Abstract
Rationale Measurement of local cerebral blood flow (LCBF) is routinely used to locate the areas involved in the generation and spread of seizures in epileptic patients. Since the spatial distribution and extent of ictal LCBF depends on the epileptogenic network, but also on the timing of injection of tracer, we used a rat model of amygdala kindled seizures to follow time-dependent changes in the distribution of seizure-induced LCBF changes. Methods Rats were implanted with a left amygdala electrode and were stimulated until reaching stage 1. LCBF was measured by the quantitative [ 14C]iodoantipyrine autoradiographic technique. The tracer was injected either at 15 s before seizure induction (early ictal) or simultaneously with the amygdala stimulation (ictal) in rats undergoing a stage 0 or 1 seizure. Results During stage 0 seizures, LCBF rates increased significantly ipsilaterally in medial and central amygdala and substantia nigra. During stage 1 seizures, LCBF increased unilaterally in amygdala, piriform cortex, substantia nigra, ventral tegmental area and cerebellum and bilaterally in several limbic and subcortical structures, excepted in hippocampus and pallidum. When pooling stages 0 and 1 but considering only tracer injection time, discrete LCBF changes occurred ipsilaterally in amygdala and substantia nigra at early ictal time. At true ictal time, significant changes occurred in several subcortical structures bilaterally while limbic structures displayed more localized and lateralized changes. Conclusion LCBF mapping appears unable to identify in rats the ictal onset zone of clinically significant amygdala-triggered seizures (stage 1), while the study of sub-clinical seizures (stage 0) allowed to correctly locate the amygdala onset of the seizures within the limbic network. Compared to human SPECT studies, this work confirms that some ictal hyperperfused areas belong to the spreading network rather than to the epileptogenic zone. The spatial recruitment of remote subcortical structures could be further investigated to strengthen the rationale of therapeutic stimulation of basal ganglia in drug-resistant epilepsies.
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