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)

Recent years have brought increased awareness of and attention to the non-motor aspects of Parkinson's disease. Non-motor features encompass a surprisingly broad clinical spectrum that includes sensory dysfunction, behavioral abnormalities, autonomic impairment, sleep disturbances, and fatigue. Some of these features, such as impaired olfaction, REM sleep behavior disorder, and constipation, may develop long before the classic motor features of Parkinson's disease make their appearance, while others emerge in concert with disease progression. The early emergence of some non-motor features presents diagnostic opportunities, while the dopa-unresponsiveness of others poses treatment challenges, especially in the advanced stages of the disease.
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PMID:Non-motor parkinsonism. 1826 38

Functional imaging can be used to detect preclinical evidence of dopamine deficiency in people deemed to be at increased risk of Parkinson's disease (PD) based on genetic or environmental risk, or because they have clinical features such as REM sleep behaviour disorder that may be a harbinger of PD. Positron emission tomography (PET) using [11C]dihydrotetrabenazine to label the vesicular monoamine transporter type 2 (VMAT2), a variety of 11C- or 18F-labeled ligands for the membrane dopamine transporter (DAT), or 6-[18F]fluoro-L-dopa (FD), which assesses uptake and decarboxylation of levodopa as well as vesicular storage of radiolabeled dopamine, can all be used, and all provide comparable, but somewhat different information. DAT binding using either PET or SPECT appears to be the most sensitive marker of dopamine denervation, while FD uptake is subject to compensatory upregulation and its reduction may more closely herald the onset of clinical disease. Alterations in glucose metabolism and in dopamine release also occur in the asymptomatic hemisphere of subjects with unilateral PD. An interesting potential application of PET is the determination of non-dopaminergic abnormalities that correlate with the presence of clinically apparent pre-motor symptoms of PD.
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PMID:Positron emission tomography in premotor Parkinson's disease. 1826 75

In the aging population of many countries in the world, neurodegenerative diseases like Parkinson's disease (PD) are becoming an increasing burden. Therefore, early therapy and ultimately disease prevention is essential, which is only possible with an early diagnosis. Besides a genetic predisposition, a number of biomarkers are being discussed to indicate vulnerability to PD, some of them many years before disease manifestation. These include hyperechogenicity of the substantia nigra as well as premotor symptoms like olfactory and autonomic dysfunction, depression, REM sleep behavior disorder, and neuropsychological impairment. Moreover, first signs of affection of the substantia nigra like PET and SPECT abnormalities and slight motor signs can be included, as they may be detected before a definite diagnosis according to motor symptoms can be made. Interestingly, other frequent neurodegenerative disorders like Alzheimer's disease (AD) are also characterized by a long preclinical period, with several biomarkers discussed as indicative for disease vulnerability including cerebrospinal fluid, serum, and neuroimaging biomarkers, olfactory dysfunction as well as subtle neuropsychological deficits. However, future studies are necessary, which establish the predictive value of these markers singularly and in combination to detect a subgroup of the population at risk for PD and AD not only to accelerate research on etiology and pathophysiology but also to promote testing for neuroprotective strategies.
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PMID:Biomarkers for the early detection of Parkinson's and Alzheimer's disease. 1832 70

Sleep disorders in Parkinson's disease (PD) are frequent and have numerous etiologies. Both nighttime sleep disturbances and daytime sleepiness can occur. The key to effective treatment is appropriate diagnosis. A careful interview of the patient and his or her bed partner provides direction for additional evaluations. Referral to a sleep specialist for quantitative studies is necessary to evaluate for rapid eye movement (REM) sleep behavior disorder, sleep apnea, periodic limb movements, and other sleep disorders. Excessive daytime sleepiness may be attributed to interrupted nighttime sleep or daytime medications (particularly the dopamine agonists) or it may be intrinsic to PD. When the diagnosis is established, treatment is directed toward the primary sleep disturbance. Fragmented sleep due to recurrence of PD symptoms may improve with the use of long-acting preparations of carbidopa/levodopa. Sleep apnea is treated using continuous positive airway pressure, and REM sleep behavior disorder may improve using pharmacologic interventions, although controlled trials are lacking. Restless legs syndrome and periodic limb movements during sleep are treated with direct dopaminergic agonists at bedtime. Excessive daytime sleepiness related to the use of direct dopaminergic agonists may improve with dosage reduction or discontinuation. Stimulants such as modafinil may provide modest benefit.
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PMID:Sleep disorders in Parkinson's disease. 1857 25

