Metabolic and electrophysiological effects of focal epileptic discharges on surrounding and remote brain tissue in the rat cortex.
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Publications and source records attributed to C Bruehl.
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Focal epileptic activity can be expected to influence distant brain areas via far reaching connections. To investigate such interactions the effects of focal epileptic activity on the metabolism of the brain were investigated in the rat cortex. Focal epileptic activity was induced by the application of penicillin onto the motor cortex. The focus, and to a lesser extent homotopic contralateral brain areas, showed an increase in the regional cerebral metabolic rate of glucose (rCMRGlc) as measured by [14C]deoxyglucose autoradiography. This focal hypermetabolism was accompanied by widespread hypometabolism lateral to the focus. The decrease of rCMRGlc occurred in somatosensory cortical areas but not in the motor cortex behind or in front of the focus, the perirhinal cortex or the occipital cortex. It was associated with an increase in metabolic rate in the ventrolateral, ventroposteromedial, ventroposterolateral and, in particular, posterior nuclei of the thalamus. It is hypothesized that the widespread reduction of rCMRGlc in the somatosensory cortical areas is due to inhibition via thalamic nuclei caused by activity in the motor cortex.
Demonstration of focal alterations of brain metabolism with positron emission tomography has become a widely used method for identifying epileptic foci. Here we investigated how neuronal and glial cell activity relates to alterations of brain metabolism. Acutely induced epileptic activity in the motor cortex of rat brain increased metabolism in the focus and homotopic contralateral areas, and decreased metabolism in the ipsilateral somatosensory area. Increases and decreases of deoxyglucose uptake did not directly correlate with excitations and inhibitions; instead, deoxyglucose uptake was related to the overall strength of synaptic activity, and both strong excitations and strong inhibitions increased brain metabolism. Reduction of metabolism below normal values was associated with reduced synaptic activity and with tonic hyperpolarization of the cells. Our results show that in the absence of structural abnormalities, hypometabolism indicates functional disturbances which may be both reversible and remote from the epileptogenic focus.
The interictal hypometabolism in patients with focal epilepsy is usually regarded as stationary. In this study we investigated to which extent the hypometabolism may depend on the activity of the epileptic focus. In focal penicillin-induced epilepsy in rats the epileptic focus is hypermetabolic. This focus is accompanied by hypometabolism in widespread areas of adjacent cerebral cortex. The experiments revealed that these metabolic alterations are transient. Data from a patient experiencing a focal seizure during PET scanning gave similar results. They showed that the transition from interictal to ictal activity was accompanied by the development of hypermetabolic epileptic focus and the dynamic enlargement of the surrounding hypometabolism. Both, the experimental and clinical data provide evidence that the cerebral hypometabolism may vary in size depending on the activity of the epileptic focus. It is hypothesized that in human PET studies the large interictal hypometabolism may prevent the identification of hyperactive interictal epileptic foci due to the partial volume effects resulting from the limited spatial resolution of PET cameras.