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Klüver-Bucy syndrome is a behavioral disorder that occurs when both the right and left medial temporal lobes of the brain malfunction. The amygdala has been a particularly implicated brain region in the pathogenesis of this syndrome.
The list of symptoms differs somewhat by source. Generally included are the following:
While this cluster of syndromes is common to such sources as 1997’s The Neuropsychiatry of Limbic and Subcortical Disorders, 2005’s Functional Neuroanatomy: Text and Atlas and 2008’s “Single-Photon Emission CT and MR Findings in Klüver-Bucy”, an article in the American Journal of Neuroradiology, the three vary thereafter.
Inconsistent criteria include:
The syndrome is named for Heinrich Klüver and Paul Bucy. As part of an investigation into the area of affect of mescaline in the 1930, Klüver arranged to have the temporal lobes of a number of rhesus monkeys bilaterally removed by neurosurgeon Bucy.[5] Klüver did not find the expected impact on response to mescaline, but did observe a series of changes in the subject animals. The six points of difference that Klüver recorded were visual agnosia, an increased tendency to explore items by mouth, hypermetamorphosis, dampening of emotional expression, altered sexual behavior and differences in diet.[5] Klüver later discovered similar observations by Sanger Brown and Edward Albert Sharpey-Schafer that had been published in 1881 and drew on these to substantiate his own observations.[6]
Monkeys in the Klüver-Bucy experiment evidently had normal vision and motor skills, but exhibited “psychic blindness”, what Rusiko Bourtchouladze described in 2004 as an inability to recognize “the emotional importance of events”.[7] They did not display fear for items that would ordinarily frighten members of their species; they displayed an appetite for improper foods such as rocks or live rats and sought intercourse with unusual partners, including members of other species.[7] They became extremely interested in exploring items in their environment and became placid when approached.[8]
Klüver-Bucy syndrome was first documented among humans who had experienced temporal lobectomy in 1955 by H. Terzian and G.D. Ore.[9] It was first noted in a human with meningoencephalitis in 1975 by Marlowe et al.[1][3] Klüver-Bucy syndrome can manifest after either of these (lobectomies can be medically required by such reasons as accidents or tumors), but may also appear in humans with acute herpes simplex encephalitis or following a stroke.[10] Other conditions may also contribute to a diagnosis of Klüver-Bucy syndrome, including Alzheimer’s Disease, Ischemia, Anoxia, progressive subcortical gliosis, Rett syndrome, porphyria and carbon monoxide poisoning, among others.[1]
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