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)

"Parkinson plus" is a group of sporadic degenerative disorders associating Parkinsonism, poorly sensitive to L-dopa, to other neurological syndromes. Thus, progressive supranuclear palsy includes Parkinson's disease, vertical gaze paralysis, nuchal dystonia and dementia; multisystem atrophies associate to different degrees Parkinson's disease (striatonigral degeneration), a cerebellar syndrome (olivopontocerebellar atrophy), dysautonomia (Shy-Drager syndrome), pyramidal syndrome, etc. Other diseases (corticobasal degeneration, diffuse Lewy body disease) also belong to the Parkinson "plus" group. Clinical differentiation between Parkinson "plus" and idiopathic Parkinson's disease is difficult. Their prognosis and treatment are substantially different. Certain diagnosis is based solely upon anatomical observations.
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PMID:[Parkinson "plus"]. 920 70

Pure autonomic failure (PAF; also known as idiopathic orthostatic hypotension or Bradbury-Eggleston syndrome) is an uncommon sporadic disorder, characterized by autonomic failure without other neurological deficits and histopathologically by cell loss in intermediolateral columns and sympathetic ganglia. Few postmortem studies of patients with PAF have been reported in the literature, and none have demonstrated Lewy bodies in distal axons, although this has been described as a feature in Parkinson's disease with autonomic failure. We report a patient with PAF who had orthostatic hypotension and urinary symptoms for 15 years prior to death at the age of 63 years. Postmortem findings included typical and atypical Lewy bodies in the substantia nigra, locus ceruleus, substantia innominata, and sympathetic ganglia, as well as in autonomic axons in the epicardial fat, autonomic nerve fascicles in periadrenal adipose tissue, and autonomic nerves in the muscularis of the urinary bladder. Sites of autonomic nerve involvement correlated with clinical symptomatology, and thus were a valuable observation in the complete autopsy. Systemic autopsy results should be reviewed carefully in patients with PAF, as Lewy bodies in this disease may be seen in distal axons at a great length from their primary cell bodies.
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PMID:The distribution of Lewy bodies in pure autonomic failure: autopsy findings and review of the literature. 925 96

Both the striatal 18F-dopa uptake and brain glucose metabolism were studied by PET with 6-L-[18F]fluorodopa (FD) and [18F]fluorodeoxyglucose (FDG) in 9 patients with multiple system atrophy (MSA) and 15 patients with idiopathic Parkinson's disease (PD). Five of the 9 MSA patients were diagnosed as having olivopontocerebellar atrophy, whereas 2 had striatonigral degeneration and 2 demonstrated Shy-Drager syndrome. The FD uptake ratios to the occipital cortex in the MSA patients at 120 min after the administration of FD were 2.07 +/- 0.31 (mean +/- SD) and 1.96 +/- 0.29 in the caudate and the putamen, respectively, and decreased compared to those in the controls (2.72 +/- 0.11, 2.71 +/- 0.10). The same ratios in the PD patients were 2.07 +/- 0.36 and 1.74 +/- 0.24, respectively, which also decreased, but the decreased uptake in the putamen was more prominent. The caudate-putamen index (CPI)(%), which was calculated by a formula based on the difference in the uptakes in the caudate and putamen divided by the caudate uptake, indicated 5.6 +/- 4.6 in the MSA patients and 14.8 +/- 5.4 in the PD patients. The CPI for all PD patients was more than 7.0, which was the mean + 2SD for the controls, but the CPI for 3 MSA patients was more than 7.0 (accuracy: 88%). The glucose metabolic rates for each region in the PD patients showed no difference from the normal controls. The frontal and the temporal cortical glucose metabolism and the caudate, the putaminal, the cerebellar and the brainstem glucose metabolism in the MSA patients decreased significantly in comparison to those in the controls. But, as the glucose metabolic rates in such regions of each patient overlapped in the two groups, the accuracy of the FDG study for differentiation was lower than that of the FD study. The putaminal glucose metabolic rates, for example, in 3 PD patients were less than 6.8 (mg/min/100 ml), which was the mean-2SD for the controls, while those in 3 MSA patients were more than 6.8 (accuracy: 75%). In addition, the combination of these two methods slightly improved the accuracy. The glucose metabolism is useful for evaluating the regional metabolic activity of the brain, and the FD study, which is specific to the dopamine system, seems to be more useful for differentiating between MSA and PD.
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PMID:Differentiating between multiple system atrophy and Parkinson's disease by positron emission tomography with 18F-dopa and 18F-FDG. 931 Jan 75

