Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients with Parkinson's disease and renal insufficiency had excessively high concentrations of amantadine hydrochloride in the blood. The amounts of the drug removed by hemodialysis and peritoneal dialysis were small. However, since extrarenal elimination is negligible in such patients, frequently repeated dialysis may be required to remove the drug.
Can Med Assoc J 1976 Sep 18
PMID:Removal of amantadine hydrochloride by dialysis in patients with renal insufficiency. 95 34

The further therapeutic benefit of piribedil when combined with amantadine or Levodopa was studied by a double-blind, cross-over trial in 15 patients with Parkinson's disease. A significant improvement at the 5 per cent level for akinesia, gait, speech disorder and facial expression occurred when piribedil was added to Levodopa; and a more highly significant improvement at the 1 per cent level for akinesia, facial expression and finger dexterity occurred with piribedil and amantadine. No significant improvement occurred for special timed tests. Improvement was associated with side effects in both groups of patients. Side effects occurred with both placebo and active piribedil. Only nausea during piribedil and Levodopa treatment reached statistical significance when compared with the placebo. Piribedil did not give rise to any haematological or biochemical complications. Our findings suggest that piribedil is of further therapeutic benefit when added to amantadine or Levodopa. It was suggested that the improvement which occurred together with amantadine could be due to the combined action of both drugs on dopamine receptors.
Acta Neurol Scand 1975 Sep
PMID:Piribedil (ET 495) in the treatment of Parkinson's disease combined with amantadine or levodopa. 109 59

Patients with Parkinson's disease are unable to adjust the firing rate of motor units that initiate contraction from zero to higher rates; the frequency modulation of motor units is not normal, but motor units recruit normally as effort is increased. Treatment with levodopa makes these motor units accessible to activation and frequency control. Elderly subjects also have difficulty in the activation of minimal contraction and in the maintenance of firing but to a significantly lesser degree than do parkinsonian patients. In this respect, the elderly patient and the parkinsonian patient are qualitatively similar.
Neurology 1975 Sep
PMID:Motor unit control in Parkinson's disease and the influence of levodopa. 117 11

A 77-year-old man developed syncope after meals at the age of 75. He had been treated with anti-Parkinson's drugs such as levodopa for 18 years as a patient with idiopathic Parkinson's disease (PD). The medications had been very effective to his parkinsonism. Ambulatory blood pressure was recorded every 20 minutes throughout one day by indirect measurement using a Colin medical instrument monitor (ABPM-630). The subsequent data disclosed that postprandial hypotension (PPH) was associated with the frequent after-meal syncope. It was also found that oral ingestion of a solution containing 50 grams of glucose caused a marked and prolonged hypotension during the resting supine position. Plasma norepinephrine failed to show any increment. Plasma vasopressin slightly increased while pulse rate, plasma renin activity, osmolality, and hematocrit did not change despite the production of severe hypotension of a relative acute onset. Signs of glucose intolerance and hyperinsulinemic response were observed. Indications of systemic autonomic nervous dysfunctions were revealed in various autonomic nervous function tests. Physical treatment combined with medication such as droxidopa, midodrine and especially caffeine and fludrocortisone proved to be effective on PPH. The authors confirmed the existence of PD with symptomatic PPH. In addition, we considered this present case as an example of "progressive autonomic failure with PD" (Bannister, 1988).
Rinsho Shinkeigaku 1992 Sep
PMID:[Parkinson's disease with syncope as a chief complaint induced by prominent postprandial hypotension]. 130 Feb 58

