A patient with bilateral medial temporal lobe damage (Klüver-Bucy syndrome) demonstrates hyperphagia, hypersexuality, and visual agnosia. The structure most critically damaged to produce the core emotional-behavioral features is:

• A Hippocampus, impairing memory consolidation and emotional context
• B Cingulate cortex, disrupting motivational behavior and error monitoring
• C Entorhinal cortex, disrupting polymodal sensory input to the limbic system
• D Amygdala, which normally assigns emotional salience and mediates fear responses to stimuli ✓

Explanation

Klüver-Bucy syndrome results from bilateral amygdala damage (along with adjacent temporal neocortex). The amygdala is the critical structure for assigning emotional valence to sensory stimuli — it determines whether a stimulus is threatening, rewarding, or aversive. Bilateral amygdalectomy removes fear responses (placidity), causes hypersexuality (loss of appropriate social inhibition), hyperphagia (loss of aversion to inappropriate oral stimuli), and visual agnosia/psychic blindness. The hippocampus is critical for declarative memory consolidation but is not primarily responsible for these affective features.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.