Milovanovic Maja, Grujicic Roberto
Department for Epilepsy and Clinical Neurophysiology, Institute of Mental Health, Belgrade, Serbia.
Faculty for Special Education and Rehabilitation, University of Belgrade, Belgrade, Serbia.
Front Psychiatry. 2021 Sep 29;12:686021. doi: 10.3389/fpsyt.2021.686021. eCollection 2021.
Electroencephalography (EEG) can further out our understanding of autistic spectrum disorders (ASD) neurophysiology. Epilepsy and ASD comorbidity range between 5 and 46%, but its temporal relationship, causal mechanisms and interplay with intellectual disability are still unknown. Epileptiform discharges with or without seizures go as high as 60%, and associate with epileptic encephalopathies, conceptual term suggesting that epileptic activity can lead to cognitive and behavioral impairment beyond the underlying pathology. Seizures and ASD may be the result of similar mechanisms, such as abnormalities in GABAergic fibers or GABA receptor function. Epilepsy and ASD are caused by a number of genetic disorders and variations that induce such dysregulation. Similarly, initial epilepsy may influence synaptic plasticity and cortical connection, predisposing a growing brain to cognitive delays and behavioral abnormalities. The quantitative EEG techniques could be a useful tool in detecting and possibly measuring dysfunctions in specific brain regions and neuronal regulation in ASD. Power spectra analysis reveals a U-shaped pattern of power abnormalities, with excess power in the low and high frequency bands. These might be the consequence of a complicated network of neurochemical changes affecting the inhibitory GABAergic interneurons and their regulation of excitatory activity in pyramidal cells. EEG coherence studies of functional connectivity found general local over-connectivity and long-range under-connectivity between different brain areas. GABAergic interneuron growth and connections are presumably impaired in the prefrontal and temporal cortices in ASD, which is important for excitatory/inhibitory balance. Recent advances in quantitative EEG data analysis and well-known epilepsy ASD co-morbidity consistently indicate a role of aberrant GABAergic transmission that has consequences on neuronal organization and connectivity especially in the frontal cortex.
脑电图（EEG）能够进一步拓展我们对自闭症谱系障碍（ASD）神经生理学的理解。癫痫与ASD的共病率在5%至46%之间，但其时间关系、因果机制以及与智力残疾的相互作用仍不明确。伴有或不伴有癫痫发作的癫痫样放电高达60%，并与癫痫性脑病相关，这一概念术语表明癫痫活动可导致超出潜在病理的认知和行为损害。癫痫发作和ASD可能是由类似机制引起的，例如γ-氨基丁酸（GABA）能纤维或GABA受体功能异常。癫痫和ASD是由多种导致这种失调的遗传疾病和变异引起的。同样，初期癫痫可能会影响突触可塑性和皮质连接，使发育中的大脑易出现认知延迟和行为异常。定量脑电图技术可能是检测并有可能测量ASD中特定脑区功能障碍和神经元调节的有用工具。功率谱分析揭示了功率异常的U形模式，低频和高频带功率过高。这些可能是影响抑制性GABA能中间神经元及其对锥体细胞兴奋性活动调节的复杂神经化学变化网络的结果。功能连接性的脑电图相干性研究发现不同脑区之间普遍存在局部过度连接和长程连接不足。ASD患者前额叶和颞叶皮质中GABA能中间神经元的生长和连接可能受损，这对兴奋性/抑制性平衡很重要。定量脑电图数据分析的最新进展以及癫痫与ASD的众所周知的共病情况一致表明，异常的GABA能传递起了作用，这对神经元组织和连接性有影响，尤其是在额叶皮质。