The clinical management of Parkinson's disease has been revolutionized by the introduction of levodopa therapy. It has significantly reduced disability and has extended life expectancies of patients with Parkinson's disease. However, motor response fluctuations frequently appear in patients after long-term treatment with levodopa. In this study, we investigated the effect of protein-restricted diet on fluctuations in eight patients with Parkinson's disease who had been receiving long-term levodopa treatment (mean 12.5 years). Two weeks of protein-restricted daytime diet (7.5 g total at breakfast and lunch) was followed by 12.5 g total at breakfast and lunch. At night, high-protein diet (40-50 g at dinner) was offered to the patients in order to maintain total daily protein intake at Japanese standard level. The medication schedule of levodopa and other antiparkinsonian drugs was not changed within 2 weeks after the study was began. Fluctuations were reduced in 7 of the 8 patients. But in only one patient (case 6), dyskinesia and general condition got worse and stopped this therapy. Body weight, serum protein and albumin levels did not change significantly for at least three month after the study was begun in every 6 patients who were examined. Homovanillic acid level of cerebrospinal fluid reduced in every 4 patients who were examined. We concluded that protein-restricted diet during the daytime offers a fascinating technique for the control of motor response fluctuations in patients with Parkinson's disease undergoing long-term levodopa treatment. But this therapy must be indicated carefully. Mechanism of this therapy may has something to do with improvement of dopamine metabolism in the brain.
Rinsho Shinkeigaku 1992 Sep
PMID:[Influence of protein-restricted diet on motor response fluctuations in Parkinson's disease]. 130 Feb 70

It is now well recognized that the hypothalamus is an important site of neuropathology in Parkinson's disease (PD). Lewy bodies, a marker of nerve cell degeneration and a pathological hallmark of PD, have been observed frequently in the hypothalamus of PD patients by Lewy (1923) and other investigators and confirmed by more recent systematic studies by Langston & Forno (1978). Both Lewy and Langston & Forno found a predilection of Lewy body formation in specific hypothalamic nuclei with the tuberomammillary, lateral, and posterior areas containing by far the highest average counts per nucleus. Selective vulnerability of the tuberomammillary, lateral, and posterior hypothalamic cell groups to degeneration has been observed also in aging, postencephalitic Parkinsonism, Alzheimer's disease, and schizophrenia. The susceptibility of these particular nuclei to degenerative changes including Lewy body formation is not presently understood nor are the mechanisms by which Lewy bodies are formed in PD and other CNS disorders. Accumulation of amines, a pathological process which follows degeneration of catecholamine-containing neurons in experimental animals, also occurs most frequently in the lateral and posterior hypothalamic areas. In the present communication we propose that in PD, amine accumulation may be a precursor to Lewy body formation and that the susceptibility of certain hypothalamic areas to Lewy body formation may be related to their propensity to accumulate amines. Furthermore, the frequent co-existence of Lewy bodies and Alzheimer's neurofibrillary tangles in the lateral and posterior hypothalamic nuclei suggest that they may share a common pathogenetic etiology. If confirmed, this hypothesis may provide an experimental model by which the formation of Lewy bodies and neurofibrillary tangles may be investigated.
Int J Neurosci 1992 Sep
PMID:Amine accumulation: a possible precursor of Lewy body formation in Parkinson's disease. 130 71

Application of external weak magnetic fields recently has been reported to be efficacious in the treatment of a 62-year-old patient with idiopathic Parkinson's disease (PD) complicated by levodopa-induced fluctuations in motor response ("on-off"). I report an additional case of a 67-year-old man with idiopathic PD and levodopa-related motor fluctuations who likewise experienced marked and sustained improvement in Parkinsonian symptoms and amelioration of "on-off" symptoms following the application of external weak magnetic fields. Based on these observations it is concluded that artificial weak magnetic fields may be beneficial for the treatment of PD complicated by levodopa-related "on-off" phenomenon. Furthermore, since in experimental animals external magnetic fields alter the secretion of melatonin, which in turn has been shown to regulate striatal and mesolimbic dopamine-mediated behaviors, it is proposed that the antiParkinsonian effects of weak magnetic fields are mediated via the pineal gland.
Int J Neurosci 1992 Sep
PMID:Weak magnetic fields in the treatment of Parkinson's disease with the "on-off" phenomenon. 130 75

