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)

The prevalence of gait disorders among neurological inpatients is unknown, although disturbed gait is a common symptom. Gait disorders often lead to loss of independence with restraints for the patients and caregivers and costs for the health system. We designed a prospective study and investigated all patients admitted to a neurological hospital during a 100-day period for the presence of a gait disorder. Clinical investigation and several disease-specific rating scales were carried out for 493 patients. In 60% of the patients, a disturbance of gait was diagnosed. Most frequent diagnoses were stroke (21%), Parkinson's disease (17%), and polyneuropathy (7%). Within these diagnoses, the rate of patients with disturbed gait was high in Parkinson's disease (93%), subcortical arteriosclerotic encephalopathy (85%), and motor neuron disease (83%). Advanced age, dementia, alcohol abuse, and treatment with antiepileptics, neuroleptics, benzodiazepines, and chemotherapeutics were identified as risk factors for a gait disorder. A decline of cognitive function was accompanied by a reduction of walking speed. According to these results, gait disorders are among the most frequent symptoms in neurology.
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PMID:Prevalence of gait disorders in hospitalized neurological patients. 1539 43

We tested the characteristics and the differential pattern of upper extremity motor compromise, comparing hand tapping in patients with subcortical vascular encephalopathy (SVE; n = 18), idiopathic Parkinson's disease (PD; n = 18), and in healthy controls (n = 18). Both patient groups showed significant compromise in hand tapping compared with that in controls, with higher coefficients of variability (CV) regarding tapping amplitude and angular velocity, determined using a computerized movement analysis system. A differential tapping pattern in both patient groups could be demonstrated in that patients with PD showed lower tapping amplitudes than patients with SVE. Both patient groups displayed abnormalities in tapping rhythmicity compared with that in the control group.
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PMID:Differential pattern of hand-tapping compromise in vascular versus idiopathic parkinsonism: a study based on computerized movement analysis. 1564 33

Approximately 25% of patients with idiopathic Parkinson's disease (IPD) later develop dementia, with the typical characteristics as detailed in ICD-10 and DSM-IV. Differential diagnosis has to exclude dementia due to Lewy bodies, subcortical vascular encephalopathy and subcortical dementia due to progressive supranuclear paralysis or corticobasal degeneration. Several studies showed promising results for cholinesterase inhibitors such as donepezile, rivastigmine and galantamine. The demented Parkinsonian patients then present with improvement in cognitive function while motor skills do not deteriorate.
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PMID:Dementia in idiopathic Parkinson's syndrome. 1567 22

Whether chronic hallucinations belong to the natural history of untreated Parkinson disease (PD) remains undetermined. For early authors such as Gowers or Charcot and his followers, hallucinations that occurred in the course of PD either accompanied the final phase of the disease or reflected comorbidities. However, a few authors observed that hallucinations could occur in PD patients with severe depression, confusion, or dementia. Interest in hallucinations with parkinsonism increased with the outbreak of von Economo encephalitis, as they were more frequent than in PD, provoking new pathophysiologic questions. Later studies on mental symptoms in parkinsonism were often based on series that pooled patients with PD and postencephalitic syndromes, confounding a clear analysis. It remains difficult to estimate the prevalence of hallucinations in the natural course of PD before the introduction of levodopa therapy. The lack of prospective studies, the wide early use of anticholinergics and ergots compounds, and the absence of dementia with Lewy bodies in the nosology of the time are further limitations. Even with these limitations, historical descriptions of PD from the prelevodopa era suggest that hallucinations may be part of PD itself, especially in the context of late dementia, depression, or nonspecific encephalopathy.
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PMID:Hallucinations in Parkinson disease in the prelevodopa era. 1640 53

The management of Parkinson's disease (PD) tends to focus on the presenting motor syndrome; yet, in the long term, nonmotor complications of the illness and complications of treatment become increasingly troublesome. The aims of this study were to review the reasons for 761 hospital admissions for patients with a diagnosis of PD and to determine the cause of hospitalization. Only 15% were admitted for primary management of the motor syndrome. PD was the secondary diagnosis in 645 admissions. Of the latter, 39% were admitted because of falls leading to fracture, pneumonia, encephalopathy or dementia and hypotension with syncope. Cardiac and gastrointestinal diseases accounted for a further 22% of admissions. Complications of the later stages of PD and associated treatments are more likely to lead to hospital admission than management of the primary motor syndrome. Some of the emergency hospital admissions for PD may be potentially avoidable with better planning of management in the outpatient and community setting.
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PMID:Reasons for admission to hospital for Parkinson's disease. 1686 58

