KlüverBucy

Klüver–Bucy syndrome is a behavioral and emotional syndrome that results from bilateral lesions of the anterior temporal lobes, particularly the amygdala. It was first described in 1937 by Heinrich Klüver and Paul Bucy after their experimental ablation of the temporal lobes in rhesus monkeys, and has since been observed in humans with bilateral temporal lobe damage from trauma, infection, stroke, tumors, or neurodegenerative disease.

Clinical features typically occur in several domains. Visual processing is affected, producing psychic blindness (visual agnosia) where objects can be seen but not properly recognized. There is hyperorality and hyperphagia with indiscriminate eating, and patients often engage in oral exploration of objects. Hypermetamorphosis, an exaggerated attention to visual stimuli, is common. Emotional and social changes include placidity or reduced fear, diminished aggression, and disinhibited social behavior; some individuals exhibit hypersexuality. Memory impairment may accompany the syndrome if the hippocampal formation is involved.

Pathophysiology centers on damage to the amygdala and related temporal structures, which disrupt emotional processing, fear responses, and the evaluation of visual stimuli, leading to disinhibited and overly familiar behavior.

Diagnosis is clinical and supported by neuroimaging showing bilateral temporal lobe involvement. Management focuses on treating the underlying brain injury and addressing behavioral symptoms through rehabilitation and supportive care; pharmacological strategies may be used to manage agitation or disinhibition as needed. The syndrome remains relatively rare in humans.