Limbic System

The amygdala is connected extensively to the hypothalamus and other limbic structures. It receives input from widespread sensory cortical regions and paralimbic structures (piriform cortex, entorhinal cortex, and parahippocampal cortex on the temporal lobe medial surface and the cingulate cortex just above the corpus callosum). The amygdala is critical for channeling drive and affect. In lesion studies of monkeys, visual information from one eye was restricted to an intact amygdala, while visual information from the other eye was directed toward a lesioned amygdala. The monkey’s typical aggressive behavior when visually provoked was intact only when stimulated through the intact visual pathway. When provoked via the lesioned pathway, the monkey remained passive.

This is observed in the Klüver-Bucy syndrome that arises when the amygdala is disconnected from cortical sensory input. The typical features of the Klüver-Bucy syndrome include (1) indiscriminant sexual behavior toward objects in the immediate extrapersonal space, (2) absence of fight-flight reaction toward threat, and (3) inability to visually distinguish edible from inedible objects except by orally inspecting objects.

The amygdala channels appropriate emotional response toward sensory targets while having an important role in the interpretation and display of affective gestures, including vocalization. The right hemisphere is dominant here. The amygdala also plays an integral role in the experience of strong emotions, including fear, rage, and experiences of familiarity. The amygdala imparts the affective coloring of personal experience that reflects a person’s history, present internal state, and characteristics of their present mental experience. Certain disease states engender disruptions of this balance. Thus the affective color of a particular mental process may be distorted, amplified, or diminished, thereby changing the very meaning of the entire experience. This is witnessed in panic attacks, dissociative states, depression, and schizophreniform conditions. In humans, the amygdala does not appear to play a direct role in memory formation, although amnesia resulting from hippocampal damage seems more severe if there is additional involvement of the amygdala. This suggests the amygdala may establish an affective link in memorization. Additional amygdala roles include regulation of autonomic, endocrine, and immunologic function.

The piriform cortex is a relay area for cortical and olfactory information, much the way the thalamus is the relay area for every other sensory modality. This area also has numerous connections with hypothalamus and other limbic regions. Animal studies suggest a role in regulation of the direction of drive within extrapersonal space, such as attack or sexual behaviors.

The hippocampus receives almost all of its input from paralimbic areas, which receive their input from cortical sensory areas. Other inputs include hypothalamus, amygdala, and septal area. Its major role is memory and learning. Isolated hippocampal damage is relatively rare, but combined lesions of hippocampal and parahippocampal areas in infarcts lead to severe amnestic states, even when the amygdala is spared. These structures are necessary for the formation of new memories (recording experience) rather than storage of memories. In addition, they rekindle memories during retrieval. The motivational relevance of experience makes it more likely to be memorized and recalled. This is why storage and retrieval are affected with relative preservation of memory banks (long-term memory) in diseases affecting these structures.

The septal nuclei and substantia innominata contain the major cholinergic cells of the brain, located in the medial septal nucleus, the vertical and horizontal limb nuclei of Broca’s diagonal band, and the nucleus basalis of Meynert. These areas project to the hippocampus, olfactory region, widespread cortical regions, and the amygdala. The hypothalamus and various limbic and paralimbic structures give rise to the majority of the inputs to these structures. This cholinergic network is essential for intact memory function. Patients with anterior communicating artery aneurysms or with septal tumors may develop amnestic states. In Alzheimer disease, where memory loss is the major clinical feature, there is a profound loss of cholinergic neurons in the nucleus basalis as well as in widespread cortical regions. Septal lesions may also produce exaggerated emotional reactions to novel or threatening stimuli, hyperdipsia, hyperphagia, and altered taste preference. There is evidence suggesting a role in attaching motivational value to extrapersonal objects.

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