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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

Terguride, an analogue of lisuride, decreased locomotor activity, produced cataplexy, and blocked apomorphine-induced stereotypic behavior. It did not induce stereotypies in rodents or emesis in dogs. However, in rats with unilateral 6-hydroxydopamine lesions of the substantia nigra, terguride produced contralateral rotation. Terguride bound to D-2 striatal dopamine receptors. Terguride has both agonist and antagonist actions at striatal dopamine receptors, but chronic administration did not produce behavioral supersensitivity. These pharmacologic properties differ from those of other antiparkinsonian agents; terguride may be effective for the chronic treatment of Parkinson's disease.
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PMID:Terguride, a mixed dopamine agonist-antagonist, in animal models of Parkinson's disease. 356 89

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

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

There are many reasons for patients with idiopathic Parkinson's disease to develop sleep disorders and subsequent daytime sleepiness. Important causes are reduction of total sleep duration and sleep efficiency, and an increase in respiratory and motor arousals. This daytime sleepiness at first glance seems different from the "sleep attacks" which caused motot vehicle mishaps reported recently in persons taking pramipexole and ropinirole. There is, however, only little evidence that we deal with a new phenomenon in a new clinical situation, i. e. cataplexy-like attacks after high doses of new non-ergot dopamine-agonists. Until now there is no single case of a proven cataplexy on one hand, and older dopamine agonists like pergolide as well as L-Dopa + carbidopa have been reported to induce sudden onsets of sleep, too.
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PMID:Parkinson's disease and sleep. 1119 12

Patients with Parkinson's disease (PD) and parkinsonian syndromes (eg, dementia with Lewy bodies, multisystem atrophy, and Shy-Drager syndrome) suffer from daytime sleepiness. Sleepiness in PD is common (10% to 50% of patients) and very real, often approaching levels observed in the prototypical disorder of sudden-onset sleep, viz, and narcolepsy with cataplexy. Physicians need to be vigilant in assessing parkinsonian patients for sleepiness, because treatment can dramatically enhance quality of life and prevent the significant morbidity and mortality that attends daytime sleepiness. Men with advanced disease, cognitive impairment, drug-induced psychosis, and orthostatic hypotension are most at risk for developing pathologic sleepiness. Because primary sleep disorders can coexist with Parkinsonism (eg, sleep apnea, insufficient or interrupted sleep), these potential causes should be carefully assessed with polysomnography and treated appropriately. Dopaminomimetics may exacerbate sleepiness in a small subset of patients. The primary pathologies involved in Parkinsonism appear to be the greatest contributors to the development of daytime sleepiness. Sleepiness in Parkinsonism, especially a narcolepsy-like phenotype, may necessitate treatment with wake-promoting agents, such as bupropion, modafinil, or traditional psychostimulants.
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PMID:Sleepiness and Unintended Sleep in Parkinson's Disease. 1267 Apr 12

Patients with Parkinson's disease and parkinsonian syndromes (eg, dementia with Lewy body disease, multisystem atrophy, and Shy-Drager syndrome) suffer from daytime sleepiness. This sleepiness is common and very real, often approaching levels observed in the prototypical disorder of sudden-onset sleep, namely narcolepsy/cataplexy. Physicians need to be vigilant in assessing parkinsonian patients for sleepiness because treatment can dramatically enhance quality of life and prevent the significant morbidity and mortality that attends daytime sleepiness. Male patients with advanced disease, cognitive impairment, drug-induced psychosis, and orthostatic hypotension are most at risk for developing pathologic sleepiness. Because primary sleep disorders can coexist with parkinsonism (eg, sleep apnea, insufficient or interrupted sleep), these potential causes should be carefully assessed with polysomnography and treated appropriately. Dopaminomimetics exacerbate sleepiness in a small subset of patients in a dose-dependent fashion. Nonetheless, the primary pathologies involved in parkinsonism appear to be the greatest contributors to daytime sleepiness. Sleepiness in parkinsonism, especially a narcolepsy-like phenotype, may necessitate treatment with wake-promoting agents such as bupropion, modafinil, or traditional psychostimulants.
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PMID:Excessive daytime sleepiness and unintended sleep in Parkinson's disease. 1652 72

