A Case Of Utilization Behavior and Hyperorality Following Bilateral Anterior Cerebral Artery Infarct Partially Responsive to Carbamazepine: Can Both Behaviors Be Attributed To Lesions In Different Frontal Lobe Circuits?

Abstract

Lhermitte (1983) coined the term “utilization behavior” (UB) to define a neurobehavioral syndrome in which the visuo-tactile presentation of objects compels patients to grasp and use them, despite the fact that they have not been instructed to do so. The author suggested that UB was the consequence of frontal lobe damage. There are various interpretations as to the pathophysiology that brings about UB. Authors have described UB as an executive function deficit, intimating impairment in dorsolateral frontal-subcortical circuits. Yet, others have proposed disconnection between frontal and parietal lobe circuits or intra-frontal lobe pathology. Hyperorality and “bulimic type eating” (BTE) are symptoms of Kluver-Bucy Syndrome (KBS). While typically occurring after bilateral amygdala lesions/removal, others have suggested that symptoms of KBS may develop due to selective neurotoxicity in the basolateral amygdala and its cortical connections. Furthermore, the circuit between amygdala and cortex are reciprocal. Thus, disruption of a frontal-amygdalar circuit, with the latter projecting to the hypothalamus, may result in the production of Kluver-Bucy symptoms. We present a case of a woman with a bifrontal craniotomy and subsequent anterior cerebral artery cerebrovascular accident who developed manifestations of UB and Kluver-Bucy symptoms of hyperorality and BTE. We treated this patient with carbamazepine (CBZ), with the latter symptoms significantly improving, but the former essentially unchanged. We suggest that it is possible that this result may have occurred because while UB may not improve with CBZ, both bulimic type eating and symptoms of KBS have been reported to respond to treatment with CBZ.