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 function of neuromelanin is not known, but some properties of the pigment suggest a protective action. Its unique ability to accumulate and retain several compounds, such as various amines and a number of metals, may protect the pigment-containing neurons from high exposure to harmful substances. This possible mechanism of protection may however in certain instances be of a double-edged nature, as accumulation of neurotoxic agents with a high melanin affinity may cause toxic concentrations in the neuro-melanin-containing cells. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) seems to be such a compound, as it has been found to preferentially destroy neuromelanin-containing cells. The degree of MPTP neurotoxicity seems to be related to the amount of neuromelanin present in the particular species. It is possible that also manganese, which is known to cause an extrapyramidal disorder resembling Parkinson's disease, causes injury to neuromelanin-bearing neurons due to its melanin affinity. This mechanism may be involved in other forms of chemically induced Parkinsonism and possibly also in idiopathic Parkinson's disease, although the offending agent remains to be discovered.
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PMID:Neuromelanin and its possible protective and destructive properties. 333 86

Three patients are described who suffered from Parkinson's disease and who also experienced severe pain. In one patient who had used psychotropic medication for a long period there was evidence of associated autonomic failure. It is suggested that the pain, which has some features of central pain with ill defined areas of involvement and lack of sensory abnormality, may occasionally be an important aspect of Parkinson's disease and indeed can precede the onset of this extrapyramidal disorder. Possible mechanisms are discussed including the influence of dopaminergic pathways on pain modulation. The importance of recognising the pain of Parkinson's disease is stressed.
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PMID:Pain in Parkinson's disease. 404 9

We describe a clinical picture identical to Parkinson disease complicating postoperative hypoparathyroidism. Unlike most previously described cases, the extrapyramidal disorder was reversed completely by repletion of serum calcium.
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PMID:Reversible Parkinson syndrome complicating postoperative hypoparathyroidism. 719 11

Senile dementia of Lewy body type or Lewy body dementia (SDLT or LBD) is defined as a Lewy body associated disease presenting in the elderly primarily with dementia with variable extrapyramidal disorder. Characteristic clinical symptoms include fluctuating cognitive impairment, psychotic features such as hallucinations and a particular sensitivity to neuroleptic medication. Although apolipoprotein e4 allele is increased 2-3 fold in SDLT (as in Alzheimer's disease) and beta-amyloidosis occurs in most cases, the most robust neurobiological correlate of the dementia so far identified appears to be extensive cholinergic deficits in the neocortex. This is consistent with previously reported correlations between cortical cholinergic activity and dementia in Parkinson's disease (PD) and Alzheimer's disease. There is also a significant interaction between the density of limbic cortical Lewy bodies and dementia in both SDLT and PD, although the cortical neuronal population affected remains to be identified. Cortical Lewy body density is positively correlated with the age of disease onset in PD and SDLT. This may account for the increased incidence of psychiatric syndromes, as opposed to extrapyramidal disorder in Lewy body disease with advancing age as may age-related loss of cholinergic activity in cortical areas such as the hippocampus.
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PMID:Lewy body dementia--clinical, pathological and neurochemical interconnections. 947 Jan 31

Essential tremor (ET) is the most prevalent extrapyramidal disorder, yet its diagnosis is still controversial. This article introduces new findings that pertain to this diagnostic problem. Twenty-three patients with ET were studied. Patients with parkinsonism, cerebellar signs, severe head injury, or those under neuroleptic medication were excluded. Twenty-five normal subjects served as control subjects. Visuomotor tests involving tracking and tracing along three different paths with both the right and left hands, were used. Performance was assessed by measuring test duration, directional error, the proportion of the cumulative test time during which directional error exceeded half the maximal possible level (PT50%), the mean distance from the model path, the velocity of the hand movement, and the number of tracking interruptions. In 15 of 23 patients performance was the same as in the control subjects. These patients were defined as having a "simple condition" of ET (ETs). Considerable visuomotor impairment was found in eight patients who were regarded as having a "complex condition" of ET (ETc). Patients with ETc had significantly lower tracking speed, more tracking interruptions, longer test duration, greater directional error, greater PT50%, and greater distance from path than patients with ETs or control subjects. Most patients with ET appear to have normal visuomotor capabilities (ETs) but some display significant visuomotor disturbances (ETc). Considering the presence of similar impairments in patients with early Parkinson's disease and the increased prevalence of parkinsonism in patients with ET, it is possible that preclinical parkinsonism exists in patients with ETc. Further follow up of patients with ETc is necessary to verify this possibility.
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PMID:Visuomotor performance in patients with essential tremor. 1058 74

