Tubbs R Shane, Killingsworth Cheryl R, Rollins Dennis L, Smith William M, Ideker Raymond E, Wellons John C, Blount Jeffrey P, Oakes W Jerry
Department of Cell Biology, Division of Pediatric Neurosurgery, University of Alabama at Birmingham, Alabama 35233, USA.
J Neurosurg. 2005 Mar;102(2 Suppl):213-7. doi: 10.3171/jns.2005.102.2.0213.
Vagus nerve stimulation is known to decrease the frequency, duration, and intensity of some types of intracranial seizures in both humans and animals. Although many theories abound concerning the mechanism for this action, the true cause remains speculative. To potentially elucidate a pathway in which vagus nerve stimulation aborts seizure activity, seizures were initiated not in the cerebral cortex but in the spinal cord and then vagus nerve stimulation was performed.
Ten pigs were anesthetized and placed in the lateral position, and a small laminectomy was performed in the lumbar region. Topical penicillin, a known epileptogenic drug to the cerebral cortex and spinal cord, was applied to the dorsal surface of the exposed cord. With the exception of two animals that were used as controls, once seizure activity was discernible via motor convulsion or increased electrical activity the left vagus nerve, which had been previously isolated in the neck, was stimulated. Following multiple stimulations of the vagus nerve and with seizure activity confirmed, the cord was transected in the midthoracic region and vagus nerve stimulation was performed. Vagus nerve stimulation resulted in cessation of spinal cord seizure activity in all (87.5%) but one experimented animal. Transection of the spinal cord superior to the site of seizure induction resulted in the ineffectiveness of vagus nerve stimulation to cause cessation of seizure activity in all study animals.
The effects of vagus nerve stimulation on induced spinal cord seizures involve descending spinal pathways. The authors believe that this experiment is the first to demonstrate that spinal cord neuronal hyperactivity can be suppressed by stimulation of a cranial nerve. These data may aid in the development of alternative mechanisms for electrical stimulation in patients with medically intractable seizures. Further studies are now necessary to isolate which specific tracts, nuclei, and neurotransmitters are involved in this process.
已知迷走神经刺激可降低人类和动物某些类型颅内癫痫发作的频率、持续时间和强度。尽管关于这种作用机制的理论众多,但真正原因仍属推测。为了潜在地阐明迷走神经刺激终止癫痫活动的途径,癫痫发作并非在大脑皮层引发,而是在脊髓引发,然后进行迷走神经刺激。
十头猪麻醉后置于侧卧位,在腰椎区域进行小范围椎板切除术。将已知对大脑皮层和脊髓有致痫作用的局部青霉素应用于暴露脊髓的背表面。除两只用作对照的动物外,一旦通过运动性抽搐或电活动增加可辨别出癫痫活动,就对先前已在颈部分离的左侧迷走神经进行刺激。在多次刺激迷走神经并确认有癫痫活动后,在胸段中部横断脊髓,并进行迷走神经刺激。在所有(87.5%)实验动物中,除一只外,迷走神经刺激均导致脊髓癫痫活动停止。在癫痫发作诱导部位上方横断脊髓导致在所有研究动物中迷走神经刺激均无法有效引起癫痫活动停止。
迷走神经刺激对诱导的脊髓癫痫发作的影响涉及脊髓下行通路。作者认为该实验首次证明刺激颅神经可抑制脊髓神经元的过度活动。这些数据可能有助于为难治性癫痫患者开发电刺激的替代机制。现在需要进一步研究以确定在此过程中涉及哪些特定的神经束、神经核和神经递质。