13 research outputs found

    A retrospective study suggests that chronic insomnia behaves as a neurodegenerative disorder

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    © 2020 Neutel D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Insomnia is a prevalent sleep disorder. We examined chronic insomnia in terms of subjective and objective measures, according to self-reported duration of disorder. 443 patients were included from a sleep clinic diagnosed with chronic insomnia (ICSD3 criteria). Patients were retrospectively evaluated in terms of medical interview, sleep questionnaires, a standard polysomnography study, and subdivided in subgroups according to disorder duration. We compared patient’s results to a control group. Insomnia and control groups were significantly different in terms of TST, SE, SOL, N1 sleep, REM sleep, REM latency and number of REM episodes (p<0.05). For the group of ≤1 year of insomnia disorder all PSG parameters were statistically different from controls, except N2% and N3%, REM latency, and number of REM episodes. In the groups of 2 to 4 years, 10 to 19 years, and ≥ 20 years of insomnia we found the same differences except for REM sleep. On the contrary, in a subgroup analysis of 5 to 9 years of insomnia disorder duration, no differences to control group were found in TST, N1 or REM sleep to control group, adjusted for age. The polysomnographic sleep profile of chronic insomnia patients is different over time. It sketches an initial attempt of compensation in initial years of insomnia, which seems to disappear in long time chronic insomnia patients, as we usually see in others neurodegenerative disorders. Future studies are needed to clarify the natural history of chronic insomnia disorder and its behaviour as a neurodegenerative disorder.info:eu-repo/semantics/publishedVersio

    End of OSLER test sessions in Parkinson’s disease do not correspond to true sleep onset: results from an exploratory study

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    Copyright © 2015 Neutel, Peralta, Pires, Bentes and Ferreira. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.The aim of the present study was to evaluate the correlation between the end of an Oxford sleep resistance (OSLER) test session and a neurophysiological marker of sleep onset in Parkinson's disease (PD) patients. Single center study was conducted in PD patients with excessive daytime sleepiness [Epworth sleepiness scale (ESS) >9]. The OSLER test was conducted with a concomitant electroencephalography (EEG), electromyography (mentalis), right and left electroculogram, and video monitoring. Neurophysiological (NP) sleep onset was defined according to AASM criteria (2005). Five PD patients with mean ESS of 14 (10-16) were included. OSLER test duration was shorter than 40 min in all patients (mean duration 20 min and 39 s). No patient fulfilled neurophysiological criteria to sleep onset at the time of OSLER test termination. In 13 OSLER sessions that ended before 40 min, eight had microsleeps in the last 30 s before the end of the test. NP monitoring showed signs of sleepiness in all patients. In PD patients, the early termination of an OSLER test session may not correspond to NP criteria of sleep onset. However, in all PD patients with abnormal OSLER results, there were EEG signs of sleepiness, which do not exclude the potential utility of OSLER test to evaluate the risk of falling asleep.info:eu-repo/semantics/publishedVersio

    End of OSLER test sessions in Parkinson’s disease do not correspond to true sleep onset: results from an exploratory study

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    Copyright © 2015 Neutel, Peralta, Pires, Bentes and Ferreira. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.The aim of the present study was to evaluate the correlation between the end of an Oxford sleep resistance (OSLER) test session and a neurophysiological marker of sleep onset in Parkinson's disease (PD) patients. Single center study was conducted in PD patients with excessive daytime sleepiness [Epworth sleepiness scale (ESS) >9]. The OSLER test was conducted with a concomitant electroencephalography (EEG), electromyography (mentalis), right and left electroculogram, and video monitoring. Neurophysiological (NP) sleep onset was defined according to AASM criteria (2005). Five PD patients with mean ESS of 14 (10-16) were included. OSLER test duration was shorter than 40 min in all patients (mean duration 20 min and 39 s). No patient fulfilled neurophysiological criteria to sleep onset at the time of OSLER test termination. In 13 OSLER sessions that ended before 40 min, eight had microsleeps in the last 30 s before the end of the test. NP monitoring showed signs of sleepiness in all patients. In PD patients, the early termination of an OSLER test session may not correspond to NP criteria of sleep onset. However, in all PD patients with abnormal OSLER results, there were EEG signs of sleepiness, which do not exclude the potential utility of OSLER test to evaluate the risk of falling asleep.info:eu-repo/semantics/publishedVersio

    Delayed leukoencephalopathy after acute carbon monoxide intoxication

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    This journal provides immediate open access to its content on the principle that making research and education freely available to the public supports a greater global exchange of knowledge. This work is licensed under CC BY-NC-ND.Delayed leukoencephalopathy is an uncommon complication of hypoxicischemic events of different etiologies, including carbon monoxide intoxication. We present a case of a 40-year-old male patient who was admitted with rapidly progressive neurocognitive and behavioral deficits. There was a history of accidental carbon monoxide intoxication one month before, presenting with loss of consciousness and short hospitalization, followed by a complete clinical recovery. The imaging studies in the delayed phase depicted confluent, symmetric supra-tentorial white matter lesions in keeping with diffuse demyelinization. Restricted diffusion and metabolite abnormalities in magnetic resonance proton spectroscopy were also seen. The diagnosis of CO-mediated delayed post-hypoxic leukoencephalopathy was assumed after exclusion of other mimickers. Hyperbaric oxygen therapy was tentatively performed and the patient had a favorable clinical and radiological evolution.info:eu-repo/semantics/publishedVersio

