• 제목/요약/키워드: dementia with Lewy bodies

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치매 환자에서 나타나는 비정상적인 안구운동 (Abnormal Eye Movements in Patients with Dementia)

  • 김현;이강준
    • 정신신체의학
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    • 제15권2호
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    • pp.73-80
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    • 2007
  • 지난 여러 해 동안 치매에서 나타나는 안구운동기능부전에 대해 수많은 논문이 발표되었다. 안구운동검사는 뇌의 기능을 평가하는 비침습적인 검사이며, 치매와 연관된 뇌의 이상을 밝혀내는데 유용한 방법이다. 저자는 치매와 연관된 안구운동이상에 대한 지금까지의 여러 연구들을 고찰해 보았다. 알쯔하이머병에서는 신속안구운동의 잠재기가 증가하고 정확도가 감소하며 항신속안구운동의 오류가 증가 한다. 전측두엽 치매 환자에서는 반사성 신속안구운동 억제의 장애와 항신속안구운동 잠재기와 오류 증가 소견이 나타난다. 그리고 헌팅톤병에서는 수의적인 신속안구운동의 시작 지연, 느린 신속안구운동, 항신속안구운동의 오류와 잠재기 증가 소견이 나타난다. 파킨슨병 치매와 루이체 치매 환자에서는 반사성 신속안구운동과 복합성 신속안구운동 실행 장애가 보고되었다. 크로이츠펠트-야콥 병에 관한 연구는 많지 않으며, 안구운동장애는 치매 증상이 명확해진 이후인 질병의 말기에 나타나고, 이차적으로 소뇌와 전정기관을 침범하게 된다고 한다. 진행성 핵상마비에서는 느린 신속안구운동과 측정저하 신속안구운동이 수직방향주시 장애가 오기 이전에 나타나는 경우가 많다. 수의적인 눈꺼풀 운동의 기능부전도 진행성 핵상마비의 특징적인 증상이다. 결론적으로 치매 환자들은 다양한 비정상적인 안구운동장애를 나타내며 이는 피질, 피질하 기능부전과 연관되어 있다. 치매 환자의 안구운동장애에 대한 다음 단계 연구는 치매에서 나타나는 임상적인 증상이 뇌의 어떤 부위 이상 때문에 발생하는지를 좀 더 명확하게 밝히는 것이 될 것이다.

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Neuroanatomical Localization of Rapid Eye Movement Sleep Behavior Disorder in Human Brain Using Lesion Network Mapping

  • Taoyang Yuan;Zhentao Zuo;Jianguo Xu
    • Korean Journal of Radiology
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    • 제24권3호
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    • pp.247-258
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    • 2023
  • Objective: To localize the neuroanatomical substrate of rapid eye movement sleep behavior disorder (RBD) and to investigate the neuroanatomical locational relationship between RBD and α-synucleinopathy neurodegenerative diseases. Materials and Methods: Using a systematic PubMed search, we identified 19 patients with lesions in different brain regions that caused RBD. First, lesion network mapping was applied to confirm whether the lesion locations causing RBD corresponded to a common brain network. Second, the literature-based RBD lesion network map was validated using neuroimaging findings and locations of brain pathologies at post-mortem in patients with idiopathic RBD (iRBD) who were identified by independent systematic literature search using PubMed. Finally, we assessed the locational relationship between the sites of pathological alterations at the preclinical stage in α-synucleinopathy neurodegenerative diseases and the brain network for RBD. Results: The lesion network mapping showed lesions causing RBD to be localized to a common brain network defined by connectivity to the pons (including the locus coeruleus, dorsal raphe nucleus, central superior nucleus, and ventrolateral periaqueductal gray), regardless of the lesion location. The positive regions in the pons were replicated by the neuroimaging findings in an independent group of patients with iRBD and it coincided with the reported pathological alterations at post-mortem in patients with iRBD. Furthermore, all brain pathological sites at preclinical stages (Braak stages 1-2) in Parkinson's disease (PD) and at brainstem Lewy body disease in dementia with Lewy bodies (DLB) were involved in the brain network identified for RBD. Conclusion: The brain network defined by connectivity to positive pons regions might be the regulatory network loop inducing RBD in humans. In addition, our results suggested that the underlying cause of high phenoconversion rate from iRBD to neurodegenerative α-synucleinopathy might be pathological changes in the preclinical stage of α-synucleinopathy located at the regulatory network loop of RBD.

