Soares J C, Mann J J
Laboratory of Neuropharmacology, Western Psychiatric Institute and Clinic, University of Pittsburgh Medical Center, Pennsylvania, USA.
Biol Psychiatry. 1997 Jan 1;41(1):86-106. doi: 10.1016/s0006-3223(96)00006-6.
The structural neuroimaging findings in mood disorders were reviewed, to evaluate evidence for a neuroanatomic model of pathophysiology, involving the prefrontal cortex, the basal ganglia, the amygdala-hippocampus complex, thalamus, and connections among these structures. Global atrophy is not consistently found. The best replicated finding is an increased rate of white matter and periventricular hyperintensities. A smaller frontal lobe, cerebellum, caudate, and putamen appear present in unipolar depression. A larger third ventricle, and smaller cerebellum and perhaps temporal lobe appear present in bipolar disorder. These localized structural changes involve regions that may be critical in the pathogenesis of mood disorders. Generalized and localized anatomic alterations may be related to age or vascular disease. The clinical and biological correlates of these changes need to be investigated to allow development of a more complete model of pathophysiology of mood disorders.
对情绪障碍的结构性神经影像学研究结果进行了综述，以评估涉及前额叶皮质、基底神经节、杏仁核 - 海马复合体、丘脑以及这些结构之间连接的病理生理神经解剖模型的证据。并非始终能发现整体萎缩。得到最佳重复验证的发现是白质和脑室周围高信号发生率增加。在单相抑郁症中似乎存在较小的额叶、小脑、尾状核和壳核。在双相情感障碍中似乎存在较大的第三脑室、较小的小脑以及可能较小的颞叶。这些局部结构变化涉及可能对情绪障碍发病机制至关重要的区域。全身性和局部性解剖改变可能与年龄或血管疾病有关。需要对这些变化的临床和生物学相关性进行研究，以便建立更完整的情绪障碍病理生理模型。
