Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report longitudinal data on a group of 29 male patients 50 years of age or older who were initially diagnosed as having idiopathic REM sleep behavior disorder (RBD) after extensive polysomnographic and neurologic evaluations. Thirty-eight percent (11/29) were eventually diagnosed as having a parkinsonian disorder (presumably Parkinson's disease) at a mean interval of 3.7 +/- 1.4 (SD) years after the diagnosis of RBD+, and at a mean interval of 12.7 +/- 7.3 years after the onset of RBD. To date, only 7% (2/29) of patients have developed any other neurologic disorder. At the time of RBD diagnosis, data from the RBD group with eventual Parkinson's disease (n = 11) and the current idiopathic RBD group (n = 16) were indistinguishable, with two exceptions: the RBD-Parkinson's disease group had a significantly elevated hourly index of periodic limb movements of non-REM sleep and an elevated REM sleep percentage. RBD was fully or substantially controlled with nightly clonazepam treatment in 89% (24/27) of patients in both groups. Thus, RBD can be the heralding manifestation of Parkinson's disease in a substantial subgroup of older male RBD patients. However, a number of presumed Parkinson's disease patients may eventually be diagnosed with multiple system atrophy (striatonigral degeneration subtype). Our findings indicate the importance of serial neurologic evaluations after RBD is diagnosed and implicate the pedunculopontine nucleus as a likely site of pathology in combined RBD-Parkinson's disease, based on experimental and theoretical considerations rather than on autopsy data.
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PMID:Delayed emergence of a parkinsonian disorder in 38% of 29 older men initially diagnosed with idiopathic rapid eye movement sleep behaviour disorder. 861

Since both REM sleep deprivation and unilateral 6-OHDA lesions induce supersensitivity of DA receptors, the purpose of this study was to determine whether the response of rats with such lesions would be modified by REM sleep deprivation. In addition, the effect of grafts of dissociated chromaffin cells was also tested. Rats with 6-OHDA lesions were subjected to 24 or 72 h of REM sleep deprivation and tested with various doses of apomorphine to determine turning behavior frequencies. At end of those experiments, the animals were transplanted with dissociated chromaffin cells and turning behavior was tested again. The results showed that REM sleep deprivation nearly doubled the turning behavior frequency, that chromaffin cell grafts decreased it, but that REM deprivation in grafted animals still seemed to produce an increase of post-synaptic supersensitivity independent of denervation. The results were discussed in terms of the possible relationship of sleep with Parkinson's disease through the DA system.
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PMID:Rapid eye movement (REM) sleep deprivation in 6-OHDA nigro-striatal lesioned rats with and without transplants of dissociated chromaffin cells. 887 85

Absent or markedly reduced REM sleep with cessation of dream recall has been documented in numerous neurological disorders associated with subcortical dementia including Parkinson's disease, progressive supranuclear palsy and Huntington's chorea. This report concerns a 69 year old Parkinsonian patient who experienced complete cessation of dreaming since the onset of motor disability 13 years ago. Long term treatment with levodopa and dopamine (DA) receptor agonists (bromocriptine and pergolide mesylate) did not affect dream recall. However, dreaming was restored after the patient received three treatment sessions with AC pulsed picotesla range electromagnetic fields (EMFs) applied extracranially over three successive days. Six months later, during which time the patient received 3 additional treatment sessions with EMFs, he reported dreaming vividly with intense colored visual imagery almost every night with some of the dreams having sexual content. In addition, he began to experience hypnagogic imagery prior to the onset of sleep. Cessation of dream recall has been associated with right hemispheric dysfunction and its restoration by treatment with EMFs points to right hemispheric activation, which is supported by improvement in this patient's visual memory known to be subserved by the right temporal lobe. Moreover, since DA neurons activate REM sleep mechanisms and facilitate dream recall, it appears that application of EMFs enhanced DA activity in the mesolimbic system which has been implicated in dream recall. Also, since administration of pineal melatonin has been reported to induce vivid dreams with intense colored visual imagery in normal subjects and narcoleptic patients, it is suggested that enhanced nocturnal melatonin secretion was associated with restoration of dream recall in this patient. These findings demonstrate that unlike chronic levodopa therapy, intermittent pulsed applications of AC picotesla EMFs may induce in Parkinsonism reactivation of reticular-limbic-pineal systems involved in the generation of dreaming.
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PMID:Treatment with weak electromagnetic fields restores dream recall in a parkinsonian patient. 928 89

Sleep is normally a time of motor quiescence. Motor disorders may, however, arise during the different phases of sleep. Nocturnal myoclonus or periodic leg movements in sleep usually occur during light sleep and may be considered the motor accompaniment of the cyclic fluctuations in excitability typical of such stages. Nocturnal frontal lobe epilepsy also occurs during NREM sleep and may be misdiagnosed as parasomnia. REM behavior disorders are instead dissociated episodes of REM sleep without atonia, often associated with or even heralding Parkinson's disease or multiple system atrophy.
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PMID:Motor disorders in sleep. 936 31

The organization of components of the reticular activating system and their role in sleep-wake mechanisms and arousal are described. A functional model is proposed based on known neuroanatomical and neurophysiological findings. The involvement of these elements of the reticular activating system in various neurological and psychiatric disorders is discussed. A series of hypotheses are advanced to account for the role of these nuclei in such diverse disorders as schizophrenia, post-traumatic stress disorder, REM behavior disorder, Parkinson's disease and narcolepsy. This line of reasoning suggests that, when neurological or psychiatric disorders manifest symptoms related to arousal and sleep-wake control, disturbances of elements of the reticular activating system must be considered responsible.
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PMID:Disorders of the reticular activating system. 942 2