    Quantitative analysis versus visual assessment of Neuromelanin MR Imaging for the diagnosis of Parkinson’s disease

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    © 2015 – IOS Press and the authors. All rights reservedBackground: Specific MR sequences have been able to identify the loss of neuromelanin in the substantia nigra (SN) of early stage Parkinson's disease (PD) patients. Since this technique may have a significant impact in clinical patient management, easy and widely available imaging analysis is needed for routine use. Objective: In this study we compared a quantitative analysis with a visual assessment of SN neuromelanin-sensitive MR images in early stage PD patients, in terms of pattern changes recognition and diagnostic accuracy. Methods: The inclusion criteria were untreated "de novo" PD patients or a 2-5 year PD duration; in addition, age matched controls were enrolled. These were studied with a high-resolution T1-weighted MR imaging sequence at 3.0 Tesla to visualize neuromelanin. The primary outcome was the comparison of quantitative width measurement with visual assessment by experienced neuroradiologists of SN neuromelanin sensitive MR images for PD diagnosis. Results: A total of 12 "de novo" PD patients, 10 PD patients with 2-5 year disease duration and 10 healthy controls were evaluated. We obtained a good accuracy in discriminating early-stage PD patients from controls using either a quantitative width measurement of the T1 high signal or a simple visual image inspection of the SN region. Conclusions: Visual inspection of neuromelanin-sensitive MR images by experienced neuroradiologists provides comparable results to quantitative width measurement in the detection of early stage PD SN changes and may become a useful tool in clinical practice.info:eu-repo/semantics/publishedVersio

    Portuguese Consensus on the Diagnosis and Management of Lewy Body Dementia (PORTUCALE)

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    Lewy body dementia is a common cause of dementia leading to the progressive deterioration of cognitive function and motor skills, behavioral changes, and loss of autonomy, impairing the quality of life of patients and their families. Even though it is the second leading cause of neurodegenerative dementia, diagnosis is still challenging, due to its heterogenous clinical presentation, especially in the early stages of the disease. Accordingly, Lewy body dementia is often misdiagnosed and clinically mismanaged. The lack of diagnostic accuracy has important implications for patients, given their increased susceptibility to the adverse effects of certain drugs, such as antipsychotics, which may worsen some symptoms associated with Lewy body dementia. Therefore, a specialist consensus based on the analysis of the most updated and relevant literature, and on clinical experience, is useful to all professionals involved in the care of these patients. This work aims to inform and provide recommendations about the best diagnostic and therapeutic approaches in Lewy body dementia in Portugal. Moreover, we suggest some strategies in order to raise the awareness of physicians, policy makers, and the society at large regarding this disease.A demência com corpos de Lewy é uma causa comum de demência, provocando a perda progressiva de funções cognitivas e capacidades motoras, alterações comportamentais, e perda de autonomia, com compromisso da qualidade de vida dos doentes e seus familiares. Apesar de ser a segunda causa mais frequente de demência neurodegenerativa, o diagnóstico mantém-se um desafio, devido à sua apresentação clínica heterogénea, sobretudo nas fases iniciais da doença. Por conseguinte, a demência com corpos de Lewy é frequentemente mal diagnosticada e clinicamente gerida de forma insuficiente. A falta de acuidade diagnóstica tem implicações significativas para os doentes, dada a maior suscetibilidade aos efeitos adversos de determinados fármacos, tais como os antipsicóticos, que podem agravar alguns sintomas associados à demência com corpos de Lewy. Por conseguinte, um consenso de especialistas, baseado na análise da literatura mais atual e relevante, e na experiência clínica, é útil para todos os profissionais envolvidos no cuidado destes doentes. O objetivo deste trabalho é informar e gerar recomendações acerca das melhores abordagens diagnóstica e terapêutica da demência com corpos de Lewy em Portugal. Além disso, sugerimos estratégias para aumentar a sensibilização dos médicos, dos decisores políticos e da sociedade em geral em relação a esta doença.Este trabalho foi parcialmente financiado pela GE Healthcare Espanha para apoio à logística da realização da reunião de consenso e para apoio de medical writing no âmbito da preparação deste artigo. A GE Healthcare Espanha não teve qualquer papel no desenho do consenso, recolha, análise e interpretação de literatura, redação do manuscrito, nem na decisão de submeter o artigo para publicação. As opiniões expressas no artigo são da responsabilidade dos autores e não são necessariamente as da GE Healthcare Espanha.info:eu-repo/semantics/publishedVersio
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