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)

Sleep characteristics are studied in 7 patients with sequelae of manganese intoxication and in 8 controls. A reduction in the length of the REM stage was observed, which could be prolonged by L Dopa administration, but without achieving values comparable to the controls. No changes were noted in the non-REM stage of sleep. These results are similar to the ones obtained in Parkinson's disease, suggesting clinical and probably biochemical similarities between the 2 conditions. The blood concentrations of growth hormone during sleep in the manganic patients was lower than in the control group, and no significant variations were noted after L Dopa administration.
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PMID:[Sleep stages and growth hormone in manganese poisoning. Effects of L dopa]. 23 4

Sixty-four all-night sleep polygraphic recordings have been carried out in patients affected by Parkinson's syndrome, before and after treatment with an association of l-dopa plus a peripheral dopa-decarboxylase inhibitor. Without any drug, parkinsonian patients showed sleep disruption with frequent awakenings, reduction of total sleeping time and lessening of REM stage rather than slow sleep. Treatment with l-dopa plus inhibitor appeared to be able to restore good night sleep organization with a noteworthy increase in the REM stage.
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PMID:L-dopa plus dopa-decarboxylase inhibitor. Sleep organization in Parkinson's syndrome before and after treatment. 120 95

In a sample of 44 patients with Parkinson's disease, REM latency showed a unimodal rather than bimodal distribution, with peak frequency between 0-10 min. A total of 16 patients exhibited (36.4%) a sleep onset REM period (SOREMP-10); i.e. REM latency of 10 min during the night; an additional 4 patients (9%) showed REM latencies of 11-20 min, while 8 patients (18.2%) showed REM latencies of less than 50 min (63.6 of the total sample). Patients with REM latencies of less than 50 min were older, both at the time of study and at the age of onset of the disease. There were more patients with depressive syndrome in this group than in the other group. They also showed a higher sleep amount. No other clinical or polysomnographic differences were found between patients with short REM latencies and patients exhibiting REM latencies of more than 50 min. Very short REM latencies probably reflect depressive syndrome associated with Parkinson's disease.
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PMID:[Changes in sleep in Parkinson's disease]. 213 18

Neurophysiological studies were performed on 8 patients with group A xeroderma pigmentosum during early childhood. EEG, ABR and NCV were normal during this period. In contrast, various sleep parameters detected by polysomnography showed abnormal findings even in the neurologically normal patient. Decreased % sleep REM was seen in a case, and decreased frequency of REMs were seen in another. Body movements were extremely high or low in frequency in 3 cases in whole night sleep. The distribution of body movements were abnormal; in control subjects, the frequency was higher in SREM and stage 1 than in slow wave sleep; in 7 cases, it was higher in slow wave sleep than in stage 1 or 2, or body movements were extremely frequent. Neurological examination revealed soft signs in various systems in early childhood. All cases except one showed hypotonia. Many cases were slow in learning to walk and the gait was unstable. Speech delay and decreased deep tendon reflexes, especially of patella, were seen in most cases. Since the neural deficits in XP may be related to the DNA repair defect, these findings indicate the possibility that some endogenous compounds distributing all over the nervous system might produce the DNA damages. Because the body movements during sleep are controlled by the nigrostriatal dopaminergic system, present data indicate that the basal ganglia might be one of the earliest degenerative systems in the CNS. Recently, some studies have suggested the possibility that oxygen radical mechanisms might be involved in the development of the dopamine neurodegenerative process in Parkinson's disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Neurophysiological studies on group A xeroderma pigmentosum in early childhood]. 217 31

Previous investigations have shown that REM sleep deprived (REM SD) rats display an enhanced response to dopamine agonists. This action seems to be mediated through a supersensitivity of dopamine post-synaptic receptors. Accordingly, REM SD was performed on rats with an experimental model of Parkinson's disease. The animals were bilaterally lesioned in the nigrostriatal pathway through a stereotaxically directed electrical current. Seven days after the surgery the animals were REM SD for 72 hours and immediately after the end of this period were observed in an open field for ambulation, rearing, grooming, and latency. In comparison with non-deprived rats there was a significant increase in ambulation and rearing, a response that appeared again after a second REM SD period on day 21th after the surgery. These data of improvement of two parameters of an experimental model of Parkinson's disease suggest that SD may be useful in this condition.
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PMID:Rem sleep deprivation in an experimental model of Parkinson's disease. 332 48

