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T Grisar

Publications and source records attributed to T Grisar.

62 records · Page 4Linked to original sources
PubMed1978

[Diagnostic means to exclude deficient secretion of growth hormone in paediatric practice (author's transl)].

Growth hormone serum levels were measured radioimmunologically in 365 children with stunted growth before and after 10 minutes of stair-climbing, and in 134 children before and after 10 minutes of physical stress produced by means of a bicycle ergometer. Only 20% of the children had a growth hormone level of more than 5 ng/ml before initiation of the study. After climbing the stairs, the hormone level rose in 160 children to more than 5 ng/ml (max. 41.1 ng/ml). Growth hormone deficiency could thus be definitively eliminated as the cause of retarded growth in only 46% of the patients. In 16 (of 22) children of normal size, in 34 (of 49) chilkren with arrested growth who had a corresponding familial background, and in 33 (of 57) children with constitutionally conditioned retarded development, the growth hormone content after exercise on an rose to more than 5 ng/ml. Hence, a total of 65% of the children showed a satisfactory increase of the growth hormone. It follows from this that the ergometer exercise test is more suitable that the stair-climbing test to exclude hormone deficiency as the cause of stunted growth, and can, therefore, be recommended for use in paediatric practice as a supplementary examination method besides clinical findings, case history and determination of the growth rate.

Child↗
PubMedDate not supplied

Glial contribution to seizure: carbonic anhydrase activity in epileptic mammalian brain.

The activity of carbonic anhydrase (CA), a glial enzyme, was measured in the epileptic cortex of audiogenic DBA/2 mice and of cats with a freeze lesion. In mice, the activity increased with age from birth to 24 days, but were always higher in audiogenic mice than in normal C57/BL mice, reflecting species differences. The difference between the two strains increased sharply from 25 to 40 days of age, after the period of maximal audiogenic susceptibility. Acetazolamide, a CA-specific inhibitor, greatly decreased the seizure severity score of DBA/2 mice after a single intraperitoneal (i.p.) administration (150 mg/kg). After 24 days of age, when CA activities were high, the effect of acetazolamide was less important, suggesting that the increased cortical CA activity might reflect a protective mechanism. In cats with a freeze lesion, no significant changes in CA activities were observed in the actively discharging primary and secondary foci as compared with the nonepileptogenic perifocal cortex and the control cortex of sham-operated animals. The results indicate that the cortex of genetically susceptible audiogenic mice has an increased CA activity. The hypothesis of an adaptive glial mechanism, relating to the age-dependent decrease of seizure susceptibility in DBA/2 mice, is postulated.

Acoustic Stimulation↗
PubMedDate not supplied

Effect of milacemide on audiogenic seizures and cortical (Na+, K+)-ATPase of DBA/2J mice.

Milacemide (MLM, CP 1552 S, 2-N-pentylaminoacetamide), a glycinamide derivative, is currently being evaluated clinically for antiepileptic activity. Anticonvulsant properties have been shown in various animal models, but the mechanism of action of MLM is unclear. We studied its activity in audiogenic seizures of DBA/2J mice. MLM was effective in inhibiting the convulsions induced by sound with a biphasic dose-effect relation. The ED50 was 109 mg/kg orally against tonic extension. Higher doses were necessary to abolish clonic convulsion and running response. Because impaired cerebral (Na+, K+)-ATPase activity is supposed to play a role in epileptogenesis, we tested MLM on in vitro cortical enzymatic activity of DBA/2J mice. Basal (Na+, K+)-ATPase activity was unchanged by several concentrations of MLM in normal C57BL/6J and audiogenic DBA/2J mice. K+ activation (from 3 to 18 mM) of (Na+, K+)-ATPase is abolished in DBA/2J mice as compared with C57BL/6J mice, suggesting impaired glial (Na+, K+)-ATPase. In the presence of MLM (from 30 to 1000 mg/L), cortical (Na+, K+)-ATPase of DBA/2J mice is activated by high concentrations of K+, as in C57BL/6J mice. Results suggest that the antiepileptic activity of MLM in audiogenic mice may be secondary to an activation of a deficient glial (Na+, K+)-ATPase.

Acetamides↗
PubMedDate not supplied

Biochemical and neuroendocrine approaches to a malignant syndrome of neuroleptics.

A 20 year old patient who has been hospitalized for depressive schizoidia is treated by nomifensine (75 mg/d) plus pimozide (4 mg/d). Four days later, he shows a typical neuroleptic malignant syndrome (Syndrome malin de Delay et Deniker). The biological explorations show that inflammatory blood tests are increased, hepatic tests are disturbed and the pituitary tests suggest a hypothalamic disturbance of the balance between NE and DA (reduced STH, FHS and LH) with a relative NE predominance, but also an increase of DA (increased HVA in CSF. A pathogenic interaction between nomifensine, an antidepressant inhibiting the reuptake of NE and DA, and pimozide, a neuroleptic blocking dopaminergic postsynaptical receptors is to be considered.

Adult↗
PubMedDate not supplied

[A study of clinical signs and EEG profiles in hypercalcemic encephalopathy (author's transl)].

Eight cases of acute or subacute hypercalcemic encephalopathy are described. The symptoms comprise digestive disorders, signs of dehydration and neuropsychological anomalies. Among the latter, it is stressed that impairments of upright stance and locomotion are present in all cases. The clinical picture is not characteristic. The EEG profile is constant: a slow occipitoparietal background activity is interrupted by high-voltage anterior delta bursts of 1 to 4 second duration. When blood calcium is restored to a normal level the clinical symptoms disappear within 1-2 weeks and EEG anomalies within 3-8 weeks. The physiopathological mechanism whereby hypercalcemia cause clinical and EEG anomalies is still unknown. Blood calcium determinations should be included among the biochemical tests carried out on all patients presenting neuropsychological disorders.

Adult↗