From the Department of Psychiatry, Cumming School of Medicine, University of Calgary, Calgary, Alta. (Kahl, Swansburg, MacMaster); the Department of Pediatrics, Cumming School of Medicine, University of Calgary, Calgary, Alta. (Kahl, Swansburg, Lemay, Kirton, MacMaster); the Hotchkiss Brain Institute, University of Calgary, Calgary, Alta. (Kahl, Wrightson, Bell, Kirton, MacMaster); the Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Alta. (Kahl, Bell, Kirton, MacMaster); the Department of Educational Psychology, University of Alberta, Edmonton, Alta. (Hai); the Department of Radiology, Cumming School of Medicine, University of Calgary, Calgary, Alta. (Bell); the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, Alta. (Kirton); and the Strategic Clinical Network for Addictions and Mental Health, Calgary, Alta. (MacMaster).
From the Department of Psychiatry, Cumming School of Medicine, University of Calgary, Calgary, Alta. (Kahl, Swansburg, MacMaster); the Department of Pediatrics, Cumming School of Medicine, University of Calgary, Calgary, Alta. (Kahl, Swansburg, Lemay, Kirton, MacMaster); the Hotchkiss Brain Institute, University of Calgary, Calgary, Alta. (Kahl, Wrightson, Bell, Kirton, MacMaster); the Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Alta. (Kahl, Bell, Kirton, MacMaster); the Department of Educational Psychology, University of Alberta, Edmonton, Alta. (Hai); the Department of Radiology, Cumming School of Medicine, University of Calgary, Calgary, Alta. (Bell); the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, Alta. (Kirton); and the Strategic Clinical Network for Addictions and Mental Health, Calgary, Alta. (MacMaster)
J Psychiatry Neurosci. 2022 Jul 6;47(4):E239-E249. doi: 10.1503/jpn.210186. Print 2022 Jul-Aug.
Although much is known about cognitive dysfunction in attention-deficit/hyperactivity disorder (ADHD), few studies have examined the pathophysiology of disordered motor circuitry. We explored differences in neurometabolite levels and transcranial magnetic stimulation (TMS)-derived corticomotor representations among children with ADHD and typically developing children.
We used magnetic resonance spectroscopy (MRS) protocols to measure excitatory (glutamate + glutamine [Glx]) and inhibitory (γ-aminobutyric acid [GABA]) neurometabolite levels in the dominant primary motor cortex (M1) and the supplementary motor area (SMA) in children with ADHD and typically developing children. We used robotic neuronavigated TMS to measure corticospinal excitability and create corticomotor maps.
We collected data from 26 medication-free children with ADHD (aged 7-16 years) and 25 typically developing children (11-16 years). Children with ADHD had lower M1 Glx ( = 0.044, = 0.6); their mean resting motor threshold was lower ( = 0.029, = 0.8); their map area was smaller ( = 0.044, = 0.7); and their hotspot density was higher ( = 0.008, = 0.9). M1 GABA levels were associated with motor map area ( = 0.036). Some TMS data were lost because the threshold of some children exceeded 100% of the machine output. The relatively large MRS voxel required to obtain sufficient signal-to-noise ratio and reliably measure GABA levels encompassed tissue beyond the M1, making this measure less anatomically specific.
The neurochemistry and neurophysiology of key nodes in the motor network may be altered in children with ADHD, and the differences appear to be related to each other. These findings suggest potentially novel neuropharmacological and neuromodulatory targets for ADHD.
尽管人们对注意力缺陷多动障碍(ADHD)患者的认知功能障碍有了很多了解,但很少有研究探讨紊乱运动回路的病理生理学。我们探讨了 ADHD 患儿与正常发育儿童之间神经代谢物水平和经颅磁刺激(TMS)衍生皮质运动代表之间的差异。
我们使用磁共振波谱(MRS)方案测量 ADHD 患儿和正常发育儿童的优势初级运动皮层(M1)和辅助运动区(SMA)中的兴奋性(谷氨酸+谷氨酰胺[Glx])和抑制性(γ-氨基丁酸[GABA])神经代谢物水平。我们使用机器人神经导航 TMS 来测量皮质脊髓兴奋性并创建皮质运动图。
我们从 26 名未服用药物的 ADHD 儿童(年龄 7-16 岁)和 25 名正常发育儿童(11-16 岁)中收集了数据。ADHD 患儿的 M1 Glx 水平较低( = 0.044, = 0.6);其静息运动阈值较低( = 0.029, = 0.8);其映射区域较小( = 0.044, = 0.7);热点密度较高( = 0.008, = 0.9)。M1 GABA 水平与运动图面积相关( = 0.036)。由于一些儿童的阈值超过了机器输出的 100%,因此丢失了一些 TMS 数据。为了获得足够的信噪比并可靠地测量 GABA 水平,所需的相对较大的 MRS 体素包含了超出 M1 的组织,使得该测量不太具有解剖学特异性。
ADHD 患儿运动网络关键节点的神经化学和神经生理学可能发生改变,这些差异似乎相互关联。这些发现表明 ADHD 可能存在潜在的新型神经药理学和神经调节靶点。