Narcolepsy is a chronic neurologic disease characterized by excessive daytime sleepiness and one or more of three additional symptoms (cataplexy, or sudden loss of muscle tone; vivid hallucinations; and brief periods of total paralysis) related to the occurrence of rapid eye movement (REM) sleep at inappropriate times. The daytime sleepiness typically presents as a sudden overwhelming urge to sleep, followed by periods of sleep that last for seconds or minutes, or even longer. During daytime sleep episodes, patients may exhibit "automatic behavior," performing conventionalized functions (eg, taking notes), but not remembering having done so once they are awake. About 10% of narcoleptics are members of familial clusters; however, genetic factors alone are apparently insufficient to cause the disease, inasmuch as the most common genetic disorder, a mutation in chromosome 6 controlling the HLA antigen immune complex, although seen in 90% to 100% of patients, also occurs in as many as 50% of people without narcolepsy. A dog model of narcolepsy exhibits a mutation on chromosome 12 that disrupts the processing of the peptide neurotransmitter hypocretin. No such mutation characterizes human narcolepsy; however, cerebrospinal fluid (CSF) hypocretin levels are profoundly depressed in narcoleptic patients, and a specific reduction in hypocretin-containing neurons has been described. One hypothesis concerning the pathophysiology of narcolepsy proposes that the HLA subtype resulting from the mutation on chromosome 6 increases the susceptibility of hypocretin-containing brain neurons to immune attack. Because hypocretin may normally participate in the maintenance of wakefulness, the loss of neurons that release this peptide might allow REM sleep to occur at inappropriate times, ie, while the patient is awake, in contrast to its normal cyclic appearance after a period of slow-wave sleep. The cataplexy, hallucinations, and/or paralysis associated with REM episodes normally are unnoticed-or, at least, not remembered-when the transition to REM follows slow wave sleep, as is normally the case; however, they are remembered when, in people with narcolepsy, the REM episode starts during a period of wakefulness. The association of narcolepsy with a deficiency in a specific neurotransmitter, in this case, hypocretin, is reminiscent of the associations between Parkinson disease and dopamine, or early Alzheimer disease and acetylcholine.
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PMID:Narcolepsy and the hypocretins. 1697 25

Much has been learned about the pathophysiology of narcolepsy over the last several decades. It is likely that hypocretin-producing cells in the lateral hypothalamus are selectively destroyed in genetically susceptible individuals carrying 1 or more alleles of HLA DQB1*0602. Despite advances, the causes of narcolepsy and how to prevent it remain elusive. Classic epidemiology aims not only to enumerate occurrence of disease in populations, but also to identify etiologic risk factors. This review details what the application of classic epidemiology has taught us so far about narcolepsy and suggests directions for future studies to clarify its etiology. The prevalence of narcolepsy with cataplexy has been examined in many studies and falls between 25 and 50 per 100,000 people. Information on incidence is limited, with 1 study finding the incidence of narcolepsy with cataplexy to be 0.74 per 100,000 person-years. The search for etiologic risk factors has yet to yield important associations. Factors most thoroughly examined include body mass index, immune responses, and stressful life events. Such associations may reflect a consequence rather than a cause of disease. As with other diseases characterized by selective cell loss, such as Parkinson disease or type 1 diabetes mellitus, narcolepsy is likely caused by environmental exposures before the age of onset in genetically susceptible individuals. Matching efforts in these other diseases and using large well-designed epidemiologic studies of narcolepsy, investigators must intensify the search for these exposures, focusing on the first 2 decades of life. Identification of modifiable risk factors will help to prevent this disease.
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PMID:The epidemiology of narcolepsy. 1731 Aug 60

These practice parameters pertain to the treatment of hypersomnias of central origin. They serve as both an update of previous practice parameters for the therapy of narcolepsy and as the first practice parameters to address treatment of other hypersomnias of central origin. They are based on evidence analyzed in the accompanying review paper. The specific disorders addressed by these parameters are narcolepsy (with cataplexy, without cataplexy, due to medical condition and unspecified), idiopathic hypersomnia (with long sleep time and without long sleep time), recurrent hypersomnia and hypersomnia due to medical condition. Successful treatment of hypersomnia of central origin requires an accurate diagnosis, individual tailoring of therapy to produce the fullest possible return of normal function, and regular follow-up to monitor response to treatment. Modafinil, sodium oxybate, amphetamine, methamphetamine, dextroamphetamine, methylphenidate, and selegiline are effective treatments for excessive sleepiness associated with narcolepsy, while tricyclic antidepressants and fluoxetine are effective treatments for cataplexy, sleep paralysis, and hypnagogic hallucinations; but the quality of published clinical evidence supporting them varies. Scheduled naps can be beneficial to combat sleepiness in narcolepsy patients. Based on available evidence, modafinil is an effective therapy for sleepiness due to idiopathic hypersomnia, Parkinson's disease, myotonic dystrophy, and multiple sclerosis. Based on evidence and/or long history of use in the therapy of narcolepsy committee consensus was that modafinil, amphetamine, methamphetamine, dextroamphetamine, and methylphenidate are reasonable options for the therapy of hypersomnias of central origin.
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PMID:Practice parameters for the treatment of narcolepsy and other hypersomnias of central origin. 1824 80


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