Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Center for Psychosocial Medicine, Department of General Psychiatry, Heidelberg University, Heidelberg, Germany.
Schizophr Bull. 2020 Feb 26;46(2):272-285. doi: 10.1093/schbul/sbz074.
In 1874, Karl Kahlbaum described catatonia as an independent syndrome characterized by motor, affective, and behavioral anomalies. In the following years, various catatonia concepts were established with all sharing the prime focus on motor and behavioral symptoms while largely neglecting affective changes. In 21st century, catatonia is a well-characterized clinical syndrome. Yet, its neurobiological origin is still not clear because methodological shortcomings of hitherto studies had hampered this challenging effort. To fully capture the clinical picture of catatonia as emphasized by Karl Kahlbaum, 2 decades ago a new catatonia scale was developed (Northoff Catatonia Rating Scale [NCRS]). Since then, studies have used NCRS to allow for a more mechanistic insight of catatonia. Here, we undertook a systematic review searching for neuroimaging studies using motor/behavioral catatonia rating scales/criteria and NCRS published up to March 31, 2019. We included 19 neuroimaging studies. Studies using motor/behavioral catatonia rating scales/criteria depict cortical and subcortical motor regions mediated by dopamine as neuronal and biochemical substrates of catatonia. In contrast, studies relying on NCRS found rather aberrant higher-order frontoparietal networks which, biochemically, are insufficiently modulated by gamma-aminobutyric acid (GABA)-ergic and glutamatergic transmission. This is further supported by the high therapeutic efficacy of GABAergic agents in acute catatonia. In sum, this systematic review points out the difference between motor/behavioral and NCRS-based classification of catatonia on both neuronal and biochemical grounds. That highlights the importance of Kahlbaum's original truly psychomotor concept of catatonia for guiding both research and clinical diagnosis and therapy.
1874 年，卡尔·卡哈尔鲍姆（Karl Kahlbaum）将紧张症描述为一种以运动、情感和行为异常为特征的独立综合征。在随后的几年中，建立了各种紧张症概念，所有这些概念都主要集中在运动和行为症状上，而在很大程度上忽略了情感变化。在 21 世纪，紧张症是一种特征明确的临床综合征。然而，其神经生物学起源尚不清楚，因为迄今为止的研究方法上的缺陷阻碍了这一具有挑战性的努力。为了充分捕捉卡尔·卡哈尔鲍姆（Karl Kahlbaum）所强调的紧张症的临床特征，20 年前开发了一种新的紧张症量表（Northoff 紧张症评定量表[NCRS]）。从那时起，研究人员就使用 NCRS 来更深入地了解紧张症的发病机制。在这里，我们进行了一项系统评价，搜索了截至 2019 年 3 月 31 日使用运动/行为紧张症评定量表/标准和 NCRS 的神经影像学研究。我们纳入了 19 项神经影像学研究。使用运动/行为紧张症评定量表/标准的研究描述了由多巴胺介导的皮质和皮质下运动区域，这些区域是紧张症的神经元和生化基础。相比之下，依赖于 NCRS 的研究发现了相当异常的高阶额顶叶网络，从生化角度来看，这些网络的 GABA 能和谷氨酸能传递调节不足。这进一步得到了 GABA 能药物在急性紧张症中高治疗效果的支持。总的来说，这项系统评价指出了基于运动/行为和 NCRS 的紧张症分类在神经和生化方面的差异。这突出了卡哈尔鲍姆（Kahlbaum）原始的真正的精神运动紧张症概念对指导研究和临床诊断和治疗的重要性。
