Basilar artery involvement with memory impairment, apathy, and abulia corresponds to which syndrome?

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Multiple Choice

Basilar artery involvement with memory impairment, apathy, and abulia corresponds to which syndrome?

This pattern points to top-of-basilar syndrome, caused by occlusion of the basilar artery high in its course. When the top portion is affected, blood supply to both thalami (especially the dorsomedial nuclei) and portions of the midbrain can be disrupted. The dorsomedial thalamus is heavily connected with frontal-subcortical circuits that regulate initiation, motivation, and memory. Damage here produces memory impairment along with abulia (a loss of will or initiative) and apathy, reflecting disruption of those circuits rather than pure motor or sensory deficits. Weber’s syndrome would present with ipsilateral oculomotor nerve palsy plus contralateral motor weakness from a midbrain lesion, not the memory and behavioral changes described. Locked-in syndrome involves complete loss of voluntary movement with preserved consciousness and eye movements due to ventral pons injury, again not matching this cognitive-behavioral profile. A primary thalamic syndrome can cause sensory disturbances and thalamic pain, but the combination of memory impairment with apathy and abulia in the context of basilar artery involvement most specifically fits top-of-basilar territory.

This pattern points to top-of-basilar syndrome, caused by occlusion of the basilar artery high in its course. When the top portion is affected, blood supply to both thalami (especially the dorsomedial nuclei) and portions of the midbrain can be disrupted. The dorsomedial thalamus is heavily connected with frontal-subcortical circuits that regulate initiation, motivation, and memory. Damage here produces memory impairment along with abulia (a loss of will or initiative) and apathy, reflecting disruption of those circuits rather than pure motor or sensory deficits.

Weber’s syndrome would present with ipsilateral oculomotor nerve palsy plus contralateral motor weakness from a midbrain lesion, not the memory and behavioral changes described. Locked-in syndrome involves complete loss of voluntary movement with preserved consciousness and eye movements due to ventral pons injury, again not matching this cognitive-behavioral profile. A primary thalamic syndrome can cause sensory disturbances and thalamic pain, but the combination of memory impairment with apathy and abulia in the context of basilar artery involvement most specifically fits top-of-basilar territory.

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