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)

Narcolepsy is a severe debilitating chronic life-long sleep disorder that can be ameliorated but not cured. In the United States, its prevalence is at least 1 in 1000 making it more common than multiple sclerosis or Parkinson's disease. Its symptoms lead to severe lifestyle consequences, with profound impact on the affected persons, their interpersonal relationships, job, school experiences, and family life. Despite this, little has appeared in the nursing literature about the disorder. The most characteristic symptoms include uncontrollable excess daytime sleepiness, cataplexy (bilateral voluntary muscle weakness), sleep paralysis, hypnagogic hallucinations and disturbed night-time sleep. Characteristics of normal sleep are reviewed and compared with disturbances seen in narcolepsy. The aetiology, assessment, diagnosis, pharmacologic therapy, non-pharmacologic therapy and psychosocial issues are discussed along with needed research directions.
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PMID:Narcolepsy: a review of a common, life-long sleep disorder. 306 1

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

We report the findings of a total population survey of Thugbah community in the Eastern Province of Saudi Arabia (SA) to determine its point prevalence of neurological diseases. During this two-phase door-to-door study, all Saudi nationals living in Thugbah were first screened by trained interviewers using a pretested questionnaire (sensitivity 98%, specificity 89%) administered at a face-to-face interview. Individuals with abnormal responses were then evaluated by a neurologist using specific guidelines and defined diagnostic criteria to document neurological disease. The questionnaire was readministered blind by a neurologist to all those with abnormal responses and a 1-in-20 random sample of those without abnormal responses, respectively. The family members of an individual with an abnormal response were also screened to improve accuracy. A total of 23,227 Saudis (98% of the eligible subjects) were screened and those residing in Thugbah on the reference date (22,630) were used to calculate the point prevalence rates. Forty-two percent of those screened were in the first decade of life and only 1.5% were more than 60 years old. There were marginally more females (50.2%) than males (49.8%). Consanguineous marriages especially between first cousins were present in 54.6%. The demographic characteristics of Thugbah community were similar to those in other parts of SA. The overall crude prevalence ratio (PR) for all forms of neurological disease was 131/1,000 population. All subsequent PRs are per 1,000 population. Headache syndromes were the most prevalent disorder (PR 20.7). The PR for all seizure disorders was 7.60, and the epilepsies (6.54) were more frequent than febrile convulsions (0.84). Mental retardation, cerebral palsy syndrome, and microcephaly were common pediatric problems with PRs of 6.27, 5.30 and 1.99, respectively. Stroke, Parkinson's disease, and Alzheimer's disease were uncommon with respective PRs of 1.8, 0.27 and 0.22. Central nervous system (CNS) malformations (0.49) such as hydrocephalus and meningomyelocele were more prevalent than spinal muscular atrophy (0.13), congenital brachial palsy (0.13) and narcolepsy (0.04). Multiple sclerosis was rare (0.04). Osteoarthritis and low back pain syndromes were the main non-neurological conditions seen. The major medical diseases that may be neurologically relevant were diabetes mellitus, hypertension, and connective tissue disorders.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A community survey of neurological disorders in Saudi Arabia: the Thugbah study. 827 77

Phantom measurements were performed with a conventional single-head single-photon emission tomography (SPET) camera in order to validate the relevance of the basal ganglia/frontal cortex iodine-123 iodobenzamide (IBZM) uptake ratios measured in patients. Inside a cylindrical phantom (diameter 22 cm), two cylinders with a diameter of 3.3 cm were inserted. The activity concentrations of the cylinders ranged from 6.0 to 22.6 kBq/ml and the cylinder/background activity ratios varied from 1.4 to 3.8. From reconstructed SPET images the cylinder/background activity ratios were calculated using three different regions of interest (ROIs). A linear relationship between the measured activity ratio and the true activity ratio was obtained. In patient studies, basal ganglia/frontal cortex IBZM uptake ratios determined from the reconstructed slices using attenuation correction prior to reconstruction were 1.30 +/- 0.03 in idiopathic Parkinson's disease (n = 9), 1.33 +/- 0.09 in infantile and juvenile neuronal ceroid lipofuscinosis (n = 7) and 1.34 +/- 0.05 in narcolepsy (n = 8). Patients with Huntington's disease had significantly lower ratios (1.09 +/- 0.04, n = 5). The corrected basal ganglia/frontal cortex ratios, determined using linear regression, were about 80% higher. The use of dural-window scatter correction increased the measured ratios by about 10%. Although comprehensive correction methods can further improve the resolution in SPET images, the resolution of the SPET system used by us (1.5-2 cm) will determine what is achievable in basal ganglia D2 receptor imaging.
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PMID:Validation of quantitative brain dopamine D2 receptor imaging with a conventional single-head SPET camera. 840 54

