Neuroanatomy, neurophysiology and basic neurosciences
The exam in this domain tests whether you can derive a clinical deficit from anatomy rather than recalling syndromes in isolation. Expect questions on tract decussation levels, vascular territories, cranial nerve nuclei topography, and the physiology that underpins EEG, EMG and neuroimaging signals.
Long tracts and where they cross
- Corticospinal tract: Betz cells and premotor cortex → corona radiata → posterior limb of the internal capsule → cerebral peduncle → basis pontis → medullary pyramid → pyramidal decussation (85–90%) → lateral corticospinal tract. The minority fibres form the anterior corticospinal tract and cross segmentally.
- Dorsal column / medial lemniscus (vibration, fine touch, conscious proprioception): ascends ipsilaterally in fasciculus gracilis and cuneatus, synapses in the medullary nuclei, and crosses as internal arcuate fibres.
- Spinothalamic tract (pain, temperature, crude touch): synapses in the dorsal horn and crosses within 1–2 segments in the anterior white commissure, so cord lesions produce contralateral loss starting 1–2 segments below the level.
Cerebellum and basal ganglia
Superior cerebellar peduncle carries mainly output (dentate → contralateral ventrolateral thalamus); middle peduncle is pontocerebellar input; inferior peduncle is the restiform body (dorsal spinocerebellar and vestibular fibres). Hemispheric lesions give ipsilateral limb ataxia; vermal lesions give truncal ataxia. In the basal ganglia, the direct (D1) pathway facilitates movement and the indirect (D2) pathway inhibits it; loss of nigrostriatal dopamine disinhibits the indirect pathway and produces hypokinesia.
Vascular territories worth memorising
PCA supplies occipital cortex, thalamus (VPL/VPM) and midbrain; AICA the lateral pons; PICA the lateral medulla; the anterior choroidal artery the posterior limb of the internal capsule and hippocampus. Watershed infarcts between ACA/MCA and MCA/PCA produce proximal limb weakness.
Physiology
The resting membrane potential (about −70 mV) is set by the Na⁺/K⁺-ATPase; the action potential depends on voltage-gated Na⁺ channels and saltatory conduction in myelinated fibres. GABA-A receptors are Cl⁻ channels; NMDA receptors are Ca²⁺-permeable and mediate long-term potentiation. Cerebral blood flow is about 50 mL/100 g/min with autoregulation between roughly 50 and 150 mmHg.
Worked example
A patient has right-sided spastic weakness of the leg plus loss of vibration and joint position sense on the right below T8, with loss of pain and temperature on the left from about T10. The corticospinal and dorsal column deficits are ipsilateral because neither has crossed at T8; the spinothalamic loss is contralateral and begins below the lesion because those fibres cross segmentally. This is a right cord hemisection (Brown-Séquard).
Traps
Assuming all sensory loss below a cord lesion is contralateral; confusing AICA and PICA syndromes; forgetting that the anterior spinal artery spares the dorsal columns; treating the thalamic VPM (face) and VPL (body) as interchangeable.