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)

Idiopathic REM sleep behavior disorder (RBD) predicts Parkinson's disease (PD) and dementia. However, the nature of the disease that emerges from RBD has not been fully characterized. Since 2004, we have been conducting a prospective study of idiopathic RBD patients, providing an opportunity to directly observe patients as they transitioned to a defined neurodegenerative syndrome. Patients with idiopathic RBD underwent an extensive annual evaluation of motor function, olfaction, color vision, autonomic function, cognition and psychiatric symptoms. Neurodegenerative disease was defined according to standard criteria. We compared these measures in patients who had developed PD to those with dementia, all within the first year of developing disease. Of 67 patients, 6 developed PD and eleven developed dementia. Except for cognitive functioning, all tests of olfaction, color vision, autonomic function, depression, and quantitative measures of motor speed were similar in patients with PD and dementia. Of dementia patients, seven met criteria for probable Lewy body dementia (LBD) and four for Alzheimer's disease (or, possible LBD). In all probable LBD cases, the diagnosis was made because of parkinsonism, with no patient experiencing hallucinations or fluctuations. Patients with "Alzheimer's disease" seemed to have LBD, as they demonstrated typical LBD cognitive profiles on neuropsychological testing and were indistinguishable from LBD patients in ancillary measures. Therefore, among RBD patients with new-onset LBD, hallucinations or fluctuations are absent, suggesting that RBD is a reliable early sign of LBD. The indistinguishability of dementia and PD in all ancillary measures suggests a single unitary "RBD-then-neurodegeneration" process, the clinical presentation of which depends upon selective neuronal vulnerability.
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PMID:Idiopathic REM sleep behavior disorder in the transition to degenerative disease. 1976 14

Parkinson's disease is the second most common neurodegenerative disorder, after Alzheimer's disease. It predominantly affects the elderly. Age is the most clearly established risk factor and there is a male:female ratio of 1.5:1. Current incidence in the general population is 8.4-19 per 100,000 population per year with an approximate prevalence of 120 per 100,000 population. NICE recommends that patients with suspected Parkinson's disease should be referred untreated to a specialist with expertise in parkinsonian disorders. The diagnosis is primarily clinical. Parkinson's disease should be suspected in all patients presenting with bradykinesia (which is essential for the diagnosis of any form of parkinsonism, including Parkinson's disease), muscular rigidity, resting tremor (4-6 Hz) and postural instability not caused by a primary visual, vestibular, cerebellar, or proprioceptive dysfunction. At present, there are no specific biochemical, imaging or genetic tests to assist in the diagnosis of Parkinson's disease. Structural brain imaging (MRI or CT) has no role in the diagnosis of Parkinson's disease but may be useful to exclude cerebrovascular disease, hydrocephalus and Wilson's disease in selected cases. Parkinson's disease is a condition that results in both motor and non-motor symptoms. Morbidity associated with non-motor symptoms in Parkinson's disease is becoming increasingly recognised and some non-motor symptoms such as hyposmia, apathy, depression and REM sleep behaviour disorder may precede the onset of motor symptoms.
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PMID:Non-motor symptoms may herald Parkinson's disease. 1987 55

Autonomic dysfunction is common in Lewy body disorders (Parkinson's disease, Dementia with Lewy Bodies, Pure Autonomic Failure, and REM sleep disorder). The loss of post-ganglionic myocardial sympathetic nerve fibers is a prominent feature of autonomic dysfunction in such disorders. (123)I-metaiodobenzylguanidine (MIBG) scintigraphy that visualizes catecholaminergic terminals in vivo is a biomarker used to detect cardiac sympathetic degeneration. Abnormal MIBG uptake has been consistently reported in Lewy body disorders. Some studies agree in the notion that increasing bradykinesia is related with an incremental cardiac sympathetic denervation, whereas tremor is not closely linked to cardiac denervation. "Atypical" parkinsonian syndromes, including Multiple System Atrophy, Progressive Supranuclear Palsy, and others, show modest reductions of cardial MIBG uptake. MIBG scintigraphy is moderately sensitive and specific in differentiating Parkinson's disease from such syndromes. Conversely, its sensitivity and specificity might be better in cognitively impaired patients, helping differential diagnosis between Dementia with Lewy Bodies, and Alzheimer disease. Confounding factors (comorbidities, comedications) should be carefully controlled before analyzing MIBG scintigraphy.
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PMID:123I-metaiodobenzylguanidine scintigraphy in Parkinson's disease and related disorders. 1987 2

