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Biomedical subjects

W Birkmayer

Publications and source records attributed to W Birkmayer.

18 recordsLinked to original sources
PubMed1979

[The combined treatment of Parkinson's disease with L-dopa plus decarboxylase inhibitors (carbidopa, benserazide) (author's transl)].

An open cross-over study of 20 patients with Parkinson's disease performed with two drugs containing L-dopa and a peripheral aromatic amino acid decarboxylase inhibitor (benserazide, carbidopa) confirmed the conclusions reached in other clinical trials that this combined treatment of Parkinson's disease is the most effective form of drug therapy available at present. With both drugs, Madopar or Sinemet, an optimum therapeutic result was obtained with relatively small doses of L-dopa (the reduction in L-dopa dosage amounting to about 80%). A loss of efficacy with both drugs, which has observed during long-term treatment of patients with Parkinson's disease, could be avoided by switching the patients from Sinemet to Madopar and vice versa. Determination of L-dopa in the plasma demonstrated that with either drug similar plasma levels of L-dopa were achieved during clinically effective treatment.

Aged↗
PubMed1979

Distinction between benign and malignant type of Parkinson's disease.

Clinical data demonstrate that there is a significant difference between at least two types of idiopathic Parkinsonian patients; a benign type of Parkinson's disease and a malignant type. They can be distinguished by the time course of a disability-score, independent of the duration of the disease. The benign cases respond very well to L-Dopa (Madopar) treatment and show a long lasting (7 years) drop in the disability, whereas the improvement of disability in the malignant cases is much smaller and lasts for about one year, followed by an increase of disability. The duration of the disease is 12,5 +/- 0,4 years in the benign type but only 4,0 +/- 0,3 years in the malignant type. Akinetic crises, off-phases, hyperkinetic crises and toxic deliria after Madopar treatment can be observed later in the benign than in the malignant cases. These results suggest that the degeneration of the dopaminergic nigrostriatal system occurs much more rapidly in malignant cases than in benign cases of Parkinson's disease.

Dose-Response Relationship, Drug↗
PubMed1979

[Psychological problems of incurable patients in old age (author's transl)].

Biological functions are regulated by feedback mechanisms. In old age disorders occur in this regulation by insufficiency of biochemical transmitters. The synthesizing enzymes of Tyrosine Hydroxylase, Tryptophan Hydroxylase, Dopa Decarboxylase and 5-Hydroxytryptophan Decarboxylase are diminished in old age. Minus symptoms as depression, or exhaustion and disorders of circulation occur. A substitution by biogenic transmitters is not possible, because these don't pass the blood-brain-barriere. Therefore a medication of psychopharmacological drugs is necessary. For instance Anxiety--tranquilizer, exhaustion--anti depressive drugs.

Aged↗
PubMed1978

Dopamine-sensitive adenylate cyclase activity in the caudate nucleus and adrenal medulla in Parkinson's disease and in liver cirrhosis.

In human caudate nucleus and adrenal medulla dopamine-stimulated adenylate cyclase was measured. At a concentration of 100 microM dopamine, liver cirrhosis, carcinoma and therapy resistent parkinsonian patients showed decreased stimulation or even a reduction compared to controls. Therapy responding parkinsonian patients showed a decreased stimulation compared to controls, but this stimulation was significantly higher than in drug resistent patients.

Adenylyl Cyclases↗
PubMed1978

Toxic delirium after L-dopa medication.

L-DOPA-psychosis is a frequent side effect of the combined treatment of Parkinson's disease with L-DOPA and peripherally active decarboxylase inhibitors. Regional human post-mortem brain studies showed a significant increase of noradrenaline and serotonin particularly in extrastriatal areas, whereas the lenticular nuclei were not involved. The significance of extrastriatal neurotransmitter dysfunctions for psychiatric disorders is discussed.

Autopsy↗
PubMed1978

CNS Modulation of adrenal tyrosine hydroxylase in Parkinson's disease and metabolic encephalopathies.

