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)

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

Sleep-disordered breathing may be present in patients with degenerative diseases affecting the brainstem. Indeed, this last structure contains the executive system of rapid eye movement (REM) sleep (tegmentum of the pons), of respiratory drive (medulla oblongata and pons) and motor neurons of upper airways dilators (fifth, seventh, ninth, tenth and twelfth cranial roots). Patients with Parkinson's disease suffer frequently from insomnia, partly caused by nocturnal motor disability, and from REM sleep behavior disorder. In 20 percent of the patients, excessive daytime sleepiness is caused by a sleep apnea syndrome, with a partly levodopa-dependent upper airway dysfunction. In 40 percent of the patients, sleepiness mimics a secondary narcolepsy and may be associated with hypnagogic hallucinations. During supranuclear palsy, REM sleep is progressively curtailed with rare sleep-disordered breathing. Patients with multiple systemic atrophy may present a nocturnal stridor caused by laryngeal palsy and benefit from tracheotomy or continuous nasal positive airway pressure. Seldom sleep and respiratory studies in genetic ataxic diseases suggest a normal respiratory drive, occasional diaphragmatic dysfunction and night hypopneas. During amyotrophic lateral sclerosis, the progressive loss of phrenic nerve leads to a diaphragmatic dysfunction, dyspnea and a lesser survival. Adequate ventilation is jeopardized during REM sleep with a consequent loss of this state.
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PMID:[Respiratory disorders during sleep in degenerative diseases of the brain stem]. 1192 29

Controversial reports of sudden onset 'sleep attacks' resulting in road traffic accidents have recently been reported in patients with Parkinson's disease (PD) taking the non-ergot dopamine D(2 )/D(3) receptor agonists pramipexole and ropinirole. These reports have generated considerable debate as the concept of 'sleep attacks' is disputed amongst sleep specialists and most believe that isolated 'sleep attacks' not preceded by warning on the background of chronic sleepiness or 'unintended sleepiness' do not exist. A series of case reports suggested that this phenomenon may not be exclusive to the non-ergot dopamine agonists such as pramipexole or ropinirole and indeed may occur with most dopaminergic agents. Recent evidence suggest that a 'sleepiness' or 'hypoactivity' reaction to dopaminergic therapy may be related to underlying dopamine deficiency of PD rather than a drug effect. In this report we provide the evidence for the phenomenon being a class effect attributable to all dopamine agonists currently employed in the management of PD. Controversy surrounding excessive daytime sleepiness (EDS) in PD and the use of the Epworth Sleepiness Scale (ESS) in relation to PD is also discussed. In spite of variable reports, EDS is recognised to be common in PD and is likely to be related to both the disease process and drug therapy. Studies using multiple sleep latency tests have also reported differing results in PD although a recent study indicated that a subset of 'sleepy' patients with PD may experience pathological somnolence with resultant detrimental consequence on daytime and cognitive functions. We recommend that the issue of 'sleepiness' or 'sleep attacks' in PD should be routinely checked in all patients with PD and indirectly assessed by using either the ESS or the recently introduced Parkinson's Disease Sleep Scale. Those with reported 'sleep attacks' or 'unintended sleep episodes' and excessive daytime sleepiness while taking dopamine agonists or dopaminergic agents such as levodopa should have a review of their medication, should not be driving a car on their own and some may merit formal sleep architecture studies. The latter may identify sleep disorders such as secondary narcolepsy which may benefit from the use of a wakefulness promoting agent.
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PMID:'Sleep attacks' or 'unintended sleep episodes' occur with dopamine agonists: is this a class effect? 1209 5

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

Hallucinations (mainly visual), psychosis and excessive daytime sleepiness are potential side-effects of dopaminergic treatment. They may require a reduction or suppression of dopaminergic agonists, and the prescription of atypical neuroleptic agents or vigilance-enhancing drugs. The recent description of narcolepsy-like sleep onset in rapid eye movement sleep periods synchronous with hypnagogic hallucinations in patients with dopaminergic-induced psychosis or excessive daytime sleepiness, suggests that the mesodiencephalic lesions may predispose to the psychic effects of dopaminergic treatment. Disease-related mood disorders, sexual compulsions, gambling or levodopa addiction may also be amplified by the antiparkinsonian treatment. These complications illustrate the neuro-psychic aspect of Parkinson's disease: psychic troubles may result from a subtle balance between the direct effects of drugs, the pre-morbid pathological personality and the cortical and subcortical lesions.
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PMID:[Psychic disorders and excessive daytime sleepiness] 1269 Mar 20

Hallucinations (mainly visual), psychosis and excessive daytime sleepiness are potential side-effects of dopaminergic treatment. They may require a reduction or suppression of dopaminergic agonists, and the prescription of atypical neuroleptic agents or vigilance-enhancing drugs. The recent description of narcolepsy-like sleep onset in rapid eye movement sleep periods synchronous with hypnagogic hallucinations in patients with dopaminergic-induced psychosis or excessive daytime sleepiness, suggests that the mesodiencephalic lesions may predispose to the psychic effects of dopaminergic treatment. Disease-related mood disorders, sexual compulsions, gambling or levodopa addiction may also be amplified by the antiparkinsonian treatment. These complications illustrate the neuro-psychic aspect of Parkinson's disease: psychic troubles may result from a subtle balance between the direct effects of drugs, the pre-morbid pathological personality and the cortical and subcortical lesions.
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PMID:[Psychic disorders and somnolence]. 1269 Jun 69