This article is a review of autonomic dysfunction in idiopathic Parkinson's disease (iPD), as well as the clinical features of a specific form of PD, i.e. autonomic failure (AF) with PD, and is based mainly on the results obtained from our recent studies. Since James Parkinson's original discription, the definition of autonomic dysfunctions in iPD and their clinical characteristics have undergone changes. Autonomic dysfunction is considered to be uncommon and rarely severe on one hand, while not infrequent but not as severe as in Shy-Drager syndrome on the other hand. AF with PD is characterized by severe orthostatic hypotension, postprandial hypotension, supersensitivity to noradrenaline, low or absent uptake of m-[123I]iodobenzylguanidine scintigraphy of the limbs, and preserved arginine vasopressin response to head-up tilt, suggesting a postganglionic sympathetic lesion resembling pure AF (PAF). On the other hand, reduced cortical glucose metabolism in positron emission tomography study may indicate that AF with PD has diffuse nervous system lesions resembling diffuse Lewy body disease.
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PMID:Autonomic dysfunction in Parkinson's disease. 938 97

Over the last decade multiple system atrophy (MSA) has been confirmed as a distinct clinicopathological entity. For a long time, overlapping pathology in individual cases with striatonigral degeneration (SND), sporadic olivopontocerebellar atrophy (OPCA) or Shy-Drager syndrome (SDS) had often been a source of confusion. The recently discovered glial and neuronal inclusions indeed confirm that these three disorders represent manifestations of the same disease. Parkinsonism is the most frequent motor disorder of MSA. Early diagnosis of these patients is difficult but important, particularly in clinical trials of potential therapies. Patients with only parkinsonism (+/- autonomic failure) account for much of this diagnostic difficulty, particularly early on. Some features that have been associated with SND such as symmetry or absence of tremor are not helpful, and insistence on a poor levodopa response will miss a sizeable minority of patients. A number of further clinical 'red flags' may be helpful. MRI, MRS, PET and SPECT scanning, autonomic function tests and, especially, external sphincter EMG, may also help differentiate between idiopathic Parkinson's disease (IPD) and MSA. Available medical treatments are usually disappointing, so that good therapy services are all the more important. Better animal models of MSA and evaluation of novel treatment strategies are urgently required, and grafting techniques currently applied to IPD and Huntington's disease (HD) patients might be usefully combined in MSA. Epidemiological and case-control studies are needed to determine the prevalence, incidence and risk factors of MSA. The pathogenesis of MSA remains uncertain. Until the discovery of glial cytoplasmic inclusions (GCIs) previous studies had failed to identify abnormalities relevant to pathogenesis rather than reflecting secondary change. The abundance of GCIs points to a fundamental cytoskeletal alteration in glial cells that may eventually result in neuronal degeneration. Mechanisms of formation and distribution of GCIs as well as disordered glial-neuronal interactions should be studied in more detail in MSA brains.
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PMID:Parkinsonism. Multiple system atrophy. 942 75

Cytoplasmic RNA species have been identified recently within neurofibrillary tangles and senile plaques of Alzheimer's disease brain. To determine whether RNA sequestration is a common feature of other lesions found in progressive neurodegenerative disorders, acridine orange histofluorescence was employed, alone or in combination with immunohistochemistry and thioflavine-S staining to identify RNA species in paraffin-embedded brain tissue sections. Postmortem samples came from 39 subjects with the following diagnoses: Alzheimer's disease, amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam, corticobasal degeneration, diffuse Lewy body disease, normal controls, multiple system atrophy, Parkinson's disease, Pick's disease, progressive supranuclear palsy, and Shy-Drager syndrome. RNAs were detected in neurofibrillary tangles and neuritic senile plaques as well as in Pick bodies. However, Lewy bodies, Hirano bodies, and cytoplasmic glial inclusions did not contain abundant cytoplasmic RNA species. These observations demonstrate the selective localization of RNA species to distinct pathological lesions of neurodegenerative disease brains.
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PMID:RNA sequestration to pathological lesions of neurodegenerative diseases. 982 12