Sleep and respiration during sleep were studied in patients with idiopathic Parkinson's disease, patients with Parkinsonism with autonomic disturbance, and normal age and sex matched controls. Patients with idiopathic Parkinson's disease showed significantly reduced REM sleep, and more frequent and prolonged waking throughout the night. Hypoventilation and sleep apnoea did not occur in the idiopathic Parkinson's disease or normal groups, but respiration was disorganised with frequent central and obstructive apnoeas in the autonomic disturbance group. Respiratory rate during non rapid eye movement sleep was similar in the idiopathic Parkinson's disease and normal groups, but patients with idiopathic Parkinson's disease showed tachypnoea awake and during REM sleep.
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PMID:Respiration and sleep in Parkinson's disease. 408 99

A 71 year old retired printer developed idiopathic Parkinson's disease over a period of 3 years. On account of his worsening condition he was admitted to hospital. Following the interruption of his medication the patient developed an akinetic crisis. A 48 hour polysomnogram recording, repeated five times during hospitalization, showed severe sleep deprivation. Treatment with Pergolide alone was then started; and sleep monitoring showed suppression of REM rebound, REM only appearing when the dose of the drug was reduced. It is suggested that REM rebound phenomena produced by sleep deprivation in a Parkinson's disease patient are suppressed by the effect of the dopaminergic agent Pergolide.
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PMID:Suppression of REM rebound by Pergolide. 672 17

We treated 17 narcolepsy patients in a placebo-controlled, double-blind, crossover trial with 10-, 20-, 30-, and 40-mg daily doses of selegiline, a monoamine oxidase inhibitor widely used in Parkinson's disease. There was a dose-dependent as well as a statistically and clinically significant improvement in narcoleptic symptoms and polygraphic measures. At 40 mg, there was a 36% reduction in the number of daytime sleep episodes and a 34% reduction in their duration (compared with placebo, mean values). The number of excessive sleepiness episodes decreased by 43%, and the duration decreased by 47%. The number of cataplectic attacks was reduced by 89%. On the multiple sleep latency test, the REM sleep latency increased from 5.0 to 13.3 minutes, and the number of sleep-onset REM periods decreased from 3.1 to 0.6. Sleep (S1) latency was not changed. No intolerable adverse events occurred. The effective dose range was 20 to 40 mg, requiring a low-tyramine diet, which was easy to maintain. In conclusion, selegiline alleviates both main symptoms of narcolepsy--the abnormal sleep tendency and cataplexy. Thus, treatment with selegiline makes it possible to avoid polypharmacy and to use a potent stimulant without known addiction risk.
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PMID:Selegiline in the treatment of narcolepsy. 796 65

The objective of this questionnaire-based survey was to evaluate the prevalence and causes of sleep disturbances in 90 nondepressive patients with Parkinson's disease (PD) and 71 age-matched healthy subjects. We also assessed the prevalence and characteristics of excessive daytime sleepiness (both groups) and excessive fatigue (PD patients). A high prevalence of sleep disturbances in PD patients was found; this is to a large extent probably the result of aging. As compared with controls, patients had a more severely disturbed sleep maintenance because of nycturia, pain, stiffness, and problems with turning in bed. The prevalence of excessive dreaming is similar in both groups, but altered dream experiences almost exclusively occurred in PD. Patients rated themselves more often to be morning-types than controls. This finding may account for the reported adaptation effects in experimental settings and the reduced REM latency in PD patients. The prevalence of daytime sleepiness was similar in both groups. Excessive daytime sleepiness showed a clear diurnal pattern with a peak in the early afternoon. As for excessive fatigue, the majority of the patients did not report a preferential time for this symptom. Our findings further argue against an association of fatigue with any circadian factor, and instead suggest a relationship with the motor deficits of PD.
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PMID:Sleep, excessive daytime sleepiness and fatigue in Parkinson's disease. 836 3

Two major sources of dissatisfaction with the quality of life among Parkinsonian patients are the "locomotor disability" and the "nature of their sleep". The main focus of research was directed towards the locomotor disability, but in the last two decades some progress has been made towards the understanding of sleep in PD patients. Sleep in Parkinson's disease is light and fragmented due to an increased skeletal muscle activity, disturbed breathing, impaired biological rhythm and REM-nonREM variations of the dopaminergic receptor sensitivity.
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PMID:Sleep in Parkinson's disease. 847 84


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