Sensory processing in Parkinson's and Huntington's disease -: Investigations with 3D H215O-PET
Sensory processing in Parkinson's and Huntington's disease -: Investigations with 3D H215O-PET
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DOI：
10.1093/brain/122.9.1651
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发表时间：
1999-09-01
期刊：
影响因子：
14.5
通讯作者：
Conrad, B
中科院分区：
文献类型：
--
作者：
Boecker, H;Ceballos-Baumann, A;Conrad, B
有相关的实验和临床证据支持基底节作为参与中枢躯体感觉控制的感觉分析器的基本作用。本研究旨在研究两种以基底节功能障碍为特征的临床疾病，即帕金森氏病和亨廷顿病时感觉加工的功能解剖学。根据先前记录的体感诱发电位数据，我们预计，通过基底节接受调节性体感输入的皮质区域存在感觉诱发激活缺陷。8名帕金森病患者、8名亨廷顿病患者和8名健康对照在两种实验条件下按随机顺序重复进行(H2O)-O-15-PET激活扫描：(I)对固定的食指掌骨关节施加持续的单边高频振动刺激；(Ii)休息(无振动刺激)。在对照组中，激活模式偏向刺激呈现相反的一侧，包括皮质[初级感觉皮质(S1)；次级感觉皮质(S2)]和皮质下(苍白球、丘脑腹外侧部)局部脑血流量增加(P<；0.001)，组间比较(P<；在帕金森病患者和对照组之间，振动诱发的rCBF变化揭示了中枢感觉加工的不同：(1)帕金森病患者对侧感觉运动(S1/M1)和外侧运动前皮质、对侧S2、对侧后扣带回、双侧前额叶皮质(Brodmann区10)和对侧基底节的激活减少；(Ii)亨廷顿病患者对侧S2、顶区39和40区、舌回、双侧前额叶皮质(Brodmann区8、9、10和44区)、S1(仅趋势)和对侧基底节的激活减少；(Iii)在两种临床情况下，同侧感觉皮质区，特别是尾侧S1、S2区和岛叶皮质的相对激活增强。我们的数据显示，帕金森氏病和亨廷顿氏病，除了公认的中枢运动控制缺陷外，其特征是被动感觉刺激时皮质和皮质下的异常激活。此外，同侧感觉皮质区的激活增加可能被解释为感觉冲动的中心聚焦和门控改变的迹象，或者在存在基底节功能障碍的情况下联合感觉区的代偿性募集增强。感觉处理的改变被认为在这两种情况下都会导致相关的运动障碍。
There is conjoining experimental and clinical evidence supporting a fundamental role of the basal ganglia as a sensory analyser engaged in central somatosensory control. This study was aimed at investigating the functional anatomy of sensory processing in two clinical conditions characterized by basal ganglia dysfunction, i.e. Parkinson's and Huntington's disease. Based on previously recorded data of somatosensory evoked potentials, we expected deficient sensory-evoked activation in cortical areas that receive modulatory somatosensory input via the basal ganglia. Eight Parkinson's disease patients, eight Huntington's disease patients and eight healthy controls underwent repetitive (H2O)-O-15-PET activation scans during two experimental conditions in random order: (i) continuous unilateral high-frequency vibratory stimulation applied to the immobilized metacarpal joint of the index finger and (ii) rest (no vibratory stimulus). In the control cohort, the activation pattern was lateralized to the side opposite to stimulus presentation, including cortical [primary sensory cortex (S1); secondary sensory cortex (S2)] and subcortical (globus pallidus, ventrolateral thalamus) regional cerebral blood flow (rCBF) increases (P < 0.001), Between-group comparisons (P < 0.01) of vibration-induced rCBF changes between patients and controls revealed differences in central sensory processing: (i) in Parkinson's disease, decreased activation of contralateral sensorimotor (S1/M1) and lateral premotor cortex, contralateral S2, contralateral posterior cingulate, bilateral prefrontal cortex (Brodmann area 10) and contralateral basal ganglia; (ii) in Huntington's disease, decreased activation of contralateral S2, parietal areas 39 and 40, and lingual gyrus, bilateral prefrontal cortex (Brodmann areas 8, 9, 10 and 44), S1 (trend only) and contralateral basal ganglia; (iii) in both clinical conditions relative enhanced activation of ipsilateral sensory cortical areas, notably caudal S1, S2 and insular cortex. Our data show that Parkinson's disease and Huntington's disease, beyond well-established deficits in central motor control, are characterized by abnormal cortical and subcortical activation on passive sensory stimulation. Furthermore, the finding that activation increases in ipsilateral sensory cortical areas may be interpreted as an indication of either altered central focusing and gating of sensory impulses, or enhanced compensatory recruitment of associative sensory areas in the presence of basal ganglia dysfunction. Altered sensory processing is thought to contribute to pertinent motor deficits in both conditions.