在强迫症患者经过经直流刺激后,局部有效连接性发生变化
Hanyang Ruan1, Daniela Rodriguez Manrique2, Chelsea Winkelmann1
1School of Medicine and Health, Department of Diagnostic and Interventional Neuroradiology, Technical University of Munich, Munich, Germany; School of Medicine and Health, TUM-NIC Neuroimaging Center, Technical University of Munich, Munich, Germany.
Journal of affective disorders
|January 13, 2025
概括
跨直流刺激 (tDCS) 增强了痴迷强迫症 (OCD) 患者在感觉运动网络 (SMN) 中的局部大脑网络连接. 这表明tDCS可能有助于使强迫症患者的脑活动正常化.
科学领域:
- 神经科学是一个神经科学.
- 精神病学是一个精神病学.
- 医疗成像医学成像
背景情况:
- 强迫症 (OCD) 是通过改变大脑网络连接的特征.
- 感觉运动网络 (SMN) 在强迫症病理生理学中发挥作用.
- 像tDCS这样的非侵入性脑刺激技术正在探索强迫症的治疗潜力.
研究的目的:
- 研究跨直流刺激 (tDCS) 对强迫症患者大脑网络连接的影响.
- 确定针对右前补充运动区域 (前SMA) 的tDCS是否可以调节大脑内的有效连接.
主要方法:
- 一项随机,双盲,假控制的研究,涉及43名强迫症患者.
- 阳极tDCS应用于右侧前SMA,在左侧前SMA (2 mA) 进行阴极参考.
- 休息状态功能性MRI (fMRI) 和回归动态因果建模 (rDCM) 分析了有效连接 (EC) 和图形理论指标.
主要成果:
- 与假的相比,单个会话的tDCS显著改变了SMN内的本地有效连接.
- 积极的tDCS导致了SMN中增加的招聘水平,集群系数和本地效率.
- 在全球网络连接方面没有观察到任何重大变化.
结论:
- 一个单一的tDCS会话可以有效地调节强迫症患者在SMN内的本地有效连接.
- 针对SMN的tDCS可能提供一种潜在的干预措施,用于正常化强迫症中改变的大脑网络连接.
- 需要进一步的研究来确定tDCS在强迫症的长期影响.
相关概念视频
Long-term Potentiation
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Long-term Potentiation
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when presynaptic neurons...
Hebbian LTP
LTP can occur when presynaptic neurons...
Ligand-gated Ion Channels
Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Spinal Cord Injury ll: Pathophysiology
Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
Secondary Spinal Cord Injury llI: Pathophysiology
Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...