Tyrosine hydroxylase (TH) activity was assayed radioenzymatically in various regions of post-mortem brains of human individuals without neurologic disorders (controls), with Parkinson's disease, senile dementia, hypertensive encephalopathy, hepatic and diabetic coma, liver cirrhosis without coma, and hepatic coma treated with parenteral administration of L-valine. In addition TH activity of the post-mortem adrenal medulla was assayed in controls, in Parkinson's disease, senile dementia and hypertensive encephalopathy. In Parkinson's disease TH activity was significantly decreased in the nigrostriatal system, and less severe in other brainstem areas, while the raphé-reticular formation and limbic system showed normal values. In addition, there was significant decrease in the TH activity of the adrenal medulla, suggesting that Parkinson's disease is a generalized disorder not limited to distinct CNS areas, and that impairment of the dopaminergic niggro-striatal system may involve the TH activity in the adrenal medulla, thus inducing disorders of the peripheral sympathetic system. Senile brain atrophy showed no definite changes in brain, except the striatum, and adrenomedullary TH, while in one case of hypertensive encephalopathy due to long-term corticosteroid treatment normal TH activity in the adrenal medulla was opposed by decreased striatal TH activity, probably due to cerebral ischemia. TH activity in the caudate nucleus of individuals with both hepatic and diabetic coma were within normal ranges, suggesting a sufficient energy supply of the brain during such metabolic catastrophes, while reduced brain TH activity in patients with hepatic coma who died of acute gastrointestinal bleeding is probably due to severe final cerebral ischemia. No correlative data on brain and adrenomedullary TH activities in metabolic encephalopathies are available so far.

Aged↗
PubMed1977

Implications of combined treatment with 'Madopar' and L-deprenil in Parkinson's disease. A long-term study.

In a clinical trial the effect of L-deprenil, a selective irreversible inhibitor of monoamine oxidase (M.A.O.) "type B" in potentiating the anti-kinetic properties of levodopa has been investigated in 223 patients. Both drugs were given orally, levodopa as 'Madopar' (levodopa plus the peripherally acting decarboxylase inhibitor, benserazide) 250 mg three times daily and L-deprenil 5 mg once or twice daily. The addition of L-deprenil to madopar therapy resulted in a statistically significant (P less than 0-01-0-001) reduction in patients' functional disability on average within 60 min after a single oral dose and lasting for 1 to 3 days. Dyskinesia occurred in 16 patients, psychosis in 14, orthostatic hypotension in 5, and nausea in 8. Reduction of the L-deprenil dose to 5 mg in these patients eliminated some of the side-effects. Two-thirds of the patients with side-effects had suffered from parkinsonism for between 7 and 15 years. 14% of the patients failed to respond to madopar-deprenil therapy. It is suggested that L-deprenil may act through inhibition of brain M.A.O. as well as by a psychostimulant effect similar to that of amphetamine which occurs through the release of dopamine. Both mechanisms would make more dopamine available at dopamine receptor sites.

Administration, Oral↗
PubMed1977

Brain-noradrenaline and 3-methoxy-4-hydroxyphenylglycol in Parkinson's syndrome.

1. Significantly reduced values of noradrenaline in Parkinson's disease were observable in all brain areas which were studied. 2. A topographic distribution of free 3-methoxy-4-hydroxyphenylglycol (MHPG) can be demonstrated in the human brain. As MHPG in the various brain areas shows a different pattern of concentration it seems that this metabolite of noradrenaline is of physiological significance and is able to reflect noradrenaline turnover. The highest values of free MHPG were found in the hypothalamus, n. accumbens, thalamus and n. ruber. 3. In a limited series of patients with Parkinson's disease post mortem analysis indicated lower values of MHPG in caudate n., putamen, s. nigra, red nucleus and n. accumbens. All other brain areas did not show significant alterations. 4. Parkinsonian patients who died during Madopar therapy demonstrated a significant increase of MHPG in caudate n., putamen, s. nigra, n. ruber, n. amygdalae and n. accumbens when compared to the untreated group, indicating an enhanced turnover of noradrenaline in these areas. 5. Bound MHPG has been estimated in various brain areas as to be in the range of 13--38 percent of free MHPG.

Brain Chemistry↗
PubMed1975

On the determination of free L-tryptophan.

The determination of free L-tryptophan depends on several analytical well checked points e.g. absorbing effects, pH of the serum, dependence of the throughput, concentration dependence of retention, volume ultrafiltrated, cut-off, temperature dependence of the binding rate, purification on ion-exchange column, interfering substances of the fluorometric method. Ultrafiltration was compared to an ultracentrifugation technique. In normal human serum the concentration of free L-tryptophan is 3,1 +/- 0,6 microgram/ml and of the bound plus free form 12,2 +/- 1,12 microgram/ml. Both values are dependent on the albumin concentration.

Collodion↗