REM sleep behavioral disorder may be an independent risk factor for orthostatic hypotension in Parkinson’s disease

Yin, Kangfu; Zhou, Chen; Zhu, Yongyun; Yin, Weifang; Yin, Lu; Liu, Bin; Ren, Hui; Xu, Zhenhe; Yang, Xinglong

doi:10.1007/s40520-021-01887-y

Cited by 5 publications

(2 citation statements)

References 33 publications

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“…RBD is a strong risk factor for subsequent development of a neurodegenerative synucleinopathy ( 54 ), including a “diffuse/malignant” form of PD ( 55 ) that features OH ( 56 , 57 ). RBD is also associated with olfactory dysfunction ( 58 , 59 ) and neuroimaging evidence of cardiac noradrenergic deficiency ( 60 ).…”

Section: Discussionmentioning

confidence: 99%

Cardiac noradrenergic deficiency revealed by 18F-dopamine positron emission tomography identifies preclinical central Lewy body diseases

Goldstein,

Holmes,

Sullivan

et al. 2024

Journal of Clinical Investigation

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BACKGROUND. In Lewy body diseases (LBDs) Parkinson disease (PD), and dementia with Lewy bodies (DLB), by the time parkinsonism or cognitive dysfunction manifests clinically, substantial neurodegeneration has already occurred. Biomarkers are needed to identify central LBDs in a preclinical phase, when neurorescue strategies might forestall symptomatic disease. This phase may involve catecholamine deficiency in the autonomic nervous system. We analyzed data from the prospective, observational, long-term PDRisk study to assess the predictive value of low versus normal cardiac 18 F-dopamine positron emission tomography (PET), an index of myocardial content of the sympathetic neurotransmitter norepinephrine, in at-risk individuals. METHODS. Participants self-reported risk factor information (genetics, olfactory dysfunction, dream enactment behavior, and orthostatic intolerance or hypotension) at a protocol-specific website. Thirty-four with 3 or more confirmed risk factors underwent serial cardiac 18 F-dopamine PET at 1.5-year intervals for up to 7.5 years or until PD was diagnosed. RESULTS. Nine participants had low initial myocardial 18 F-dopamine–derived radioactivity (<6,000 nCi-kg/cc-mCi) and 25 had normal radioactivity. At 7 years of follow-up, 8 of 9 with low initial radioactivity and 1 of 11 with normal radioactivity were diagnosed with a central LBD (LBD+) ( P = 0.0009 by Fisher’s exact test). Conversely, all 9 LBD+ participants had low 18 F-dopamine–derived radioactivity before or at the time of diagnosis of a central LBD, whereas among 25 participants without a central LBD only 1 (4%) had persistently low radioactivity ( P < 0.0001 by Fisher’s exact test). CONCLUSION. Cardiac 18 F-dopamine PET highly efficiently distinguishes at-risk individuals who are diagnosed subsequently with a central LBD from those who are not. TRIAL REGISTRATION. ClinicalTrials.gov NCT00775853. FUNDING. Division of Intramural Research, NIH, NINDS.

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Section: Discussionmentioning

confidence: 99%

Cardiac noradrenergic deficiency revealed by 18F-dopamine positron emission tomography identifies preclinical central Lewy body diseases

Goldstein,

Holmes,

Sullivan

et al. 2024

Journal of Clinical Investigation

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“…Виникнення моторних проявів ХП пов'язано з загибеллю допамінергічних нейронів компактної частини чорної субстанції [9], а дегенеративне ураження постгангліонарних норадренергічних волокон периферичної нервової системи з відкладанням альфа-синуклейну та формуванням цитоплазматичних тілець Леві призводить до нейрогенної ОГ (НОГ) [3]. За останніми даними порушення поведінки фази швидкого сну (REM-фаза) має позитивну кореляцію з ОГ, що пов'язано з ураженням центральних норадренергічних структур [10,11,12]. Тому скринінг розладів REM-фази сну [15] може бути актуальним як додатковий маркер ОГ з огляду частого безсимптомного перебігу синдрому у пацієнтів з ХП [1].…”

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Orthostatic Hypotension as a Non-Motor Symptom of Parkinson’s Disease

Ovchynnykova

Trufanov

2022

East European Journal of Parkinson`s Disease and Movement Disorders

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The objective of our research was to raise awareness of neurologists about orthostatic hypotension (OH) in Parkinson’s disease (PD) and to explore the current approach to the problem. Materials and methods. This work was performed by searching for current information on OH in PD, reflecting the pathophysiology, classification, symptoms, diagnosis, and treatment. PubMed and Google Scholar resources were used to write the review. Results. An important task in the management of patients with PD is diagnostic and treatment of OH due to the negative impact of the syndrome on somatic, psychological and cognitive status. According to recent data, the prevalence of OH among PD patients is 30-50% [1] with no association with the stage of the disease [2]. OH in PD is neurogenic (NOH); it results from neurodegenerative damage to the central and peripheral structures of the sympathetic nervous system, which leads to reduced postganglionic release of epinephrine [3]. It is often asymptomatic, as a result of compensatory tolerance mechanisms [1]. In about of 50% of patients [4], OH is associated with supine hypertension [2] and may have a connection with REM-sleep disorders [5]. Classification features of OH include: onset period under orthostatic stress, the relationship of OH to different parts of the cardiac cycle, mechanism of pathophysiology, clinical course, presence of symptoms and clinical severity [20, 31, 32]. OH symptoms usually occur during orthostatic stress. They include dizziness, blurred vision, cognitive slowing, syncope, coat-hanger pain, difficulty breathing, leg buckling or leg weakness, general weakness and fatigue [1, 5, 17, 18]. Bedside orthostatic test with blood pressure measurement at the 1st, 3rd and 5th minutes of standing and ambulatory blood pressure monitoring (ABPM) are used for diagnosis [6]. The treatment strategy is to evaluate the medications taken by the patient and obligatory inclusion of non-pharmacological treatment. Pharmacological treatment for supine hypertension and OH is only given if necessary [1, 2]. Conclusions. OH is a widespread non-motor symptom of PD [1], which should be timely diagnosed and treated because of the negative impact on quality of life with increased risk of death and injuries due to falls [31, 32, 33]. The relationship between OH and other non-motor symptoms of PD should be further explored, and optimal therapeutic strategies for different functional classes and a combination of non-pharmacological and pharmacological treatments for OH should be found as well.

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A systematic review and meta-analysis on the association between orthostatic hypotension and mild cognitive impairment and dementia in Parkinson’s disease

et al. 2022

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REM sleep behavioral disorder may be an independent risk factor for orthostatic hypotension in Parkinson’s disease

Cited by 5 publications

References 33 publications

Cardiac noradrenergic deficiency revealed by 18F-dopamine positron emission tomography identifies preclinical central Lewy body diseases

Cardiac noradrenergic deficiency revealed by 18F-dopamine positron emission tomography identifies preclinical central Lewy body diseases

Orthostatic Hypotension as a Non-Motor Symptom of Parkinson’s Disease

A systematic review and meta-analysis on the association between orthostatic hypotension and mild cognitive impairment and dementia in Parkinson’s disease

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