Northoff Georg
Laboratory for Magnetic Brain Stimulation, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Behav Brain Sci. 2002 Oct;25(5):555-77; discussion 578-604. doi: 10.1017/s0140525x02000109.
Differential diagnosis of motor symptoms, for example, akinesia, may be difficult in clinical neuropsychiatry. Symptoms may be either of neurologic origin, for example, Parkinson's disease, or of psychiatric origin, for example, catatonia, leading to a so-called "conflict of paradigms." Despite their different origins, symptoms may appear more or less clinically similar. Possibility of dissociation between origin and clinical appearance may reflect functional brain organisation in general, and cortical-cortical/subcortical relations in particular. It is therefore hypothesized that similarities and differences between Parkinson's disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations. Catatonia can be characterized by concurrent motor, emotional, and behavioural symptoms. The different symptoms may be accounted for by dysfunction in orbitofrontal-prefrontal/parietal cortical connectivity reflecting "horizontal modulation" of cortico-cortical relation. Furthermore, alteration in "top-down modulation" reflecting "vertical modulation" of caudate and other basal ganglia by GABA-ergic mediated orbitofrontal cortical deficits may account for motor symptoms in catatonia. Parkinson's disease, in contrast, can be characterized by predominant motor symptoms. Motor symptoms may be accounted for by altered "bottom-up modulation" between dopaminergic mediated deficits in striatum and premotor/motor cortex. Clinical similarities between Parkinson's disease and catatonia with respect to akinesia may be related with involvement of the basal ganglia in both disorders. Clinical differences with respect to emotional and behavioural symptoms may be related with involvement of different cortical areas, that is, orbitofrontal/parietal and premotor/motor cortex implying distinct kinds of modulation--"vertical" and "horizontal" modulation, respectively.
例如，在临床神经精神病学中，运动症状（如运动不能）的鉴别诊断可能很困难。症状可能源于神经学原因，如帕金森病，也可能源于精神疾病，如紧张症，这就导致了所谓的“范式冲突”。尽管它们的起源不同，但症状在临床上可能或多或少相似。病因与临床表现之间可能存在分离，这可能反映了大脑的整体功能组织，特别是皮质 - 皮质/皮质下关系。因此，有人推测帕金森病和紧张症之间的异同可能是由皮质 - 皮质和皮质 - 皮质下关系的不同调节方式所导致的。紧张症的特征可能是同时出现运动、情感和行为症状。不同的症状可能是由于眶额 - 前额叶/顶叶皮质连接功能障碍所致，这反映了皮质 - 皮质关系的“水平调节”。此外，由GABA能介导的眶额皮质缺陷对尾状核和其他基底神经节的“自上而下调节”改变，可能是紧张症运动症状的原因。相比之下，帕金森病的特征可能是主要表现为运动症状。运动症状可能是由于纹状体中多巴胺能介导的缺陷与运动前区/运动皮质之间的“自下而上调节”改变所致。帕金森病和紧张症在运动不能方面的临床相似性可能与两种疾病中基底神经节的受累有关。在情感和行为症状方面的临床差异可能与不同皮质区域的受累有关，即眶额/顶叶和运动前区/运动皮质，这意味着分别有不同类型的调节——“垂直”和“水平”调节。
