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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synucleinopathies, with and without dementia, encompass a wide range of diseases including Parkinson's disease, multiple system atrophy, rapid eye movement (REM) sleep behavior disorder, and dementia with Lewy bodies (DLB). DLB is a neurodegenerative disorder resulting in slowly progressive and unrelenting dementia until death. Prevalence studies suggest that it is the second most common dementing illness in the elderly. The neuropathologic findings of DLB show a wide anatomic range. Lewy bodies and Lewy-related pathology are found from the brain stem to the cortex and, in many cases, associated with concurrent Alzheimer's disease pathology. A recent international consortium on DLB has resulted in revised criteria for the clinical and pathological diagnosis of DLB incorporating new information about the core clinical features and improved methods for their assessment. The presentation of DLB is typically one of cortical and subcortical cognitive impairments, with worse visuospatial and executive dysfunction than Alzheimer's disease. There may be relative sparing of memory especially in the early stages. Core clinical features of DLB include fluctuating attention, recurrent visual hallucinations, and parkinsonism. Suggestive features include REM sleep behavior disorder, severe neuroleptic sensitivity, and low dopamine transporter uptake in the basal ganglia on functional neuroimaging. Additional supportive features that commonly occur in DLB, but with lower specificity, include repeated falls and syncope, transient, unexplained loss of consciousness, severe autonomic dysfunction, hallucinations in other modalities, systematized delusions, depression, relative preservation of medial temporal lobe structures on structural neuroimaging, reduced occipital activity on functional neuroimaging, prominent slow wave activity on electroencephalogram, and low uptake myocardial scintigraphy. Management of DLB includes pharmacological and nonpharmacological interventions for its cognitive, neuropsychiatric, motor, and sleep disturbances.
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PMID:Dementia with Lewy bodies. 1722 40

Idiopathic rapid-eye-movement (REM) sleep behavior disorder (iRBD) has been suggested to be a risk factor for subsequent development of neurodegenerative disorders, especially Parkinson's disease (PD) and other alpha-synucleinopathies. At present, it is not possible to predict whether or not an iRBD patient will eventually develop PD. Here, we report 5 iRBD patients who underwent a test battery comprising a neurological examination (including UPDRS rating), mini mental state examination testing, transcranial sonography, olfactory function testing, and presynaptic dopamine transporter imaging with FP-CIT-SPECT. Our preliminary data show the diverse pattern of individual combinations of pathological findings when a multimodal assessment approach is applied in this patient group. Large-size longitudinal studies in iRBD patients are required to evaluate the usefulness of diagnostic tests to identify the subgroup of iRBD patients that is prone to develop PD.
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PMID:Assessment of idiopathic rapid-eye-movement sleep behavior disorder by transcranial sonography, olfactory function test, and FP-CIT-SPECT. 1817 46

Sleep dysfunction is common among patients with Parkinson's disease and occurs in approximately two thirds of patients. The problems range from nocturnal issues such as difficulty with sleep initiation, sleep fragmentation, disturbance of circadian rhythm, and rapid eye movement sleep behavior disorder, to daytime problems such as excessive daytime sleepiness. Frequent nighttime awakening and sleep disruption are the most common sleep problems in Parkinson's disease. Dopamine plays an important role in maintaining wakefulness. To improve sleep in Parkinson's disease, it is important to achieve the critical balance of adequate dopaminergic therapy and control of symptoms. Increased dopaminergic agents can cause dyskinesias and painful dystonia, and undertreatment can cause nighttime akinesia, rigidity, and worse quality of sleep. Other nondopaminergic drugs commonly used in Parkinson's disease can also affect sleep. In patients with advanced Parkinson's disease, deep brain stimulation of the subthalamic nucleus has a favorable impact on sleep quality and sleep architecture.
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PMID:Sleep disorders associated with Parkinson's disease: role of dopamine, epidemiology, and clinical scales of assessment. 1832 61

