Rink Claudia, Görtzen Angelika, Veh Rüdiger W, Prüss Harald
Department of Internal Medicine, St. Josef Hospital, Oberhausen, Germany.
Department of Neurology, St. Josef Hospital, Oberhausen, Germany.
J Neurol Sci. 2017 Jan 15;372:318-323. doi: 10.1016/j.jns.2016.11.078. Epub 2016 Dec 3.
Guillain-Barré syndrome (GBS) is an autoimmune disease with progressive flaccid paralysis of the extremities. Several auto-antibodies have been identified, binding to myelin, gangliosides, astrocytes or proteins at the nodes of Ranvier. Some epitopes are not confined to the peripheral nerve, suggesting that auto-antibodies may also contribute to symptoms of the central nervous system, which are common in GBS and include anxiety, depression, hallucinations, oneiroid psychosis or fatigue. This notion is supported by treating patients with plasma exchange, resulting in improvement of both central and peripheral symptoms. We analyzed binding of GBS sera to neurons of cholinergic, serotonergic, dopaminergic, nor-adrenergic or histaminergic nuclei using immunohistochemistry of the rat brain. We hypothesized that GBS sera harbor antibodies against monoaminergic structures in the brain, as these circuits influence larger neuronal networks with relevance for multiple neuropsychiatric symptoms. Indeed, several GBS sera strongly and specifically reacted with monoaminergic neurons, in particular cholinergic nuclei of the diagonal band, neurons of the basal nucleus of Meynert, nor-adrenergic neurons of the nucleus coeruleus, neurons in the raphe or the ambiguous nucleus. The frequency significantly exceeded those of sera from patients with multiple sclerosis, non-autoimmune neurological disorders and healthy controls. The binding to neuronal surfaces makes it conceivable that the auto-antibodies can interfere with ion channels and receptors and thus contribute to the variable clinical spectrum of neuropsychiatric and autonomic abnormalities in GBS. Future research should include the target identification of promising GBS sera and aim to determine the functional effects of these antibodies.
格林-巴利综合征（GBS）是一种导致四肢进行性弛缓性麻痹的自身免疫性疾病。已鉴定出几种自身抗体，它们可与髓磷脂、神经节苷脂、星形胶质细胞或郎飞结处的蛋白质结合。一些表位并不局限于周围神经，这表明自身抗体也可能导致中枢神经系统症状，这些症状在GBS中很常见，包括焦虑、抑郁、幻觉、梦样精神病或疲劳。血浆置换治疗患者后症状改善，这支持了这一观点。我们使用大鼠脑免疫组织化学分析了GBS血清与胆碱能、血清素能、多巴胺能、去甲肾上腺素能或组胺能核团神经元的结合情况。我们假设GBS血清中含有针对脑中单胺能结构的抗体，因为这些神经回路影响着与多种神经精神症状相关的更大的神经元网络。事实上，几种GBS血清与单胺能神经元发生了强烈而特异性的反应，特别是斜角带的胆碱能核团、迈内特基底核的神经元、蓝斑的去甲肾上腺素能神经元、中缝核或疑核中的神经元。其频率显著超过了多发性硬化症患者、非自身免疫性神经系统疾病患者和健康对照者的血清频率。与神经元表面的结合使得可以想象自身抗体能够干扰离子通道和受体，从而导致GBS中神经精神和自主神经异常的临床谱变化。未来的研究应包括确定有前景的GBS血清的靶标，并旨在确定这些抗体的功能作用。
