Clinic of Psychiatry, Socialpsychiatry and Psychotherapy, Hannover Medical School, Carl-Neuberg-Street 1, D-30625 Hannover, Germany.
BMC Neurosci. 2014 Jan 7;15:6. doi: 10.1186/1471-2202-15-6.
Despite strong evidence that the pathophysiology of Tourette syndrome (TS) involves structural and functional disturbances of the basal ganglia and cortical frontal areas, findings from in vivo imaging studies have provided conflicting results. In this study we used whole brain diffusion tensor imaging (DTI) to investigate the microstructural integrity of white matter pathways and brain tissue in 19 unmedicated, adult, male patients with TS "only" (without comorbid psychiatric disorders) and 20 age- and sex-matched control subjects.
Compared to normal controls, TS patients showed a decrease in the fractional anisotropy index (FA) bilaterally in the medial frontal gyrus, the pars opercularis of the left inferior frontal gyrus, the middle occipital gyrus, the right cingulate gyrus, and the medial premotor cortex. Increased apparent diffusion coefficient (ADC) maps were detected in the left cingulate gyrus, prefrontal areas, left precentral gyrus, and left putamen. There was a negative correlation between tic severity and FA values in the left superior frontal gyrus, medial frontal gyrus bilaterally, cingulate gyrus bilaterally, and ventral posterior lateral nucleus of the right thalamus, and a positive correlation in the body of the corpus callosum, left thalamus, right superior temporal gyrus, and left parahippocampal gyrus. There was also a positive correlation between regional ADC values and tic severity in the left cingulate gyrus, putamen bilaterally, medial frontal gyrus bilaterally, left precentral gyrus, and ventral anterior nucleus of the left thalamus.
Our results confirm prior studies suggesting that tics are caused by alterations in prefrontal areas, thalamus and putamen, while changes in the cingulate gyrus seem to reflect secondary compensatory mechanisms. Due to the study design, influences from comorbidities, gender, medication and age can be excluded.
尽管有强有力的证据表明妥瑞氏综合征（TS）的病理生理学涉及基底神经节和皮质额区的结构和功能障碍，但活体成像研究的结果却提供了相互矛盾的结果。在这项研究中，我们使用全脑弥散张量成像（DTI）来研究 19 名未经药物治疗的成年男性 TS 患者（无合并精神疾病）和 20 名年龄和性别匹配的对照组的白质通路和脑组织的微观结构完整性。
与正常对照组相比，TS 患者双侧额内侧回、左侧额下回的额眶部、中枕叶、右侧扣带回和内侧运动前皮质的分数各向异性指数（FA）降低。左扣带回、前额区、左中央前回和左壳核的表观扩散系数（ADC）图增加。左侧额上回、双侧额内侧回、双侧扣带回和右侧丘脑腹后外侧核的 tic 严重程度与 FA 值呈负相关，胼胝体体部、左侧丘脑、右侧颞上回和左侧海马旁回的 FA 值与 tic 严重程度呈正相关。左侧扣带回、双侧壳核、双侧额内侧回、左侧中央前回和左侧丘脑腹前核的局部 ADC 值与 tic 严重程度呈正相关。
我们的结果证实了先前的研究，即 tic 是由前额叶区域、丘脑和壳核的改变引起的，而扣带回的变化似乎反映了继发性代偿机制。由于研究设计，可以排除合并症、性别、药物和年龄的影响。