REM sleep behavior disorder (RBD) is commonly associated with Parkinson disease (PD), but it is unclear whether this association has implications for disease manifestations. We evaluated 36 PD patients for the presence of RBD by polysomnography. Patients underwent an extensive evaluation by a movement disorders specialist blinded to polysomnography results. Severity of motor manifestations, autonomic, visual, psychiatric, and olfactory dysfunctions and quality of life (QOL) were assessed, and compared using regression analysis that adjusted for disease duration, age and sex. Severity of motor manifestations did not differ between groups. However, the presence of RBD in PD was strongly associated with symptoms and signs of orthostatic hypotension (systolic blood pressure lying to standing = -25.7 +/- 13.0 mmHg vs. -4.9 +/-14.1, P < 0.001); and orthostatic symptom prevalence = 71% vs. 27%, P = 0.0076). There was no association between RBD and other autonomic symptoms. Color vision was worse in patients with RBD, but olfactory dysfunction did not differ between groups. The prevalence of depression, hallucinations, paranoia, and impulse disorders did not differ between groups. Emotional functioning and general health QOL measures were lower in those with RBD, but there were no differences between groups on disease-specific indices or on measures of overall physical QOL. These findings suggest that the pathophysiology of RBD and nonmotor manifestations of PD, particularly autonomic dysfunction, are linked.
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PMID:Manifestations of Parkinson disease differ in association with REM sleep behavior disorder. 1870 86

Rapid eye movement sleep behaviour disorder (RBD) may serve as a useful indicator to approach Parkinson's disease (PD); however, PD patients do not always exhibit RBD. We wondered whether the presence of RBD would be reflected in the expansion of PD lesions and represent the same PD entity. We examined the clinical differences between PD with and without RBD and studied the frequency of RBD-like symptoms (RBD-s) and clinical differences in 150 PD patients, including 81 patients (54.0%) who satisfied the International Classification of Sleep Disorders, Revised, minimum clinical criteria for RBD. RBD-s preceding the appearance of parkinsonism were found in 44.4% of patients. Statistically, the presence of RBD-s was associated with ages above 65 years, male gender, constipation, dopa-induced dyskinesia and 'sleep attack', with odds ratios of 3.709, 2.469, 2.184, 5.046 and 6.562, respectively. No differences were found between the 2 groups with regard to symptoms at PD onset, disease duration, Hoehn-Yahr stage, hallucination, dementia, wearing-off, orthostatic hypotension, cerebral blood flow and antiparkinsonism drugs. In the early stage, RBD and autonomic system dysfunction are important factors in the progression of PD.
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PMID:Parkinson's disease with and without REM sleep behaviour disorder: are there any clinical differences? 1912 3

Substantia nigra (SN) hyperechogenicity--a sonographic vulnerability marker for Parkinson's disease (PD)--has been recently described in patients with idiopathic REM sleep behaviour disorder (RBD). It is not known whether subjects with narcolepsy (who frequently have associated RBD) also show SN hyperechogenicity. The aim of this study was to (1) evaluate SN echogenicity in narcolepsy and (2) determine whether transcranial sonography (TCS) differs in narcoleptic subjects with and without RBD. A total of 16 patients with narcolepsy-cataplexy (7 had a concomitant, video-polysomnographically based diagnosis of RBD) were examined with TCS by two investigators blinded to the clinical data. The size of the SN echogenic area in both subgroups was within the range previously described for healthy subjects. The brainstem raphe, however, was reduced in five of seven narcoleptic subjects with RBD, whereas only two of nine narcoleptic subjects without RBD exhibited this TCS finding. We conclude that evaluation of SN echogenicity does not discriminate between both subgroups. The absence of SN hyperechogenicity in narcoleptic patients with RBD supports the hypothesis that SN hyperechogenicity in patients with presumed idiopathic RBD is an additional risk marker for subsequent evolvement of PD rather than an RBD-immanent finding. Reduced echogenicity of the brainstem raphe might indicate an involvement of the serotonergic system in narcoleptic subjects with RBD.
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PMID:Transcranial midbrain sonography in narcoleptic subjects with and without concomitant REM sleep behaviour disorder. 1925 99

