Department of Neuroscience, Imaging, and Clinical Sciences, University G. d'Annunzio of Chieti-Pescara, Chieti, Italy.
Institute for Advanced Biomedical Technologies (ITAB), University G. d'Annunzio of Chieti- Pescara, Chieti, Italy.
Mov Disord. 2022 Nov;37(11):2226-2235. doi: 10.1002/mds.29187. Epub 2022 Aug 22.
The high co-occurrence of somatic symptom disorder (SSD) in Parkinson's disease (PD) patients suggests overlapping pathophysiology. However, little is known about the neural correlates of SSD and their possible interactions with PD. Existing studies have shown that SSD is associated with reduced task-evoked activity in the medial prefrontal cortex (mPFC), a central node of the default-mode network (DMN). SSD is also associated with abnormal γ-aminobutyric acid (GABA) content, a marker of local inhibitory tone and regional hypoactivity, in the same area when SSD co-occurs with PD.
To disentangle the individual and shared effects of SSD and PD on mPFC neurotransmission and connectivity patterns and help disclose the neural mechanisms of comorbidity in the PD population.
The study cohort included 18 PD patients with SSD (PD + SSD), 18 PD patients, 13 SSD patients who did not exhibit neurologic disorders, and 17 healthy subjects (HC). Proton magnetic resonance (MR) spectroscopy evaluated GABA levels within a volume of interest centered on the mPFC. Resting-state functional MR imaging investigated the region's functional connectivity patterns.
Compared to HC or PD groups, the mPFC of SSD subjects exhibited higher GABA levels and connectivity. Higher mPFC connectivity involved DMN regions in SSD patients without PD and regions of the executive and attentional networks (EAN) in patients with PD comorbidity.
Aberrant reconfigurations of connectivity patterns between the mPFC and the EAN are distinct features of the PD + SSD comorbidity. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
帕金森病(PD)患者躯体症状障碍(SSD)的高共病发生率表明其存在重叠的病理生理学机制。然而,SSD 的神经相关性及其与 PD 的可能相互作用知之甚少。现有研究表明,SSD 与内侧前额叶皮层(mPFC)的任务诱发活动减少有关,mPFC 是默认模式网络(DMN)的一个中枢节点。SSD 还与 PD 伴 SSD 时同一区域的γ-氨基丁酸(GABA)含量异常有关,GABA 是局部抑制性张力和区域活动减少的标志物。
厘清 SSD 和 PD 对 mPFC 神经传递和连接模式的单独和共同影响,帮助揭示 PD 人群共病的神经机制。
研究队列包括 18 例 PD 伴 SSD(PD+SSD)患者、18 例 PD 患者、13 例未出现神经系统疾病的 SSD 患者和 17 名健康对照(HC)。质子磁共振波谱(MR)评估了以 mPFC 为中心的感兴趣区内的 GABA 水平。静息态功能磁共振成像(rs-fMRI)研究了该区域的功能连接模式。
与 HC 或 PD 组相比,SSD 患者的 mPFC 区域 GABA 水平和连接性更高。更高的 mPFC 连接性涉及 SSD 患者无 PD 时的 DMN 区域以及 PD 共病患者的执行和注意力网络(EAN)区域。
mPFC 与 EAN 之间连接模式的异常重构是 PD+SSD 共病的独特特征。© 2022 作者。运动障碍由 Wiley 期刊代表国际帕金森和运动障碍协会出版。