LAUSR

Sir, The Kluver–Bucy syndrome (KBS) is a rare neurobehavioral disorder characterized by hyperorality, hypersexuality, short-term memory loss, placidity, hypermetamorphosis, visual agnosia, mutism, and seizures.[1,2] At least three main symptoms are required to make a diagnosis of KBS.[2] This condition was first described in 1939 by Heinrich Kluver and Paul Bucy in a rhesus monkey following removal of a portion of temporal lobes and rhinencephalon. The first human case was described by Terzian and Ore in 1955, following bilateral temporal lobectomy for epilepsy surgery. The pathogenesis of KBS is secondary to dysfunction of temporal lobes, particularly amygdale, hippocampus, and white matter tracts.[1,2]Any infiltrative, infectious, degenerative disorder, infarct, and surgical resection of temporal lobe can lead to KBS. Disruption of pathways connecting the dorsomedial thalamus to the prefrontal cortex and/or other limbic areas may also lead to KBS. Most cases of KBS have been reported in adults. In children, KBS has been reported in association with herpes encephalitis,[1] Listeria monocytogenes meningoencephalitis, metabolic/hypoxic encephalopathy, congenital temporal lobe malformations, and following surgical resection of temporal lobes.[2] We describe a case of KBS in a girl with autoimmune encephalitis.