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Epilepsia. 1998 Apr;39(4):339-46.

Brain hypometabolism in a model of chronic focal epilepsy in rat neocortex.

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Department of Neurology, Heinrich-Heine-University, Duesseldorf, Germany.



Metabolic mapping of the human brain has become a widely used method for identifying and localizing epileptic foci. A reduction of glucose consumption usually is found interictally in the area of the focus. By contrast, animal models of acute epilepsy show a hypermetabolism in the epileptic focus. Here we investigated how metabolism is altered in an animal model of chronic epilepsy caused by focal injection of tetanus toxin into rat neocortex.


A total of 27 male Wistar rats were anesthetized and injected into the motor or sensory cortex either with dissolved tetanus toxin or with the solvent only. Animals recovered for 7, 14, or 30 days and then were anesthetized again for quantitative 14C-deoxyglucose autoradiography. Data were analyzed with an imaging program, and regional cerebral glucose metabolism (rCMRGlc) was determined.


Injection of tetanus toxin into the motor cortex caused a focal hypometabolism which was confined to the cytoarchitectonic boundaries of the injected area, whereas sensory cortex injection caused a more widespread hypometabolism in all sensory cortical and connected, areas. None of the animals displayed focal hypermetabolism and we observed no significant time-dependent alteration of brain metabolism.


Tetanus toxin injection into the cortex of the rat induces chronic epileptic activity accompanied by a focal hypometabolism. The data suggest that the spread of the metabolic alterations depends on the connectivity of the injected cortical area.

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