Frontal Syndrome due to Striato-Capsular Infarction

The frontal lobes have an important role in human cognition, including executive functions and social cognition. These domains are broadly subsumed under the rubric of frontal functions. Human cognition is subserved by large-scale neural networks, which have subcortical as well as cortical components. Therefore, the frontal syndrome should be understood as the clinical consequence of the damaged parallel frontostriatal circuits residing in the frontal lobes. While these manifestations may evolve progressively during neurodegenerative processes (e.g., frontotemporal dementia), they may appear acutely, full-blown after a strategically located infarction within a specific neural network, be it a cortical or subcortical hub. Here I report a case of a 70-year-old woman with acute onset of apathy, restlessness, and hyperorality. Mental status examination showed perseverations, decreased resistance to interference, and a left-sided hemineglect. Magnetic resonance imaging revealed a right striato-capsular infarction. An FDG-PET one year later showed large ipsilateral frontal and contralateral cerebellar hypometabolism compatible with diaschisis. Acute onset of a complex clinical presentation, including the majority of the functions of a single hemisphere, may be seen after a strategically located single cerebral infarction. Basal ganglia structures such as rightsided caudate and anterior putamen may host the hubs for the large-scale networks for executive functions, social cognition, and directed attention. Behavioral-cognitive syndromes should be evaluated as a manifestation of network damage.