Hirato Masafumi, Miyagishima Takaaki, Takahashi Akio, Yoshimoto Yuhei
Department of Neurosurgery, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Department of Neurosurgery, National Hospital Organization Shibukawa Medical Center, Shibukawa, Gunma, Japan.
Acta Neurochir (Wien). 2021 Aug;163(8):2121-2133. doi: 10.1007/s00701-021-04743-0. Epub 2021 May 14.
The genesis of central post-stroke pain (CPSP) is important but difficult to understand. We evaluated the involvement of the thalamic anterior part of the ventral posterolateral nucleus (VPLa) and central lateral nucleus (CL) in the occurrence of CPSP.
Stereotactic thalamotomy was performed on the posterior part of the ventral lateral nucleus (VLp)-VPLa and CL in 9 patients with CPSP caused by deep-seated intracerebral hemorrhage. Computed tomography (CT) did not reveal definite thalamic lesion in 5 patients but did in 4 patients. Electrophysiological studies of these thalamic nuclei were carried out during the surgery. Anatomical studies using CT were performed in another 20 patients with thalamic hemorrhage who had clear consciousness but had sensory disturbance at onset.
Neural activities were preserved and hyperactive and unstable discharges (HUDs) were often recognized along the trajectory in the thalamic VLp-VPLa in 5 patients without thalamic lesion. Surgical modification of this area ameliorated pain, particularly movement-related pain. Neural activities were hypoactive in the other 4 patients with thalamic lesion. However, neural activities were preserved and HUDs were sometimes recognized in the CL. Sensory responses were seen, but at low rate, in the sensory thalamus. Anatomical study showed that the thalamic lesion was obviously smaller in the patients with developing pain in the chronic stage.
Change in neural activities around the cerebrovascular disease lesion in the thalamic VPLa or CL might affect the perception of sensory impulses or sensory processing in those thalamic nuclei, resulting in the genesis of CPSP.
脑卒中后中枢性疼痛(CPSP)的发病机制很重要但难以理解。我们评估了丘脑腹后外侧核前部(VPLa)和中央外侧核(CL)在CPSP发生中的作用。
对9例由深部脑出血导致CPSP的患者,在腹外侧核后部(VLp)-VPLa和CL进行立体定向丘脑切开术。5例患者的计算机断层扫描(CT)未显示明确的丘脑病变,4例显示有病变。手术期间对这些丘脑核进行了电生理研究。对另外20例丘脑出血且起病时意识清醒但有感觉障碍的患者进行了CT解剖学研究。
5例无丘脑病变的患者,其神经活动得以保留,且在丘脑VLp-VPLa的轨迹上常可识别到活动亢进和不稳定放电(HUDs)。对该区域进行手术干预可缓解疼痛,尤其是与运动相关的疼痛。另外4例有丘脑病变的患者神经活动减弱。然而,CL中的神经活动得以保留,有时可识别到HUDs。在感觉丘脑中可观察到感觉反应,但发生率较低。解剖学研究表明,慢性期出现疼痛的患者丘脑病变明显较小。
丘脑VPLa或CL中脑血管病病变周围神经活动的改变可能会影响这些丘脑核中感觉冲动的感知或感觉处理,从而导致CPSP的发生。