelopathy pattern
| Syndrome | Features |
|---|---|
| Brown-Sequard | Ipsilateral motor + dorsal column loss, contralateral spinothalamic loss |
| Anterior cord | Bilateral motor + spinothalamic loss; dorsal columns SPARED (anterior spinal artery infarct) |
| Central cord | Upper limbs > lower limbs, "cape" dissociated sensory loss (syringomyelia, hyperextension injury) |
| Posterior cord | Dorsal column loss with sensory ataxia (B12, copper, tabes) |
| Complete transverse | All modalities lost below a level, with early sphincter involvement |
| Conus / cauda equina | Saddle anaesthesia, early bladder and bowel involvement, LMN signs |
Management
Management is management of the cause. The syndrome itself directs urgency, not treatment.
A. Immediate
- Urgent MRI and neurosurgical referral for any compressive lesion - the deficit becomes fixed
- Spinal immobilisation if trauma; avoid hypotension (maintain mean arterial pressure ~85-90 mmHg for the first week after acute traumatic cord injury to preserve cord perfusion)
- *High-dose methylprednisolone is NOT recommended in acute traumatic spinal cord injury* - the harms outweigh any benefit
- Dexamethasone for malignant compression; urgent radiation oncology and oncology referral
B. By cause
| Cause | Treatment |
|---|---|
| Trauma / fracture-dislocation | Early surgical decompression and stabilisation |
| Disc or spondylotic compression | Decompression |
| Epidural abscess | Blood cultures, surgical drainage + prolonged IV antibiotics |
| Epidural haematoma | Reverse anticoagulation, urgent evacuation |
| Tumour | Dexamethasone, surgery and/or radiotherapy; systemic therapy for the primary |
| Multiple sclerosis | IV methylprednisolone 1 g daily for 3-5 days, then commence or escalate disease-modifying therapy |
| NMOSD / MOGAD | High-dose corticosteroid + plasma exchange early; then rituximab, eculizumab, satralizumab or inebilizumab. *MS DMTs make NMOSD worse - check the antibodies* |
| Infective myelitis | Aciclovir for HSV/VZV; antimicrobials per organism |
| Vascular malformation | Endovascular embolisation or surgery |
| Radiation myelopathy | Corticosteroid, supportive; consider bevacizumab and hyperbaric oxygen |
C. Rehabilitation - where the functional gain happens
- Specialist spinal rehabilitation unit referral
- Bladder: post-void residuals, intermittent self-catheterisation, urodynamics
- Bowel: regimen from day 1, aperients, digital stimulation
- Spasticity: physiotherapy and stretching, baclofen, tizanidine, botulinum toxin
- Neuropathic pain: amitriptyline, duloxetine, gabapentin or pregabalin
- VTE prophylaxis, pressure area care, contracture prevention
- Sexual function - address explicitly; fertility advice
- Autonomic dysreflexia education for lesions at or above T6 - patient, family and ambulance card
- Psychological support, vocational rehabilitation, home and vehicle modification
Associations
- Penetrating trauma - stabbing, gunshot; motor vehicle and sporting injury
- Multiple sclerosis and other demyelinating disease (NMOSD, MOGAD, ADEM)
- Spinal AVM and dural arteriovenous fistula; cavernoma
- Spinal tumours - meningioma, schwannoma, ependymoma, glioma, metastasis
- Radiation to the spine or adjacent structures
- Infection - HSV, VZV, HIV, HTLV-1, TB (Pott disease), syphilis, schistosomiasis
- Anticoagulation and neuraxial procedures (epidural haematoma)
- Cervical spondylosis; rheumatoid atlantoaxial subluxation; ankylosing spondylitis
- Horner syndrome when the lesion is at or above T1
Natural history & complications
- *Brown-Sequard has the BEST prognosis of any incomplete spinal cord syndrome*
- Over 75-90% regain ambulation, and most regain bladder and bowel continence
- The intact contralateral corticospinal tract does the work
- Recovery sequence: proximal extensor then distal flexor power returns; motor recovery precedes sensory
- Most recovery occurs in the first 3-6 months, continuing up to 2 years
- Better prognosis: incomplete lesion, younger age, traumatic (rather than infiltrative) cause, early decompression, preserved sacral sensation
Complications
- Neuropathic pain below the level - common and often the dominant long-term symptom
- Spasticity and contracture
- Neurogenic bladder -> recurrent UTI, hydronephrosis, renal impairment
- Autonomic dysreflexia (lesions at or above T6) - a hypertensive emergency triggered by a distended bladder, constipation or a pressure sore; sit the patient up, remove the trigger, then treat the blood pressure
- Pressure injury, VTE, osteoporosis and fragility fracture below the level
- Sexual dysfunction and infertility
- Post-traumatic syringomyelia - late deterioration, ascending dissociated sensory loss; requires repeat MRI
- Depression and adjustment disorder
Monitor
- Serial ASIA/ISNCSCI motor and sensory examination
- Bladder residuals, renal tract imaging, urodynamics
- Skin integrity, spasticity, pain scores
- Any late deterioration -> repeat MRI for syrinx, tethering or recurrent disease
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