The caudate’s elongated, c-shaped course tracking the lateral ventricle reflects its embryological origin from a continuous striatal anlage that was bent over by the developing temporal lobe. Slice atlases that show caudate at multiple coronal levels reveal the same nucleus appearing in different positions: head superior near the ventricle, body running along the dorsolateral wall of the ventricle, tail descending into the roof of the temporal horn near the amygdala.

The basal-ganglia direct/indirect pathway model, developed by DeLong and colleagues in the 1980s, frames the striatum as the gateway through which cortex selects actions. The direct pathway disinhibits thalamus (facilitating action); the indirect pathway inhibits thalamus (suppressing alternatives). Dopaminergic input from substantia nigra biases the balance: D1-expressing direct-pathway neurons are excited by dopamine, while D2-expressing indirect-pathway neurons are inhibited.

Huntington’s disease is the canonical caudate-degenerative disorder, with selective loss of medium-spiny indirect-pathway neurons in the striatum. The disinhibited direct pathway facilitates inappropriate movements (chorea), and selective sparing of cortical and limbic afferents to caudate in the early disease produces the characteristic combination of preserved language with progressive cognitive and motor decline.