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)

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

Patients suffering from Parkinson's disease (PD) often report about sleep disorders and excessive daytime sleepiness. To some extent, motor disabilities or neural degeneration of sleep modulating structures may be responsible for these effects. Depressive disorders also contribute to the occurrence of insomnia and daytime sleepiness. Nevertheless, dopaminergic, anticholinergic, and other drugs used in PD have a great impact on sleep/wakefulness mechanisms. They may indirectly improve or worsen sleep by changing motor symptoms such as akinesia, hyperkinesia, or tremor. Although their is only little information on the complex regulation of vigilance, it is well known that monoaminergic and cholinergic drugs could influence it directly. Data from animal experiments and clinical experiences led to the hypothesis of a biphasic influence on sleep by dopaminergic substances: small doses of L-Dopa e. g. appear to improve sleep whilst higher doses led to insomnia. Different dopaminergic receptor types or changes in receptor sensitivity may explain these phenomena. Dopaminergic and anticholinergic drugs suppress REM sleep. Recently, initial data on 'sleep attacks' after pramipexole or ropinirole treatment were published. Our preliminary results using 24 h polygraphic recordings showed excessive daytime sleepiness in patients taking ropinirole and L-Dopa which disappeared when changed to ropinirole monotherapy. Sleepiness did never appear as an irresistible attack. Current hypotheses on this topic are reviewed.
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PMID:Effects of parkinsonian medication on sleep. 1119 13

This study reports the current neurobiologic data on REM sleep including psychoanalysis, distinguishing between the "instincts of pleasure" and the "instincts of death" (Beyond the principles of pleasure, S. Freud, 1920). The award and punishment systems are also reported and current data related to nightmares and mainly dream behavior during REM sleep without atonia are presented underlining the frequency of parasomnia in ponto-cerebellous atrophy and Parkinson's disease. The author emphasizes the need for establishing discussions among the different neuroscientific fields related to these questions.
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PMID:[Nightmares and behavior during REM sleep]. 1141 20

We reviewed the polysomnograms (PSGs) of 292 consecutive patients with sleep disorders (Parkinson's disease (PD), n=19, other sleep disorders, n=273) to investigate the sensitivity and specificity of the clinical diagnosis of rapid eye movement behavior disorder (RBD) compared with polysomnographic diagnosis. Patients with dementia, multiple system atrophy, or any other neurodegenerative disease were excluded. RBD was diagnosed clinically if the minimal criteria, according to the guidelines given in the International Sleep Disorders Classification, were fulfilled. The following PSG criteria were required for diagnosis of RBD: REM sleep without muscle atonia seen in PSG associated with motor behavior visible in the PSG-synchronized videotape. Nine of nineteen PD patients (47%) had RBD. RBD occurred in only four patients without PD (1.8%). The sensitivity of specialized interviews for identifying RBD clinically was good in non-PD patients (sensitivity: 100%, specificity: 99.6%). However, the sensitivity was poor (33%) with a specificity of 90%, in patients with PD. We conclude that the diagnosis of RBD in patients with PD requires PSG, whereas interviews are sufficient for diagnosing RBD in non-PD patients.
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PMID:REM sleep behavior disorder in sleep-disordered patients with versus without Parkinson's disease: is there a need for polysomnography? 1141 65

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

Parkinson's disease (PD) is associated with sleep disorders which are attributed mainly to dopamine deficiency, nocturnal akinesia, drug therapy, and cofactors such as age and depression. These disturbances affect the macro- and microstructure of both REM and non-REM sleep and motor, respiratory, and autonomic functions. Excessive daytime sleepiness and the interactions between sleep and daytime motor performance in PD are not yet completely understood. Correct diagnosis and treatment of sleep disorders is essential due to the risk of harm to the patient and others and due to their effect on quality of life for all concerned. As sleep disorders in PD are extremely common (about 70%) and may have severe consequences, a systematic sleep history and specific therapy should be considered integral to treatment in every PD patient.
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PMID:[Pathophysiology, clinical aspects and therapy of sleep disorders in Parkinson disease]. 1143

