著者
上田 明広 小松 研一 髙橋 牧郎
出版者
日本神経学会
雑誌
臨床神経学 (ISSN:0009918X)
巻号頁・発行日
vol.63, no.2, pp.85-91, 2023 (Released:2023-02-25)
参考文献数
35

症例1は80歳女性.アルツハイマー病でドネペジル塩酸塩(donepezil hydrochloride,以下DNPと略記)を増量した2ヶ月後に首下がり症状が出現した.頸部伸筋のミオパチーを思わせる軽度の筋力低下やMRIでのT2高信号,針筋電図での筋原性変化を認めたが,DNP中止2ヶ月後に姿勢異常は消失した.症例2は78歳男性.レビー小体型認知症でレボドパ,プラミペキソール(pramipexole,以下PPXと略記)を服用していた.レボドパ減量4週後にDNPを開始,10日後に右前方への体幹屈曲が生じた.DNP・PPXの中止とレボドパ増量を行い5ヶ月後に姿勢異常はほぼ消失した.コリンエステラーゼ阻害薬の稀な副作用として体幹の姿勢異常が報告されており,注意が必要である.
著者
髙橋 牧郎
出版者
日本神経治療学会
雑誌
神経治療学 (ISSN:09168443)
巻号頁・発行日
vol.36, no.4, pp.404-409, 2019 (Released:2020-04-24)
参考文献数
13

Parkinson's disease (PD) exhibits motor symptoms such as resting tremor, bradykinesia, and rigidity for which levodopa is successful, but often needs to be differentiated from other PD–related disorders resistant to levodopa. In PD, non–motor symptoms including autonomic symptoms such as constipation, hyperhidrosis, orthostatic hypotension, REM sleep behavior disorder (RBD), psychological symptoms such as depression and apathy, and olfactory dysfunction are merged at a high rate. Since non–motor symptoms develop before the onset of motor symptoms in PD, most of the PD cases are judged from the initial symptoms, however, atypical cases often encountered. Although conventional MRI do not show any abnormalities in PD, disappearance of nigrosome 1 can be confirmed by high magnetic field MRI susceptibility weighted images. Further, dopamine transporter scintigraphy (DaT–SPECT) is a sensitive for parkinsonism and iodine–123–metaiodobenzylguanidine (123I–MIBG) has higher specificity of PD diagnosis myocardial scintigraphy. However, the advanced stage of PD involves dementia with overlapping Aβ and tau pathology, leading to the mixed pathology of PDD/DLB which are clinically problematic. Differentiation from DLB, AD, PSP, CBD is also enabled by brain SPECT. Progress of these diagnostic tools is improving the correct diagnosis of PD, but quite a few familial PD and atypical cases exist. In this lecture, the tips as the clinical and pathological discrimination points of PD and other parkinsonian syndromes are outlined with specific cases. Further, not only various pathological background but also trauma and inflammation of the brain are required to consider the modifying factor for the diagnosis and treatment of PD.
著者
髙橋 牧郎
出版者
日本神経治療学会
雑誌
神経治療学 (ISSN:09168443)
巻号頁・発行日
vol.34, no.3, pp.182-187, 2017 (Released:2017-10-14)
参考文献数
18

As the clarification of the nature of Parkinson's disease progresses, many drugs have been developed, and clinicians have been asked to make judgments as to their proper use. Until now, various dopaminergic drugs have been developed against the motor symptoms such as tremor, rigidity, akinesia and postural reflex disturbance as the main therapeutic targets. Recently, due to aging and prolonged disease duration of Parkinson's disease patients, it has become problematic and can not be ignored as a treatment target that includes autonomic symptoms such as constipation and orthostatic hypotension, REM sleep behavioral disorder (RBD), mental disorders such as depression, apathy, delusion/hallucination, performance impairment and cognitive disorders. Moreover, the manifestation of non–motor symptoms such as pain, fatigue, camptocormia, dropped head are focused as the cardinal symptom of Parkinson's complex. Further, these symptoms correlate well with the progression of α–synuclein pathological stage of Parkinson's disease reported by Braak et al. It is awaited to develop disease modifying drugs that suppress not only symptoms but also pathological progress itself. At the same time, it is also required to develop biomarkers that can be accurately used in the preclinical phase from the viewpoint of early detection and early prevention as well as risk factor analysis. In addition, intestinal microbiota dysbiosis and gut–brain axis via the vagus nerve are attracting attention as a new pathogenic mechanism of Parkinson's disease. In this presentation, I will present my personal opinion of various anti–Parkinson's disease treatment based on clinical evidences and its current use, as well as the molecular mechanisms concerning α–synuclein's pathology. Recent trial of immunotherapy targeting α–synuclein proteins and the suppression of the protein aggregation will also be outlined.