1,721,137 research outputs found

    Sleep disorders in Parkinson's disease

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    Sleep disorders are commonly reported by patients with Parkinson's Disease (PD) both in early and in advanced stage of illness. Furthermore, some sleep disorders, namely REM Behaviour Disorders (RBD), have been hypothesized to herald PD. Awareness of the clinical and pathophysiological importance of sleep disorders in PD has been growing in recent years. Sleep disorders are now regarded as the most frequent and disabling non-motor complications of PD and as a significant variable of PD-related quality of life. The common subjective reports of disrupted nocturnal sleep and daytime sleepiness find confirmation in the objective findings of various sleep alterations at neurophysiological investigations. Sleep alterations in PD are to be viewed from the multifactorial perspective of a picture build up by interacting factors: involvement of dopaminergic, serotoninergic, noradrenergic and cholinergic neural networks, neuro-degeneration linked to the disease itself, chronic use of antiparkinsonian drugs, sleep-related motor symptoms, aging, cognitive and psychiatric alterations, Restless legs syndrome, Periodic Limb Movements (PMLs) and sleep-disordered breathing. The use of ad hoc questionnaires and scales is advisable for the evaluation of disordered sleep in PD patients for preliminary screening of sleep disorders in PD. In a few cases neurophysiological investigations (i.e. the video-polysomnography in primis) are needed in order to confirm a diagnosis of sleep disorder in PD. It is true particularly in diagnosing RBD. The correct diagnosis unlock the way to the correct treatment, and combined pharmacological and non-pharmacological protocols appear to be particularly suitable in the treatment of sleep disorders in PD

    Interictal, potentially misleading, epileptiform EEG abnormalities in REM sleep behavior disorder

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    Study Objectives: To examine the implications of interictal epileptiform abnormalities (IEA) in idiopathic REM-sleep behavior disorder (RBD), particularly the risk of misdiagnosing RBD episodes as epileptic nocturnal seizures. Design: Observational analysis and review. Setting: Tertiary sleep center. Patients: Thirty patients (28 men; mean age 66.3 ± 7.5 years) referred to our sleep unit for a definite diagnosis of nocturnal sleep-related motor and behavioral paroxysmal episodes. Interventions: N/A. Measurements and Results: All the patients were found to be affected by idiopathic RBD according to standard clinical and videopolysomnographic criteria. IEA(sporadic, fronto-temporal sharp-waves) were detected in 8 subjects (26.6%) during routine electroencephalogram and/or nocturnal in-lab videopolysomnography with extended EEG montages. In 2 of these 8 patients, IEA occurred during REM sleep. Conclusions: When only the clinical history is considered, RBD episodes may be confused with nocturnal epileptic focal seizures. The presence of IEA either on routine awake electroencephalograms, or during sleep electroencephalograms, may add support for a diagnosis of epileptic nocturnal seizures. Our data show that IEA may occur in wake and sleep (non rapid eye movement and rapid eye movement sleep) tracings of subjects with episodes of idiopathic RBD. However full-night extended electroencephalogram montages and polysomnography recording of an episode proved useful in establishing a definite diagnosis of RBD in these potentially misleading cases. Comparison of the patients' demographic data and RBD features revealed no differences between RBD with IEA and without IEA. On this basis-and given that these abnormalities have also been described in elderly people with wakefulness-related nonepileptic disorders-IEA in RBD could simply be interpreted as a nonspecific phenomenon, probably related to brain aging

    Complex paroxysmal nocturnal behaviors in Parkinson's disease

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    Complex paroxysmal nocturnal motor behavioral disorders (CPNBs) are frequently reported in patients with Parkinson's disease (PD). REM sleep behavior disorder (RBD) is reported in at least a third of PD patients, although CPNB episodes can also occur on arousal from NREM sleep. It is important to establish the nature of CPNBs occurring in PD, as the different types have different neurobiological significance and clinical importance, and also different treatments. Ninety-six PD patients with and without CPNBs were submitted to overnight in-hospital video-polysomnography. Of these, 76 (47 men) were included in the study analysis: these were patients in whom it was possible to establish the presence or absence of CPNBs and to obtain a clear-cut diagnosis of the nature of the CPNBs reported. The CPNBs were found to be RBD episodes in 39 cases (87%) and nonRBD episodes in 6 (13%) (arousal-related episodes arising from NREM sleep in 3 cases and from REM sleep in 2 cases, parasomnia overlapping syndrome in 1 case). In 4 of the 6 subjects with nonRBD episodes, these occurred upon arousal at the end of an obstructive apnoeic event. Our data confirm that CPNBs in PD are, in most cases, RBD episodes. However, arousal-related episodes accounted for 13% of the CPNBs observed in our sample and occurred in close temporal association with sleep-disordered breathing (SDB). The arousal system is defective in extrapyramidal diseases due to neurodegenerative changes involving the brain stem reticular network; against this background, a trigger effect of SDB on CPNBs, through induction of abrupt arousal, may be hypothesized. © 2010 Movement Disorder Society

    Abnormal pro-opiomelanocortin processing in Alzheimer's disease. A case report.

