Department of Neuropsychiatry, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui 910-1193, Japan.
Department of Neuropsychiatry, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui 910-1193, Japan; Psychiatric Medical Center, Fukui Prefectural Hospital, 2-8-1 Yotsui, Fukui-City, Fukui 910-8526, Japan.
Med Hypotheses. 2019 Mar;124:37-39. doi: 10.1016/j.mehy.2019.02.001. Epub 2019 Feb 2.
We previously hypothesized that depressive and manic states may be consecutive presentations of the same underlying neuronal plasticity, and that moderate impairments in neuronal plasticity cause depressive states while further impairment to neuronal plasticity causes manic states. Psychopathological or biological relationships between bipolar disorder and schizophrenia have also been revealed. Therefore, in addition to depressive and manic states, psychosis may also be considered a manifestation resulting from additional impairments to neuronal plasticity. In the present manuscript, we hypothesize that moderate and more severe impairments to neuronal plasticity cause depressive and manic states, respectively, and that more serious impairments to neuronal plasticity cause psychosis. Many studies have suggested that impairments in neuronal plasticity contribute to schizophrenia and other mental disorders with psychotic features, and that the impairment of neuronal plasticity in schizophrenia is more severe than that in bipolar disorder. Therefore, we hypothesize more specifically that impairments in neuronal plasticity may be more severe in the order of the cases featuring psychosis, mania, and depression. This progression notably overlaps with the arrangement of schizophrenia, bipolar disorder, and depressive disorder in the DSM-5. Psychotic symptoms are thought to appear further towards the base of the psychopathological hierarchy than are manic or depressive symptoms. If impairments to neuronal plasticity contribute to this psychopathological hierarchy, as we contest that they do, our hypothesis may serve as a bridge between clinical psychopathology, diagnosis, and biological psychiatry.
我们之前假设抑郁和躁狂状态可能是同一潜在神经元可塑性的连续表现，而神经元可塑性的适度损伤导致抑郁状态，而进一步的神经元可塑性损伤导致躁狂状态。双相情感障碍和精神分裂症之间的精神病理学或生物学关系也已经揭示出来。因此，除了抑郁和躁狂状态外，精神病也可能被认为是神经元可塑性进一步损伤的结果。在本手稿中，我们假设神经元可塑性的适度和更严重损伤分别导致抑郁和躁狂状态，而神经元可塑性的更严重损伤导致精神病。许多研究表明，神经元可塑性的损伤导致精神分裂症和其他具有精神病特征的精神障碍，并且精神分裂症中的神经元可塑性损伤比双相情感障碍中的更严重。因此，我们更具体地假设神经元可塑性的损伤可能按照精神病、躁狂和抑郁的病例特征依次变得更严重。这种进展与 DSM-5 中精神分裂症、双相情感障碍和抑郁症的排列明显重叠。精神病症状被认为比躁狂或抑郁症状更接近精神病理学层次的基础。如果神经元可塑性的损伤有助于这种精神病理学层次，正如我们所争论的那样，我们的假设可能成为临床精神病理学、诊断和生物精神病学之间的桥梁。
