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Biomedical subjects

W Birkmayer

Publications and source records attributed to W Birkmayer.

At least 55 records · Page 3Linked to original sources
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

The potentiation of the anti akinetic effect after L-dopa treatment by an inhibitor of MAO-B, Deprenil.

The potentiation of the anti akinetic effect after L-Dopa treatment by an inhibitor of monoamine oxidase (MAO) "B", Deprenil, has been demonstrated in parkinsonian patients with or without previous L-Dopa theapy. Application of the drug has been performed orally, intravenously and intramuscularly. Excellent kinetic effects resulted when combined with Madopar. The combined treatment with L-Dopa was highly effective when applicated i.v. or i.m. Deprenil is an inhibitor of MAO-B and is characterized by less frequent side effects. These are predominantly involuntary movements and confusion, which can be eliminated by lowering the dosage of Deprenil. A daily rhythm of MAO could be demonstrated in several areas of human brains as well as in a control group as in parkinsonian patients with or without L-Dopa therapy. Maximal activity of MAO occurs between noon and 6p.m. The clinical and biochemical data are discussed regarding the off-phenomenons as Deprenil is an excellent drug for preventing these.

Administration, Oral↗
PubMed1975

Biochemical post-mortem findings in depressed patients.

Biochemical human post-mortem studies on depressed patients indicate an unspecific deficiency of neurotransmitters in several brain areas. The loss of drive of these patients could be correlated with a decrease of striatal dopamine concentration. Noradrenaline was significantly diminished in red nucleus, a fact which points to the characteristic posture of depressed patients. Serotonin was diminished in all brain areas. During remission all values trended to be normal. There also exists a circadian disrhythm in depressed patients resulting in lowered VMA- and HVA-levels in urines during the morning and a remission to normal values in the evening. This agrees with the findings of lowered blood tyrosine levels in the morning. The ratio of blood tyrosine and tryptophan is disturbed during depression and recovers during remission. Central and peripheral biochemical mechanisms seems to be involved in depression syndrom.

Aged↗
PubMed1975

Responsibility of extrastriatal areas for the appearance of psychotic symptoms (clinical and biochemical human post-mortem findings).

1. A Dopa-medication leads sometimes in Parkinsonian patients to a psychosis. 2. The diminished capacity of striatal dopaminergic neurons to store DA leads to a storage of DA in serotoninergic or noradrenergic neurons. 3. Extrastriatal noradrenergic and/or serotoninergic neurons are involved. 4. Dopaminergic receptors of the striatium are not involved because of a lack of kinetic response after L-Dopa application in Parkinsonian patients with akinetic crises. 5. Extrastriatal dopaminergic receptors of DA as "false transmitter" at serotoninergic receptors seem to be responsible for the production of psychotic symptoms, whereas noradrenaline is not responsible. Psychotic symptoms can be imagined to be triggered by a contact of a transmitter to a nonspecific receptor.

Brain↗
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↗