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Cortical inhibitory dysfunction in epilepsia partialis continua: A high frequency oscillation somatosensory evoked potential study.
OBJECTIVE: The pathophysiology of epilepsia partialis continua (EPC) is still unclear, a thalamo-cortical circuit dysfunction has been hypothesized. The aim of present study is the functional evaluation of the thalamo-cortical network in EPC by means of the study of low- and high-frequency somatosensory evoked potentials (LF-SEP and HF-SEP).
METHODS: Median LF-SEP and HF-SEP were recorded in 3 patients with EPC and in 2 patients with rolandic lesions without EPC (non-EPC). Recording electrodes were placed on P3, C3, F3 and P4, C4, F4 of scalp regions. HF-SEP were obtained by an offline 400-800 Hz filtering of P3-F3 and P4-F4 traces.
RESULTS: In EPC patients, we found a significant suppression of post-synaptic HF-SEP burst and an amplitude reduction of the P24 wave of the LF-SEPs. Both these components are related to cortical inhibitory interneuron activity. HF-SEP and LF-SEP were normal in non-EPC patients.
CONCLUSION: The different results obtained in patients with a rolandic lesion with and without EPC supports the hypothesis that EPC might be correlated to a dysfunction of gabaergic interneurons of a cortical sensory-motor network.
SIGNIFICANCE: Our results might contribute to the understanding of the physiological basis of the cortical dysfunction causing epilepsia partialis continua.
METHODS: Median LF-SEP and HF-SEP were recorded in 3 patients with EPC and in 2 patients with rolandic lesions without EPC (non-EPC). Recording electrodes were placed on P3, C3, F3 and P4, C4, F4 of scalp regions. HF-SEP were obtained by an offline 400-800 Hz filtering of P3-F3 and P4-F4 traces.
RESULTS: In EPC patients, we found a significant suppression of post-synaptic HF-SEP burst and an amplitude reduction of the P24 wave of the LF-SEPs. Both these components are related to cortical inhibitory interneuron activity. HF-SEP and LF-SEP were normal in non-EPC patients.
CONCLUSION: The different results obtained in patients with a rolandic lesion with and without EPC supports the hypothesis that EPC might be correlated to a dysfunction of gabaergic interneurons of a cortical sensory-motor network.
SIGNIFICANCE: Our results might contribute to the understanding of the physiological basis of the cortical dysfunction causing epilepsia partialis continua.
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