Neurodevelopmental long-term outcome in children with hydrocephalus requiring neonatal surgical treatment.

PURPOSE: To assess long-term neurodevelopmental outcome in children with hydrocephalus requiring neurosurgical treatment during the neonatal period. METHODS: This prospective longitudinal population-based study included 43 children with neonatal shunted hydrocephalus. The 43 children were prospectively reviewed in the presence of their parents at the outpatient clinic. Cognitive and motor outcomes were assessed respectively using different Wechsler scales according to age and Gross Motor Function Classification System (GMFCS). Postoperative MRI was routinely performed. RESULTS: The mean gestational age at birth of the 43 consecutive children with neonatal hydrocephalus (sex ratio M/F: 1.39) was 34.5±5.4 weeks of gestation. At mean follow-up of 10.4±4 years, mean total IQ was 73±27.7, with equivalent results in mean verbal and mean performance IQ. Of the 33 children with IQ evaluation, 18 presented an IQ≥85 (41.9%). Efficiency in walking without a mobility device (GMFCS≤2) was obtained in 37 children (86%). Only severity of postoperative ventricular dilation was significantly associated with unfavorable outcome (Evans index>0.37; odds ratio: 0.16, P=0.03). CONCLUSION: This information could be provided to those families concerned who often experience anxiety when multi-disciplinary management of neonatal hydrocephalus is required.

[Is it possible to protect the preterm infant brain and to decrease later neurodevelopmental disabilities?]. / Est-il possible de protéger le cerveau de l'enfant né prématuré et de diminuer le taux de séquelles neuro-développementales ?

With improving neonatal survival for very premature babies, the challenge for neonatalogists is to ameliorate outcome of surviving babies. Several pharmacological molecules have been shown to have protective effects in different types of in vitro or in vivo animal models of acquired cerebral brain damages. However translational research and conduction of therapeutic trials in human remain difficult due to failure to recognize start of deleterious cascade leading to cerebral damage and additional toxic effect of potential protective molecules. This review concentrates on best evidence emerging in recent years on prevention on brain damage by early drug administration. It has been shown in two randomised trials that prenatal low-dose of magnesium sulphate does not increase paediatric mortality in very-preterm infants and has non significant neuroprotective effects on occurrence of motor dysfunction (with a 0.62 odds ratio in the French trial Premag and 0.71 relative risk in the Australian trial ACTOMgSO4), justifying that magnesium sulphate should be discussed as a stand-alone treatment or as part of a combination treatment, at least in the context of clinical trials. Antenatal corticosteroid therapy increases the survival of very-preterm infants, including the most immature. Moreover in an observational recent study of the Epipage cohort, it has been observed a significant decrease in white matter injury in the 28-32 weeks' gestation group but no effect on long term outcome and behaviour. Conversely in the most immature of the 24-27 weeks' gestation group, no effect has been detected either in white matter injury incidence or in long term outcome rates. Caffeine has a protective effect since a decrease in cerebral palsy has been noted in the caffeine group in a randomised trial studying caffeine versus placebo. For what concern other widely used potential protective molecules during the perinatal period, there is no evidence of cerebral protection with indometacine, nitric oxide, eythropoietin, phenobarbital, and etamsylate. Due to their specific properties, a careful evaluation of aspirin, anaesthetic drugs and tocolytics should be done in the next months.

Reflex sympathetic dystrophy in a dog.

Reflex sympathetic dystrophy is a well-recognized syndrome in human patients following injury to an extremity. The syndrome may include hyperesthesia and autonomic changes. The autonomic changes are initial vasodilatation followed by vasoconstriction (e.g., edema followed by cyanosis, and cool skin); hyper- or hypohydrosis; atrophic changes in the skin, subcutis, and muscles; and osteoporosis. Early treatment with a short course of steroids and infiltration of the painful site with lidocaine may alleviate symptoms. If that fails, sympathetic ganglionic block with lidocaine (and possibly steroids) or surgical sympathectomy may provide resolution. A case of reflex sympathetic dystrophy in a dog is presented, involving bilateral distal hind-limb edema and hyperesthesia.

Addition of sorbitol to a milk substitute for veal calves. II. Effects on plasma, liver and muscle lipids.

Two homologous groups of preruminant male calves (10 control and 9 sorbitol) of the Friesian X Holstein crossbreed were used to study the effects of sorbitol on lipid metabolism. Between 1 and 8 weeks of age they received two diets (IC, IS) with high levels of protein and fat (23% of DM), and then between 8 and 19 weeks two diets (FC, FS) containing lower levels of protein and fat (21% of DM). Diets IC and FC contained no sorbitol, while in the IS and FS diets it accounted for 0.8% of DM. Blood samples were taken at 2, 3, 4, 7, 12 and 19 weeks of age and at the following times: 2 h before (T-2), and then 1/2 (T1/2), 2 (T2), 3 (T3), 5 (T5) and 7 (T7) hours after ingestion of the morning meal. At slaughter (19 weeks), samples of liver and of rectus abdominis muscle were taken from the carcasses. The addition of sorbitol to the replacer milks had no effect on plasma levels of nonesterified fatty acids or triglycerides. However at weeks 2, 7 and 12, the levels of free and esterified cholesterol decreased significantly by a mean of 60 and 15% respectively. Sorbitol intake significantly reduced muscle levels of triglycerides (6.8 mg/g of fresh tissue vs 18.6 mg/g), free cholesterol (0.41 mg/g vs 0.66) and total lipids (13.6 mg/g vs 26.1). Lipid composition of liver was not modified by sorbitol ingestion. An histological study confirmed that the diets caused no serious lesions. Generally, the results were more dispersed in the control group than in the sorbitol group.

Electrophysiologic effects of disopyramide phosphate on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered disopyramide (2 mg/kg) on three parameters of sinus node function were examined in 16 symptomatic patients with sinus node dysfunction. Based on their ECG data before study, patients were subdivided into group A (n = 8), those with sinus pauses and/or sinoatrial (SA) exit block; and group B (n = 8), those with sinus bradycardia. Disopyramide shortened spontaneous cycle length in 10 of 16 patients and lengthened it in six--markedly so (91%) in one patient. Estimated SA conduction time decreased in seven of 14 patients and increased in seven. Two patients developed second degree SA exit block after disopyramide. Maximum sinus node recovery time was prolonged by disopyramide in 11 of 16 patients and markedly so in four. For the group as a whole there was no significant difference in spontaneous cycle length, maximum sinus node recovery time or estimated SA conduction time. P-wave and QRS durations and H-V intervals were significantly lengthened by disopyramide. Marked depression of the three parameters of sinus node function occurred in three group A patients and in one group B patient who had persistent severe sinus bradycardia. These four patients also had secondary pauses after termination of rapid atrial pacing under control conditions. Disopyramide should be administered cautiously to patients with sinus node dysfunction, particularly those with sinus pauses, SA exit block or secondary pauses.