Klüver-Bucy Syndrome

Original Editor - Kehinde Fatola
Top Contributors - Kehinde Fatola, Rucha Gadgil and Cindy John-Chu

Introduction[edit | edit source]

Klüver-Bucy Syndrome (KBS) is a dysfunction arising from lesions of bilateral medial temporal lobes, including nucleus of the amygdala.[1] Though, it is a neurologic dysfunction, it may also be classified under “psychiatry”. It was first recorded among humans who had undergone temporal lobectomy in 1955[2].

The investigation leading to the discovery was carried out by Heinrich Klüver and Paul Bucy, a neurosurgeon on a number of rhesus monkeys in the 1930s.[3]

Mainly KBS presented with:

  1. psychic blindness or visual agnosia,
  2. strong oral tendencies,
  3. hypermetamorphosis or excessive tendency to react to every visual stimulation,
  4. decrease in aggressive behavior and fear reaction, and
  5. hypersexuality[4].

Clinical Presentation[edit | edit source]

Clinical presentations are not agreed upon and vary in literature according to source. Generally, it includes the following;[5][6][7]

  • Amnesia: this is essentially inability to recall past experiences (memories) which may be anterograde – inability to recall events from the period of the amnesic episode, or retrograde – loss of memory from the period before the amnesic episode.
  • Tameness: also termed “placidity” or “docility”, it is characterized by showing reduced ‘flight or fight’ response.
  • Hyperphagia and dietary changes: this can present as pica (eating inappropriate objects) and/or overeating
  • Hyperorality: “oral tendency or compulsion to examine objects by mouth”
  • Hypersexuality: manifested as a heightened sex drive and propensity to seek sexual stimulation from unusual and inappropriate objects.
  • Visual agnosia: inability to identify familial items and people.


Some presentations which are found to be inconsistent include;

  • Hypermetamorphorsis; “an irresistible impulse to notice and react to everything in sight”
  • Diminished or lack of emotional response

Diagnostic Procedures[edit | edit source]

It is uncommon for patients to manifest all symptoms, three or more of which is essential for diagnosis. The commonest symptoms in humans include tameness, hyperorality and dietary changes.[5]

Pathophysiology[edit | edit source]

The clinical symptoms of KBS are mainly due to[8]:

  1. destruction of either the temporal neocortex
  2. the amygdala bilaterally.
  3. The disturbances in the temporal portions of limbic networks that connect with multiple cortical and subcortical circuits to modulate emotional behavior and affect.
  4. injury to the amygdala, uncus, hippocampus, orbitofrontal and cingulate gyri, and insular cortex.[8]

This syndrome is uncommon in humans because the anterior temporal lobe dysfunction is usually less severe as compared to that following total temporal lobe resection in monkeys.

Herpes simplex encephalitis (HSE) is one of the causes of KBS, as the herpes virus can cause dysfunction/destruction of the temporal lobes[9].

Predisposing Conditions[edit | edit source]

Conditions which predisposes an individual to the diagnosis of KBS include;[5][10]

Management / Interventions[edit | edit source]

Studies have shown pharmacotherapy as an effective way of combating KBS. Pharmacological interventions have been known to include treatment with;[11]

  • Carbamezine
  • Valproate
  • Topiramate
  • Quetiapine,
  • Propranolol
  • Benztropine
  • Haloperidol
  • Trazodone
  • Sertraline
  • Olanzapine
  • Lorazepam
  • Valproic acid
  • Thiothixene
  • Bromocriptine

Physiotherapy Management[edit | edit source]

There are no studies related to the physiotherapy management in KBS. One reason for this might be that KBS has been reported in only a few of human individuals[4].

Management can be tailored according to the signs and symptoms shown by the individual.

References[edit | edit source]

  1. Afifi A, Bergman R. Functional Neuroanatomy. McGraw-Hill. The Kluver-Bucy syndrome is a clinical syndrome observed in humans and other animals after bilateral lesions in the temporal lobe that involve the amygdala, hippocampal formation, and adjacent neural structures,1998.
  2. Terzian H, Ore GD. Syndrome of Klüver and Bucy; reproduced in man by bilateral removal of the temporal lobes. Neurology. 1955 Jun;5(6):373-80.
  3. Klüver H, Bucy P. Preliminary analysis of functions of the temporal lobes in monkeys. Arch Neurol Psychiatry. 1939; 42:979-1000
  4. 4.0 4.1 Hooshmand H, Sepdham T, Vries JK. Klüver-Bucy Syndrome: Successful Treatment With Carbamazepine. JAMA. 1974;229(13):1782. doi:10.1001/jama.1974.03230510056026
  5. 5.0 5.1 5.2 Salloway S, Malloy P; Cummings. The Neuropsychiatry of Limbic and Subcortical Disorders. American Psychiatric Pub.1997. p. 125. ISBN 0-88048-942-1.
  6. Ozawa H, Sasaki M; Sugai K; Hashimoto T; Matsuda H, Takashima S, Uno A, Okawa T. "Single-Photon Emission CT and MR Findings in Klüver-Bucy" (PDF). American journal of neuroradiology (Oak Brook, IL,: American Society of Neuroradiology), 1997, 18 (3): 540–542. ISSN 0195-6108. PMID 9090419
  7. Afifi, Adel K., Bergman R. Functional Neuroanatomy: Text and Atlas. McGraw-Hill Professional. 2005, p. 299. ISBN 0-07-140812-6.
  8. 8.0 8.1 Lanska DJ. The Klüver-Bucy Syndrome. Front Neurol Neurosci. 2018;41:77-89.
  9. Costa R, Fontes J, Mendes T, Pereira M, Gonçalves C. Kluver-Bucy Syndrome: A Rare Complication of Herpes Simplex Encephalitis. Eur J Case Rep Intern Med. 2021 Jul 22;8(7):002725. doi: 10.12890/2021_002725. PMID: 34377704; PMCID: PMC8336756.
  10. Tancredi, Laurence R. Hardwired Behavior: What Neuroscience Reveals about Morality. Cambridge University Press. 2005. pp. 98–99. ISBN 0-521-86001-6.
  11. Clay FJ, Kiriakose A, Lesche D, Hicks AJ, zaman H, Azizi E, Ponsford JL, Jayaram M. Hopwood M. Klüver-Bucy Syndrome following Traumatic Brain Injury: a systematic synthesis and review of pharmacological treatment from case in adolescent and adult. Journal of neuropsychiatry and clinical neurosciences. 2019:31:1, 6-16