A 70-year-old man develops progressive gait instability described as wide-based with inability to tandem walk, past-pointing on finger-nose test, and scanning dysarthria. Imaging shows atrophy of the vermis and anterior cerebellar lobe. Which specific cerebellar circuit abnormality explains the gait ataxia?

• A Loss of Purkinje cell inhibition over deep cerebellar nuclei (dentate nucleus) causing uncontrolled excitatory output to thalamus
• B Disruption of the spinocerebellar tract input to vermal/intermediate zone → impaired proprioceptive regulation of limb and trunk coordination via fastigial nucleus → lateral vestibular nucleus and spinal cord pathway ✓
• C Disruption of the cortico-ponto-cerebellar pathway to lateral cerebellar hemispheres causing limb ataxia
• D Degeneration of climbing fibers from inferior olive causing loss of error correction signals to Purkinje cells

Explanation

The vermis receives spinocerebellar inputs (dorsal/ventral spinocerebellar tracts carrying proprioceptive and load information from trunk and legs). Vermal Purkinje cells project to the fastigial nucleus, which projects via the fastigiospinal and fastigiobulbar tracts to the reticulospinal and vestibulospinal systems controlling axial and proximal limb muscles for balance and gait. Vermis/anterior lobe atrophy (as in alcoholic cerebellar degeneration or spinocerebellar ataxias) disrupts this pathway, causing truncal and gait ataxia. Option C (lateral hemispheres → dentate → thalamus → motor cortex) would cause ipsilateral limb ataxia but not predominantly gait/truncal ataxia. Option A is a general circuit statement, not specific to gait ataxia.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.