Amygdala

The majority of afferent information arises from the glutamatergic projections arising from pyramidal neurons in layer V of the cortex. These projections largely travel ipsilaterally via the extreme capsule. Information from sensory association areas and memory-related structures, such as the hippocampus, are relayed via cortical and thalamic inputs. Autonomic and behavioral inputs arise from the hypothalamus and brainstem.

Afferents to the corticomedial nuclei arrive primarily from subcortical limbic sources, including the olfactory bulb, septal nuclei, and hypothalamic nuclei (ventromedial [VM], lateral hypothalamic area [LHA]); the thalamus (intralaminar nuclei); the stria terminalis; and excessive numbers of autonomic nuclei and monoamine nuclei of the brainstem. Afferents to the basolateral nuclei arrive mainly from the cortical areas, including extensive sensory association cortices, the prefrontal cortex, the cingulate cortex, and the subiculum.

In the late 1930s Klüver and Bucy described a behavioral syndrome characterized by hypersexuality, hyperorality, excessive exploration of visual stimuli (hypermetamorphosis), visual agnosia, apathy, and withdrawal. They linked this behavior to bilateral amygdaloid complex lesions. This syndrome has been described in patients with neurodegenerative diseases, such as Alzheimer disease and even frontotemporal dementia. Because the amygdala processes sensory information for emotional relevance, it is not surprising that atypical emotional responses, such as anger, aggressive behavior, and even apathy, can evolve in these patients. Damage to the hypothalamic connectivity of the amygdala is responsible for hyperphagia, hypersexuality, and overeating/obesity. Likewise, alterations of the visual association cortical afferent projections to the amygdala result in hypermetamorphosis and visual agnosia (patients cannot recognize facial expressions that indicate fear).

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