Pedunculopontine tegmental nucleus is formed by an ensemble of cholinergic and non-cholinergic neurons located in the caudal pontomesencephalic tegmentum, surrounding the superior cerebellar peduncle. It is an integral part of the reticulate formation of the brain stem, with extensive anatomical connections and highly varied functions. By means of ascendant projections that it sends to the thalamus, it intervenes in the waking-sleep cycle. Besides, it constitutes the most caudal nucleus of the neuroaxis, receiving connections from the basal ganglia, for which reason it has attracted the interest of those researchers concerned with the study of these structures. Thanks to its reciprocal connections with the basal ganglia, as well as to its descending projections to different structures of the pons, medulla and spinal cord; it has been related to the control of locomotion. Recently, it has also been considered as a possible centre for the integration of the motor information provided by the dorsal striatum with the motivational or limbic information proceeding from the ventral striatum, to permit its direct access to bulbar or spinal motor centres. In this work we will review its anatomical and functional characteristics, as well as its implication in some diseases of the nervous system such as narcolepsy, progressive supranuclear paralysis, schizophrenia and Parkinson's disease.
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PMID:[Pedunculopontine tegmental nucleus. Anatomy, functional considerations and physiopathological implications]. 1288 47

The spectrum of rapid eye movement behavior disorders (RBD) spans various age groups, with the greatest prevalence in elderly men. Major diagnostic features include harmful or potentially harmful sleep behaviors that disrupt sleep continuity and dream enactment during rapid eye movement sleep. In RBD patients, the polysomnogram during rapid eye movement sleep demonstrates excessive augmentation of chin electromyogram or excessive chin or limb phasic electromyogram twitching. RBD may be associated with various neurodegenerative disorders, such as multiple system atrophy, Parkinson's disease, and dementia with Lewy bodies. Other co-morbid conditions may include narcolepsy, agrypnia excitata, sleepwalking, and sleep terrors. RBD is hypothesized to be caused by primary dysfunction of the pedunculo-pontine nucleus or other key brainstem structures associated with basal ganglia pathology or, alternatively, from abnormal afferent signals in the basal ganglia leading to dysfunction in the midbrain extrapyramidal area/ pedunculo-pontine nucleus regions.
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PMID:Review of rapid eye movement behavior sleep disorders. 1498 89

REM sleep behaviour disorder (RBD) and olfactory dysfunction are common and very early features of alpha-synucleinopathies, in particular Parkinson's disease. To investigate the hypothesis that these two clinical features in combination are an indicator of evolving alpha-synucleinopathy, olfactory function was assessed in RBD. We studied 30 patients (18 male, 12 female; mean age 48 +/- 14 years, range 19-78 years) with clinical (idiopathic, n = 6; symptomatic, n = 13, mostly associated with narcolepsy) or subclinical (n = 11, associated with narcolepsy) RBD according to standard criteria and 30 age- and gender-matched healthy control subjects using standardized 'Sniffin' Sticks'. RBD patients had a significantly higher olfactory threshold (P = 0.0001), lower discrimination score (P = 0.003), and lower identification score (P = 0.001). Compared with normative data, 97% of the RBD patients had a pathologically increased olfactory threshold, 63% an impaired odour discrimination score, and 63% a decreased identification score. On neurological examination, signs of parkinsonism were newly found in five patients with clinical RBD (not associated with narcolepsy), who usually had a long history of 'idiopathic' RBD. Four of the five patients fulfilled the UK Brain Bank criteria for the clinical diagnosis of Parkinson's disease. The underlying nigrostriatal degeneration of clinical Parkinson's disease was confirmed by I-123-FP-CIT SPECT in one patient and early nigrostriatal degeneration was identified by SPECT in a further two patients with 'idiopathic' clinical RBD out of 11 RBD patients who agreed to undergo SPECT studies. Our study shows that RBD patients have a profound impairment of olfactory function. Five patients with clinical RBD not associated with narcolepsy had clinical or imaging signs of nigrostriatal degeneration. This new clinical finding correlates with the neuropathological staging of Parkinson's disease (stages 1-3) as proposed by Braak. In stage 1, the anterior olfactory nucleus or the olfactory bulb is affected (along with the dorsal motor nucleus of the glossopharyngeal and vagal nerves). In stage 2, additional lesions consistently remain confined to the medulla oblongata and pontine tegmentum, which are critical areas for RBD. Midbrain lesions are found only in stage 3, in particular degeneration of dopaminergic neurons in the substantia nigra pars compacta. Thus, 'idiopathic' RBD patients with olfactory impairment might present with stage 2 preclinical alpha-synucleinopathy. Since narcoleptic patients are not known to have an increased risk of developing parkinsonism, the pathophysiology and clinical relevance of hyposmia in RBD/narcolepsy patients requires further research.
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PMID:Combination of 'idiopathic' REM sleep behaviour disorder and olfactory dysfunction as possible indicator for alpha-synucleinopathy demonstrated by dopamine transporter FP-CIT-SPECT. 1554 52


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