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<p><b>BACKGROUND</b>The antiepileptic effect of the anterior thalamic nuclei (ANT) stimulation has been demonstrated; however, its underlying mechanism remains unclear. The aim of this study was to investigate the effect of chronic ANT stimulation on hippocampal neuron loss and apoptosis.</p><p><b>METHODS</b>Sixty-four rats were divided into four groups: The control group, the kainic acid (KA) group, the sham-deep brain stimulation (DBS) group, and the DBS group. KA was used to induce epilepsy. Seizure count and latency to the first spontaneous seizures were calculated. Nissl staining was used to analyze hippocampal neuronal loss. Polymerase chain reaction and Western blotting were conducted to assess the expression of caspase-3 (Casp3), B-cell lymphoma-2 (Bcl2), and Bcl2-associated X protein (Bax) in the hippocampal CA3 region. One-way analysis of variance was used to determine the differences between the four groups.</p><p><b>RESULTS</b>The latency to the first spontaneous seizures in the DBS group was significantly longer than that in the KA group (27.50 ± 8.05 vs. 16.38 ± 7.25 days, P = 0.0005). The total seizure number in the DBS group was also significantly reduced (DBS vs. KA group: 11.75 ± 6.80 vs. 23.25 ± 7.72, P = 0.0002). Chronic ANT-DBS reduced neuronal loss in the hippocampal CA3 region (DBS vs. KA group: 23.58 ± 6.34 vs. 13.13 ± 4.00, P = 0.0012). After chronic DBS, the relative mRNA expression level of Casp3 was decreased (DBS vs. KA group: 1.18 ± 0.37 vs. 2.09 ± 0.46, P = 0.0003), and the relative mRNA expression level of Bcl2 was increased (DBS vs. KA group: 0.92 ± 0.21 vs. 0.48 ± 0.16, P = 0.0004). The protein expression levels of CASP3 (DBS vs. KA group: 1.25 ± 0.26 vs. 2.49 ± 0.38, P < 0.0001) and BAX (DBS vs. KA group: 1.57 ± 0.49 vs. 2.80 ± 0.63, P = 0.0012) both declined in the DBS group whereas the protein expression level of BCL2 (DBS vs. KA group: 0.78 ± 0.32 vs. 0.36 ± 0.17, P = 0.0086) increased in the DBS group.</p><p><b>CONCLUSIONS</b>This study demonstrated that chronic ANT stimulation could exert a neuroprotective effect on hippocampal neurons. This neuroprotective effect is likely to be mediated by the inhibition of apoptosis in the epileptic hippocampus.</p>

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Deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) is a novel therapy developed to treat Parkinson's disease. We report a patient who underwent bilateral DBS of the PPN and subthalamic nucleus (STN). He suffered from freezing of gait (FOG), bradykinesia, rigidity and mild tremors. The patient underwent bilateral DBS of the PPN and STN. We compared the benefits of PPN-DBS and STN-DBS using motor and gait subscores. The PPN-DBS provided modest improvements in the gait disorder and freezing episodes, while the STN-DBS failed to improve the dominant problems. This special case suggests that PPN-DBS may have a unique role in ameliorating the locomotor symptoms and has the potential to provide improvement in FOG.

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Objective To explore the treatment efficacy of deep brain stimulation (DBS) of the pedunculopontine nucleus (PPN) in a patient with Parkinson's disease (PD).Methods The patient,admitted to our hospital in August 10,2010,was chosen in the study; in the first stage of surgery,PPN and STN stimulation tests were performed; Unified Parkinson's disease rating scale,freezing gait questionnaire,and posture and fall assessment questionnaire were employed to compare the treatment efficacy.According to these results,PPN-DBS was performed in the patient in the second stage of surgery,and the above the rating scale,questionnaires were also performed to compare the treatment efficacy.Results PPN-DBS provided modest improvements in the gait disorder and freezing episodes,while STN-DBS failed to improve the dominant problems.The patient accepted PPN-DBS treatment with obvious improvement in movement and gait; with the follow-up being prolonged,the alleviation trend was weakening.Conclusion PPN-DBS may have a unique role in ameliorating frozen gait,bradykinesia and other symptoms of PD.

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<p><b>BACKGROUND</b>Electrical stimulation of the anterior nucleus of the thalamus (ANT) appears to be effective against seizures. In this study, we investigated changes in glucose metabolism during high-frequency stimulation of ANT in epileptic rats.</p><p><b>METHODS</b>Three groups of rats were used: (1) a stimulation group (n = 12), (2) a sham stimulation group (n = 12) with seizures induced by stereotactic administration of kainic acid (KA), and (3) a control group (n = 12) with sham surgery. Concentric bipolar electrodes were stereotaxically implanted unilaterally in the ANT. High-frequency stimulation was performed in each group except the sham stimulation group. Microdialysis probes were lowered into the CA3 region of the hippocampus unilaterally but bilaterally in the stimulation group. The concentrations of glucose, lactate, and pyruvate in dialysate samples were determined by an ISCUS microdialysis analyzer.</p><p><b>RESULTS</b>The extracellular concentrations of lactate and lactate/pyruvate ratio (LPR) of epileptic rats were significantly higher than in control rats (P = 0.020, P = 0.001; respectively). However, no significant difference in the concentration of glucose and pyruvate was found between these groups (P > 0.05). Electrical stimulation of ANT induced decreases in lactate and LPR in the ipsilateral hippocampus (KA injected) of the stimulation group (P < 0.05), but it did not influence the glucose metabolism in the contralateral hippocampus (P > 0.05).</p><p><b>CONCLUSIONS</b>This study demonstrated that the glycolysis was inhibited in the ipsilateral hippocampus of epileptic rats during electrical ANT stimulation. These findings may provide useful information for better understanding the mechanism of ANT-deep brain stimulation.</p>

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Refractory gelastic seizure is one of the most common clinical manifestations in patients with hypothalamic hamartoma (HH) and HH is usually regarded as the epileptogenic focus. A young female patient with a small HH and refractory seizures is reported here. However, both the seizure semiology and results of electroencephalogram monitoring indicated the right temporal region was the epileptogenic focus. Thus a standard right anterior temporal lobectomy was performed while the hamartoma preserved. There was a marked improvement in both seizure frequency and quality of life during a 13-month follow-up. The outcome supported the concept that independent epileptogenic focus outside of the hypothalamus might occur in patients with HH.

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Objective To observe the behavioral changes of rats with 3-nitropropionic acid (3-NP) induced secondary dystonia to set up a kind of reliable secondary dystonia models. Methods Thirty-six SD rats were equally divided into control group and low-dosage 3-NP treatment group (2000nmol) and high-dosage 3-NP treatment group (4000 nmol). The 3-NP was injected into the left caudate putamen (CPU) in rats of the later 2 groups and sodium chloride solution was injected into the left CPU in rats of control group. Narrow board training was proceeded and camera was employed to record the dystonic posture and both the time and steps passing the board. Results As compared with the control group, 3-NP treatment groups had obvious ipsilateral dystonic posturing (P＜0.05), and the scores of dystonic posturing in the high-dosage 3-NP treatment group were significantly higher than those of that in the low-dosage 3-NP treatment group (P＜0.05). Narrow board experimental results indicated that the time was significantly extended and length of step was significantly shortened in rats of 3-NP treatment groups as compared with those in the control group (P＜0.05); rats in the treatment groups walked towards the lateral side of the boared, these symptoms became much severe following the increase of 3-NP dosage.While rats in the control group had no dystonic posture, and they can go though the board without retention. Conclusion The 3-NP injecting into the CPU of rats can induce a kind of stable animal models with secondary dystonia.