Approach to unilateral UMNL and Brown Sequard Syndrome Flashcards
What are the causes of unilateral UMNL?
Cortical, subcortical and brainstem
1. Stroke - cortical, subcortical, brainstem
2. Multiple sclerosis affecting unilateral
3. Neoplastic - tumours
4. Infective - abscess
Spinal cord
5. Brown sequard syndrome
6. Multiple sclerosis
Possible distribution of UMN weakness
Exceptions:
1. Patchy UMN weakness or multiple UMN deficits that do not fit into a single lesion
- Multiple sclerosis.
- Multiple cortical strokes.
2. Brown sequard syndrome:
- Ipsilateral spastic hemiparesis with DCML loss + contralateral loss of pinprick sensation
Unilateral UMNL Dance
- Examine UL or LL as per stem
- Identifying unilateral UMNL pattern with spasticity, contracture, hyperreflexia, weakness
- Look out for distribution of sensation loss
> Ipsilateral unilateral DCML loss + contralateral spinothalamic loss -> think Brown Sequard syndrome
> Ipsilateral spinothalamic loss + examine CN -> think cortical/subcortical/brainstem - Cerebellar signs
- Cranial neuropathy
- Cortical: contralateral CN + limb
- Brainstem: ipsilateral uncrossed CN nuclei + contralateral crossed descending corticospinal fibres
- Distinguish between UMN vs. LMN CN VII palsy - Higher cortical signs
- Frontal: gaze preference, acalculia, personality change
> Broca area: non-fluent expressive aphasia
- Parietal: hemineglect, abnormal line bisection
- Temporal: memory loss
> Wernicke area: fluent receptive dysphasia
- Occipital: visual field defect with macular sparing - Complications
- Fine motor tasks (button shirt, use handphone).
- Mobility - use of walking aid or wheelchair.
- Swallowing - nasogastric tube.
- Urinary function - urinary catheter or diapers. - Exploring mechanisms of infarct
A. Haemorrhagic: signs of anticoagulation, injuries
B. lschaemic
- Cardioembolic: irregularly irregular pulse
- Artery-to-artery embolism: carotid bruit
- Large vessel disease: atherosclerosis (xanthalesma, archus senilis)
- Small vessel disease: diabetes (BGM marks, request blood pressure)
- Existing cardiovascular disease: sternotomy scar, lower limb amputations
Neuro-localisation of unilateral UMNL
Assume initial examination of left hemiparesis
Brown-sequard syndrome is a hemiscection (one-sided injury) of the spinal cord
Resulting in: (MVP same side, pain other side):
- Ipsilateral UMN spastic paralysis
- Ipsilateral DCML loss
- Contralateral spinothalamic loss
+/- LMN at level (anterior horn) and Horner’s syndrome (cervical)
Causes:
1. Trauma and wound
2. Spinal cord tumours
3. Multiple sclerosis
4. Vascular - infarct, AVM
5. Transverse myelitis
6. Infectious - TB, syphilis
7. Radiation myeloapthy
8. Syringomyelia - rarely presents this way
Examination findings and signs of Brown-Sequard Syndrome
- Ipsilateral UMN below level
- Hemiparesis/hemiplegia, spasticity, hyperreflexia, muscle weakness, positive Babinski - Ipsilateral DCML loss below level
- Loss of vibration, proprioception, 2-point discrimination - Contralateral spinothalamic loss below level
- Loss of pain and temperature
- Usually 1-2 segments below level of lesion (fibres decussate 1-2 segments before ascending) - Entire hemi-cord damage - LMNL at level
- Ipsilateral LMN (anterior horn damage)
- Ipsilateral pan-sensory loss (dorsal horn damage) - Additional features
- Neuropathic pain
- Bladder and bowel dysfunction
- Respiratory failure (high cervical)
- Ipsilateral Horner (above T1)
Investigations of unilateral UMNL
- CT and MRI brain and spine
- Cervical cord evoked potential (in BSS)
- CVRF screening - HbA1c, lipid panel
- Lumbar puncture - oligoclonal IgG bands (in MS), identifying inflammatory or infections
- NCS and EMG - demyelination vs axonal
- Evoked potentials (SEP and MEP)
Management of unilateral UMN
General
1. Multidisciplinary team: PT, OT, psychologist, Neurology
Symptomatic
2. Spasticity: baclofen, diazepam
3. Neuropathic pain: gabapentin, TCA, SSRI
4. Bladder/bowel dysfunction
5. DVT prophylaxis
Definitive
6. Ischaemic stroke: aspirin, statin, control CVRF
7. Acute Brown-Sequard:
- Methylprednisolone
- Haemodynamic support MAP >85-90
- Orthospine surgery
8. Multiple sclerosis: methylprednisolone, PLEX, interferon beta, natalizumab
Comparison of other spinal cord syndromes
Cortical/subcortical strokes affect cerebral cortex and descending white matter tracts. The lesions damage UMN of corticobulbar tract before they reach cranial nerve nuclei in brainstem.
A. Contralateral UMNL of cranial nerves:
1. CN7 - contralateral facial weakness with forehead sparing
2. CN12 - contralateral tongue weakness with deviation away from lesion, NO atrophy or fasciculations
3. CN 5, 9, 10, 11 - contralateral jaw weakness, shoulder shrug, SCM weakness
B. Contralateral UMNL of limbs:
1. Hypertonia, hyperreflexia - loss of central inhibition
2. Muscle weakness
Brainstem strokes affect structures within brainstem, which contain LMN cranial nerve nuclei at the level (brainstem) and UMN descending corticobulbar tracts (below level)
A. Ipsilateral LMNL of cranial nerves:
- Pontine infarct CN7 - ipsilateral whole hemiface palsy with fasciculations/atrophy
- Medullary infarct CN12 - ipsilateral tongue weakness with deviation towards lesion, atrophy and fasciculation
B. Contralateral UMNL of limbs
Comparison between cortical/subcortical vs brainstem stroke
Cranial nerves UMNL vs LMNL
CN 5(V3) (Motor): Mild contralateral weakness, brisk jaw jerk (UMN) vs. ipsilateral weakness/atrophy, jaw deviates towards lesion, reduced/absent jaw jerk (LMN).
CN 7: Forehead sparing (UMN) vs. full hemiface weakness (LMN).
CN 9/10: Uvula deviates away from lesion (both UMN/LMN), but LMN has ipsilateral absent gag, hoarseness, significant palatal droop.
CN 11: Contralateral trapezius / ipsilateral SCM weakness (UMN) vs. ipsilateral weakness of both (LMN).
CN 12: Tongue deviates away from UMN lesion vs. towards LMN lesion (LMN also has atrophy/fasciculations).
