Focal cortical seizures cause distant thalamic lesions.
Topical application of convulsants to the rat sensorimotor cortex in concentrations sufficient to cause repetitive focal motor seizures resulted in acute neuropathology (dark cell neuronal degeneration and spongiform neurophil changes) involving both the cortical seizure focus and certain thalamic nuclei within seizure pathways. Changes in the cortex were localized primarily in layer IV and those in the thalamus in nuclei having reciprocal connections with the cortical focus. The spongiform neuropil changes consisted of massively dilated presynaptic axon terminals in the cortex and postsynaptic dendrites in the thalamus. The dendritic and dark cell changes resemble the excitotoxic damage caused by glutamate and aspartate. Since these putative transmitters may be released locally from recurrent collaterals and remotely from corticothalamic axons, excessive release of glutamate or aspartate may account for the changes in both sites. The abnormal axons in sensory cortex appear to be terminals of thalamocortical neurons. Swelling of these axons may be caused by excessive anti- and orthodromic firing in the course of focal motor seizures.
D000818:Animals; D001369:Axons / Q000648:ultrastructure; D002540:Cerebral Cortex / Q000503:physiopathology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D009474:Neurons / Q000502:physiology / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000503:physiopathology*; D013788:Thalamus / Q000503:physiopathology*