目前，一项发表在Bipolar Disord杂志上的研究"White matter microstructure in untreated first episode bipolar disorder with psychosis: comparison with schizophrenia"指出，与精神分裂症患者相比，双相障碍患者的脑白质微结构异常可能涉及不同的病理生理学机制。
Lisa Lu（Roosevelt University, Chicago, Illinois）和她的同事们指出，先前的、有关双相障碍患者脑白质微结构异常的弥散张量成像（DTI）研究有多种不同的试验结果，一些研究发现各向异性分数（FA）值降低，而另有一些研究指出FA值增加或无结果。导致结果不一致的可能的原因是样本的异质性。大多数受试者在纳入研究前，已有多年的疾病史和异质性药物治疗史。此外，很少有研究对双相障碍和精神分裂症患者的脑白质微结构异常进行对照评估。
本研究采用DTI技术，对13例未治疗、首次精神病性发作的双相障碍患者、21例未治疗、首次精神分裂症发作患者以及18例健康对照者的脑白质完整性进行了评估。三组在年龄、性别、受教育程度以及智能方面无差异。
基于体素的形态学研究指出，与对照组相比，双相障碍患者脑部多个联合、投射和相关部位的FA值降低；相反地，精神分裂症患者与健康对照组在FA值方面的差异无统计学意义。
与精神分裂症患者相比，双相障碍患者在扣带回、内囊、后脑部区域（后胼胝体、脑毯以及枕叶白质包括后丘脑辐射区、下纵束以及下额枕束）等部位FA值降低。
与健康对照者相比，双相障碍和精神分裂症患者在以下脑部区域的的平均扩散率（水分子的扩散大小）均增加，包括扣带回、内囊、脑毯、枕叶白质（包括后丘脑辐射区、下纵束以及下额枕束）。双相障碍和精神分裂症患者在平均扩散率方面无统计学差异。
研究指出，双相障碍和精神分裂症患者脑部区域的FA值存在差异，与对照组相比，精神分裂症患者轴向和径向扩散率均增加；FA值降低的双相障碍患者，沿着纤维束方向，其径向扩散率增加（而非轴向扩散率）。
研究者们指出，精神分裂症患者的脑内轴向和径向扩散率均增加，这可能能够解释为何精神分裂症患者与对照组在FA值方面无差异。原因是轴向和径向扩散率同时增加可能不会导致FA值变化。
Lisa Lu和她的同事们总结到：“双相障碍患者选择性的轴向扩散率增加，提示纤维束结构异常与髓鞘神经发育或改变相一致。相反地，精神分裂症患者轴向和径向扩散率均增加，提示轴突外空间内的水内容物增多。”
本项研究提示双相障碍和精神分裂症患者脑白质微结构异常可能存在不同的生理病理学机制。（生物谷Bioon.com）
doi:10.1111/j.1399-5618.2011.00958.x
PMC:
PMID:
White matter microstructure in untreated first episode bipolar disorder with psychosis: comparison with schizophrenia
Lisa H Lu1,2, Xiaohong Joe Zhou3, Sarah K Keedy2, James L Reilly2, John A Sweeney2
Objectives:White matter abnormalities have been reported in bipolar disorder. The present study aimed to investigate white matter integrity in untreated first episode patients with psychotic bipolar disorder using diffusion tensor imaging, and to compare observations with those from untreated first episode schizophrenia patients.
Methods:Fractional anisotropy and mean diffusivity were measured in first episode psychotic patients with bipolar disorder (n = 13) or schizophrenia (n = 21) and healthy individuals (n = 18). Group differences were evaluated using voxel-based morphometry. Axial and radial diffusivity were examined in regions with altered fractional anisotropy in post-hoc analyses.
Results:Patients with bipolar disorder showed lower fractional anisotropy than healthy controls in several white matter tracts. Compared with schizophrenia patients, bipolar disorder patients showed lower fractional anisotropy in the cingulum, internal capsule, posterior corpus callosum, tapetum, and occipital white matter including posterior thalamic radiation and inferior longitudinal fasciculus/inferior fronto-occipital fasciculus. Lower fractional anisotropy in bipolar disorder was characterized by increased radial diffusion rather than axial diffusion along the orientation of fiber tracts. Across several white matter tracts, both patient groups showed greater mean diffusivity than healthy individuals.
Conclusions:Selectively increased radial diffusivity in bipolar disorder patients suggests structural disorganization in fiber tract coherence of neurodevelopmental origin or alterations in myelin sheaths along fiber tracts. In contrast, increased isotropic diffusion along white matter tracts in schizophrenia patients with alterations in both radial and axial diffusivity suggests increased water content outside the axonal space. Thus, the present results suggest that different pathophysiological mechanisms may underlie white matter microstructural abnormalities in bipolar disorder and schizophrenia.