Parkinson's disease (PD) is the second most common neurodegenerative disease and primarily considered as a movement disorder defined by the presence of motor symptoms, such as bradykinesia, tremor and rigidity. However, it is nowadays widely recognized that in addition there is impairment of cognitive function, mood and the autonomic nervous system in a high percentage of PD patients, which is sometimes even more harming quality of life. These symptoms not only occur during the course of the disease but may even precede the onset of motor symptoms. Typical examples of non-motor features of PD are depression, constipation, REM sleep behaviour disorder, and hyposmia.
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PMID:Non-motor features of Parkinson's disease: depression and dementia. 2008 17

Altered sleep is a common non motor symptom in Parkinson's disease. Sleep dysfunction has been reported to occur in 60-90% of all PD patients, having a detrimental impact on quality of life and increasing disability. alpha-Synuclein deposits in the lower brainstem affecting autonomic and sleep regions have been identified in the pathophysiology. The resultant non motor symptoms such as REM sleep behaviour disorder (RBD) can precede the motor symptoms by years. RBD is violent, enacted dreams that expose the patient or their sleeping partner to night-time injuries. Excessive daytime sleepiness, sometimes with a narcolepsy-like phenotype, is a common occurrence in PD, owing to lesions in the arousal systems of the brain. Restless legs syndrome and sleep disordered breathing can all affect daytime alertness of PD patients. Autonomic deregulation can also negatively affect sleep patterns, by adding to night-time wakening and disrupting sleep.
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PMID:Sleep dysfunction and role of dysautonomia in Parkinson's disease. 2008 18

We investigated cardiac uptake of (123)I-metaiodobenzylguanidine (MIBG) in patients with REM sleep behavior disorder (RBD) and compared the findings with those of idiopathic Parkinson's disease (IPD). Thirteen RBD, 222 IPD and 50 controls underwent cardiac (123)I-MIBG scintigraphy. Resulting heart-to-mediastinum (H/M) ratios were significantly lower in patients with RBD and IPD as compared to the control ratios. H/M ratios were lower for delayed than for early images in patients with RBD and IPD; whereas, the controls had higher ratios for delayed images. H/M ratios were significantly lower for patients with RBD than for those with IPD at Hoehn and Yahr stages 1 and 2. Disease duration did not differ between the two groups. Our study revealed that cardiac (123)I-MIBG uptake was more markedly reduced in patients with RBD than in those with early stage IPD. RBD may not necessarily be a prodromal condition of IPD with respect to cardiac (123)I-MIBG uptake results.
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PMID:Cardiac 123I-MIBG uptake is reduced more markedly in patients with REM sleep behavior disorder than in those with early stage Parkinson's disease. 2009 95

Meta-iodbenzylguanidine scintigraphy (MIBG scintigraphy) shows reduced uptake in idiopathic Parkinson's disease (IPD), idiopathic REM sleep behavior disorder (IRBD) and Lewy body dementia (LBD), but not in other parkinsonian or dementia syndromes. We retrospectively reevaluated 50 patients. Concordance rate between last clinical diagnosis and scintigraphy diagnosis was only given in two-thirds of the patients. Confounding factors were: decreasing heart/mediastinum ratio (HMR) with progressive age, higher HMR in women and possibly interference with antihypertensive medication. Standardization of the methods and precise clinical guidelines are warranted for better clinical use.
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PMID:Myocardial MIBG scintigraphy: a useful clinical tool? : A retrospective study in 50 parkinsonian patients. 2015 79

