Deep brain stimulation of the anterior nucleus of the thalamus: Effects of electrical stimulation on pilocarpine-induced seizures and status epilepticus

Favorable modulation in neurotransmitters: Effects of chronic anterior thalamic nuclei stimulation observed in epileptic monkeys

“…Successful establishment of the KA-TLE model was confirmed by video recordings of spontaneous epileptic seizures in KA-treated monkeys. Our results showed that the mean number of total seizures was significantly lower in the ATN-stimulation group compared with the shamstimulation group, indicating that ATN-stimulation was effective in seizure reduction,which is consistent with previous studies (Fisher et al, 2010;Hamani et al, 2008;Hodaie et al, 2002;Jou et al, 2013;Kerrigan et al, 2004;Lim et al, 2007;Mirski et al, 1997;Takebayashi et al, 2007). Moreover, our results revealed that the changes in the amino acid levels in the ATN-stimulation group were significantly different from those changes in the sham-stimulation group.…”

Outcome based definition of the anterior thalamic deep brain stimulation target in refractory epilepsy

“…In a study by Stypulkowski et al, authors observed powerful inhibitory effect upon hippocampal electrical activity using most cranially located contacts at ANT, whereas adjacent more deeply located contact was not associated with suppression of neuronal activity [36]. Hamani et al reported in pilocarpine model of SE in rats that the latency for SE onset was increased after stimulation of all different subnuclei in ANT complex (anteromedial, anterior principal and anterior dorsal nucleus) [37]. Finally, in an earlier study by Mirski et al, behavioural seizure scores were decreased with high frequency ANT stimulation compared to stimulation at striatum or posterior thalamus in a PTZ model in rat [17].…”

Development of a Large Animal Model for Investigation of Deep Brain Stimulation for Epilepsy

“…The rationale for the AN target comes from the early work of Mirski et al [11][12][13] who demonstrated a reduction in drug-induced seizures in a rodent model with interruption, or high-fre-quency stimulation, of the Papez circuit. Subsequent preclinical studies [14][15][16][17] have confirmed that the AN is a key node in this pathway that can influence seizure initiation and propagation. Electrophysiologic mapping of this circuit has also been conducted in patients undergoing investigational AN DBS.…”