1043-3155 Pediatr Neurol Briefs pedneurbriefs Pediatr Neurol Briefs Pediatric Neurology Briefs Pediatr Neurol Briefs 2166-6482 1043-3155 2166-3155 Pediatric Neurology Briefs Publishers Chicago, IL, USA PNB-9-19-a 10.15844/pedneurbriefs-9-3-4 Seizure Disorders Neurology Pediatrics Nervous System Diseases Child Development Brain Diseases Neurosurgery Child Infant Mechanisms of Absence Seizures http://orcid.org/0000-0002-0173-7931 Millichap J. Gordon MD 1 2 * Division of Neurology, Children's Memorial Hospital, Chicago, IL Departments of Pediatrics and Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL Correspondence: Dr. J. Gordon Millichap, E-mail: jgmillichap@northwestern.edu 03 1995 01 06 2016 9 3 19 19 Copyright: © 1995 The Author(s) 1995 This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Basic mechanisms of generalized absence seizures

A unifying hypothesis for the pathogenesis of absence seizures, involving the thalamocortical circuitry, is proposed in a neurological progress report from the University of Southern California School of Medicine, Childrens Hospital Los Angeles.

 G-Aminobutyric Acid Absence Seizures Synchronous Spike

A unifying hypothesis for the pathogenesis of absence seizures, involving the thalamocortical circuitry, is proposed in a neurological progress report from the University of Southern California School of Medicine, Childrens Hospital Los Angeles. Abnormal oscillatory rhythms generated in the circuit involve g-aminobutyric acid (GABA)B-mediated inhibition alternating with glutamate-mediated excitation which triggers a low-threshold calcium current in neurons of the nucleus reticularis thalami. The process is modulated by pathways utilizing various neurotransmitters and projected onto the thalamus and cortex, generating bilaterally synchronous spike wave discharges and absence seizures. Ethosuximide and trimethadione block absence seizures by reducing the low-threshold calcium current via a direct action at the T-type calcium channel. Other anti-absence seizure medications have indirect effects on this calcium current within the thalamus. [1]

COMMENT. A knowledge of the mechanisms of absence seizures should facilitate the development of more specific antiepileptic medications and the avoidance of drugs (eg. phenytoin and carbamazepine) that exacerbate absence attacks. For an excellent review of mechanisms of antiepileptic drug action see Talwar D, 1990, and commentary, Progress in Pediatric Neurology I, 1991, pp94-5.

 Snead OC 3rd Basic mechanisms of generalized absence seizures Ann Neurol 1995 Feb 37 2 146 57 7847856 10.1002/ana.410370204