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)

This article summarizes sleep disturbances in a variety of neuro-degenerative diseases, including Parkinson's disease, multiple system atrophy, and amyotrophic lateral sclerosis. Sleep complaints in these conditions include insomnia, hypersomnia, abnormal motor activity and behavior during sleep, sleep-related breathing problems, and circadian rhythm sleep disturbances. Clinical examination followed in selected cases by polysomnographic, multiple sleep latency, and other laboratory tests is essential for correct diagnosis and treatment of these sleep disturbances.
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PMID:Sleep and degenerative neurologic disorders. 892 96

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

The newly identified association of human nonnarcoleptic rapid eye movement (REM) sleep behavior disorder (RBD) with human leukocyte antigen (HLA) DQw1 class II genes raises the possibility that RBD may arise from autoimmune mechanisms. Two recent case reports involving postmortem brain stem histochemical analyses in elderly males with RBD identified severe monoaminergic cell loss in the locus ceruleus (LC). Thus, we designed a study to detect anti-LC antibodies in RBD. Ten Caucasian males (mean age, 66 years) with polygraphically confirmed RBD (n = 5, idiopathic RBD: n = 5, RBD with Parkinson's disease), but without narcolepsy, idiopathic hypersomnia, or autoimmune disease, were recruited for this study, along with 10 Caucasian male controls (mean age, 63 years) without a history of sleep disorder or autoimmune disease. In a blinded design, sera from the RBD patients and their controls were tested against human LC and other brainstem neurons. Brainstem tissue was obtained from autopsies of neurologically normal individuals. The presence of anti-LC antibodies was examined using immunohistochemistry on brainstem sections. Sections incubated with sera from normal individuals and sera from patients with paraneoplastic antineuronal antibodies (anti-Hu and anti-Ri) were used as controls. No reactivity with LC or any other brainstem area was identified with sera from either RBD patients or their controls, or from the other group of normal individuals. In contrast, sera from patients with paraneoplastic anti-Hu and anti-Ri antibodies reacted strongly with nuclei of LC and other brainstem neurons, sparing the nucleoli, and reacted to a lesser extent with the cytoplasm of these neurons. Therefore, it is unlikely that human RBD is associated with anti-LC antibodies. However, an autoimmune process in RBD has not been excluded by this study.
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PMID:A controlled study of serum anti-locus ceruleus antibodies in REM sleep behavior disorder. 938 Oct 56

We report a 63-years old patient with Parkinson's disease, who experienced slight fluctuations 10 years after first signs of the disease and two years after initiation of levodopa/carbidopa and biperiden therapy. He was enrolled in a double blind, placebo controlled study with the dopamine agonist pramipexole. This study was extended to an open phase. During this phase we were able to reduce levodopa/carbidopa down to zero, while fluctuations and peak dose dyskinesias ceased. The most important adverse event were hypersomnia and very slight persistent dyskinesias, which were reported tolerable by the patient. Treatment without levodopa/carbidopa could be maintained for 31 months. We conclude that in selected cases patients in Hoehn and Yahrs stages II to III and with mild fluctuations might be treated with pramipexole without levodopa.
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PMID:[High dosage therapy of Parkinson disease. New dopamine agonist pramipexol allows reduction of L-dopa dose down to zero]. 1048 75

Up to 40% of cases of Parkinson's disease are associated with the occurrence of depression. The symptoms of the patients' depressive state may be factors such as significant weight change, insomnia or hypersomnia, psychomotor retardation, fatigue or loss of energy, feelings of worthlessness or inappropriate guilt, decreased concentration and indecisiveness, and recurrent thoughts of death or suicidal ideation. Given these conditions, drugs prove ineffective in many cases. Electroconvulsive therapy (ECT) has been reported to be beneficial in cases of drug-resistant depression. ECT has also been applied to Parkinsonian patients with depression and found to be effective with both depression and the Parkinsonian symptom. Transcranial magnetic stimulation(TMS) has recently been investigated for application in cases of depression and has become known as a valuable tool for depression therapy. TMS is easily implemented even in outpatient therapy. TMS will make a great contribution to the therapy of depression with Parkinson's disease.
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PMID:[Parkinson's disease and depression]. 1106 58