This pilot study characterizes memory functioning of 11 men with occupational chronic solvent encephalopathy (CSE). Pattern (PRM) and spatial recognition (SRM), spatial span (SSP), spatial working memory (SWM), and paired associate learning (PAL) from Cambridge Neuropsychological Test Automated Battery were performed twice. The most sensitive variables to show impairment were PAL trials, SRM total correct, and SWM number of between-search errors. The majority of the CSE patients demonstrated mild deficits. The most persistent dysfunction was in tasks demanding working memory processing, which predicted well the CSE status. Qualitatively, the memory deficits resemble those seen in moderate or severe Parkinson's disease.
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PMID:Memory performance profile in occupational chronic solvent encephalopathy suggests working memory dysfunction. 1705 Feb 60

Intracellular protein deposition due to aggregation caused by conformational alteration is the hallmark of a number of neurodegenerative disorders, including Parkinson's disease, tauopathies, Huntington's disease, and familial encephalopathy with neuroserpin inclusion bodies. The latter is an autosomal dominant disorder caused by point mutations in neuroserpin resulting in its destabilization. Mutant neuroserpin polymerizes and forms intracellular aggregates that eventually lead to neurodegeneration. We generated genetically modified mice expressing the late-onset S49P-Syracuse or the early-onset S52R-Portland mutation of neuroserpin in central nervous system neurons. Mice exhibited morphological, biochemical, and clinical features resembling those found in the human disease. Analysis of brains revealed large intraneuronal inclusions composed exclusively of mutant neuroserpin, accumulating long before the development of clinical symptoms in a time-dependent manner. Clinical symptoms and amount of neuroserpin inclusions correlated with the predicted instability of the protein. The presence of inclusion bodies in subclinical mice indicates that in humans the prevalence of the disease could be higher than anticipated. In addition to shedding light on the pathophysiology of the human disorder, these mice provide an excellent model to study mechanisms of neurodegeneration or establish novel therapies for familial encephalopathy with neuroserpin inclusion bodies and other neurodegenerative diseases with intracellular protein deposition.
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PMID:Accumulation of mutant neuroserpin precedes development of clinical symptoms in familial encephalopathy with neuroserpin inclusion bodies. 1739 69

Central nervous system (CNS) concentrates almost 10% of total zinc in the human body. Imbalances in zinc concentration are associated with numerous CNS diseases. Zinc deficiency is associated with nervous anorexia, major depression, cognitive impairment, and uncontrolled behavior. Our data reveal that plasma zinc concentration is decreased in major depression and it significantly increases following sertraline or amitriptyline treatment. Also, we found that ZnCl2 administration while inducing morphine-dependence in rats significantly decreases the symptoms of opioid-withdrawal syndrome. Recent data incriminate zinc deficit in the development of encephalopathy following severe impairment of hepatic function. On the other hand, zinc content of certain brain areas in Alzheimer disease is twice that in controls. Parkinson disease is also associated with higher zinc concentrations in the brain than normal. The ratio plasma zinc- other bivalent cations is also important for normal brain function.
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PMID:[Zinc involvements in the brain]. 1838 91

Calpain is a ubiquitous calcium-sensitive protease that is essential for normal physiologic neuronal function. However, alterations in calcium homeostasis lead to persistent, pathologic activation of calpain in a number of neurodegenerative diseases. Pathologic activation of calpain results in the cleavage of a number of neuronal substrates that negatively affect neuronal structure and function, leading to inhibition of essential neuronal survival mechanisms. In this review, we examine the mechanistic underpinnings of calcium dysregulation resulting in calpain activation in the acute neurodegenerative diseases such as cerebral ischemia and in the chronic neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, prion-related encephalopathy, and amylotrophic lateral sclerosis. The premise of this paper is that analysis of the signaling and transcriptional consequences of calpain-mediated cleavage of its various substrates for any neurodegenerative disease can be extrapolated to all of the neurodegenerative diseases vulnerable to calcium dysregulation.
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PMID:Calpain-mediated signaling mechanisms in neuronal injury and neurodegeneration. 1868 46

Parkinson's disease is a debilitating neurological disorder that affects 1-2% of the adult population over 55 years of age. For the vast majority of cases, the etiology of this disorder is unknown, although it is generally accepted that there is a genetic susceptibility to any number of environmental agents. One such agent may be viruses. It has been shown that numerous viruses can enter the nervous system, i.e. they are neurotropic, and induce a number of encephalopathies. One of the secondary consequences of these encephalopathies can be parkinsonism, that is both transient as well as permanent. One of the most highlighted and controversial cases of viral parkinsonism is that which followed the 1918 influenza outbreak and the subsequent induction of von Economo's encephalopathy. In this review, we discuss the neurological sequelae of infection by influenza virus as well as that of other viruses known to induce parkinsonism including Coxsackie, Japanese encephalitis B, St. Louis, West Nile and HIV viruses.
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PMID:Viral parkinsonism. 1876 Mar 50


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