Treatment of infantile spasms with sodium valproate followed by benzodiazepines.

OBJECTIVE: To review the result of the infantile spasms' treatment with sodium valproate followed by nitrazepam or clonazepam. STUDY DESIGN: Descriptive retrospective study. SETTING: Srinagarind Hospital, Department of Pediatrics, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. MATERIAL AND METHOD: Twenty-four infantile spasms admitted between January 1994 and December 2003 were analyzed. The inclusion criteria were the patients with infantile spasms clinically diagnosed by the pediatric neurologist, having hypsarrhythmic pattern EEG, and receiving sodium valproate with or without nitrazepam or clonazepam. The patients who had an uncertain diagnosis, incomplete medical record, or that were incompletely followed up were excluded. Data were collected on sex, age at onset of seizure, type of infantile spasms, associated type of seizure, predisposing etiological factor, neuroimaging study, and the result of treatment including cessation of spasms, subsequent development of other seizure types, quantitative reduction of spasms, relapse rates of spasms, psychomotor development, and adverse effects of AEDs. RESULTS: The mean age at onset was 177 days. The male-to-female ratio was 1:1.2. There were 13 cryptogenic (54.2%) and 11 symptomatic (45.8%) infantile spasms. The most common predisposing etiological factors in symptomatic cases were hypoxic ischemic encephalopathy (45.5%) and microcephaly (36.4%), respectively. Ten patients received sodium valproate (41.7%), another 10 received sodium valproate with clonazepam (41.7%), and four received sodium valproate with nitrazepam (16.7%). Both, the complete cessation rate and the 50% reduction of spasms rate were 45.8%. The duration to complete cessation was 70 days. The relapse rate was 18.2%. The rate of delayed psychomotor development was 83.3%. The mean duration of follow-up was 49.6 months. CONCLUSION: The authors propose to use sodium valproate concomitantly with benzodiazepines, especially clonazepam, in situations such as unavailability, intolerability, or adverse effects of ACTH or vigabatrin, or in a patient who does not respond to ACTH or vigabatrin.

Effect of equine hypothalamic extract on hormone secretion by the adenohypophysis of rats

The effect of Equine Hypothalamic Extract (EHE) on pituitary weight and secretion of TSH, FSH-LH and ACTH was studied in the rat. The pituitary respponse to EHE was assessed by measuring (131) I uptake by the thyroid and by weight changes of the pituituray glands, thyroids, adrenals, ovaries and uteri. (131) I uptake of the thyroid and weights of the pituitary, thyroid, adrenal and uterus increased in the treated rats, whereas ovarian weights were similar to control groups. These findings indicate that the EHE containes hypophysiotropic peptides which can stimulate the secretion of pituitary hormones in the rat.

Efectos endócrinos de la hipnosis con tiopental sódico en los perros / Endocrine effects of thiopental anaesthesia in dogs

se estudiaron los efectos endócrinos de la hipnosis con tiopental sódico (TPS) en perros con respiración espontánea (RE) y controlada mecánicamente (RC) durante tres horas. Se emplearon 18 perros divididos en tres grupos: 1-controles no anestesiados (CNA). 2-anestesiados con TPS y RE y 3-anestesiados con TPC y RC. Se controló la: tensión arterial media, frecuencia cardíaca, frecuencia respiratoria y temperatura rectal. Se efectuaron extracciones de sangre antes de la inducción y luego periódicamente para controlar la glucemia y los niveles de: ácidos grasos no esterificados ACTH, cortisol, catecolaminas, insulina, T3, T4 junto con las concentraciones plasmáticas de TPS. También se monitoreó el pH, gases en sangre, exceso de base y bicarbonato standard. La técnica anestésica descrita con RE y RC no modificó los niveles séricos y plasmáticos de insulina, T3 y catecolaminas, pero provocó una disminución importante en los ácidos grasos no esterificados séricos y en las concentraciones de T4, sin embargo, no logró suprimir totalmente la respuesta tardía del eje hipófiso-suprarrenal al stress anestésico.