特发性帕金森病和非典型帕金森综合征患者的诱发电位反应:比较研究

Manoj Roy, A. Misra, Joydeep Mukherjee, Manamita Mandal, Jasodhara Chaudhuri, Kartik Chandra Ghosh, B. Mohanty
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引用次数: 0

摘要

特发性帕金森病(IPD)和非典型帕金森综合征(APS)患者患有一系列障碍,尤其是在平衡和运动方面,这些障碍需要视觉、听觉和体感输入。在这项研究中,IPD 患者、APS 患者和健康对照组(每组 50 人)接受了一系列评估,包括视觉诱发电位(VEP)、脑干听觉诱发反应(BAER)和短时躯体感觉诱发电位(SSEP)。结果显示,多系统萎缩-小脑型(MSA-C)、多系统萎缩-帕金森病型(MSA-P)和皮质基底节变性(CBD)患者的 VEP P100 潜伏期延长。在 IPD、MSA-C、路易体痴呆(DLB)和帕金森病痴呆(PDD)患者中,III 峰和 V 峰的潜伏期延长。在IPD、DLB和PDD中,BAER I-III和I-V峰间潜伏期延长,而在MSA-C中,BAER I-III、III-V和I-V峰间潜伏期延长,V/I振幅比降低。在 SSEP 中,MSA-P 和 MSA-C 的中枢感觉传导时间(N20-N13)增加。IPD 患者的 VEP P100 潜伏期延长(P < 0.001),VEP N75-P100 振幅降低(P < 0.001),BAER I、II、II、IV、V 峰潜伏期延长(P < 0.001),I-III、I-V 峰间潜伏期(P < 0.001),BAER V/I 振幅比值较低(P < 0.001),SSEP N13、N20、中央感觉传导时间(N20-N13)比 HC 延长(P < 0.001)。与 APS 患者相比,IPD 患者的 BAER I、II、II、IV、V 峰潜伏期延长(P < 0.001),I-III、I-V 峰间潜伏期延长(P < 0.001),SSEP N13、N20、中枢感觉传导时间(N20-N13)缩短(P < 0.001)。此外,与 HCs 相比,APS 患者的 VEP P100 和 N145 潜伏期延长(P < 0.001),N75-N145 振幅降低(P < 0.001)。与 HC 相比,APS 患者的 BAER II、II、IV、V 峰潜伏期延长(P < 0.001),I-III、III-V、I-V 峰间潜伏期延长(P < 0.001),V/I 振幅比降低,SSEP N13、N20 和中央感觉传导时间(N20-N13)延长(P < 0.001)。与震颤为主的 IPD 相比,姿势不稳和步态障碍 (PIGD) IPD 的 BAER III、V 峰潜伏期明显延长(P < 0.05),III-V 峰间潜伏期也明显延长(P < 0.05)。总体而言,IPD 和 APS 患者的视觉、听觉和躯体感觉通路存在明显的 VEP、BAER 和 SSEP 异常,表现为脱髓鞘和轴突多样性。这些变化还与病程和严重程度相关。虽然这些疾病主要是运动性疾病,但也有重要的非运动性成分,这些电生理异常可能为评估非运动性症状开辟了一条新途径。
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Evoked potential response in patients with idiopathic Parkinson’s disease and atypical parkinsonian syndromes: A comparative study
Patients with idiopathic Parkinson’s disease (IPD) and atypical parkinsonian syndromes (APSs) suffer from a range of disorders, especially in balance and locomotion, which necessitate visual, auditory, and somatosensory inputs. In this study, IPD patients, APS patients, and healthy controls (HCs) (n = 50 per group) underwent a series of assessments for visual evoked potentials (VEP), brainstem auditory evoked response (BAER), and short-latency somatosensory evoked potentials (SSEP). Results showed that VEP P100 latency was prolonged in multiple system atrophy-cerebellar type (MSA-C), multiple system atrophy-parkinsonian type (MSA-P), and corticobasal ganglionic degeneration (CBD) patients. The latency of peaks III and V was prolonged in IPD, MSA-C, dementia with Lewy bodies (DLB), and Parkinson’s disease dementia (PDD). BAER I-III and I-V interpeak latency were prolonged in IPD, DLB, and PDD, whereas BAER I-III, III-V, and I-V interpeak latencies were increased and the V/I amplitude ratio was decreased in MSA-C. The central sensory conduction time (N20-N13) was increased in MSA-P and MSA-C in SSEP. IPD patients had prolonged VEP P100 latency (P < 0.001), lower VEP N75-P100 amplitude (P < 0.001), prolonged BAER I, II, II, IV, V peak latencies (P < 0.001), I-III, I-V interpeak latencies (P < 0.001), lower BAER V/I amplitude ratio (P < 0.001), and prolonged SSEP N13, N20, central sensory conduction time (N20-N13) (P < 0.001) than HCs. IPD patients also had prolonged BAER I, II, II, IV, V peak latencies (P < 0.001), prolonged I-III, I-V interpeak latencies (P < 0.001), and shorter SSEP N13, N20, central sensory conduction time (N20-N13) (P < 0.001) than APS patients. Moreover, APS patients had prolonged VEP P100 and N145 latencies (P < 0.001) and decreased N75-N145 amplitude (P < 0.001) compared to HCs. APS patients also had prolonged BAER II, II, IV, V peak latencies (P < 0.001), prolonged I-III, III-V, I-V interpeak latencies (P < 0.001), decreased V/I amplitude ratio, and prolonged SSEP N13, N20, central sensory conduction time (N20-N13) (P < 0.001) than HCs. Postural instability and gait disorder (PIGD) IPD had significantly prolonged BAER III, V peak latencies (P < 0.05), and prolonged III-V interpeak latencies (P < 0.05) compared to tremor-dominant IPD. Overall, the IPD and APS patients had significant VEP, BAER, and SSEP abnormalities of demyelination and axonal variety in the visual, auditory, and somatosensory pathways. The changes were also correlated with the disease duration and severity. Although the diseases are predominantly motor disorders with significant non-motor components, these electrophysiological abnormalities might open a new avenue to assess the non-motor symptoms.
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