Basic neuroscience: neuroanatomy, neurophysiology, neuropathology, neuropharmacology
Basic neuroscience underpins every other domain. Board questions rarely ask an isolated fact; they present a deficit, a drug effect, or a histological pattern and expect you to move from mechanism to localisation to clinical consequence in one step.
Neuroanatomy anchors
- Corticospinal fibres decussate in the medulla; dorsal column fibres also decussate in the medulla. Spinothalamic fibres cross within one or two segments of entry, so a cord hemisection gives ipsilateral dorsal column loss and contralateral pain/temperature loss beginning one or two levels below the lesion.
- The facial nucleus lies in the pons. An upper motor neuron lesion spares the forehead because the upper face receives bilateral cortical input; a nuclear or nerve lesion paralyses the whole half of the face.
- Eye movement localises well: CN III palsy gives ptosis, a dilated pupil and a down-and-out eye; internuclear ophthalmoplegia (MLF) gives impaired adduction on the side of the lesion with nystagmus of the abducting eye.
Physiology and pharmacology
The action potential depends on voltage-gated sodium channels (upstroke) and potassium channels (repolarisation); synaptic release is calcium-dependent. This maps directly onto mechanisms: phenytoin and carbamazepine prolong sodium-channel inactivation; valproate and ethosuximide act on T-type calcium channels (absence); vigabatrin inhibits GABA transaminase; levodopa is decarboxylated to dopamine and paired with carbidopa to block peripheral metabolism; pyridostigmine inhibits acetylcholinesterase at the neuromuscular junction.
Neuropathology
The ischaemic cascade runs from energy failure and depolarisation through glutamate excitotoxicity, calcium influx, free-radical generation, and delayed apoptosis in the penumbra. Demyelination spares axons initially (relative axonal preservation with macrophage-mediated myelin loss), which is why conduction block in inflammatory demyelination can recover. Alzheimer pathology is amyloid plaques plus tau neurofibrillary tangles; Lewy body disease shows alpha-synuclein inclusions.
Worked example
A patient has right-sided facial weakness sparing the forehead, right hemiparesis, and normal sensation. The lesion lies on the left, above the facial nucleus: corticobulbar fibres to the lower face cross, and the corticospinal tract crosses in the medulla, so a left hemisphere lesion explains both. A CN VII nuclear lesion would paralyse the entire right face and often spare the limbs.
Traps
Confusing upper and lower motor neuron facial patterns is the commonest error. The second is forgetting that dorsal column and corticospinal crossings occur in the medulla while spinothalamic crossings are segmental. Remember that the cerebellum compares intended with actual movement rather than initiating it, and the basal ganglia select and scale movement - phrases that decide many "which structure" items.