The nature of sleep is one of the major sources of dissatisfaction with the quality of life among patients with Parkinson's disease (PD). Difficult sleep maintenance (light and fragmented sleep) and difficulties with sleep initiation are the earliest and most frequent sleep disorders observed in these patients. Sleep disorders are also common in the normal elderly population, suggesting that normal aging may play a role in the etiology of sleep disorders in PD. Factor et al. examined the frequency of various sleep disorders in PD and compared them to those of normal elderly subjects. Sleep fragmentation and spontaneous daytime dozing occurred much more frequently in PD patients than in controls. Sleep fragmentation in PD may be due to an increased skeletal muscle activity, disturbed breathing and REM/non-REM variations of the dopaminergic receptor sensitivity. In parkinsonian patients who developed motor fluctuations (on-off phenomenon, wearing-off) during the day, other common sleep-related motor complaints including nocturnal akinesia, dystonia and painful cramps are observed. In a double-blind cross-over study, we compared the efficacy of a single dose of a chronic release formulation of levodopa/carbidopa (Sinemet CR) with that of a placebo in improving sleep-related motor disturbances in a group of 40 fluctuating PD patients. Sinemet CR significantly improved nocturnal akinesia and increased the hours of sleep in this group of patients. Initiation and maintenance of sleep are problems that may not be solved with antiparkinsonian treatment.
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PMID:Sleep disorders in Parkinson's disease. 961 17

The cholinergic system is one of the most important modulatory neurotransmitter systems in the brain and controls activities that depend on selective attention, which are an essential component of conscious awareness. Psychopharmacological and pathological evidence supports the concept of a 'cholinergic component' of conscious awareness. Drugs that antagonize muscarinic receptors induce hallucinations and reduce the level of consciousness, while the nicotinic receptor is implicated as being involved in the mechanism of action of general (inhalational) anaesthetics. In degenerative diseases of the brain, alterations in consciousness are associated with regional deficits in the cholinergic system. In Alzheimer's disease (AD), there is a loss of explicit (more than implicit) memory and hypoactivity of cholinergic projections to the hippocampus and cortex, while the visual hallucinations experienced by subjects with Dementia with Lewy bodies (DLB) are associated with reductions in neocortical ACh-related activity. In Parkinson's disease, the additional loss of pedunculopontine cholinergic neurones, which control REM (rapid eye movement) sleep or dreaming, is likely to contribute to REM abnormalities, which also occur in DLB. Widespread basal-forebrain and rostral brainstem cholinergic pathways, which include converging projections to the thalamus, appear to be located strategically for generating and integrating conscious awareness. Alleviation of a range of cognitive and non-cognitive symptoms by drugs that modulate the cholinergic system, which are being developed for the treatment of AD and related disorders, could be caused by changes in consciousness.
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PMID:Acetylcholine in mind: a neurotransmitter correlate of consciousness? 1054 30

We describe multiple sleep latency test (MSLT) results in 27 adult patients with idiopathic Parkinson's disease (PD). Pathological sleepiness (i.e. mean sleep latency </=5 min) was common (40 of 134 nap opportunities), and sleep-onset REM periods were also observed (13 of 134 nap opportunities). These findings bore little relationship to disease specific variables (e.g. level of disability, medication use), or sleep architecture measures (e.g. total sleep time, sleep stage percentage's). Our findings speak against a simple association of excessive sleepiness and the quality and quantity of prior night's sleep, but rather, argue for primary impairments of waking arousal and REM-sleep expression in a sizeable subpopulation of PD patients.
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PMID:FAST TRACK: daytime sleepiness in Parkinson's disease. 1073 91

Autonomic dysfunction, neuropsychiatric problems, axial signs and sleep disorders are common complications of advanced Parkinson's disease (PD). Urinary disturbance due to detrusor hyperreflexia and iatrogenic orthostatic hypotension are prominent dysautonomic signs. Depression and anxiety are frequent but can occur exclusively during off periods. A fronto-sub cortical dementia occurs in 30% of PD patients, but anti-parkinsoniens drugs (APD) can cause hallucinations even in non demented PD patients. Axial signs, such as freezing, postural instabily or dysarthria become doparesistant. Insomnia, REM sleep disorders. At least, pain is very frequent. Exact analysis of these signs is important for an adequate treatement: most of them are improved by APD but some of them, like orthostatic hypotension or hallucinations, are increased by these drugs.
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PMID:[Other symptoms of advanced stage Parkinson's disease]. 1091 48

Recently described functional connections between basal ganglia and brainstem circuits provide a neurobiologic basis for the absence of REM sleep atonia in Parkinson's disease (PD). However, identifying atypical REM sleep in PD may be problematic. Reliable sleep staging has never been demonstrated in such patients. In this study, 3 experienced scorers independently evaluated overnight polysomnograms from 10 (PD) patients. Results indicated good agreement for distinguishing REM from NREM sleep and waking. Reliable differentiation among NREM stages was more difficult to achieve. The results suggest that, despite suspension of REM sleep atonia accompanying PD, trained scorers can distinguish REM from wakefulness and NREM sleep.
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PMID:Inter-rater reliability for identification of REM sleep in Parkinson's disease. 1094 35


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