Neuroanatomy and Neurophysiology
Domain 1 rewards pure localisation: the examiner supplies a sign and expects a level, a side and a tract. Most marks come from knowing where each pathway crosses and which brainstem structure sits where.
The three long tracts and their crossings
- Corticospinal fibres decussate at the cervicomedullary junction, so a spinal lesion gives ipsilateral upper motor neuron signs while a hemispheric lesion gives contralateral signs.
- Dorsal column fibres (fine touch, vibration, proprioception) ascend to nucleus gracilis and cuneatus, cross as internal arcuate fibres, and travel in the medial lemniscus.
- Spinothalamic fibres synapse in the dorsal horn and cross within one or two segments in the anterior white commissure, so cord lesions produce contralateral pain loss beginning one to two segments below the level.
Brainstem syndromes worth memorising
- Lateral medullary (PICA or vertebral artery): ipsilateral Horner syndrome, facial numbness, ataxia, dysphagia and hoarseness from nucleus ambiguus, with contralateral body pain loss.
- Medial medullary (anterior spinal artery): ipsilateral tongue deviation, contralateral hemiparesis and vibration loss.
- Internuclear ophthalmoplegia from a medial longitudinal fasciculus lesion: failure of adduction on the affected side with abducting nystagmus of the fellow eye.
Worked example
A 30-year-old woman has subacute painful right visual loss, then left leg numbness. She has a right relative afferent pupillary defect with reduced colour vision, a sensory level at T8, and bilateral extensor plantars. Localisation is right optic nerve plus spinal cord: two sites in space. That points to neuromyelitis optica spectrum disorder, MOG antibody disease or multiple sclerosis. Next: MRI brain and whole spine, aquaporin-4 and MOG antibodies, CSF with oligoclonal bands.
Traps that cost marks
Mixing up the level of decussation; attributing ipsilateral weakness to a cortical lesion; forgetting that the Horner syndrome in Wallenberg syndrome is ipsilateral; missing that a cortical lesion causes contralateral lower facial weakness with spared forehead.