Sheikhi Koohsar Javad, Faeghi Fariborz, Rafaiee Raheleh, Niroumand Sarvandani Mohammad, Masjoodi Sadegh, Kalalian Moghaddam Hamid
Department of Medical Imaging, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Neuroscience, School of Advanced Technologies in Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Iran J Psychiatry. 2022 Jan;17(1):91-98. doi: 10.18502/ijps.v17i1.8053.
Chronic METH use results in neurodegenerative alternations in the human brain. The present study aimed to assess the long-term METH impact on brain metabolite concentrations in cases meeting the DSM-5 criteria regarding METH use. We recruited 42 METH users meeting the DSM-5 criteria and 21 healthy controls. Psychotic signs were measured using the Positive and Negative Syndrome Scale (PANSS). Proton magnetic resonance spectroscopy (1HMRS) evaluating Myo-inositol (Ml), Choline (Cho), Glutamine plus Glutamate (Glx), N-acetyl aspartate (NAA), and Creatine (Cre) were obtained in the dopaminergic pathway (Frontal Cortex, Substantia nigra, Ventral Tegmental Area (VTA), Nucleus Accumbens (NAc), Hippocampus, Striatum,) the subjects. All participants collected urine specimens for 24 hours to measure presence of specific metabolites including METH metabolite level, 5-Hydroxy indoleacetic acid metabolite (for serotonin level monitoring), and metanephrine metabolite (for dopamine level monitoring). Dopamine and Serotonin increased in the METH group (P < 0.001). METH caused an increase in the Cre (P < 0.001) and a decline in the Glx (P < 0.001), NAA (P = 0.008), and MI (P < 0.001) metabolite concentrations of dopamine circuits in METH users in comparison with healthy subjects. We found no change in Cho metabolite concentration. Psychological data and the neurometabolite concentrations in the studied area of the brain were significantly correlated. There is an association between METH use and active neurodegeneration in the dopamine circuit, and it causes serious mental illness. 1HMRS can detect patient's deterioration and progression of disease as well as follow-up management in patients with METH use disorder.
长期使用甲基苯丙胺会导致人脑发生神经退行性改变。本研究旨在评估符合《精神疾病诊断与统计手册》第五版(DSM-5)甲基苯丙胺使用标准的病例中,甲基苯丙胺对脑代谢物浓度的长期影响。我们招募了42名符合DSM-5标准的甲基苯丙胺使用者和21名健康对照者。使用阳性和阴性症状量表(PANSS)测量精神病症状。通过质子磁共振波谱(1HMRS)评估了受试者多巴胺能通路(额叶皮质、黑质、腹侧被盖区(VTA)、伏隔核(NAc)、海马体、纹状体)中的肌醇(Ml)、胆碱(Cho)、谷氨酰胺加谷氨酸(Glx)、N-乙酰天门冬氨酸(NAA)和肌酸(Cre)。所有参与者收集24小时尿液样本,以测量特定代谢物的存在情况,包括甲基苯丙胺代谢物水平、5-羟色胺酸代谢物(用于监测血清素水平)和间甲肾上腺素代谢物(用于监测多巴胺水平)。甲基苯丙胺组的多巴胺和血清素水平升高(P < 0.001)。与健康受试者相比,甲基苯丙胺导致甲基苯丙胺使用者多巴胺回路中的Cre升高(P < 0.001),Glx(P < 0.001)、NAA(P = 0.008)和MI(P < 0.001)代谢物浓度下降。我们发现Cho代谢物浓度没有变化。心理数据与大脑研究区域的神经代谢物浓度显著相关。甲基苯丙胺使用与多巴胺回路中的活动性神经退行性变之间存在关联,并且会导致严重精神疾病。1HMRS可以检测甲基苯丙胺使用障碍患者的病情恶化和进展情况以及进行随访管理。