Psychiatry Neuroimaging Branch, Department of Psychiatry and Psychotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Psychiatry Neuroimaging Laboratory, Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Psychiatry Neuroimaging Branch, Department of Psychiatry and Psychotherapy, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Int J Psychophysiol. 2019 Nov;145:83-90. doi: 10.1016/j.ijpsycho.2019.02.002. Epub 2019 Feb 7.
Auditory verbal hallucinations (AVH) are hallmark symptoms of schizophrenia and have been linked to abnormal activation, connectivity and integration within the auditory, language, and memory brain networks. The interhemispheric miscommunication theory of AVH is based on a steadily growing number of studies using a variety of modalities (EEG, fMRI, DTI) reporting that both altered integrity of the interhemispheric auditory pathways and disturbed functional gamma-band synchrony between right and left auditory cortices significantly contribute to abnormal auditory processing and the emergence of AVH. Moreover, initial studies using pharmacological EEG and H MR spectroscopy provided first insights into the underlying neurochemistry of AVH. It has been suggested that the observed interhemispheric gamma-band alterations might be mediated by an excitatory-to-inhibitory (E/I) imbalance due to dysfunction of N-methyl-d-aspartate receptor (NMDAR). In support, a potential NMDAR hypofunction is proposed to be compensated by increased levels of glutamate in prefrontal and auditory brain areas. In this mini-review paper, we used the levels of explanation approach and present how interhemispheric brain connectivity (brain-imaging level) corresponds to auditory perception (cognitive level), and eventually how these parameters are related to changes in neurotransmission (cellular level) and to the occurrence of AVH (clinical level). To the best of our knowledge, this is the first overview that overcomes traditional boundaries and presents converging evidence from different levels of knowledge that validate and support each other, and particularly point toward the role of an interhemispheric miscommunication in AVH.
听觉言语幻觉 (AVH) 是精神分裂症的标志性症状，与听觉、语言和记忆大脑网络内的异常激活、连接和整合有关。AVH 的大脑两半球间通讯错误理论基于越来越多的研究，这些研究使用各种模态（EEG、fMRI、DTI）报告称，大脑两半球间听觉通路的完整性改变以及左右听觉皮质之间功能γ 波段同步的紊乱，均显著导致听觉处理异常和 AVH 的出现。此外，使用药理学 EEG 和 H 磁共振波谱的初步研究首次深入了解了 AVH 的潜在神经化学。有人提出，观察到的大脑两半球间 γ 波段改变可能是由于 N-甲基-D-天冬氨酸受体 (NMDAR) 功能障碍导致的兴奋性-抑制性 (E/I) 失衡介导的。有研究支持认为，由于前额叶和听觉脑区谷氨酸水平升高，潜在的 NMDAR 功能低下可能得到补偿。在这篇小型综述论文中，我们使用解释水平方法，展示了大脑两半球间连通性（脑成像水平）如何对应于听觉感知（认知水平），最终这些参数如何与神经递质传递的变化（细胞水平）以及 AVH 的发生（临床水平）相关。据我们所知，这是第一篇克服传统界限的综述，呈现了来自不同知识水平的收敛性证据，相互验证和支持，特别是指出了大脑两半球间通讯错误在 AVH 中的作用。