The Usefulness of 18F-FDG PET to Differentiate Subtypes of Dementia: The Systematic Review and Meta-Analysis

  • Seunghee Na;Dong Woo Kang;Geon Ha Kim;Ko Woon Kim;Yeshin Kim;Hee-Jin Kim;Kee Hyung Park;Young Ho Park;Gihwan Byeon;Jeewon Suh;Joon Hyun Shin;YongSoo Shim;YoungSoon Yang;Yoo Hyun Um;Seong-il Oh;Sheng-Min Wang;Bora Yoon;Hai-Jeon Yoon;Sun Min Lee;Juyoun Lee;Jin San Lee;Hak Young Rhee;Jae-Sung Lim;Young Hee Jung;Juhee Chin;Yun Jeong Hong;Hyemin Jang;Hongyoon Choi;Miyoung Choi;Jae-Won Jang;Korean Dementia Association
    • 대한치매학회지
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    • 제23권1호
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    • pp.54-66
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    • 2024
  • Background and Purpose: Dementia subtypes, including Alzheimer's dementia (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD), pose diagnostic challenges. This review examines the effectiveness of 18F-Fluorodeoxyglucose Positron Emission Tomography (18F-FDG PET) in differentiating these subtypes for precise treatment and management. Methods: A systematic review following Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines was conducted using databases like PubMed and Embase to identify studies on the diagnostic utility of 18F-FDG PET in dementia. The search included studies up to November 16, 2022, focusing on peer-reviewed journals and applying the goldstandard clinical diagnosis for dementia subtypes. Results: From 12,815 articles, 14 were selected for final analysis. For AD versus FTD, the sensitivity was 0.96 (95% confidence interval [CI], 0.88-0.98) and specificity was 0.84 (95% CI, 0.70-0.92). In the case of AD versus DLB, 18F-FDG PET showed a sensitivity of 0.93 (95% CI 0.88-0.98) and specificity of 0.92 (95% CI, 0.70-0.92). Lastly, when differentiating AD from non-AD dementias, the sensitivity was 0.86 (95% CI, 0.80-0.91) and the specificity was 0.88 (95% CI, 0.80-0.91). The studies mostly used case-control designs with visual and quantitative assessments. Conclusions: 18F-FDG PET exhibits high sensitivity and specificity in differentiating dementia subtypes, particularly AD, FTD, and DLB. This method, while not a standalone diagnostic tool, significantly enhances diagnostic accuracy in uncertain cases, complementing clinical assessments and structural imaging.

I-123 MIBG Cardiac SPECT의 임상적 적응증 (Clinical Application of I-123 MIBG Cardiac Imaging)

  • 강도영
    • 대한핵의학회지
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    • 제38권5호
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    • pp.331-337
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    • 2004
  • Cardiac neurotransmission imaging allows in vivo assessment of presynaptic reuptake, neurotransmitter storage and postsynaptic receptors. Among the various neurotransmitter, I-123 MIBG is most available and relatively well-established. Metaiodobenzylguanidine (MIBG) is an analogue of the false neurotransmitter guanethidine. It is taken up to adrenergic neurons by uptake-1 mechanism as same as norepinephrine. As tagged with I-123, it can be used to image sympathetic function in various organs including heart with planar or SPECT techniques. I-123 MIBG imaging has a unique advantage to evaluate myocardial neuronal activity in which the heart has no significant structural abnormality or even no functional derangement measured with other conventional examination. In patients with cardiomyopathy and heart failure, this imaging has most sensitive technique to predict prognosis and treatment response of betablocker or ACE inhibitor. In diabetic patients, it allow very early detection of autonomic neuropathy. In patients with dangerous arrhythmia such as ventricular tachycardia or fibrillation, MIBG imaging may be only an abnormal result among various exams. In patients with ischemic heart disease, sympathetic derangement may be used as the method of risk stratification. In heart transplanted patients, sympathetic reinnervation is well evaluated. Adriamycin-induced cardiotoxicity is detected earlier than ventricular dysfunction with sympathetic dysfunction. Neurodegenerative disorder such as Parkinson's disease or dementia with Lewy bodies has also cardiac sympathetic dysfunction. Noninvasive assessment of cardiac sympathetic nerve activity with I-123 MIBG imaging nay be improve understanding of the pathophysiology of cardiac disease and make a contribution to predict survival and therapy efficacy.