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)

Delirium is commonly defined as a transient organic brain syndrome characterized by concurrent disorders of attention, perception, thinking, memory, psychomotor behavior, and the sleep-wake cycle. One of the difficulties in studying delirium is that symptoms tend to fluctuate over the course of the day. Pre-existing organic brain disease appears to be a significant risk factor for the development of delirium, and numerous studies have shown a high rate of delirium in patients with cerebrovascular disease, Parkinson's disease, and Alzheimer's disease. The cognitive deficits associated with delirium have not been widely studied in a systematic, quantitative fashion. Following resolution of the frank delirium, documented cognitive deficits can be observed, and may persist in a diluted form for a period of months. Residual cognitive deficits may be due to a minimal and persistent confusion or to an underlying brain disorder.
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PMID:Cognitive deficits in delirium: assessment over time. 129 18

We measured CSF and plasma contents of beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and ACTH in 24 patients with Parkinson's disease; 14 had not been treated. CSF beta-EP concentrations in untreated patients were lower than in 15 controls (p less than 0.005), but values did not differ significantly in treated and untreated patients. In untreated and treated patients, ACTH and beta-LPH CSF, and beta-EP, beta-LPH, and ACTH plasma concentrations were in the same range as controls. The Parkinson's disease-related decrease of CSF beta-EP levels further supports the concept that there is a generalized brain disorder in Parkinson's disease affecting more than dopaminergic neurons in the substantia nigra.
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PMID:beta-Endorphin cerebrospinal fluid decrease in untreated parkinsonian patients. 299 18

Thirty newly diagnosed patients with Parkinson's disease and 30 patients with primary depressive illness showed slowing of response on a computerized digit symbol substitution test when compared with 30 matched normal control subjects. Significant slowing was related, in the parkinsonian patients, to structural brain disorder and affective impairment and, in the depressed patients, to motor impairment. A second computerized test, cognitively simpler but requiring the same motor response, was also administered to each subject. Both cognitive and motor slowing seemed to contribute to slowing of response in the digit symbol test in both parkinsonian and depressed patients. The tests were repeated after about six months in 12 subjects from each group. The parkinsonian patients, on dopaminergic treatment, showed neither significant change in motor or affective impairment, nor improvement in response time for the digit symbol test, but change in response time was related to change in depression rating. The depressed patients, on conventional treatment, showed significant improvement in both affective and motor impairment and improvement in response time for the digit symbol test, due to improvement in cognitive slowing. It is proposed that bradyphrenia in Parkinson's disease and psychomotor retardation in depressive illness are closely related, and that impairment of dopaminergic systems may be involved in both.
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PMID:Bradyphrenia in Parkinson's disease and psychomotor retardation in depressive illness. An experimental study. 310 50

In order to determine whether, besides the severe striatal dopamine (DA) loss, other brain neurotransmitter changes may be a constant biochemical feature of idiopathic Parkinson's disease (iPD), we measured the concentration of the three major brain monoamines noradrenaline (NA), DA, and serotonin (5-HT) and their metabolites in five rostro-caudal subdivisions of the hypothalamus of eight control patients and nine patients with morphologically confirmed iPD. In the whole hypothalamus of the iPD patients we found a mild to moderate mean reduction of NA (-52%, P < 0.05), DA (-25%), and 5-HT (-26%). At the subregional level, the most consistently affected area was the intermediate subdivision of the hypothalamus proper where all three monoamines were statistically significantly reduced. Evaluation of individual patient values indicated that, in contrast to the constant and severe DA reduction present in putamen of each of the iPD patients (DA loss ranging from 96% to 99%), several of these patients had whole (and subregional) hypothalamic monoamine values well within the range of controls. We conclude that, although possibly involved in autonomic and/or endocrine disturbances in some patients with iPD, none of the observed monoamine changes in the hypothalamus is an obligatory feature of iPD. Our study demonstrates the need for evaluation of individual patient values rather than mean differences in order to permit valid conclusions to be drawn as to whether an observed neurochemical change can be regarded as specific to a given brain disorder.
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PMID:Noradrenaline, dopamine and serotonin levels and metabolism in the human hypothalamus: observations in Parkinson's disease and normal subjects. 818 Aug 36