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    Several authors have reported reduced levels of pro-opiomelanocortin (POMC)-related peptides in the cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD), but the mechanisms regulating the CSF content of these substances are still debated. In this case report the processing of POMC peptides has been investigated post-mortem (HPLC and RIA methods) at the pituitary and hypothalamic level in an AD patient and in a control subject. From the results obtained it seems likely that defects of axonal transport and/or secretion rather than synthesis could account for the abnormalities of POMC peptides in the CSF

    Sleep disorders in Parkinson's disease: Facts and new perspectives

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    Awareness of the clinical and pathophysiological importance of sleep disorders in Parkinson's disease (PD) has been growing in recent years. Sleep disorders are now regarded as important among non-motor symptoms in PD and as a significant variable of PD-related quality of life. Furthermore, some sleep disorders, namely REM behaviour disorder (RBD), has been hypothesised to herald PD by years. Subjective reports of disrupted nocturnal sleep and daytime sleepiness appear to be supported by descriptions of several sleep alterations at nocturnal polysomnographic investigation and Multiple Sleep Latency Test findings. Sleep alterations in PD are to be viewed from the multifactorial perspective of a framework of reciprocally interacting factors: pathophysiology of the disease itself, sleep-related motor symptoms, dopaminergic treatments, ageing, depression, restless legs, periodic limb movements (PMLs) and sleep-disordered breathing. Ad hoc questionnaires and scales such as the Parkinson's Disease Sleep Scale and the Short and Practical (SCOPA) Sleep Scale are now available for the evaluation of disordered sleep in PD patients and have been proved to be useful for preliminary screening of sleep disorders in PD. However in a few cases a video-polysomnography (V-PSG) is needed in order to confirm a diagnosis of sleep disorder in PD, particularly in diagnosing RBD. As for treatment of sleep disorders, combined pharmacological and non-pharmacological protocols appear to be particularly suitable in their treatment in PD. © Springer-Verlag Italia 2007

    Dopamine agonists and sleepiness in PD: Review of the literature and personal findings

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    Background and purpose: This study is aimed at evaluating daytime sleepiness in a series of Parkinson's disease (PD) patients chronically treated with dopamine agonists (DAs) alone or in combination with l-Dopa. Patients and methods: A preliminary series of 22 non-demented, adult PD patients (mean age 68.9, 13 men and 9 women) were evaluated by means of structured sleep interview, Epworth sleepiness scale (ESS) and 24-h ambulatory polysomnography (A-PSG). Results: Sleep attacks (SAs) were reported by 32% of the patients, in three of them (43%) after DA treatment was initiated (alone or in addition to l-Dopa). In two patients, both with chronic use of ropinirole, we documented NREM SAs during a continuous ambulatory polysomnography (A-PSG) performed in the patients' real-life settings. The subjects experiencing SAs showed a higher degree of daytime sleep propensity than those without SA, having higher ESS scores and a higher proportion of microsleeps and intentional naps on A-PSG. Interestingly, we found that nocturnal total sleep time is higher in PD patients with SAs than in the others. Conclusions: All in all, our data indicate that SAs are an extreme manifestation of increased daytime sleepiness. The occurrence of SAs in our series of PD patients is unlikely to depend simply on the demands of homeostatic mechanisms. © 2004 Elsevier B.V. All rights reserved

    Cerebrospinal fluid norepinephrine, 3-methoxy-4-hydroxyphenylglycol and neuropeptide Y levels in Parkinson's disease, multiple system atrophy and dementia of the Alzheimer type.

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    Neuropeptide Y, one of the most abundant polypeptides within the nervous system, is co-stored with catecholamines, especially norepinephrine (NE), thus suggesting its possible involvement in pathologies characterized by a noradrenergic impairment. In Parkinson's disease (PD), as well as in multiple system atrophy (MSA), a central noradrenergic deficit has been demonstrated, and in the dementia of Alzheimer type (DAT) an impaired noradrenergic transmission has been postulated. In this study we determined CSF NE and MHPG levels in 29 PD, 15 MSA, 22 DAT patients and in 36 controls, while CSF NPY-immunoreactivity (NPY-ir) levels were measured in 10 PD, 7 MSA, 10 DAT patients and 20 controls. PD, MSA, and DAT patients showed a significant reduction in CSF NPY-ir and NE levels compared with controls, while CSF MHPG levels resulted in a reduction in only the MSA group. Furthermore, an inverse correlation between either NE or MHPG levels and the duration of the orthostatic hypotension was found in MSA patients while for DAT patients the MHPG levels were directly correlated to the severity of cognitive impairment, and inversely to the duration of illness
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