Complex paroxysmal nocturnal motor behavioral disorders (CPNBs) are frequently reported in patients with Parkinson's disease (PD). REM sleep behavior disorder (RBD) is reported in at least a third of PD patients, although CPNB episodes can also occur on arousal from NREM sleep. It is important to establish the nature of CPNBs occurring in PD, as the different types have different neurobiological significance and clinical importance, and also different treatments. Ninety-six PD patients with and without CPNBs were submitted to overnight in-hospital video-polysomnography. Of these, 76 (47 men) were included in the study analysis: these were patients in whom it was possible to establish the presence or absence of CPNBs and to obtain a clear-cut diagnosis of the nature of the CPNBs reported. The CPNBs were found to be RBD episodes in 39 cases (87%) and nonRBD episodes in 6 (13%) (arousal-related episodes arising from NREM sleep in 3 cases and from REM sleep in 2 cases, parasomnia overlapping syndrome in 1 case). In 4 of the 6 subjects with nonRBD episodes, these occurred upon arousal at the end of an obstructive apnoeic event. Our data confirm that CPNBs in PD are, in most cases, RBD episodes. However, arousal-related episodes accounted for 13% of the CPNBs observed in our sample and occurred in close temporal association with sleep-disordered breathing (SDB). The arousal system is defective in extrapyramidal diseases due to neurodegenerative changes involving the brain stem reticular network; against this background, a trigger effect of SDB on CPNBs, through induction of abrupt arousal, may be hypothesized.
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PMID:Complex paroxysmal nocturnal behaviors in Parkinson's disease. 2019 16

Sleep in dementias has been mainly studied in Alzheimer disease (AD). Sleep disturbances are found in 25 to 35% of subjects with AD. Subjective and objective disturbances are described. Long nocturnal awakenings disrupt sleep; total sleep time and sleep efficiency are reduced. Slow wave sleep is decreased and sometimes disappears. REM sleep percentage is also reduced and at a later stage of the disease, REM latency is increased. Sleep fragmentation can be associated with excessive daytime napping and sleepiness, and with other behavioral symptoms such as the sundowning syndrome and nocturnal agitation. Sleep abnormalities closely parallel the level of severity of dementia. The rest/activity ratio and the sleep-wake rhythms are more and more disturbed; the phase delay of the temperature rhythm is associated with the severity of the sundowning syndrome. Sleep disturbances and behavioral symptoms are the main reasons to institutionalize the patient. Sleep disturbances are related to multiple factors. Pathophysiological changes resulting of the disease itself, such as damage to the cholinergic pathways and to the circadian pacemaker in the suprachiasmatic nucleus, contribute to sleep changes in AD. Associated medical and psychiatric illness and their different treatments as well as environmental factors also induced sleep disturbances. Sleep-disordered breathing is a highly prevalent condition in AD patients and restless leg syndrome may account for nocturnal agitation. In Parkinson and in Lewy body dementias, sleep disturbances are more severe than in DA and REM sleep behavior disorder can precede by several years these diseases. Sleep attacks and sleepiness are very frequent in Parkinson disease. Specific etiologies should drive specific treatment. Several non pharmacologic treatments are usually associated to treat sleep disturbances in AD: information, increased daytime physical, social activities to minimize daytime naps and exposure to bright light. Some studies found advantages to associate melatonin in the evening.
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PMID:[Sleep disturbances in Alzheimer's disease and other dementias]. 2021 95

Mild cognitive impairment (MCI) is a frequent feature in idiopathic REM sleep behavior disorder (RBD), a sleep disturbance that can be a preclinical stage of Parkinson's disease or Lewy body dementia. We evaluated the sensitivity and specificity of two brief screening tools, the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE), in detecting MCI in idiopathic RBD. Thirty-eight idiopathic RBD patients underwent a comprehensive neuropsychological assessment, including the MoCA and the MMSE. Receiver operating characteristic curves were created for the MoCA and the MMSE to assess their ability to identify MCI in idiopathic RBD patients, with neuropsychological assessment as the gold standard. For the MoCA, a normality cutoff of 26 yielded the best balance between sensitivity (76%) and specificity (85%) with a correct classification of 79%. For the MMSE, the optimal normality cutoff was 30, with a sensitivity of 84% and a specificity of 54% and a correct classification of 74%. The MoCA is superior to the MMSE in detecting MCI in idiopathic RBD patients, showing good sensitivity and very good specificity.
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PMID:The Montreal Cognitive Assessment: a screening tool for mild cognitive impairment in REM sleep behavior disorder. 2031 38


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