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High Frequency Deep Brain Stimulation in the Hippocampus Modifies Seizure Characteristics in Kindled Rats
Author(s) -
Wyckhuys Tine,
De Smedt Tim,
Claeys Pieter,
Raedt Robrecht,
Waterschoot Liesbeth,
Vonck Kristl,
Broecke Caroline Van den,
Mabilde Cyriel,
Leybaert Luc,
Wadman Wytse,
Boon Paul
Publication year - 2007
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2007.01038.x
Subject(s) - hippocampus , neuroscience , epilepsy , deep brain stimulation , epileptogenesis , stimulation , kindling , medicine , psychology , disease , parkinson's disease
Summary: Purpose: This experimental animal study evaluates the effect of high frequency deep brain stimulation (HFS DBS) on seizures in the Alternate Day Rapid Kindling model for temporal lobe epilepsy (TLE). The target for HFS is the hippocampus, as this structure is often presumed to be the seizure focus in human TLE. Methods: Rats (n = 12) were fully kindled in the hippocampus according to the Alternate Day Rapid Kindling protocol. Characteristics of the evoked afterdischarges (AD) were determined in the baseline period using AD threshold, AD latency, and AD duration as parameters. Rats were divided into a treated group (n = 7) that received 130 Hz HFS for 1 week, and a control group (n = 5) that did not receive HFS. Rats were retested in the following week. After 1 additional week of rest, the HFS group was continuously stimulated again for 1 week, during which AD evoked by kindling stimuli were characterized again. Results: HFS had a direct effect on evoked AD: during HFS, it increased AD threshold to 203 ± 13% of controls (p < 0.01) and increased AD latency to 191 ± 19% (p < 0.05). It decreased AD duration to 71 ± 9% (p < 0.05) of controls. The effect outlasted the HFS stimulation as in the week following HFS similar differences, but smaller in size, could still be established. Conclusion: Continuous HFS (130 Hz) in the hippocampus of epileptic rats modulates the characteristics of evoked AD in a way that reflects a reduction in excitability of the target region.