白质
胼胝体
磁共振弥散成像
内囊
部分各向异性
神经科学
心理学
医学
前额叶皮质
认知
磁共振成像
放射科
作者
Massieh Moayedi,Irit Weissman-Fogel,Tim V. Salomons,Adrian Crawley,Michael B. Goldberg,Bruce V. Freeman,Howard C. Tenenbaum,Karen D. Davis
出处
期刊:Pain
[Ovid Technologies (Wolters Kluwer)]
日期:2012-07-01
卷期号:153 (7): 1467-1477
被引量:126
标识
DOI:10.1016/j.pain.2012.04.003
摘要
Summary Temporomandibular disorder patients have white matter abnormalities along the trigeminal nerve and pain-related brain pathways, and abnormal connectivity of cognitive-affective brain regions. Temporomandibular disorder (TMD) is a prevalent chronic pain disorder that remains poorly understood. Recent imaging studies reported functional and gray matter abnormalities in brain areas implicated in sensorimotor, modulatory, and cognitive function in TMD, but it is not known whether there are white matter (WM) abnormalities along the trigeminal nerve (CNV) or in the brain. Here, we used diffusion tensor imaging, and found that, compared to healthy controls, TMD patients had 1) lower fractional anisotropy (FA) in both CNVs; 2) a negative correlation between FA of the right CNV and pain duration; and 3) diffuse abnormalities in the microstructure of WM tracts related to sensory, motor, cognitive, and pain functions, with a highly significant focal abnormality in the corpus callosum. Using probabilistic tractography, we found that the corpus callosum in patients had a higher connection probability to the frontal pole, and a lower connection probability to the dorsolateral prefrontal cortex, compared to controls. Finally, we found that 1) FA in tracts adjacent to the ventrolateral prefrontal cortex and tracts coursing through the thalamus negatively correlated with pain intensity; 2) FA in the internal capsule negatively correlated with pain intensity and unpleasantness; and 3) decreases in brain FA were associated with increases in mean diffusivity and radial diffusivity, markers of inflammation and oedema. These data provide novel evidence for CNV microstructural abnormalities that may be caused by increased nociceptive activity, accompanied by abnormalities along central WM pathways in TMD.
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