Department of Cognitive Science, University of California, La Jolla, CA 92093-0515, USA.
Med Hypotheses. 2012 Dec;79(6):790-8. doi: 10.1016/j.mehy.2012.08.031. Epub 2012 Sep 20.
Autism is a highly varied developmental disorder typically characterized by deficits in reciprocal social interaction, difficulties with verbal and nonverbal communication, and restricted interests and repetitive behaviors. Although a wide range of behavioral, pharmacological, and alternative medicine strategies have been reported to ameliorate specific symptoms for some individuals, there is at present no cure for the condition. Nonetheless, among the many incompatible observations about aspects of the development, anatomy, and functionality of the autistic brain, it is widely agreed that it is characterized by widespread aberrant connectivity. Such disordered connectivity, be it increased, decreased, or otherwise compromised, may complicate healthy synchronization and communication among and within different neural circuits, thereby producing abnormal processing of sensory inputs necessary for normal social life. It is widely accepted that the innate properties of brain electrical activity produce pacemaker elements and linked networks that oscillate synchronously or asynchronously, likely reflecting a type of functional connectivity. Using phase coherence in multiple frequency EEG bands as a measure of functional connectivity, studies have shown evidence for both global hypoconnectivity and local hyperconnectivity in individuals with ASD. However, the nature of the brain's experience-dependent structural plasticity suggests that these abnormal patterns may be reversed with the proper type of treatment. Indeed, neurofeedback (NF) training, an intervention based on operant conditioning that results in self-regulation of brain electrical oscillations, has shown promise in addressing marked abnormalities in functional and structural connectivity. It is hypothesized that neurofeedback produces positive behavioral changes in ASD children by normalizing the aberrant connections within and between neural circuits. NF exploits the brain's plasticity to normalize aberrant connectivity patterns apparent in the autistic brain. By grounding this training in known anatomical (e.g., mirror neuron system) and functional markers (e.g., mu rhythms) of autism, NF training holds promise to support current treatments for this complex disorder. The proposed hypothesis specifically states that neurofeedback-induced alpha mu (8-12Hz) rhythm suppression or desynchronization, a marker of cortical activation, should induce neuroplastic changes and lead to normalization in relevant mirroring networks that have been associated with higher-order social cognition.
自闭症是一种高度多样化的发育障碍，通常表现为互惠性社交互动缺陷、言语和非言语沟通困难以及兴趣受限和重复行为。尽管已经报道了广泛的行为、药物和替代医学策略来改善某些个体的特定症状，但目前尚无治愈该疾病的方法。尽管自闭症患者大脑的发育、解剖结构和功能方面存在许多不兼容的观察结果，但人们普遍认为其特征是广泛的异常连接。这种异常的连接，无论是增加、减少还是受损，都可能使不同神经回路之间和内部的正常同步和通信复杂化，从而导致对正常社交生活所需的感觉输入的异常处理。人们普遍认为，大脑电活动的固有特性产生起搏器元件和相连的网络，这些网络同步或异步振荡，可能反映出某种类型的功能连接。使用多频 EEG 波段的相位相干性作为功能连接的度量，研究表明 ASD 个体存在全局连接不足和局部连接过度的证据。然而，大脑依赖经验的结构可塑性的性质表明，这些异常模式可能会随着适当类型的治疗而逆转。事实上，神经反馈（NF）训练是一种基于操作性条件反射的干预措施，可导致大脑电活动的自我调节，已显示出在解决功能和结构连接的明显异常方面具有潜力。假设神经反馈通过使神经回路内部和之间的异常连接正常化，在 ASD 儿童中产生积极的行为变化。NF 利用大脑的可塑性来使自闭症大脑中明显的异常连接模式正常化。通过将这种训练建立在已知的自闭症解剖学（例如镜像神经元系统）和功能标志物（例如 mu 节律）之上，NF 训练有望为这种复杂疾病的当前治疗提供支持。拟议的假设特别指出，神经反馈诱导的 alpha mu（8-12Hz）节律抑制或去同步化，即皮质激活的标志物，应该引起神经可塑性变化，并导致与更高阶社会认知相关的相关镜像网络的正常化。
