The amygdala, a core limbic structure, plays a critical role in epilepsy due to its structural and functional heterogeneity. Its major subnuclei—the basolateral, centromedial, and superficial cortical nuclei—differ in cellular composition, connectivity, and function, and form extensive circuits with the prefrontal cortex, hippocampus, and hypothalamus. In epilepsy, the amygdala may become a hyperexcitable microcircuit through impaired GABAergic inhibition, ion channel dysfunction, altered synaptic plasticity, and neuroinflammation, thereby lowering seizure threshold. Abnormal amygdalar activity can propagate to the frontotemporal cortex via the uncinate fasciculus or influence autonomic centers through the stria terminalis. Theta/gamma coupling and high-frequency oscillations within the amygdala–hippocampal network are key electrophysiological markers of seizure spread. Clinically, different subnuclei are associated with distinct seizure symptoms: the basolateral nucleus is linked to affective auras such as fear, the centromedial nucleus to autonomic symptoms such as palpitations, and the superficial cortical nuclei to olfactory or gustatory auras. Stereotactic electroencephalography and multimodal neuroimaging improve epileptogenic zone localization and support precise surgical or neuromodulatory treatment targeting the amygdala. Future research should further clarify subnucleus-specific mechanisms, developmental dynamics, and cross-species differences to advance targeted therapies for amygdala-related epilepsy.