We investigated the frequency and severity of depressive symptoms among patients with Shy-Drager Syndrome (SDS) and correlated depression with the extent of the patients' disability. Data were collected from 15 patients and their spouse caregivers through a mailed questionnaire. The patients were asked to complete the Beck Depression Inventory (BDI) questionnaire, while caregivers were asked to complete the self-assessment Parkinson's Disease Disability Scale and The Northwestern University Disability Scale for Parkinson's Disease. Data were statistically analyzed using descriptive statistics and Pearson-Product moment correlations. The prevalence of depressive symptoms was 85.7%; 28.6% of SDS patients scored in the moderately to severely depressed range. There was no significant correlation between the severity of depressive symptoms and disability (r = 0.02, p = 0.94) and the ability to perform activities of daily living (r = 0.0, p = 1.0). The prevalence of depressive symptoms in patients with SDS is common. The patient's level of depression does not correlate with physical disability. Pharmacologic management and interventions aimed at increasing active coping methods should improve quality of life.
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PMID:Occurrence of depressive symptoms in Shy-Drager syndrome. 1021 41

On the basis of current literature, clinical and neuropathologic features of idiopathic autonomic neuropathy is presented. Idiopathic autonomic neuropathy is a disease characterized by acute or subacute onset, monophasic course over a period of several years, it is often preceded by an infection. The spectrum of autonomic changes ranges from cholinergic or adrenergic dysfunction to pandysautonomia, leading to heterogeneity of its clinical features. Possible sympathetic system abnormalities found in autonomic neuropathy are: poor pupillary response to light in darkness, orthostatic hypotension leading to syncope, hypotension without compensatory tachycardia, ejaculation disturbances and vasomotor instability. Possible parasympathetic dysfunctions are: salivation and lacrimation disturbances, absent pupillary constriction to light and near gaze, gastrointestinal tract immobility and impairment of gastrointestinal function, atonic bladder with large residual volume, erectile impotence. Pandysautonomia is thought to result from an immune mediated mechanism and responds well to plasmaferesis and intravenous immunoglobin therapy leading to gradual, sometimes not full, recovery. Moreover in this article we pay attention to the clinical value of many tests like cardiovascular or pharmacological studies in the diagnosis of pandysautonomia and in differentiation of pre- and postganglionic changes. In order to diagnose idiopathic autonomic neuropathy one has to rule out a large number of diseases with autonomic dysfunction e.g.: diabetes, malignant neoplasms, acute intermittent porphyria, Shy-Drager syndrome, Riley-Day's dysautonomia, Parkinson's disease, amyloidosis and others.
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PMID:[Idiopathic autonomic neuropathy (pandysautonomia)]. 1173 67

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

SEVERAL EXPLANATIONS FOR THE HIGH PREVALENCE: In Parkinson's disease, the prevalence of symptomatic orthostatic hypotension (OH) concerns more than 20% of the patients. At least 2 factors explain this high prevalence. Dopamine-mimetic drugs may induce or enhance the occurrence of OH. Parkinson's disease is a cause of primary autonomic failure with involvement of the peripheral nervous system. CHARACTERISTIC HISTOLOGICAL AND PHARMACOLOGICAL ELEMENTS: Histology indicates that Lewy bodies exist in the sympathetic glands. Pharmacology reveals cardiac sympathetic denervation. These histological and pharmacological characteristics clearly differentiate autonomic failure of Parkinson's disease from multiple system atrophy (Shy-Drager's syndrome). If autonomic abnormalities appear to be present since the early stages of the disease, the early onset, within the first year, of symptomatic OH in the course of a parkinsonian syndrome can be considered as an exclusion criterion for idiopathic Parkinson's disease. REGARDING TREATMENT: No specific clinical trials have assessed the efficacy of antihypotensive drugs in the treatment of OH in Parkinson's disease. The management of this symptom requires education of the patient and the development of non-pharmacological measures. Drug therapy should be reserved for symptomatic patients who do not improve with the preceding methods. Among the drugs available, domperidone, although widely used, has no proven effect on OH like the cardiovascular analeptics. The alpha1-adrenergic agonists (midodrine) or mineralocorticosteroids (fludrocortisone) are the most frequently used drugs.
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PMID:[Blood pressure disorders during idiopathic Parkinson's disease]. 1450 67


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