There is some evidence that Parkinson's disease (PD) seems to be a heterogenous and generalized brain disorder reflecting a degeneration of multiple neuronal networks, including somatostatinergic neurons. Somatostatin-like immunoreactivity (SLI) and its molecular forms, high molecular weight form (HMV-SST), somatostatin-14 (SST-14), somatostatin-25/28 (SST-25/28) and Des-ala-somatostatin (Des-ala-SST), as well as homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were estimated using HPLC and radioimmunoassay in the cerebrospinal fluid (CSF) of 35 aged parkinsonian patients with different stages of intellectual deterioration. The influence of L-dopa-treatment on these neurochemical parameters was evaluated. Without a correlation with dementia scores (p = 0.11), SLI was significantly reduced in PD in comparison to the control group (p < 0.05). The reduction was related to the progression of the disease. Correlations between SLI, HVA and 5-HIAA indicate a heterogenous brain disorder in PD with alterations of several transmitter systems and functions. Complex qualitative and quantitative changes in the molecular pattern of SLI are compatible with a dysregulated synthesis and/or posttranslational processing. L-dopa-treatment was associated with a significant increase of HVA (p < 0.05) and HMV-SST (p < 0.05) and a slight, but insignificant increase of SLI (p = 0.11).
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PMID:Somatostatin-like immunoreactivity, its molecular forms and monoaminergic metabolites in aged and demented patients with Parkinson's disease--effect of L-Dopa. 881 4

Stroke remains a major brain disorder that often renders patients severely impaired and permanently disabled. There is no available treatment for reversing these deficits. Hippocampal, striatal and cortical grafting studies demonstrate that fetal cells/tissues, immortalized cells, and engineered cell lines can survive grafting into the ischemic adult brain, correct neurotransmitter release, establish both afferent and efferent connections with the host brain, and restore functional and cognitive deficits in specific models of stroke. The success of neural transplantation depends on several factors: the stroke model (location, extent, and degree of infarction), the donor cell viability and survival at pre- and post-transplantation, and the surgical technique, among others. Further exploitation of knowledge of neural transplantation therapy already available from our experience in treating Parkinson's disease needs to be critically considered for stroke therapy. While the consensus is to create a functional neuronal circuitry in the damaged host brain, there is growing evidence that trophic action of the grafts and host, as well as exogenous application of trophic factors may facilitate functional recovery in stroke. Current treatment modules, specifically that of rehabilitative medicine, should also be explored with neural transplantation therapy. However, validation of neural transplantation and any other treatment for stroke should be critically assessed in laboratory experiments and limited clinical trials. No direct treatment is recognized as safe and effective for reversing the stroke-induced brain damage and functional/cognitive deficits. The first clinical trial of neural transplantation in stroke patients is a mile-stone in stroke therapy, but subsequent large-scale trials should be approached with caution.
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PMID:Restoration of function by neural transplantation in the ischemic brain. 1114 41

This article presents the data on cost of the major brain disorders in Belgium which were retrieved from "Cost of Disorders of the Brain in Europe" study sponsored by the European Brain Council and performed by Stockholm Health Economics. The disorders selected were: addiction, depression, anxiety disorders, brain tumours, dementia, epilepsy, migraine and other headaches, multiple sclerosis, Parkinson's disease, psychotic disorders, stroke and trauma. Figures for prevalence of disorders and direct medical, direct non-medical and indirect costs are based on data coming from available electronic data bases, or when missing for Belgium, best possible estimates or extrapolated data were used. All economic data were transformed to Euro's for 2004 and adjusted for purchasing power parity (PPP). The results show that the total number of people with any brain disorder in Belgium amounts to 2.9 million in 2004, the most prevalent being anxiety disorders 1.1 million, migraine 860000, addiction (any) 800,000 and depression 500,000 cases. The total cost of all included brain disorders in Belgium was estimated at 10.6 billion Euros. Most costly per case are brain tumours, multiple sclerosis, stroke and dementia. Because of their higher prevalence, however depression, dementia, addiction, anxiety disorders and migraine have the highest total costs. Taken together brain disorders consume 4% of the gross national product and cost each citizen of Belgium 1029 Euros per year. The drug costs for brain disorders constitute only 10% of the total drug market in Belgium, and only 4% of the total cost of brain disorders in Belgium. This should be compared to the cost estimates and to a previous study which showed that brain disorders are responsible for 35% of the total burden of all disorders in Europe. This study suggests therefore that the direct healthcare resources, including expenses for drug therapies, allocated to brain disorders in Belgium are not leveled to the indirect costs and burden of these disorders. A comparison with data available from a direct prospective study in demented Belgian patients suggests that the mathematical estimates presented here reflect quite accurately the real average cost for dementia, although there are large variations depending on disease severity. As, in addition, subjects with brain disorders face collateral costs which have not been taken into associations, a complementary survey in the Belgian ecosystem to establish the cost profile of representative patients for the major brain disorders. Such a survey is being organized by a task force of the Belgian Brain Council.
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PMID:Cost estimates of brain disorders in Belgium. 1732 38