The aim of our study was to assess the prevalence of the specific disorders of the circadian rhythm of cortisol and melatonin in the patients with sleep disorders. The group of our patients consisted of 93 persons (25 men, 68 women), from 4-72 years (mean age 38.3 years) with a sleep disorders. These patients were studied on Department of Neurology of 1st Medical Faculty of Charles University in Prague during years 1997-1999. Patients were divided by the clinical diagnosis into many subgroups: idiopathic hypersomnia (IH) 24 patients and other hypersomnias 8, narcolepsy 22, degenerative disorders 9, delay sleep phase syndrome (DSPS) 7, periodic leg movements syndrome (PLMS) 6, insomnia 7 and Parkinson's disease 10 patients. Twelve salivary samples were taken from each patient during a period of 24 hours in order to investigate the circadian secretion pattern of melatonin and cortisol. Salivary melatonin and cortisol levels were estimated by radioimmunoassay in the Department of Physiology of the Academy of Science, Czech Republic. Significant differences were found between our patients and the control group in idiopathic hypersomnia--acrophase of melatonin was delayed and secretion was prolonged. Patients suffered from narcolepsy often displayed multiple peak of melatonin secretion. The peak of the melatonin concentration occurred later in DSPS (non significantly). Low level of melatonin and prolonged signal of melatonin was in Parkinson's disease patients.
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PMID:[Sleep disorders and the 24-hour profile of melatonin and cortisol]. 1170 73

We present a comprehensive review of sleep studies performed in patients with brain lesions complemented by 16 additional personal selected cases and by discussion of the corresponding animal data. The reader is cautioned about the risk of establishing an erroneous correlation between abnormal sleep and a given disorder due to the important inter and intra variability of sleep parameters among individuals. Salient points are stressed: the high frequency of post-stroke sleep breathing disorders is becoming increasingly recognised and may, in the near future, change the way this condition is managed. Meso-diencephalic bilateral infarcts induce a variable degree of damage to both waking and non-REM sleep networks producing and abnormal waking and sometimes a stage 1 hypersomnia reduced by modafinil or bromocriptine, which can be considered as a syndrome of cathecholaminergic deficiency. Central pontine lesions induce REM and non-REM sleep insomnia with bilateral lateral gaze paralysis. Bulbar stroke leads to frequent sleep breathing disorders. Polysomnography can help define the extent of involvement of various degenerative diseases. Fragmented sleep in Parkinson's disease may be preceded by REM sleep behavioural disorders. Multiple system atrophies are characterised by important sleep disorganization. Sleep waking disorganization and a specific ocular REM pattern are often seen in supra-nuclear ophtalmoplegia. In Alzheimer patients, sleep perturbations parallel the mental deterioration and are possibly related to cholinergic deficiency. Fronto-temporal dementia may be associated with an important decrease in REM sleep. Few narcoleptic syndromes are reported to be associated with a tumour of the third ventricle or a multiple sclerosis or to follow a brain trauma; all these cases raise the question whether this is a simple coincidence, a revelation of a latent narcolepsy or, as in non-DR16/DQ5 patients, a genuine symptomatic narcolepsy. Trypanosomiasis and the abnormal prion protein precociously after sleep patterns. Polysomnography is a precious tool for evaluating brain function provided it is realised under optimal conditions in stable patients and interpreted with caution. Several unpublished cases are presented: one case of pseudohypersomnia due to a bilateral thalamic infarct and corrected by modafinil, four probable late-onset autosomal recessive cerebellar ataxias without sleep pattern anomalies, six cases of fronto-temporal dementia with strong reduction in total sleep time and REMS percentage on the first polysomnographic night, one case of periodic hypersomnia associated with a Rathke's cleft cyst and four cases of suspected symptomatic narcolepsy with a DR16-DQ5 haplotype, three of which were post-traumatic without MRI anomalies, and one associated with multiple sclerosis exhibiting pontine hyper signals on MRI.
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PMID:Sleep and brain lesions: a critical review of the literature and additional new cases. 1181 Sep 86

