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)

Levodopa is at present the most effective treatment of Parkinson's disease. Its use in combination with a peripheral decarboxylase inhibitor prolongs the elevation of plasma levels and decreases the incidence of peripheral side effects. Severe psychiatric and neurologic side-effects may necessitate reduction or cessation of the drug.
Prim Care 1977 Sep
PMID:Levodopa in the treatment of Parkinson's disease. 26 29

Psychiatric problems constitute one of the prime reasons for failure in levodopa therapy in Parkinson's disease. While a variety of symptoms may be seen, the levodopa itself does not produce a defined set of psychiatric symptoms. The single most important factor determining the psychiatric response to levodopa therapy is the mental state of the patient before therapy.
Prim Care 1977 Sep
PMID:Psychiatric disturbances occurring during levodopa therapy of Parkinson's disease. 26 30

Two recent sporadic cases of progressive Parkinsonism after encephalitis are described. Both patients had two oligoclonal protein bands in their CSF. These bands were not present in patients with idiopathic Parkinson's disease and might, therefore, be useful for diagnostic purposes, particularly when the history of encephalitis is uncertain.
J Neurol Neurosurg Psychiatry 1979 Sep
PMID:Oligoclonal banding in the cerebrospinal fluid of patients with postencephalitic Parkinsonism. 50 78

Virological studies were performed on brain material from 9 patients with idiopathic Parkinson disease and 3 matched controls. Electron microscopy and indirect immunofluorescent study were carried out directly on autopsy material from substantia nigra, caudate nucleus, and hypothalamus and on primary tissue culture explants of these brain areas grown alone or in cocultivation with virus-susceptible indicator cell lines. All studies were negative for the presence of viral particles, viral inclusions, or cellular changes suggestive of virus infection. All materials were negative for antigens of herpes simplex type 1, influenza A/NWS, and measles (Edmonston strain) viruses. Within the limits of these tehcniques, there is no evidence at this time that viruses are an important etiological agent in idiopathic Parkinson disease.
Ann Neurol 1979 Sep
PMID:Search for viral particles and virus-specific products in idiopathic Parkinson disease brain material. 53 25

The nicotinic cholinergic amine piperidine diminished both the dyskinesia and the symptomatic control in some patients with Parkinson disease receiving levodopa. Since the piperdine configuration is contained in the molecules of the apomorphine and N-propylnoraporphine, it might be responsible for the antagonism of these drugs to some effects of levodopa in Parkinson disease and for the palliation by apomorphine of some dopamine-mediated symptoms in other extrapyramidal disorders.
Neurology 1977 Sep
PMID:Antagonism by piperidine of levodopa effects in Parkinson disease. 56 44

In four patients with Parkinson disease, we compared carbidopa combined with levodopa (Sinemet) and benserazide combined with levodopa (Madopar). All of these patients had responded to treatment, first with levodopa and then with Sinemet; after 6 years two continued to show a good response, while two developed marked "on-off" phenomena. Clinically, Sinemet and Madopar were similar; however, DOPA levels were higher, but with a shorter half-life, on Madopar. The higher DOPA levels may have been offset by the shorter half-life, resulting in no clinical change. DOPA levels were lower and half-life was shorter in patients with on-off phenomena. These differences may be responsible in part for the on-off phenomena.
Neurology 1978 Sep
PMID:Comparative effectiveness of two extracerebral DOPA decarboxylase inhibitors in Parkinson disease. 56 68

Thirty-four autopsy cases conforming to the standard neuropathologic criteria of Parkinson disease were sex- and age-matched with controls who had died of infarct or trauma. All brains were reviewed for changes compatible with Alzheimer disease, and available clinical data were retrospectively reviewed. Nineteen (56 percent) of the Parkinson cases had shown some degree of dementia. The average parkinsonian brain weight was 1281 gm; it was 1365 gm for the controls (p less than 0.02). Plaques, neurofibrillary tangles, granulovacuolar degeneration, and cortical cell loss were present in all but one of the parkinsonian brains; these pathologic changes were present in fewer controls and to a lesser degree. The higher incidence of dementia in patients with Parkinson disease may be explained by the simultaneous presence of Alzheimer disease.
Neurology 1979 Sep
PMID:Dementia in Parkinson disease: a neuropathologic study. 57 1

Vascular siderosis (VS) refers to the presence of mineralized small and medium-sized arteries in the globus pallidus, usually regarded as reflecting an aging process. The electron probe analysis of deposits in vascular siderosis in 10 patients dying of parkinsonism and in 8 other patients without parkinsonism is reported here. The microprobes identified a total of 11 elements in the VS in these 18 patients. Five elements--lead, aluminum, sulfur, manganese, and barium--were present only in VS associated with parkinsonism. Statistically, the association of lead was highly significant while that of aluminum and sulfur in 4. The significance of the presence of sulfur is difficult to assess since its compounds are normally present in large quantities in the brain. These findings raise the question whether lead and aluminum may be associated in some way with the pathogenesis of certain forms of Parkinson disease.
Ann Neurol 1977 Sep
PMID:The relationship between Parkinson syndrome and vascular siderosis: an electron microprobe study. 61 68

Using high-performance liquid chromatography with electrochemical detection, we determined serotonin in plasma from parkinsonian patients being treated with L-3,4-dihydroxyphenylalanine or N-(DL-seryl)-N'(2,3,4-trihydroxybenzyl)hydrochloride plus L-3,4-dihydroxyphenylalanine ("Sinemet") and in serum from a blood bank, from "normal" persons, and a pooled specimen from a hospital clinical laboratory. The values obtained for the two groups of Parkinson's disease patients showed no significant difference. Long-term storage on solid CO2 was xhown to be an adequate technique for preserving samples. The mean (+/-SEAM) normal value obtained for serotonin in serum was 146 +/- 46 microgram/liter (n = 23), a result in harmony with that previously obtained [Clin. Chem. 20, 812 (1974)] by fluorometry. In comparison to other methods for measurement of serotonin in serum or plasma, we believe that the present scheme offers greater selectivity, sensitivity, and precision.
Clin Chem 1978 Sep
PMID:Liquid-chromatographic determination of serotonin in serum and plasma. 68 9

The relationship between dopamine receptor stimulation by bromocriptine or levodopa and the relief of parkinsonism was studied in 24 patients with Parkinson disease. Bromocriptine, 30 mg daily for 20 weeks, elicited an improvement in the parkinsonian clinical features, but this was less than the subsequent improvement with levodopa and benserazide, 800 mg and 200 mg daily, respectively. There was a negative correlation between the pretreatment severity of the disease or changes in cerebrospinal fluid homovanillic acid (HVA) and improvement in parkinsonian disability during bromocriptine treatment. Futhermore, it was found that clinical improvement and HVA responses in the cerebrospinal fluid after dopamine receptor stimulation by bromocriptine may predict the clinical response to levodopa.
Ann Neurol 1978 Sep
PMID:Brain dopamine receptor stimulation and the relief of Parkinsonism: relationship between bromocriptine and levodopa. 71 39


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