Neurology

A progressive, acquired decline in cognitive function severe enough to impair daily function, whose pattern of deficits directly reflects which brain networks the underlying pathology, most often amyloid and tau, Lewy bodies, or vascular injury, has damaged.

A tendency to recurrent unprovoked seizures caused by abnormal, excessive, hypersynchronous electrical discharge of cortical neurons, with seizure semiology directly reflecting which part of the cortex fires and how far the discharge spreads.

An acute, immune-mediated attack on peripheral nerves, typically triggered by molecular mimicry after infection, that strips myelin or damages axons from the roots outward, producing an ascending, symmetrical weakness that can progress to respiratory failure within days, which is why forced vital capacity is monitored more closely than the limb weakness itself.

A primary headache disorder driven by transient neuronal and vascular dysfunction (cortical spreading depression generates the aura, trigeminovascular activation generates the pain), producing a stereotyped, self-limiting attack rather than a structural lesion.

An autoimmune, T-cell-mediated attack on CNS myelin that produces neurological deficits disseminated in time and space, because demyelinating plaques occur at different sites of the central nervous system on different occasions, each slowing or blocking conduction along the affected pathway.

An autoimmune attack on the postsynaptic acetylcholine receptor at the neuromuscular junction reduces the safety margin for transmission, so muscle strength fails progressively with repeated use, fatigable weakness, because each successive nerve impulse recruits an ever smaller pool of intact receptors.

Progressive loss of dopaminergic neurons in the substantia nigra disinhibits the basal ganglia's motor-suppressing output, producing the triad of bradykinesia, rigidity and tremor because movement is constantly being over-restrained rather than driven.

Sudden focal neurological deficit from disrupted blood supply to the brain (ischaemic in the majority from vessel occlusion, haemorrhagic in the rest from vessel rupture), and telling the two apart with an urgent CT head is the single decision that determines whether thrombolysis can be given.

Sudden rupture of a blood vessel, most often a berry aneurysm, into the subarachnoid space causes an instantaneous, maximal-at-onset thunderclap headache as blood irritates the meninges and abruptly raises intracranial pressure, making the pattern of onset itself the diagnostic clue.

A focal neurological deficit from transient cerebral ischaemia that resolves completely within 24 hours, usually much sooner, because the occlusion is brief enough that no tissue infarcts, but it is a warning sign of impending full stroke that demands the same urgent work-up.