Frontal Lobe Syndrome Due to Striatocapsular Infarction

The frontal lobes are important in human cognition and are involved in aspects such as executive functioning and social cognition. These domains are broadly subsumed under the rubric of frontal functions. Human cognition is subserved by large-scale neural networks with subcortical and cortical components. Therefore, frontal lobe syndrome should be understood as the clinical consequence of damaged parallel frontostriatal circuits in the frontal lobes. While these manifestations may evolve progressively during neurodegenerative processes (e.g., frontotemporal dementia), they may appear acutely or full-blown after a strategically located infarction within a specific neural network, whether a cortical or subcortical hub. Here, the author reports a case of a 70-year-old woman with acute onset of apathy, restlessness, and hyperorality. A mental status examination showed perseverations, decreased resistance to interference, and a left-sided hemineglect. Magnetic resonance imaging revealed a right-sided striatocapsular infarction. One year later, a 18F-fluorodeoxyglucose-positron emission tomography scan showed large ipsilateral frontal and contralateral cerebellar hypometabolism compatible with diaschisis. An acute onset of a complex clinical presentation involving most of the functions of a single hemisphere may be seen after a strategically located single cerebral infarction. Basal ganglia structures, such as the right-sided caudate and anterior putamen, may host the hubs that comprise large-scale networks for executive functions, social cognition, and directed attention. Behavioral-cognitive syndromes should be evaluated as a manifestation of network damage.