Epilepsy, Schizophrenia, and the Extended Amygdala

• Published in: Annals of the New York Academy of Sciences 1999-06, Vol.877 (1), p.548-561
• Main Author: STEVENS, JANICE R.
• Format: Article
• Language: English
• Subjects: Amygdala - physiopathology; Biogenic Monoamines - physiology; Epilepsy - physiopathology; gamma-Aminobutyric Acid - physiology; Humans; Nerve Net; Neurons - physiology; Nucleus Accumbens - physiopathology; Schizophrenia - physiopathology
• ISSN: 0077-8923; 1749-6632
• DOI: 10.1111/j.1749-6632.1999.tb09288.x

Propagation and prolongation of rapid neuronal discharge underlies the epilepsies. However, episodic focal rapid neuronal discharges limited to discrete nuclei and pathways of the amygdala‐hippocampal‐septal‐hypothalamic networks are the language of physiologic message systems for endocrine regulation and reproductive activities vital to the survival of the organism and the species. To prevent prolongation and propagation of physiologic pulsed excitation to areas outside specific networks and resultant epileptic seizures, these discharges must be limited in extent and time by powerful inhibitory processes. The nucleus accumbens, a unit of the extended amygdala, and the monoamines and GABA are components of the inhibitory networks that restrict physiologic rapid discharge in duration and in location. In parallel to the relationship of excessive neuronal excitation to epilepsy, evidence will be presented that excessive inhibition via one or more components of these inhibitory networks or diminished excitation underlies development of some psychoses, including schizophrenia.