Department of Neurology, Movement Disorders Center, The Neuroscience Institute, University of Cincinnati, Cincinnati, Ohio, USA.
J Neurol Neurosurg Psychiatry. 2011 Jul;82(7):751-3. doi: 10.1136/jnnp.2009.201608. Epub 2010 Jun 28.
To report the rare but distinct clinical and neuropathological phenotype of non-familial, rapidly progressive parkinsonism and dementia associated with frontotemporal lobar degeneration with motor neuron disease (FTLD-MND).
Subjects included two 70-year-old women presenting with rapidly progressive severe postural instability, axial-predominant parkinsonism, oculomotor dysfunction and frontal-predominant dementia with language impairment and pseudobulbar palsy. One had diffuse weakness without signs of lower motor neuron disease. Post-mortem evaluations included immunohistochemistry with antiphospho-TAR DNA-binding protein 43 (TDP-43) and genetic analysis of the TARDBP and PGRN genes.
Subjects died within 14 months from symptom onset. TDP-43-positive neuronal intracytoplasmic inclusions were prominent in the primary motor cortex, granule cell layer of the hippocampus, and several cranial and spinal cord nuclei. TDP-43 globular glial inclusions (GGI) were identified in one case. There were no mutations in PGRN or TARDBP genes.
FTLD-MND due to TDP-43-proteinopathy should be considered in patients with rapidly progressive parkinsonism and dementia phenotype, especially when aphasia and/or weakness are also present.
报告与额颞叶变性伴运动神经元病(FTLD-MND)相关的非家族性、快速进展性帕金森病和痴呆的罕见但独特的临床和神经病理学表型。
研究对象包括两名 70 岁女性,均表现为快速进展性严重姿势不稳、以轴性为主的帕金森病、眼球运动功能障碍、以额叶为主的痴呆伴语言障碍和假性延髓性麻痹。其中 1 例有弥漫性无力而无运动神经元病的迹象。尸检评估包括抗磷酸化 TAR DNA 结合蛋白 43(TDP-43)的免疫组织化学检查和 TARDBP 和 PGRN 基因的遗传分析。
患者从症状出现到死亡的时间均在 14 个月内。原发性运动皮层、海马颗粒细胞层以及多个颅神经核和脊髓核中存在明显的 TDP-43 阳性神经元胞质内包涵体。在 1 例患者中发现 TDP-43 球样神经胶质包涵体(GGI)。PGRN 或 TARDBP 基因均无突变。
对于以快速进展性帕金森病和痴呆为表现的患者,尤其是同时存在失语症和/或无力的患者,应考虑由 TDP-43 蛋白病引起的 FTLD-MND。