Excessive daytime sleepiness has been widely accepted as a common problem not only in Parkinson's disease (PD) but also in other related disorders. Lowered excretion of orexin A (hypocretin 1) into the cerebrospinal fluid (CSF) is known to play a pathological role in narcolepsy and secondary hypersomnia due to hypothalamic dysfunction. Although the levels of CSF orexin in PD have been previously examined, the results have been controversial, and no systematic investigation of CSF orexin excretion has been conducted on PD related disorders. In this study, orexin was measured in CSF collected by lumbar puncture in 62 patients with PD, 13 patients with dementia with Lewy bodies (DLB), 16 patients with progressive supranuclear palsy (PSP), and 7 patients with corticobasal degeneration (CBD). Levels of CSF orexin (mean+/-SD pg/ml) were 302+/-38 in PD, 297+/-48 in DLB, 258+/-37 in PSP, 246+/-90 in CBD. The occurrence of low orexin levels (<or=110pg/ml) was rare in both PD and DLB, and orexin levels were significantly lower in the PSP and CBD groups compared to PD (PSP: p<0.001, CBD: p<0.05). Orexin levels were inversely correlated with duration of morbidity in PSP but not in the other conditions studied. These findings suggest that loss of orexin neurons or impaired orexin neurotransmission might exist as a part of the neurodegeneration associated with advanced PSP with long duration of morbidity.
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PMID:CSF orexin levels of Parkinson's disease, dementia with Lewy bodies, progressive supranuclear palsy and corticobasal degeneration. 1700 2

About 90% of neurodegenerative diseases with parkinsonism are associated with sleep disorders including daytime sleepiness, sleep-related breathing disorders and parasomnias. It is hard to define what ratio of insomnia and daytime hypersomnia is caused by the antiparkinsonian treatment, by the somatic and mental-emotional symptoms of the neurodegenerative disease and by the neurodegenerative brain process itself. Recent research suggests that the latter group is more important than expected. In Parkinson syndromes the structures included in sleep regulation--mainly within the brainstem--are also affected resulting in specific sleep disorders being the primary biological symptoms of these diseases. The recently described parasomnia--REM sleep behavior disorder--has a specific significance in this respect: it may prevent by several years a high ratio of the parkinsonian disorders--especially synucleinopathies--offering the possibility of prevention by identifying the affected individuals. There seems to exist a similar although less clarified association between daytime sleepiness and Parkinson disease. Analysing the behavior of the orexin system in neurodegenerative diseases may help to learn more about this, recently described neurohumoral system and may clear the association of narcolepsy with neurodegeneration. By understanding the associations of parkinsonian disorders and sleep disorders new therapeutical strategies may be invented and may offer new aspects to understand the mechanism of them.
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PMID:[Sleep disorders in Parkinson syndromes]. 1757 69

The present study explores the frequency of RLS in PD and focuses on the clinical differences between patients with and without restless legs syndrome (RLS). A cross-sectional study was designed, comprising 114 patients diagnosed with PD. Those patients positive for RLS were assessed for intensity of the syndrome (IRLS). We compared the clinical characteristics of the patients with and without RLS, using specific scales: Unified Parkinson's Disease Rating Scale (UPDRS I-IV), quality of life (Parkinson's Disease Questionnaire, PDQ 39), sleep symptoms (Parkinson's Disease Sleep Scale, PDSS), and diurnal hypersomnia (Epworth Sleepiness Scale). Twenty-five patients (21.9%) out of a total of 114 subjects diagnosed with PD met the RLS diagnostic criteria. RLS was more frequent in women (68%). The patients with RLS showed poorer scores on the PDSS (PD-RLS+: 102.4 +/- 15.1 vs PD-RLS-: 113.2 +/- 16.4) (P = 0.005) and in the bodily discomfort dimension of the PDQ-39 (PD-RLS+ 6.1 +/- 3.4 vs PD-RLS- 3.8 +/- 2.6) (P = 0.002). Analysis of the subscales of the PDSS showed significant differences (P < 0.001) between both groups of patients in items 4 and 10, and to a lesser degree in items 5 (P = 0.01) and 11 (P = 0.02) There was no increased incidence of diurnal hypersomnia in the group of patients with RLS. There were no differences in the rest of the variables. RLS is frequent in patients with PD, though this condition doesn't apparently affect quality of life or lead to an increased presence of diurnal hypersomnia. It would be advisable to validate the diagnostic criteria of RLS in this specific group of patients.
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PMID:Restless legs syndrome in Parkinson's disease. 1757 69


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