Traumatic brain injury can reduce striatal dopamine levels. The cause of this is uncertain, but is likely to be related to damage to the nigrostriatal system. We investigated the pattern of striatal dopamine abnormalities using ¹²³I-Ioflupane single-photon emission computed tomography (SPECT) scans and their relationship to nigrostriatal damage and clinical features. We studied 42 moderate–severe traumatic brain injury patients with cognitive impairments but no motor parkinsonism signs and 20 healthy controls. ¹²³I-Ioflupane scanning was used to assess dopamine transporter levels. Clinical scan reports were compared to quantitative dopamine transporter results. Advanced MRI methods were used to assess the nigrostriatal system, including the area through which the nigrostriatal projections pass as defined from high-resolution Human Connectome data. Detailed clinical and neuropsychological assessments were performed. Around 20% of our moderate–severe patients had clear evidence of reduced specific binding ratios for the dopamine transporter in the striatum measured using ¹²³I-Ioflupane SPECT. The caudate was affected more consistently than other striatal regions. Dopamine transporter abnormalities were associated with reduced substantia nigra volume. In addition, diffusion MRI provided evidence of damage to the regions through which the nigrostriatal tract passes, particularly the area traversed by dopaminergic projections to the caudate. Only a small percentage of patients had evidence of macroscopic lesions in the striatum and there was no relationship between presence of lesions and dopamine transporter specific binding ratio abnormalities. There was also no relationship between reduced volume in the striatal subregions and reduced dopamine transporter specific binding ratios. Patients with low caudate dopamine transporter specific binding ratios show impaired processing speed and executive dysfunction compared to patients with normal levels. Taken together, our results suggest that the dopaminergic system is affected by a moderate–severe traumatic brain injury in a significant proportion of patients, even in the absence of clinical motor parkinsonism. Reduced dopamine transporter levels are most commonly seen in the caudate and this is likely to reflect the pattern of nigrostriatal tract damage produced by axonal injury and associated midbrain damage.

中文翻译：

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创伤性脑损伤后的多巴胺能异常

创伤性脑损伤可降低纹状体多巴胺水平。其原因尚不确定，但可能与黑质纹状体系统受损有关。^{我们使用123} I-Ioflupane 单光子发射计算机断层扫描 (SPECT) 扫描研究了纹状体多巴胺异常的模式及其与黑质纹状体损伤和临床特征的关系。我们研究了 42 名有认知障碍但没有运动帕金森症状的中重度创伤性脑损伤患者和 20 名健康对照者。¹²³I-Ioflupan 扫描用于评估多巴胺转运蛋白水平。将临床扫描报告与定量多巴胺转运蛋白结果进行比较。先进的 MRI 方法用于评估黑质纹状体系统，包括根据高分辨率人类连接组数据定义的黑质纹状体投影通过的区域。进行了详细的临床和神经心理学评估。大约 20% 的中重度患者有明确的证据表明纹状体中多巴胺转运蛋白的特异性结合率降低，使用^123测量I-碘氟烷 SPECT。尾状核的影响比其他纹状体区域更一致。多巴胺转运蛋白异常与黑质体积减少有关。此外，弥散 MRI 提供了对黑质纹状体束通过的区域的损害的证据，特别是多巴胺能投射到尾状核的区域。只有一小部分患者有纹状体肉眼可见病变的证据，并且病变的存在与多巴胺转运蛋白特异性结合率异常之间没有关系。纹状体亚区域体积减少与多巴胺转运蛋白特异性结合率降低之间也没有关系。与正常水平的患者相比，尾状多巴胺转运蛋白特异性结合率低的患者显示处理速度受损和执行功能障碍。总之，我们的研究结果表明，即使在没有临床运动性帕金森病的情况下，大部分患者的多巴胺能系统也会受到中度至重度创伤性脑损伤的影响。多巴胺转运蛋白水平降低最常见于尾状核，这可能反映了由轴突损伤和相关中脑损伤产生的黑质纹状体束损伤模式。