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Symptomatic ventricular coaptation, or the slit ventricle syndrome, is frequently described and recognized as a clinical entity in the pediatric population. It is characterized by symptoms of shunt failure (i.e., ataxia, obtundation, nausea, vomiting, lethargy, irritability, and complaints of headache) and the CT findings of ventricular coaptation (slit-like ventricles). This study of twenty-two children with this syndrome reflects the variety of possible clinical presentations, and the variety of available treatment modalities. Multiple therapeutic approaches were required in seven of the patients. This illustrates not only an evolving treatment regimen, but also that a single treatment modality is not universally effective. Six patients needed only occasional symptomatic support. Blockage and/or removal of the shunt system was the definitive therapy in six patients, pressure augmentation in nine patients, and subtemporal craniectomy in one. This article outlines the theoretical pathophysiology, and a scheme for the management of patients with this syndrome.

Clinical manifestations, findings, management and outcome of a series of 177 cases with tumours of the limbic and paralimbic systems are presented. There was no operative mortality. Postoperatively 95% of them had no or only minor neurological deficits. Most of them were able to resume work. Pre-operatively 77% of the patients had epilepsy, but 84% became seizure-free after tumour removal. All 77 cases with malignant tumours died within 1-5 years. In the past many neurosurgeons were reluctant to attempt complete tumour removal in these areas. This series demonstrates the efficacy of highly skilled microneurosurgery.

The purpose of this study was to evaluate the need for separate Hb screening criteria according to race by evaluating the Hb response to a therapeutic trial of iron in 1-yr-old infants. Among the 1128 infants who were screened, a significantly larger percentage of blacks (37%) than Caucasians (22%) had a Hb less than 11.5 g/dl. However, when these screen-positive infants were treated with oral iron for 3 months, the percentage who had a greater than or equal to g/dl response was similar in blacks (38%) and Caucasians (35%). Our results indicated that a slight but significant inherent tendency to lower Hb values among the black infants was counter-balanced by a substantially higher prevalence of iron deficiency anemia. These findings are in favor of using uniform Hb screening criteria in similar populations.

An evaluation was made of 278 healthy-appearing 1-year-old infants who were tested for iron deficiency to determine the relative frequency of adverse side effects attributable to oral iron treatment. After obtaining parental informed consent, laboratory tests of iron status were performed on venous blood and infants with hemoglobin level greater than 10.5 g/dL were randomly chosen to receive 1.2 mL of ferrous sulfate (FeSO4) drops (about 3 mg of iron per kilogram per day) or equal volume of placebo for 3 months. After 3 months of treatment, infants were to return to the clinic for repeat blood testing, compliance estimation, and evaluation for possible adverse side effects. There was no significant difference (P greater than .50) in the frequency of vomiting, diarrhea, or fussiness in iron-treated infants (6%) compared with placebo-treated infants (9%). Constipation was slightly more frequently reported (P = .03) in placebo-treated infants (9%) than in iron-treated infants (1%). Compliance with therapy was confirmed in 179 completely evaluated infants by the lack of remaining medication at 3 months, the higher incidence (P less than .0001) of dark stools reported among iron-treated infants, and the changes in laboratory tests of iron status. No parents reported dark stools as an adverse effect of therapy. It is concluded that once daily, moderate-dose FeSO4 therapy given to fasting 1-year-old infants results in no more gastrointestinal side effects than placebo therapy.

Iron deficiency is a common problem in otherwise healthy children and in children with systemic disease. We have reviewed the pathophysiology, laboratory diagnosis, and systemic effects of iron deficiency. We have emphasized that routine screening procedures do not efficiently predict those otherwise healthy children who will demonstrate a therapeutic response to iron. Furthermore, in patients with certain systemic diseases the diagnosis of iron deficiency is complicated by the inflammatory process and the response to a therapeutic trial of oral iron is often blunted. Since the potential adverse effects of iron deficiency may be extensive, a therapeutic trial of iron is indicated to establish the diagnosis of iron deficiency if the index of suspicion is high and laboratory results are equivocal.

Since infants with malignant osteopetrosis often die from infection at an early age, we studied several aspects of host defense in five such infants. No consistent abnormality was found in cellular or humoral immunity. Monocyte cellular chemotaxis and phagocytosis were normal in four tested infants. However, all four of these infants had decreased intracellular bacterial killing by monocytes. Neutrophil function tests in five infants showed that two had defective bacterial phagocytosis and four had reduced cellular chemotaxis, decreased nitroblue tetrazolium reduction, and decreased intracellular bacterial killing. The severity of the decreased bactericidal capacity of granulocytes did not correlate with the number of circulating immature granulocytes. Our data suggest that abnormal function of circulating monocytes and granulocytes may contribute to impaired host resistance to infection. We postulate that this defect may reflect a more generalized inherited abnormality of phagocytic cells and perhaps osteoclasts that plays a role in the pathogenesis of infantile osteopetrosis.

Iron supplements are commonly administered to infants in order to prevent iron deficiency. We wished to determine whether iron administration could compromise zinc nutrition as might be suspected from previous studies. Measures of iron nutrition, serum zinc, and serum copper were measured before and after randomization of 291 healthy 1-yr-old infants to a 3 mo course of placebo or iron treatment (30 mg iron as ferrous sulfate given before a meal). There was no significant difference in serum zinc or copper in the two groups before or after treatment; thus iron administration did not result in any evidence of zinc deficiency in a healthy, well-nourished group of T-yr-old infants.