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

Reduction of olfactory function in idiopathic rapid-eye-movement (REM) sleep behavior disorder (iRBD) is of the same magnitude as that found in patients with Parkinson's disease (PD) and dementia with Lewy bodies (DLB). We assessed olfactory function using the Odor Stick Identification Test for Japanese (OSIT-J) in 48 Japanese patients with iRBD, 21 with PD, and 34 with obstructive sleep apnea syndrome (OSAS). Possible score of the OSIT-J ranges from 0 to 12. OSIT-J scores were 4.9 +/- 2.8 in patients with iRBD, 4.8 +/- 2.8 in patients with PD, and 9.9 +/- 1.4 in OSAS patients. An OSIT-J score of 8.5 was associated with a sensitivity of 88.2 and 85.3%, respectively, and specificity of 83.3 and 85.7%, respectively, in differentiating iRBD or PD patients from OSAS patients. Odor identification is impaired in Japanese patients with iRBD and PD. The results suggest that OSIT-J, which is a short and simple nonlexical olfactory identification test, can be useful as a clinical indicator for iRBD with Lewy body formation and is appropriate in the Japanese elderly population.
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PMID:Odor identification test as an indicator of idiopathic REM sleep behavior disorder. 1897 47

Pathology and imaging studies have shown that patients with Parkinson disease (PD) have a prolonged period of uncertain duration when vulnerable neuronal populations are degenerating, but typical motor symptoms have not yet developed. This provides both an opportunity-it may be best to test new medications and, ultimately, treat PD patients during this early phase of disease--and a challenge--how to find these premotor PD subjects? Imaging biomarkers targeting the premotor period are critical to elucidate both the onset and progression of premotor PD. Widespread data have demonstrated that dopaminergic imaging can detect PD subjects at the motor symptom threshold. Novel strategies combining dopaminergic imaging with known genetic mutations for PD or early clinical signs and PD-associated symptoms, such as olfactory loss and sleep disturbances like REM behavior disorder, have begun to be used to identify individuals at risk for PD before motor symptoms become manifest. Early studies also have used imaging targeting norepinephrine, serotonin, cholinergic, or other neuronal systems to focus on early cardiac, cognitive, and behavioral symptoms. Imaging of nondopaminergic targets such as inflammation or alpha-synuclein deposition may provide further insight into the etiology of PD. Given the multiple genetic etiologies for PD already identified, the marked variability in the loss of dopaminergic markers measured by imaging at motor symptom onset, and the clear heterogeneity of clinical symptoms at PD onset, it is certain that many imaging biomarkers with a focus ranging from clinical symptoms to PD pathobiology to molecular genetic mechanisms, will be necessary to fully map PD risk.
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PMID:Can we image premotor Parkinson disease? 1922 10

The proteinopathy sporadic Parkinson's disease (sPD) is the second most frequent degenerative disorder of the human nervous system after Alzheimer's disease. The alpha-synuclein inclusion body pathology (Lewy pathology) associated with sPD is distributed throughout the central, peripheral, and enteric nervous systems. The resulting nonrandom neuronal dysfunction and, in some regions, neuronal loss is reflected in a topographic distribution pattern of the Lewy pathology that, in the brain, can be staged. Except for olfactory structures and spinal cord constituents of the pain system, sensory components of the nervous system remain uninvolved or virtually intact. The most disease-related damage revolves around motor areas--particularly around superordinate centers of the limbic and visceromotor systems as well as portions of the somatomotor system. Vulnerable regions are interconnected anatomically and susceptible nerve cell types are not neurotransmitter-dependent. Not all clinical symptoms emerging in the course of sPD can be explained by a lack of dopamine in the nigrostriatal system. These include autonomic dysfunction, pain, hyposmia or anosmia, excessive daytime sleepiness, rapid eye movement (REM) sleep behavioral disorder, depression, anxiety, cognitive decline, and dementia. Against the background of the normal morphology and anatomy, the authors analyze the pathoanatomy of sPD in the nervous system at various neuropathological stages and summarize the potential functional consequences of the lesions.
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PMID:Neuroanatomy and pathology of sporadic Parkinson's disease. 1923 May 52

