Jørgensen K N, Nerland S, Norbom L B, Doan N T, Nesvåg R, Mørch-Johnsen L, Haukvik U K, Melle I, Andreassen O A, Westlye L T, Agartz I
Department of Psychiatric Research,Diakonhjemmet Hospital,Oslo,Norway.
NORMENT and K. G. Jebsen Center for Psychosis Research, Institute of Clinical Medicine, University of Oslo,Norway.
Psychol Med. 2016 Jul;46(9):1971-85. doi: 10.1017/S0033291716000593. Epub 2016 Apr 6.
Schizophrenia and bipolar disorder share genetic risk factors and one possible illness mechanism is abnormal myelination. T1-weighted magnetic resonance imaging (MRI) tissue intensities are sensitive to myelin content. Therefore, the contrast between grey- and white-matter intensities may reflect myelination along the cortical surface.
MRI images were obtained from patients with schizophrenia (n = 214), bipolar disorder (n = 185), and healthy controls (n = 278) and processed in FreeSurfer. The grey/white-matter contrast was computed at each vertex as the difference between average grey-matter intensity (sampled 0-60% into the cortical ribbon) and average white-matter intensity (sampled 0-1.5 mm into subcortical white matter), normalized by their average. Group differences were tested using linear models covarying for age and sex.
Patients with schizophrenia had increased contrast compared to controls bilaterally in the post- and precentral gyri, the transverse temporal gyri and posterior insulae, and in parieto-occipital regions. In bipolar disorder, increased contrast was primarily localized in the left precentral gyrus. There were no significant differences between schizophrenia and bipolar disorder. Findings of increased contrast remained after adjusting for cortical area, thickness, and gyrification. We found no association with antipsychotic medication dose.
Increased contrast was found in highly myelinated low-level sensory and motor regions in schizophrenia, and to a lesser extent in bipolar disorder. We propose that these findings indicate reduced intracortical myelin. In accordance with the corollary discharge hypothesis, this could cause disinhibition of sensory input, resulting in distorted perceptual processing leading to the characteristic positive symptoms of schizophrenia.
精神分裂症和双相情感障碍存在共同的遗传风险因素，一种可能的发病机制是髓鞘形成异常。T1加权磁共振成像（MRI）组织强度对髓鞘含量敏感。因此，灰质和白质强度之间的对比度可能反映皮质表面的髓鞘形成情况。
从精神分裂症患者（n = 214）、双相情感障碍患者（n = 185）和健康对照者（n = 278）获取MRI图像，并在FreeSurfer中进行处理。计算每个顶点处的灰/白质对比度，即平均灰质强度（在皮质带中0 - 60%采样）与平均白质强度（在皮质下白质中0 - 1.5 mm采样）之间的差值，并通过它们的平均值进行归一化。使用对年龄和性别进行协变量调整的线性模型检验组间差异。
与对照组相比，精神分裂症患者在双侧中央后回、中央前回、颞横回和岛叶后部以及顶枕区域的对比度增加。在双相情感障碍中，对比度增加主要局限于左侧中央前回。精神分裂症和双相情感障碍之间无显著差异。在调整皮质面积、厚度和脑回化后，对比度增加的结果仍然存在。我们未发现与抗精神病药物剂量有关联。
在精神分裂症中，高度髓鞘化的低级感觉和运动区域对比度增加，在双相情感障碍中程度较轻。我们认为这些发现表明皮质内髓鞘减少。根据推论放电假说，这可能导致感觉输入的去抑制，从而导致感知处理失真，进而产生精神分裂症的特征性阳性症状。
