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Biomedical subjects

K Ekbom

Publications and source records attributed to K Ekbom.

At least 73 records · Page 4Linked to original sources

Oxprenolol in the treatment of migraine.

Thirty migraine patients received oxprenolol (Trasicor), which is an adrenergic beta-receptor blocking agent with weak beta-stimulating intrinsic activity. The dosage was 80 mg three times a day. The treatment was given by a double blind cross-over technique in which the effect was compared with placebo. Each compound was administered for 8 weeks with an intermediate week without medication (wash-out). Oxprenolol had no significant effects in the prevention of migraine attacks. Our study lends further support to the assumption that differences may exist between different beta-receptor blocking agents in their effectiveness in migraine prophylaxis.

Adolescent↗

Plasma kinetics of carbamazepine and its epoxide metabolite in man after single and multiple doses.

Carbamazepine (Tegretol) was administered orally to four patients as a single dose, and one week later three times daily for 15-21 days. The plasma half-lives of the drug were shorter in all patients after multiple doses (20.9 +/- 5.0 hours) than after the initial single dose (35.6 +/- 15.3 hours). During the multiple dose the plasma concentrations of the metabolite carbamazepine-10,11-epoxide followed those of the parent drug. The steady-state plasma concentrations expected during multiple doses were calculated from the pharmacokinetic parameters obtained in the single dose studies. The calculated levels were higher (17.2+/-7.2 mug/ml) than the observed maximal concentrations (8.4+/-1.6 mug/ml on day 4), which were obtained 3-4 days after starting the multiple doses. The levels tended to decrease further during the experimental period. The results suggest that carbamazepine induces its own metabolism in man.

Carbamazepine↗

Hereditary ataxia, photomyoclonus, skeletal deformities and lipoma.

An account is given of a form of hereditary, cerebellar ataxia and photomyoclonus. Eight cases from 5 generations were affected. The disease seemed to be transmitted as an autosomal dominant trait. The age at onset usually varied between 35 to 40 years. The symptoms and signs consisted of a cerebellar ataxia, dysarthria and intention tremor. There was no nystagmus. All patients exhibited photomyoclonus and were extremely sensitive to photic stimuli. Other signs were dementia, kyphosis, pes cavus and lipoma localized in the nape of the neck, shoulders and back. Two patients had a partial syndrome with photonyoclonus and skeletal deformities. None of the patients suffered from epilepsy, In one case, histopathological examination revealed atrophy within the cerebellar cortex, dentate nucleus and the posterior columns of the spinal cord. It is concluded that this syndrome belongs to a groups of hereditary ataxias and myoclonus, and differs from myoclonic cerebellar dyssynergia (Ramsay Hunt) and alos from a variety of familial myoclonus and ataxia (Gilbert et al. 1963);

Adult↗