This article reviews the results of clinical studies with Deprenyl in various neurologic and psychiatric disorders except Parkinson's disease. Promising results could be observed both in narcolepsy in a dose of at least 20 mg/day in three different trials and in one study of Tourette's syndrome including attention hyperactivity disorders using an average dosis of 8.1 mg/ day. Controversial results were reported for Alzheimer's disease. On the one hand significant improvement of cognitive functions was found by various authors. On the other hand in a more recent study no effect on the progression of the disease could be observed. For depression a higher dosage of deprenyl between 30 to 60 mg/day appears to be necessary for effective treatment. No positive results were found in amyotrophic lateral sclerosis and in tardive dyskinesias.
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PMID:The clinical potential of Deprenyl in neurologic and psychiatric disorders. 898 64

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

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

Disorders of excessive daytime sleepiness (EDS) constitute a major health hazard, since impaired alertness may lead to accidents and poor quality of life, and some of them are associated with increased cardiovascular morbidity and mortality. Many disorders of EDS are neurological diseases (e.g. narcolepsy and periodic limb movements in sleep, PLMS). The largest group of disorders causing EDS consists of sleep-related disturbances of breathing, where neuroregulatory mechanisms play a major role in pathophysiology. Many patients with neurodegenerative and neuromuscular diseases suffer from sleep disturbances associated with EDS. Therefore, neurologists must be acquainted with the differential diagnosis of EDS and the major categories of sleep disorders causing it. The present update focuses on major sleep disorders causing EDS, and approaches the topic from the neurologist's perspective. Rather than being an extensive review, this update includes recent data on epidemiology, pathophysiology, diagnosis and treatment of obstructive sleep apnea and related conditions (increased upper airway resistance syndrome, central sleep apnea), as well as of narcolepsy and PLMS. Also included are recent data concerning EDS in neurodegenerative (Alzheimer's disease, Parkinson's disease, multiple system atrophy) and neuromuscular disorders.
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PMID:Disorders of excessive daytime sleepiness--an update. 951 78

Complex visual hallucinations may affect some normal individuals on going to sleep and are also seen in pathological states, often in association with a sleep disturbance. The content of these hallucinations is striking and relatively stereotyped, often involving animals and human figures in bright colours and dramatic settings. Conditions causing these hallucinations include narcolepsy-cataplexy syndrome, peduncular hallucinosis, treated idiopathic Parkinson's disease, Lewy body dementia without treatment, migraine coma, Charles Bonnet syndrome (visual hallucinations of the blind), schizophrenia, hallucinogen-induced states and epilepsy. We describe cases of hallucinosis due to several of these causes and expand on previous hypotheses to suggest three mechanisms underlying complex visual hallucinations. (i) Epileptic hallucinations are probably due to a direct irritative process acting on cortical centres integrating complex visual information. (ii) Visual pathway lesions cause defective visual input and may result in hallucinations from defective visual processing or an abnormal cortical release phenomenon. (iii) Brainstem lesions appear to affect ascending cholinergic and serotonergic pathways, and may also be implicated in Parkinson's disease. These brainstem abnormalities are often associated with disturbances of sleep. We discuss how these lesions, outside the primary visual system, may cause defective modulation of thalamocortical relationships leading to a release phenomenon. We suggest that perturbation of a distributed matrix may explain the production of similar, complex mental phenomena by relatively blunt insults at disparate sites.
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PMID:Complex visual hallucinations. Clinical and neurobiological insights. 979 40

Recently, sudden "sleep attacks" have been described in parkinsonian patients taking the nonergoline dopamine agonists pramipexole and ropinirole. Due to this possible side effect, patients must be instructed not to drive vehicles and to refrain from other activities carrying the risk of self-injury. However, the very existence of sleep attacks remains controversial in sleep medicine, since a gradual transition from wakefulness to sleep is normally observed. Accordingly, sudden onset of sleep, e.g., in narcolepsy or sleep apnea syndrome, is usually associated with excessive daytime sleepiness. Prevalence of sleep disorders and daytime sleepiness have been shown to be increased in Parkinson's disease. Nonergoline dopamine agonists are already known to induce somnolence. Currently, it is not predictable whether sleep attacks represent a sudden transition from wakefulness to sleep or result from an increased propensity to fall asleep, with patients perceiving a sudden onset. Possible pathophysiological mechanisms and legal implications of sleep attacks are discussed.
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PMID:["Sleep attacks" in Parkinson patients. A side effect of nonergoline dopamine agonists or a class effect of dopamine agonists?]. 1099 19


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