Maguire Gerald A, Yoo Bo Ram, SheikhBahaei Shahriar
School of Medicine, University of California, Riverside, Riverside, CA, United States.
National Institute of Neurological Disorders and Stroke/National Institutes of Health, Bethesda, MD, United States.
Front Neurosci. 2021 Feb 12;15:598949. doi: 10.3389/fnins.2021.598949. eCollection 2021.
Stuttering is a childhood onset fluency disorder that leads to impairment in speech. A randomized, double-blinded placebo-controlled study was conducted with 10 adult subjects to observe the effects of risperidone (a dopamine receptor 2/serotonin receptor 2 antagonist) on brain metabolism, using [F] deoxyglucose as the marker. At baseline and after 6 weeks of taking risperidone (0.5-2.0 mg/day) or a placebo pill, participants were assigned to a solo reading aloud task for 30 min and subsequently underwent a 90-min positron emission tomography scan. Paired -tests were performed to compare the pre-treatment vs. post-treatment in groups. After imaging and analysis, the blind was broken, which revealed an equal number of subjects of those on risperidone and those on placebo. There were no significant differences in the baseline scans taken before medication randomization. However, scans taken after active treatment demonstrated higher glucose uptake in the specific regions of the brain for those in the risperidone treatment group ( < 0.05). Risperidone treatment was associated with increased metabolism in the left striatum, which consists of the caudate and putamen, and the Broca's area. The current study strengthens previous research that suggests the role of elevated dopamine activity and striatal hypometabolism in stuttering. We propose that the mechanism of risperidone's action in stuttering, in part, involves increased metabolism of striatal astrocytes. We conclude that using neuroimaging techniques to visualize changes in the brain of those who stutter can provide valuable insights into the pathophysiology of the disorder and guide the development of future interventions.
口吃是一种始于童年的流畅性言语障碍，会导致言语功能受损。对10名成年受试者进行了一项随机、双盲、安慰剂对照研究，以[F]脱氧葡萄糖为标记物，观察利培酮（一种多巴胺受体2/5-羟色胺受体2拮抗剂）对脑代谢的影响。在基线期以及服用利培酮（0.5 - 2.0毫克/天）或安慰剂丸6周后，参与者被安排进行30分钟的独自大声朗读任务，随后接受90分钟的正电子发射断层扫描。进行配对检验以比较各组治疗前与治疗后的情况。成像和分析之后，揭盲显示服用利培酮的受试者与服用安慰剂的受试者数量相等。在药物随机分组前进行的基线扫描中没有显著差异。然而，积极治疗后的扫描显示，利培酮治疗组受试者大脑特定区域的葡萄糖摄取更高（<0.05）。利培酮治疗与左侧纹状体（由尾状核和壳核组成）以及布洛卡区的代谢增加有关。当前的研究强化了先前的研究，即表明多巴胺活性升高和纹状体代谢减退在口吃中的作用。我们提出，利培酮对口吃的作用机制部分涉及纹状体星形胶质细胞代谢增加。我们得出结论，使用神经成像技术可视化口吃者大脑的变化，可以为该疾病的病理生理学提供有价值的见解，并指导未来干预措施的开发。