A patient in stage 3-4 of the Unified Parkinson's Disease Rating Scale (UPDRS), or in stage 4-5 of Hoehn and Yahr staging scale, or a patient with 0-50% activities of daily living scale of Schwab and England is considered a Late Parkinson's Disease (LPD) patient. The prevalence of disturbed sleep in Parkinson's Disease (PD) was found to vary according to an objective rating, from 60 to 98%. The factors predicting the quality of life in PD patients are: depression, sleep disturbances and dependence. The present article proposes the insertion of the following items as a chapter in a revised UPDRS based on updated knowledge in sleep arousal disturbances in PD. V. SLEEP-AROUSAL DISTURBANCES: Sleep disturbances 43. Light fragment sleep (LFS) 44. Sleep-related breathing disorders (SRBD) 45. Restless legs-periodic leg movements during sleep (RLS-PLM) 46. REM behavioral disorders (RBD) 47. Sleep-related hallucinations (SRH) 48. Sleep-related psychotic behavior (SRPB) Arousal disturbances 49. Sleep attacks (SA) 50. Excessive daytime sleepiness (EDS). Approaching the treatment of disturbed sleep in LPD means postponement of the institutionalization of the LPD patient, allowing the spouse or the caregiver a quiet nights sleep. This approach consists of three steps, each one of major importance. (1) Correct diagnosis based on detailed anamnesis of the patient, of the spouse or of the caregiver; a one week recording on a symptom diary (log) by the patient or the caregiver; excluding co morbidities. Then choosing the most appropriate sleep test, if necessary: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), actigraphy or video-PSG. This first step allows the diagnosis of one of the above mentioned sleep-arousal disturbances. (2) The non-specific therapeutic approach consists of: (a) checking the sleep effect on motor performance: beneficial, worse or neutral. (b) Dopaminergic adjustment is necessary due to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals which alter the normal modulator mechanisms of motor centers in LPD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and non-REM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates LPD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. L-Dopa has also an arousal effect on Non-REM sleep, repeatedly awakening the patient and enhancing the fragmentation due to the involuntary movements. (c) Socio-physical assistance. (3) The specific therapy consists of: LFS-Sinemet CR, Tolcapone, Intranasal Desmopressin, Domperidon, Cisapride and neurosurgery; SRBD-CPAP, UPPP, nasal interventions, losing weight; RLS-PLM-Benzodiazepine (Clonazepam), Opioid, Apomorphine infusion; RBD-Clonazepam and dopaminergic agonists; SRH-Clozapine, Risperidone; SRPD-Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual LPD patient.
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PMID:Approaching disturbed sleep in late Parkinson's Disease: first step toward a proposal for a revised UPDRS. 1148 77

REM sleep behaviour disorder (RBD) is characterized by savage extremities movements and by vocalizations associated with vivid dreams in REM sleep and by insufficient muscle atonia in REM sleep. Videopolysomnography was performed in nine patients (six men and three women, average age 59.8, SD +/- 7.2 years) suffering from Parkinson's disease (PD). The insufficient muscle atonia was found in the records of four subjects. No behavioural symptoms of RBD were observed. The authors stress on the disposition to RBD in great number of patients with RBD and on the necessity to look for RBD by detailed disease history.
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PMID:[Manifestations of abnormal behavior during REM sleep in all-night polysomnography in patients with Parkinson disease]. 1170 74

We compared the sleep structure including a quantitative electroencephalographic (EEG) analysis and the frequency of periodic limb movements (PLM) in 17 patients with Parkinson's disease (PD; 10 men, seven women, mean age 65.9 years, mean Hoehn and Yahr stage 1.8) who had never been treated with dopaminergic agents (de novo), and 10 healthy controls (six men, four women, mean age 64.5 years). The REM sleep EEG of the PD patients was characterized by a sustained increase in the high-theta/alpha (7.8-10.5 Hz) frequency range during the first one-third (i.e., 11.00 p.m. to 01.40 a.m.) of the night. There was no significant difference in the sleep continuity and sleep architecture as well as in the PLM index between both groups. The analysis of the temporal dynamics of the observed changes suggests a dysregulation of the REM sleep homeostasis in the patients with PD.
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PMID:Increased alpha activity in REM sleep in de novo patients with Parkinson's disease. 1174 25

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


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