REM sleep behavior disorder (RBD) is characterized by vigorous movements associated with unpleasant dreams and increased electromyographic activity during REM sleep. Polysomnography with audiovisual recording is needed to confirm the diagnosis of RBD and to exclude other sleep disorders that can mimic its symptoms including obstructive sleep apnea, nocturnal hallucinations and confusional awakenings. RBD may be idiopathic or related to neurodegenerative diseases, particularly multiple system atrophy, Parkinson's disease and dementia with Lewy bodies. RBD may be the first manifestation of these disorders, antedating the onset of parkinsonism, cerebellar syndrome, dysautonomia, and dementia by several years. RBD should thus be considered an integral part of the disease process. When effective, neuroprotective strategies should be considered in subjects with idiopathic RBD. Patients with other neurodegenerative diseases, though, such as spinocerebellar ataxias, may also present with RBD. When clinically required, clonazepam at bedtime is effective in decreasing the intensity of dream-enacting behaviors and unpleasant dreams in both the idiopathic and secondary forms. When part of a neurodegenerative disorder the development of RBD is thought to reflect the location and extent of the underlying lesions involving the REM sleep centers of the brain (e.g., locus subceruleus, amygdala, etc.), leading to a complex multiple neurotransmitter dysfunction that involves GABAergic, glutamatergic and monoaminergic systems. RBD is mediated neither by direct abnormal alpha-synuclein inclusions nor by striatonigral dopaminergic deficiency alone.
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PMID:The clinical and pathophysiological relevance of REM sleep behavior disorder in neurodegenerative diseases. 1939 52

Parkin gene mutations cause a juvenile parkinsonism. Patients with these mutations may commonly exhibit REM sleep behaviour disorders, but other sleep problems (insomnia, sleepiness, restless legs syndrome) have not been studied. The aim of this study was to evaluate the sleep-wake phenotype in patients with two parkin mutations, compared with patients with idiopathic Parkinson's disease (iPD). Sleep interview and overnight video-polysomnography, followed by multiple sleep latency tests, were assessed in 11 consecutive patients with two parkin mutations (aged 35-60 years, from seven families) and 11 sex-matched patients with iPD (aged 51-65 years). Sleep complaints in the parkin group included insomnia (73% patients versus 45% in the iPD group), restless legs syndrome (45%, versus none in the iPD group, P = 0.04), and daytime sleepiness (45%, versus 54% in the iPD group). Of the parkin patients, 45% had REM sleep without atonia, but only 9% had a definite REM sleep behavior disorder. All sleep measures were similar in the parkin and iPD groups. Two parkin siblings had a central hypersomnia, characterized by mean daytime sleep latencies of 3 min, no sleep onset REM periods, and normal nighttime sleep. Although the patients with two parkin mutations were young, their sleep phenotype paralleled the clinical and polygraphic sleep recording abnormalities reported in iPD, except that restless legs syndrome was more prevalent and secondary narcolepsy was absent.
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PMID:Restless legs syndrome, rapid eye movement sleep behavior disorder, and hypersomnia in patients with two parkin mutations. 1967 85

Rapid eye movement sleep behavior disorder (RBD) is commonly accompanied in Parkinson disease (PD). However, the underlying mechanism linking RBD to PD remains unclear. We interviewed and examined 447 consecutive patients with PD to investigate factors associated with the presence of RBD in PD patients. Using the minimal diagnostic criteria for parasomnias provided in the International Classification of Sleep Disorders-Revised (ICSD-R), 164 patients (36.5%) were diagnosed with clinically probable RBD (cpRBD). PD patients with cpRBD were older, had a longer duration of PD, a more severe level of disability, a longer duration of antiparkinsonian medication, and a lower proportion of their Unified Parkinson Disease Rating Scale (UPDRS) scores accounted for by tremor than those without RBD. Multivariate and univariate logistic regression analyses revealed that patient age, PD symptom duration (and, accordingly, more severe motor disability), tremor score, and proportion of the UPDRS score accounted for by tremor were significant factors associated with the presence of RBD in PD patients. The results of the present study support previous observations that PD with RBD may result from a different underlying pattern of neurodegeneration than PD without RBD.
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PMID:Factors related to clinically probable REM sleep behavior disorder in Parkinson disease. 1971 33


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