The aim of this study was to estimate the cost of "brain" disorders in Italy. Country-specific prevalence and health-economic data on addiction, affective, anxiety and psychotic disorders, tumours, dementia, epilepsy, migraine/other headaches, multiple sclerosis, Parkinson's disease, stroke and head trauma were reviewed. Direct medical/non-medical and indirect costs were computed. Population-based samples and national or regional registries were used. The Italian population expected with a brain disorder was 12.4 million in 2004. The highest cost per case was for tumours and multiple sclerosis; the lowest was for anxiety disorders and migraine. Dementia (8.6 billion euros), psychotic and affective disorders (18.7 billion euros), migraine (3.5 billion euros) and stroke (3.4 billion euros) represented the highest total costs. Direct medical costs were predominant for psychiatric and neurosurgical disorders, direct non-medical costs for dementia, and indirect costs for neurological disorders. The total cost of brain disorders in Italy was 40.8 billion euros, 3% of the gross national product, and 706 euros per Italian citizen/year. This figure is however likely to be underestimated as it is based on retrospective methodology and samples of brain disorders, and does not include intangible costs.
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PMID:Cost of disorders of the brain in Italy. 1848 7

In neurologic disorders, there are progressive losses in regional brain structural integrity, circuitry, and neuronal process that threaten individuals' ability to express functional capacity at several levels of severity. The classification of (a) patients on the basis of diagnosis, risk prognosis, and intervention outcome forms the basis of clinical staging and (b) laboratory animals on the basis of animal model of brain disorder, extent of insult and dysfunctional expression, provides the components for the clinical staging and preclinical staging, respectively, of the disease state with certain associated epidemiological, biological, and genetic characteristics. The investigation of epigenetics and biomarkers is intrinsic to any analysis of the progressive nature of the neurogenerative disorders, in the present account disorders relating to Alzheimer's disease, Parkinson's disease, depression, and diabetes.
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PMID:Staging neurological disorders: expressions of cognitive and motor disorder. 1994 Nov 73

The notion of staging in the neurodegenerative disorders is modulated by the constant and progressive loss of several aspects of brain structural integrity, circuitry, and neuronal processes. These destructive processes eventually remove individuals' abilities to perform at sufficient and necessary functional capacity at several levels of disease severity. The classification of (a) patients on the basis of diagnosis, risk prognosis, and intervention outcome, forms the basis of clinical staging, and (b) laboratory animals on the basis of animal model of brain disorder, extent of insult, and dysfunctional expression, provides the components for the clinical staging and preclinical staging, respectively, expressing associated epidemiological, biological, and genetic characteristics. The major focus of clinical staging in the present account stems from the fundamental notions of Braak staging as they describe the course and eventual prognosis for Alzheimer's disease, Lewy Body dementia, and Parkinson's disease. Mild cognitive impairment, which expresses the decline in episodic and semantic memory performance below the age-adjusted normal range without marked loss of global cognition or activities of daily living, and the applications of longitudinal magnetic resonance imaging, major instruments for the monitoring of either disease progression in dementia, present important challenges for staging concepts. Although Braak notions present the essential basis for further developments, current staging conceptualizations seem inadequate to comply with the massive influx of information dealing with neurodegenerative processes in brain, advanced both under clinical realities, and discoveries in the laboratory setting. The contributions of various biomarkers of disease progression, e.g., amyloid precursor protein, and neurotransmitter system imbalances, e.g., dopamine receptor supersensitivity and interactive propensities, await their incorporation into the existing staging models thereby underlining the ongoing, dynamic feature of the staging of brain disorders.
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PMID:Staging neurodegenerative disorders: structural, regional, biomarker, and functional progressions. 2039 91


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