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Biomedical subjects

D B Calne

Publications and source records attributed to D B Calne.

At least 37 records · Page 2Linked to original sources
PubMed1978

Parkinsonism. Clinical and neuropharmacologic aspects.

While the etiology of the most common form of parkinsonism (idiopathic) remains elusive, studies of the regional biochemistry and pharmacology of the brain have led to recognition of the importance of certain pathways, such as the nigrostriatal system. This information evolved from the discovery that the neurotransmitter dopamine is depleted in parkinsonism and that restoration of dopamine by administration of its precursor, levodopa, induces a dramatic therapeutic response in many patients. Such studies have initiated and sustained a major surge in neuropharmacologic advances, but the tangible benefits, in the form of therapeutic results, have undergone some critical reappraisal with the appearance of late adverse reactions to levodopa. One practical approach to this problem is deliberate delay in starting levodopa therapy and the use of lower doses. Use of artificial dopaminergic agonists and selective inhibitors of monoamine oxidase B has also been investigated.

Animals↗
PubMed1977

Treatment of parkinsonism.

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Aromatic Amino Acid Decarboxylase Inhibitors↗
PubMed1977

Experiences with a new ergoline (CF 25-397) in parkinsonism.

Studies on rats with unilateral nigral lesions suggest that a new ergoline, CF 25-397, is a dopaminergic agonist that might improve parkinsonism. CF 25-397 induces less stereotyped behavior than other dopaminergic agents in rats, and might therefore cause less dyskinesia than levodopa in man. We investigated the clinical actions of CF 25-397 in nine patients. During treatment, severe deterioration resulted in hypokinesia and rigidity; five patients showed marked dysphagia and dysphonia. There was statistically significant deterioration in four timed tests. Mild improvement, not statistically significant, was noted in tremor. These results indicate that clinical implication of the response to potential therapeutic agents in rodent models of parkinsonism must be interpreted with caution.

Aged↗
PubMed1977

Antiparkinsonian therapy.

Powerful new tools for the treatment of parkinsonism include levodopa, decarboxylase inhibitors, and dopaminergic agonists. Yet earlier drugs still have a useful role to play. The decision to begin pharmacotherapy must be adjusted individually for each patient.

Antiparkinson Agents↗
PubMed1976

Bromocriptine and levodopa (with or without carbidopa) in parkinsonism.

Bromocriptine, a dopamine receptor agonist, was administered to 20 patients with idiopathic parkinsonism taking levodopa (L-dopa) or "Sinemet" (levodopa combined with carbidopa in a 10/1 ratio) at optimum doses. In a double-blind randomised cross-over study lasting 6 months, the addition of bromocriptine (mean daily dose 79 mg) led to a significant (P less than 0.01) 74% reduction in the dose of sinemet and levodopa. "Total disability score" showed a significant (P less than 0.01) improvement at both low and high doses of bromocriptine. Tremor improved 50% (P less than 0.01), with significant improvements in gait, posture, writing, balance, rigidity, finger dexterity, and drooling. Adverse reactions were similar to those observed with sinemet and levodopa. Although both the cause and the cure of idiopathic parkinsonism remain elusive, bromocriptine appears to represent a therapeutic advance.

Aged↗
PubMed1976

Bromocriptine in Huntington chorea.

Following a recent report that apomorphine hydrochloride alleviates the involuntary movements of Huntington chorea, we have investigated another dopamine receptor agonist, bromocriptine, in this disease. A double-blind crossover study in six patients showed that rather than improving chorea, bromocriptine induced an exacerbation. This finding supports the view that choreatic movements correlate with overactivity in dopaminergic systems.

Adult↗
PubMed1976

The encephalopathic action of five-carbon-atom fatty acids in the rabbit.

1. Five-carbon-atom organic acids (C-5 acids) have been administered intravenously to rabbits with ventriculocisternal perfusion and continuous electroencephalographic recording (EEG). The concentration of the acids in the cerebrospinal fluid (CSF) perfusate have been compared with changes in integrated low-frequency activity in the EEG. 2. The C-5 acids investigated were those accumulating in inborn errors of metabolism, i.e. isovaleric acid, beta-methylcrotonic acid, tiglic acid and alpha-keto- and alpha-hydroxy-isovaleric acid. There activity was compared with that of valeric acid. 3. Valeric acid and isovaleric acid produced coma and pronounced increase in slow-wave electrical activity and these changes paralleled the increase in concentration of the acids in the CSF perfusate. 4. The concentration of beta-methylcrotonic acid and tiglic acid in the CSF perfusate reached values comparable with valeric acid and isovaleric acid but showed less encephalopathic activity. An interaction between beta-methylcrotonic acid and isovaleric acid was observed. 5. Although the concentrations of alpha-ketoisovaleric acid and alpha-hydroxyisovaleric acid rose to the lesser extent in the CSF perfusate, changes in rousability of the animal and in the EEG recording were demonstrated. 6. It is concluded that all the C-5 acids tested have encephalopathic activity although this is lessened by the presence of either a double bond or an oxygenated functional group.

Animals↗
PubMed1976

Nomifensine in parkinsonism.

Nomifensine, a tetrahydroisoquinolone antidepressant which facilitates dopaminergic and noradrenergic transmission, was studied in 28 Parkinsonism patients most of whom were also receiving conventional medications. Double-blind evaluations revealed a moderate therapeutic action at a mean dose level of 150 mg daily. Adverse reactions were encountered, similar to those identical by levodopa.

Aged↗
PubMed1976

Penicillin transport from cerebrospinal fluid.

The passage of penicillin G from cerebrospinal fluid (CSF) was studied by continuous ventriculocisternal perfusion in conscious rabbits. The concentration of penicillin G in the perfusate, collected from the cisterna magna, was 76.5 percent +/- 1.0 (SEM) of that entering the ventricles (having adjusted for normal secretion of CSF). The mean concentration of penicillin G rose 15 percent (p less than 0.005) in the cisternal CSF after probenecid (2 mg per milliliter) was added to the perfusion fluid. We conclude that an active transport system removes penicillin G from the CSF; this mechanism can be inhibited by intraventricular probenecid. Our results are in accord with observations deriving from studies on anesthetized animals given probenecid intravenously or intraperitoneally.

Animals↗