SIR: Classic Klüver-Bucy syndrome (KBS) has been considered a direct consequence of bilateral anterior temporal horn damage resulting from disease or injury.1,2 Hayman et al.3 recently described a case with MRI evidence of bilateral damage to the basolateral amygdala. Unfortunately, no autopsy was reported.
Currently, the clinician is required to document the clinical features of KBS ("psychic blindness," hypersexuality, hyperorality, hypermetamorphosis, altered emotional behavior, and memory deficits) and to demonstrate the existence of a bilateral lesion in the anterior temporal horn or amygdala.2 Gloor4 has reported that lesions in the amygdala are not necessary for KBS in animals or humans. Brain imaging is frequently abnormal but not specific for lesions in these areas in cases of KBS.5
We have reported 2 cases exhibiting the clinical features of KBS (B.T. Carroll et al., unpublished). These cases lacked brain imaging evidence of bilateral damage to either the amygdala or the anterior temporal areas. However, KBS may still be present in such instances because of disruption of the limbic circuitry at the site of the mediodorsal thalamic relay.6
We applaud the efforts of Dr. Hayman and colleagues3 to further the understanding of the anatomic basis of KBS. We feel that the present approach may limit the study of KBS in that cases of KBS may be rejected for lack of the designated anatomic lesions.
There is some evidence to indicate that some of the clinical features of KBS may respond to carbamazepine treatment.7,8 In our 2 cases, antipsychotics were associated with clinical improvement. Management of KBS remains a challenging area. Treatment response to cases of KBS that lack the designated anatomic lesions may help to elucidate functional understanding of KBS.