The pedunculopontine tegmental nucleus (PPTg) has been shown to have cholinergic connections with the thalamus and basal ganglia. The ability of various doses of the excitotoxins (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) (AMPA), folate, ibotenate, kainate, N-methyl-D-aspartate (NMDA), quinolinate and quisqualate to make lesions in the PPTg was examined, with particular reference to their ability to destroy cholinergic neurons identified using choline acetyltransferase (ChAT) immunohistochemistry. All of the toxins induced convulsive activity on recovery from surgical anesthesia and all except folate made lesions in the PPTg and surrounding structures. The size of the lesions was computed following examination of Cresyl violet stained sections. The largest lesions were made by kainate = AMPA greater than NMDA = ibotenate greater than quisqualate = quinolinate. All of the toxins destroyed cholinergic neurons, higher doses producing greater loss than lower. The ratio of cholinergic cell loss to general neuronal loss (assessed by Cresyl violet staining) was also computed, revealing marked differences between the toxins. Statistical analysis showed that there were significant differences between excitotoxins in terms of this ratio, but these were accounted for by the low dose of quinolinate (24 nmol) producing a significantly greater ratio of damage (12.18:1) than every other toxin. (Next highest ratio: quisqualate 60 nmol, 6.22:1.) Between the other toxins (kainate, AMPA, ibotenate, quisqualate, NMDA and the high dose of quinolinate) there were no statistically significant differences. Intense calcium deposits (stained by Alizarin red) were found frequently and often defined the borders of the lesion. Tyrosine hydroxylase immunohistochemistry revealed axons running below and into the area of lesioned tissue suggesting strongly that fibers were undamaged by the lesions. We conclude that in the PPTg, different excitotoxins make discriminably different lesions, both quantitatively and qualitatively. Unlike excitotoxic lesions in the basal forebrain quinolinate, not quisqualate, made the most selective lesions of cholinergic neurons and, unlike excitotoxic lesions in the septal nuclei, non-myelinated fibers were spared by ibotenate. The implications of these data for research into brainstem mechanisms of Parkinson's disease are discussed.
Brain Res 1992 Sep 04
PMID:Excitotoxic lesions of the pedunculopontine tegmental nucleus of the rat. I. Comparison of the effects of various excitotoxins, with particular reference to the loss of immunohistochemically identified cholinergic neurons. 138 12

We measured regional cerebral glucose metabolism using 2-[18F]-fluoro-2-deoxy-D-glucose and positron emission tomography in depressed and nondepressed patients with early Huntington's disease (HD), compared with appropriately matched controls. Caudate, putamen, and cingulate metabolism was significantly lower in patients with HD than in control subjects, independent of mood state. Orbital frontal-inferior prefrontal cortex hypometabolism, however, differentiated depressed patients from both nondepressed patients and normal controls. These findings implicate selective dysfunction of the paralimbic regions of the frontal lobes in the mood disorder of HD. The metabolic pattern is similar to that in depression associated with Parkinson's disease, suggesting that the integrity of pathways linking paralimbic frontal cortex and the basal ganglia may be integral to the normal regulation of mood.
Neurology 1992 Sep
PMID:Paralimbic frontal lobe hypometabolism in depression associated with Huntington's disease. 138 63

A 55-year-old man presented with a 5-year history of Parkinson's disease and a 6-month history of major depression. The patient's depressive symptoms responded to treatment with fluvoxamine, a selective and potent serotonin reuptake inhibitor. Tryptophan depletion testing, which acutely lowers central serotonin levels, caused a brief exacerbation of the depressive illness, which resolved upon tryptophan repletion. Serotonergic dysfunction may be an etiologic factor in depression that occurs in Parkinson's disease.
Neurology 1992 Sep
PMID:Serotonergic dysfunction in depression associated with Parkinson's disease. 835 Oct 31


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>