Centromedian–Thalamic and Hippocampal Electrical Stimulation for the Control of Intractable Epileptic Seizures
Centromedian–Thalamic and Hippocampal Electrical Stimulation for the Control of Intractable Epileptic Seizures
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DOI：
10.1097/00004691-200111000-00001
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发表时间：
2001-11
影响因子：
2.4
通讯作者：
M. Velasco;F. Velasco;A. Velasco
中科院分区：
文献类型：
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作者：
M. Velasco;F. Velasco;A. Velasco
综述了控制难治性癫痫发作的两种不同的调制方法：(1)慢性电刺激丘脑中央中核(ESCM)以控制全身性强直阵挛发作和不典型发作；(2)亚急性海马刺激(SAHCS)和慢性海马刺激(CPH)控制非损伤性颞叶癫痫发作。ESCM的抗癫痫作用似乎是激活一个非特异性网状丘脑皮质系统的结果，该系统负责全身性皮质反应(重新募集、去同步化、负的直流电漂移和每秒三个棘波复合波)。ESCM手术的成功取决于以下预测因素：病例选择(原发性和继发性强直阵挛发作以及Lennox Gastaut综合征的不典型缺失)，最佳立体定向靶点的脑室造影和电生理学定义(基于前连合、后连合和垂直于后连合的垂直线和皮质招募反应)，在患者没有主观感觉和完全内化皮下刺激系统的情况下对ESCM的可靠性进行定期电生理监测(通过记录头皮皮质电刺激、去同步化和直流电反应)，临床和EEG改善的定量评估，以及开关效应的分析考虑到ESCM的长期(可能是塑料)影响。SAHCS可阻断颞叶癫痫的临床和脑电迹象，而不会对刺激的海马区组织造成额外的损害。初步结果表明，这种抗癫痫作用至少部分是由于对受刺激的海马区组织的生理抑制所致，因为作者发现：(1)SAHCS后，伴随着海马区后放电的临床体征的阈值增加，持续时间、传播和阻断减少；(2)海马区诱发的反应恢复周期变平；(3)单光子发射计算机断层扫描显示低灌注量；(4)受刺激的海马区苯二氮卓类受体结合浓度增加。在24个月中，在开放方案下，慢性海马区刺激持续阻止了一名患者的颞叶癫痫发生，近期记忆中没有明显的额外改变。
Summary The following two different modulatory procedures to control intractable epileptic seizures are presented: (1) chronic electrical stimulation of the centromedian–thalamic nucleus (ESCM) for control of generalized tonic–clonic seizures and atypical absences, and (2) subacute hippocampal stimulation (SAHCS) and chronic hippocampal stimulation for control of nonlesional temporal lobe seizures. The ESCM antiepileptic effect seems to be the result of activation of a nonspecific reticulothalamocortical system responsible for generalized electrocortical responses (recruiting, desynchronization, negative direct current shifts, and three spike–wave complexes per second). The success of the ESCM procedure depends on the following predictor factors: case selection (primary and secondary tonic–clonic seizures and atypical absences of the Lennox Gastaut syndrome), ventriculographic and electrophysiologic definition of the optimal stereotactic targets (based on the anterior commissure, posterior commissure, and the vertical line perpendicular to the posterior commissure and electrocortical recruiting responses), periodic electrophysiologic monitoring of the reliability of ESCM in the absence of the patient’s subjective sensations and with totally internalized subcutaneous stimulation systems (by recording scalp electrocortical recruiting, desynchronizing, and direct current responses), quantitative evaluation of clinical and EEG improvement, and analysis of the ON and OFF effects, taking into account a long-lasting (possibly plastic) effect of ESCM. SAHCS blocks clinical and EEG signs of temporal lobe epileptogenesis with no additional damage of the stimulated hippocampal tissue. Preliminary results suggest that this antiepileptic effect is, at least in part, the result of a physiologic inhibition of the stimulated hippocampal tissue, because after SAHCS the authors found the following: (1) increased threshold and decreased duration, propagation, and blockage of the clinical signs accompanied with the hippocampal afterdischarge; (2) flattening of the hippocampal-evoked response recovery cycles; (3) single photon emission computed tomographic hypoperfusion; and (4) increased concentration of benzodiazepine receptor binding at the stimulated hippocampal region. Chronic hippocampal stimulation persistently blocked temporal lobe epileptogenesis in one patient under open protocols during 24 months with no apparent additional alterations in recent memory.