Extrapyramidal system, a rich network of nerve and glial cells consists of subcortical and cortical grey matter. The system serves as an integrator of unaware, automatic, repeated, spontaneous, complicated and purposeful motor samples. Muscle tone regulation and its distribution is another decisive extrapyramidal function. This review article concerns to some degradation mechanisms in extrapyramidal system, as either the programmed cell death or apoptosis. The physiologic extracellular decreasing signals creating apoptosis (nerve growth factor--fall) are either genetically expressed or there are neuropathophysiologic processes that may activate pathways leading to apoptosis, namely oxidative stress, glutamate toxicity and calcium homeostasis disruption. The level of dopamine transporter expression (mRNA, methyl-phenyl-pyridinium) might determine the vulnerability of the nigral neurons to the Parkinsonian insult. The most common clinical picture of extrapyramidal disorder-Parkinson's disease-consists of an active dopamine cell death-apoptosis, which is partially programmed like as programmed cell death and partially accidentally installed chain of events. Without morphological criteria, biochemical indicators such as laddered DNA fragmentation pattern and/or the requirement for macromolecular synthesis merely suggest but do not provide unequivocal evidence for apoptosis. There are either genetic or acquired conditions creating unbalance of Bax/Bcl-2 families-proapoptotic and prooncogenic factors, respectively. The first Bax gene cooperates with other genes coding the new transmembrane proteins into the mitochondrial megapores determinating transition by means of death receptors. Bcl-2 codes prooncogenic mitoses and tissue proliferation. The neuroprotective hypothesis of the dopamine agonist action is a very attractive working hypothesis and some of its tenets are derived from the oxidative stress hypothesis for neurodegeneration, but this hypothesis is still controversial.
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PMID:Possible extrapyramidal system degradation in Parkinson's disease. 1113 99

The etiology of a high-incidence focus of amyotrophic lateral sclerosis and parkinsonism-dementia (ALS/P-D) in south West Papua (Irian Jaya, Indonesia), first described in the 1960s and 1970s, has been attributed to mineral deficiencies, hyperparathyroidism, and metal neurotoxicity arising from reliance on drinking water obtained from springs and shallow wells. More recent visits (1987 and 1990) to the south West Papua focus of neurodegenerative disease cast doubt on this explanation by revealing changes in disease prevalence in communities with an unchanged water supply. These communities have experienced a dramatic decline in ALS and a reversal in the relative prevalence of ALS and parkinsonism. The extrapyramidal disorder can be distinguished from Parkinson disease by pyramidal features (and dementia) reminiscent of Guam P-D. Topical use of cycad seed (termed kurru) gametophyte to treat large skin lesions is advanced as a plausible but unproven etiologic factor. Medicinal use of untreated cycad seed (Cycas sp.) has also been linked with ALS foci in Japan (oral use) and Guam (topical use), with the additional consumption on Guam of food items prepared from Cycas sp. seed or animals that consume cycad seed components.
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PMID:On the decline and etiology of high-incidence motor system disease in West Papua (southwest New Guinea). 1609 1

A primary mitochondrial dysfunction has been recently hypothesized in the pathogenesis of Parkinson's disease (PD). As a matter of fact, MPTP (a drug able to induce neuronal loss in substantia nigra) is a specific inhibitor of Complex I, while controversial data on Complex I deficiency have been reported in platelets, muscle and brain of patients affected by Parkinson's disease. Here we report data on respiratory chain enzyme activities in isolated muscle mitochondria from 6 patients with classical PD (two with the hereditary form, HPD), and in 6 patients with a multisystem extrapyramidal disorder (MSED) with parkinsonsim as the main clinical feature. While histological and biochemical evidence of mitochondrial dysfunction has been detected in 1 case with PD and in 3 cases with MSED, normal results have been obtained in the other cases confirming the extreme clinical and biochemical heterogeneity of these disorders.
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PMID:Muscle respiratory chain enzyme activities in parkinson's disease and in multisystem extrapyramidal disorders with parkinsonism as the main clinical feature. 1864 55

Drug induced parkinsonism is the second most common cause of parkinsonism in older people after idiopathic Parkinson's disease (PD). Risk factors for developing drug induced parkinsonism include: older age; female gender; dose and duration of treatment; type of agent used; cognitive impairment; acquired immunodeficiency syndrome (AIDS); tardive dyskinesia; and pre-existing extrapyramidal disorder. In most patients parkinsonism is reversible upon stopping the offending drug, though it may take several months to resolve fully and in some patients it may even persist. In this case, one needs to consider the possibility of PD which has been unmasked by the offending drug, and treatment with dopaminergic agents may be warranted. Drug induced parkinsonism adversely affects the quality of life in older patients and is potentially reversible, highlighting the importance of early recognition of this condition. This article discusses the drugs implicated, as well as the epidemiology, pathophysiology, clinical features, and management of drug induced parkinsonism.
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PMID:Drug induced parkinsonism: a common cause of parkinsonism in older people. 1952 8

Parkinsonism is an extrapyramidal disorder characterised by tremor, muscle rigidity, bradykinesia and postural instability. The most common cause of parkinsonism is idiopathic Parkinson disease. Another common cause is drug-induced parkinsonism. Various drugs can cause parkinsonian symptoms. Many patients exhibiting these side-effects are mistakenly treated with dopaminergic medication. We present two patients with drug-induced parkinsonism induced by sodium valproate and cinnarizine, respectively. The symptoms disappeared after they stopped taking this medication.
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PMID:[Parkinsonism due to the medication]. 1990 Mar 8


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