Gene/Protein Disease Symptom Drug Enzyme Compound
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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

Rapid eye movement sleep behavior disorder may herald several neurodegenerative disorders associated with parkinsonism, including Parkinson's disease. A 72-year-old man with a 17-year history of rapid eye movement sleep behavior disorder confirmed by polysomnography developed a progressive dementia that met operational clinical criteria for diffuse Lewy body disease. The differential diagnosis of progressive neurodegenerative disorders heralding as rapid eye movement sleep behavior disorder should now include diffuse Lewy body disease.
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PMID:Probable diffuse Lewy body disease presenting as REM sleep behavior disorder. 927 May 89

A clinically relevant sleep-wake disturbance is found in up to half the patients with dementia, and the sundowning agitation is a common cause of institutionalisation of demented geriatric patients. The circadian rhythm of demented patients is levelled off with increased daytime sleep and disrupted night sleep. Particularly in vascular dementia, Korsakow syndrome, Parkinson's disease, and depression the alteration of sleep architecture may be pronounced, whereas in Alzheimer's disease prominent hypersomnolence or insomnia is typically only found in later stages of the diseases. Greatly increased daytime sleepiness or striking insomnia at the very beginning of suspected dementia should thus prompt the search for other, possibly treatable causes of dementia. Neuropathological and neurophysiological studies support the hypothesis of a deteriorated hypothalamic suprachiasmatic nucleus (harbouring the biological clock) as a cause for the deranged circadian sleep-wake system in dementia. Management of sundowning behaviour includes restriction of daytime sleep, exposure to bright lights, and social interaction schedules during the day. The benzodiazepines and analogues usually not being sufficiently effectual, low doses of mild neuroleptics are often needed. Whether recent reports on efficacy of melatonin in elderly insomniacs also apply to demented patients is yet uncertain. The careful search and treatment of possible extracerebral physiologic factors causing reversible hypersomnia or insomnia is an important requisite. Polysomnographic studies are needed to recognise treatable sleep disturbance which could deteriorate or mimic dementia and sundowning. Particularly, a sleep-apnea-hypopnea syndrome must be searched for at the beginning of a suspected dementia, when successful treatment is still possible. Sleep studies should also identify periodic leg movements of sleep with restless legs and/or increased daytime sleepiness, and hyperkinetic parasomnias such as REM sleep behaviour disorder which may complicate or imitate sundowning.
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PMID:[Sleep disorders and dementia]. 938 Oct 26

Behavioral disturbances in Parkinson's disease (PD) are a common source of disability to both patients and their families, but there is a considerable controversy regarding their frequency and their neuropathological and neurochemical bases. Since they are so common, the disorders associated with PD should be well recognized, and proper management by neurologists is required. The most frequent behavioral disturbances encountered in patients with PD are depression, anxiety, cognitive impairment and dementia. Also frequent are sleep disorders such as sleep fragmentation, REM sleep behavior disorder, insomnia and altered dreaming. The most troublesome situations come from drug-induced psychiatric states, such as delusional states, hallucinations, paranoid ideation, delirium, and confusion. The treatment of these behaviors is reviewed here.
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PMID:Therapy of behavioral disorders in Parkinson's disease. 1034 4

The frequency of sleep complaints in patients with Parkinson's disease (PD) is estimated to be between 60-90% and a variety of either disease-related or secondary mechanisms and the dopaminergic treatment itself contributes to the development of different sleep disturbances. These comprise slight, fragmented sleep with increased number of arousals and awakenings, and PD-specific motor phenomena such as nocturnal immobility, rest tremor, eye-blinking, dyskinesias, and other phenomena such as periodic and nonperiodic limb movements in sleep, restless legs syndrome, fragmentary myoclonus, and respiratory dysfunction in sleep. Depression and hallucinations/psychosis further complicate the picture. The incidence of REM sleep behavior disorder (RBD) with nightmares and violent behavior is increased in PD and may occur as a preclinical disease-related symptom. A careful sleep history of patients and their partners, polysomnograms when necessary, motor and psychiatric assessments should precede individual treatment strategies, which include adjusting dopaminergic daytime treatment, benzodiazepines for RBD, reduction of anticholinergic drugs, and, if necessary, clozapine for nocturnal psychosis.
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PMID:Sleep dysfunction in Parkinson's disease. 1078 36

REM sleep is the stage associated with vivid dream mentation, desynchronous cortical EEG, and atonia of antigravitary muscles. REM sleep behavior disorder (RBD) is characterized by the intermittent loss of REM sleep atonia and by the appearance of elaborate motor activity associated with dream mentation. The animal model of REM sleep without atonia indicates that lesions to the perilocus coeruleus disrupt the excitatory connection to the nucleus reticularis magnocellularis in the descending medullary reticular formation and disable the hyperpolarization of the alpha spinal motoneurons. Extensive neurologic evaluations in humans suffering from both idiopathic and symptomatic forms have not identified specific lesions; however, findings in some patients suggest that diffuse lesions of the hemispheres, bilateral thalamic abnormalities, or primary brain-stem lesions may result in the RBD. Symptomatic RBD cases are associated with several neurologic disorders such as dementia, cerebrovascular diseases, multiple sclerosis, brain-stem neoplasm. RBD has been often documented to precede or to co-occur with neurodegenerative disorders, such as dementia, Parkinson's disease and multiple system atrophy. Most importantly, RBD is readily diagnosable and treatable. Patients and their bed partners usually report immediate improvement in sleep-related motor behavior with small doses of clonazepam.
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PMID:REM sleep behavior disorder. 1099 67

