Németh G, Hegedüs K, Molnár L
Department of Neurology and Psychiatry, University Medical School, Debrecen, Hungary.
Eur Arch Psychiatry Neurol Sci. 1988;237(4):218-22. doi: 10.1007/BF00449910.
The clinical symptoms and neuropathological findings of three patients suffering from akinetic mutism were summarized. The patients showed almost absolute mutism and immobility and were unable to communicate in any way. The neurological signs varied from case to case. The pathological features common to all of the cases were bilateral lesions of the rostral part of the anterior cingulate gyri which overlapped onto the neighboring supplementary motor area, while differing as regards other damage. With the help of more recent neurobiochemical findings we tried to analyze the pathomechanism of akinetic mutism on the basis of the structures damaged. There seems to be an anatomic correspondence between the mesolimbocortical dopaminergic system and the circumscribed bilateral lesions of the medial prefrontal cortex. The study suggests that damage of the mesolimbocortical dopaminergic terminal fields in the anteromedial frontal cortex is essential for this specific type of akinetic mutism.
总结了3例运动不能性缄默症患者的临床症状和神经病理学发现。这些患者表现出几乎完全缄默和不动,无法以任何方式进行交流。神经体征因病例而异。所有病例共有的病理特征是双侧前扣带回前部病变,该病变延伸至邻近的辅助运动区,而其他损伤情况则有所不同。借助最近的神经生化研究结果,我们试图根据受损结构分析运动不能性缄默症的发病机制。中脑边缘皮质多巴胺能系统与内侧前额叶皮质局限性双侧病变之间似乎存在解剖学对应关系。该研究表明,前额叶内侧皮质中脑边缘皮质多巴胺能终末场的损伤对于这种特定类型的运动不能性缄默症至关重要。