The motor symptoms of Parkinson's disease (PD), bradykinesia, muscular rigidity, and tremor depend upon degeneration of the dopaminergic neurons in the substantia nigra pars compacta. Recent neuropathological studies show that the Lewy bodies, the intraneuronal landmark of PD, accumulate in several neuronal cell types in the brain. An ascending gradient of pathological involvement, from the medulla oblongata to neocortical areas has been reported. Thus the original view of PD as a disease characterized by selective damage of the dopaminergic neurons in the mesencephalon should be updated into the concept of a severe multisystemic neurodegenerative disorder. Additionally, the neuropathological alterations outside the substantia nigra are soundly correlated with the non-motor symptoms of PD. As a result of these findings, interest is growing in the identification of prodromal non-motor symptoms of PD. Indeed, data from the literature suggest that autonomic disturbances, olfactory dysfunctions, depression and sleep disorders (in particular REM-sleep behavior disorder) may represent prodromal non-motor symptoms of PD. Several tests are available to detect most of these symptoms. Thus, the identification of prodromal non-motor symptoms may contribute to the precocious diagnosis of PD, and might be useful in the future to test the efficacy of neuroprotective agents.
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PMID:Prodromal non-motor symptoms of Parkinson's disease. 1930 May 44

Rapid eye movement (REM) sleep behavior disorder (RBD), which is characterized by dream-enacted, sometimes violent and aggressive, behaviors was firstly reported by Schenck and his colleagues in 1986; thereafter, it was incorporated as parasomnia in the International Classification of Sleep Disorders 1st edition (ICSD-1). The polysomnographical hallmarks of RBD include intermittent/sustained loss of the skeletal muscle atonia of REM sleep (REM sleep without atonia [RWA]); further, this finding has been mandatory in the diagnostic criterion (requiring polysomnographic [PSG] monitoring) in the ICSD-2 in 2005. The animal equivalent of RBD was previously described by Jouvet's and Morrison's groups, dated back to 1965, when Jouvet's group firstly created experimentally lesioned cats (in the bilateral pontine tegmentum areas) presenting with "oneiric behaviors". In 1970s Hishikawa's group had also described peculiar sleep state in alcoholics and other subjects of drug withdrawal with rapid eye movements and tonically increased chin muscle activity (reffered to as "Stage 1-REM with tonic EMG" [Stage 1-REM]). It was difficult to determine from the polysomnographical features whether Stage 1-REM was REM sleep or not, as this state did not preserve proper cyclic appearance of REM sleep. They also reported Stage 1-REM in patients with Shy-Drager syndrome in 1981. The latter finding of Hishikawa's group, together with RBD observed in multiple system atrophy (MSA) reported by other groups, could be best explained by the experimental cat model because of its presumed extensive brainstem pathology. However, neurophysiology of withdrawal states has not been well understood; therefore, Stage 1-REM should be reappraised from new perspectives. After 1990, more extensive studies on RBD revealed that about half of RBD cases were associated with neurological disorders, especially neurodegenerative diseases pathologically known as syncleiopathies (Parkinson disease [PD], dementia with Lewy bodies, and MSA). In addition, it has been shown that a substantial number of idiopathic RBD (iRBD) patients eventually developed Parkinsonian diseases. In accordance with accumulative data indicating that various non-parkinsonian features can precede the onset of motor symptoms of PD (or pathologically Lewy body diseases), a search of early PD markers in patients with iRBD has been performed. The results of the studies support the hypothesis of RBD as an early sign of a neurodegenerative disorder. More recently, it was reported that RBD is frequently symptomatic of narcolepsy, although the pathophysiological mechanism of this state was still unknown. RBD in stroke patients have been anecdotal; however, under such conditions, specific lesion studies can be possible, as data in the experimental RBD rats have been accumulated during these few years. In conclusion, RBD is observed in a wide range of neurological disorders, and the causative mechanism of RWA and behavioral manifestations may not only be attributable to brainstem lesions. RBD is not a homogeneous clinical entity, and further refinement of its diagnostic classification is warranted to avoid diagnostic confusion.
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PMID:[Historical overview of REM sleep behavior disorder in relation to its pathophysiology]. 1951 16

Sleep disorders occur commonly in Parkinson's disease (PD), and reduce quality of life. Sleep-related problems in PD include insomnia, restless legs syndrome, rapid eye movement sleep behavior disorder, sleep apnea, parasomnias, excessive daytime sleepiness, and sleep attacks. This article reviews sleep disorders and their treatment in PD.
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PMID:Sleep disorders in Parkinson's disease. 1989 67


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