Rapid eye movement sleep behavior disorder (RBD) is a rare but clinically distinct disorder which is easily overlooked. It commonly occurs in older men and, because of its similarity to epileptic seizures, is often misdiagnosed. The etiology of RBD is still unknown. However, there is an interesting association with Parkinson's disease which presents some pathophysiological hypotheses. Treatment is usually successful with clonazepam.
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PMID:[REM sleep behavior disorder]. 1108 10

Dementia with Lewy bodies (DLB) is the second most frequent neuropathologically diagnosed degenerative dementing illness. The clinical characteristics are progressive dementia, parkinsonian syndrome, fluctuations of cognitive functions, alertness, and attention, visual hallucinations (usually detailed and well described), depression, REM sleep behavior disorder, adverse responses to standard neuroleptics doses, falls, syncopes, systematized delusions, and other modalities of hallucinations. Specificity of the clinical diagnostic criteria is high (95%), and sensitivity is considerably lower. Mean age at disease onset ranges between 60 and 68 years. The male gender prevails. Disease duration is 6 to 8 years. The differential diagnoses of DLB are dementia of the Alzheimer type, Parkinson's disease, subcortical arteriosclerotic encephalopathy, progressive supranuclear palsy, multiple system atrophy, and rarely Creutzfeldt-Jakob disease. The genetic background of the disease is unclear. Magnetic resonance imaging and single photon emission tomography can contribute to the diagnosis. Controlled pharmacological studies have so far not been published. The disease is treated with L-dopa, atypical neuroleptics, acetylcholine esterase inhibitors, antihypotensive agents, and peripheral anticholinergic and alpha receptor-blocking medications to improve neurogenic bladder dysfunction.
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PMID:[Dementia with Lewy bodies]. 1113 88

We report a case of Parkinson's disease (PD) diagnosed by REM sleep behavior disorder (RBD). The patient was a 68-year-old man. On admission, rigidity in the left upper and lower extremities, bradykinesia, and gait disturbance were noted. In addition, polysomnography revealed REM sleep without atonia (RWA), and a diagnosis of untreated PD associated with RBD was made. Polysomnographic data showed that REM density decreased and RWA tended to increase after administration of a combination of L-DOPA and DCI (L-DOPA/DCI). Thus, we considered that the pathophysiological mechanism of RBD in this case was based not only on the dysfunction of the brainstem mechanism of RWA, but also on the impairment of dopaminergic neuron.
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PMID:Parasomnia as an occasion for the diagnosis of Parkinson's disease. 1142 72

Our objective was to examine whether rapid eye movement (REM) sleep behavior disorder occurs in disproportionally greater frequency in multiple system atrophy (MSA), Parkinson's disease (PD), and dementia with Lewy bodies (DLB), collectively known as the synucleinopathies, compared to other nonsynucleinopathy neurodegenerative disorders. In study 1, we reviewed the clinical records of 398 consecutive patients evaluated at Mayo Clinic Rochester for parkinsonism and/or cognitive impairment. The frequency of suspected and polysomnogram (PSG)-confirmed REM sleep behavior disorder (RBD) among subjects with the synucleinopathies MSA, PD, or DLB was compared to the frequency among subjects with the nonsynucleinopathies Alzheimer's disease (AD), frontotemporal dementia (FTD), corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), mild cognitive impairment (MCI), primary progressive aphasia (PPA), and posterior cortical atrophy (PCA). In study 2, we reviewed the clinical records of 360 consecutive patients evaluated at Mayo Clinic Jacksonville for parkinsonism and/or cognitive impairment. The frequency of probable RBD among patients with PD and DLB was compared to the frequency among patients with AD and MCI. In study 3, we reviewed the brain biopsy or postmortem autopsy diagnoses of 23 Mayo Clinic Rochester patients who had been clinically examined for possible RBD and a neurodegenerative disorder. In study 1, patients with MSA, PD, or DLB were more likely to have probable and PSG-confirmed RBD compared to subjects with the nonsynucleinopathies (probable RBD 77/120=64% vs. 7/278=3%, p < 0.01; PSG-confirmed RBD 47/120=39% vs. 1/278=0%, p < 0.01). In study 2, patients with PD and DLB were more likely to have probable RBD compared to those with AD and MCI (56% vs. 2%, p < 0.01). In study 3, of the 23 autopsied patients who had been questioned about possible RBD, 10 were clinically diagnosed with RBD. The neuropathologic diagnoses in these 10 included Lewy body disease in nine, and MSA in one. Of the other 13 cases, 12 did not have a history suggesting RBD, and the one case who did had normal electromyographic atonia during REM sleep on PSG and autopsy findings of PSP. Only one of these 13 had a synucleinopathy. The positive predictive values for RBD indicating a synucleinopathy for studies 1-3 were 91.7%, 94.3%, and 100.0%, respectively. Clinically suspected and PSG-proven RBD occurs with disproportionally greater frequency in MSA, PD, and DLB compared to other neurodegenerative disorders. In the setting of degenerative dementia and/or parkinsonism, we hypothesize that RBD is a manifestation of an evolving synucleinopathy.
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PMID:Association of REM sleep behavior disorder and neurodegenerative disease may reflect an underlying synucleinopathy. 1148 85


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