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Biomedical subjects

R D Sheth

Publications and source records attributed to R D Sheth.

At least 37 records · Page 2Linked to original sources
PubMed1998

Trends in incidence and severity of intraventricular hemorrhage.

The incidence of germinal matrix-intraventricular hemorrhages declined from 50% in 1977 to 24% in 1985. Over the last decade intraventricular hemorrhage rates ranging from 8% to 56% were reported, leaving uncertainty as to the direction of recent intraventricular hemorrhage trends. Records of all 1950 neonates weighing 2250 g or less at birth (867 weighing 1500 g or less and 1083 weighing 1501-2250 g) at a university neonatal intensive care unit between 1986 and 1995 were studied. Intraventricular hemorrhage rate declined by 53%, from 11.5% in 1986 to 5.5% in 1995 (P < .01), and was consistent across all birthweight groups: 750 g or less from 36% to 24%, 751-1000 g from 38% to 22%, 1001-1250 g from 19% to 13%, 1251-1500 g from 12% to 2% and 1551-2250 g from 3% to 0.2% (P < .05). Proportionately, severe intraventricular hemorrhage (grades 3 +/- intraparenchymal hemorrhage) declined from 70% of all intraventricular hemorrhages in 1986 to 23% in 1995 (P < .005). Overall mortality declined by 65% between 1986 and 1995 (P < .001), whereas mortality associated with intraventricular hemorrhage declined by 30% (P = .34). Despite dramatic declines in intraventricular hemorrhage rates, 21% of infants weighing less than 1000 g and 12% of those weighing less than 1500 g at birth were affected in 1995.

Birth Weight↗
PubMed1998

Frequency of neurologic disorders in the neonatal intensive care unit.

Neonatal intensive care unit survival rates have improved significantly over the past decade. This improvement primarily reflects declining mortality rates among preterm infants. Neurologic morbidity increases with prematurity and is the major predictor of long-term disability. Accordingly, concern has been expressed that the burden of neurologic dysfunction among contemporary neonatal intensive care unit survivors may be increasing. To define the trends of neurologic disorders in the contemporary neonatal intensive care unit, all 4164 admissions between 1986 and 1995 to a tertiary neonatal intensive care unit were examined. Neonatal intensive care unit admissions (413 +/- 49 per year), proportion of births at less than 37 weeks (70 +/- 3% per year), and referral patterns were stable between 1986 and 1995. Over the study period, 773 (18%) of 4164 neonatal intensive care unit infants had a total of 1062 neurologic disorders. The neonatal intensive care unit mortality rate declined from 12% in 1986 to 4.2% in 1995 (P < .01). Neurologic disorders declined, from 27% of infants born in 1986 to 12% in 1995 (P < .001): 356 had seizures (14% in 1986 to 4% in 1995; P < .001), 235 had hypoxic-ischemic encephalopathy (8% in 1986 to 4% in 1995, P < .01), and 167 had intraventricular hemorrhage (7% in 1986 to 1.4% in 1995, P < .005). Frequency of congenital or chromosomal aberration affecting the nervous system was relatively constant (4.5% per year). Despite a three-fold improvement in neonatal intensive care unit survival between 1986 and 1995, the frequency of perinatally acquired neurologic disorders declined by more than 50%.

Female↗
PubMed1997

Rolandic epilepsy and cortical dysplasia: MRI correlation of epileptiform discharges.

An 8 year-old girl presented with simple facial motor seizures. Although the electroencephalogram (EEG) demonstrated left hemisphere centrotemporal spikes with features consistent with benign rolandic epilepsy, magnetic resonance imaging (MRI) indicated a left hemisphere focal cortical dysplasia. MRI-assisted EEG dipole analysis of the spikes suggested that the rolandic fissure rather than the focal cortical dysplasia was the origin of the epileptic spike discharge. This noninvasive method may be a useful adjunct in evaluation of some patients with epilepsy and focal superficial cerebral lesions.

Brain Mapping↗
PubMed1996

Mental retardation plus macrocephaly in a 16-year-old boy.

The evaluation of mental retardation is a frequent and challenging problem in pediatric neurology. Often clues obtained on history or by physical examination will help to direct the evaluation in the appropriate channel. This 16-year-old boy had clinical features which suggested the appropriate diagnostic studies.

Adolescent↗
PubMed1996

Neck pain and headache in an afebrile 15-year-old.

Nuchal rigidity and headache are important signs of bacterial meningitis, although, in the absence of fever other etiologies would be considered. An evaluation of a 15-year-old boy with the above features, focal neurological deficits, and two cerebral contrast enhancing ring lesions is discussed.

Adolescent↗
PubMed1996

Recurrent coma.

Recurrent episodes of coma are usually associated with a metabolic disorder. A healthy 9-year-old boy of normal intellect and intact corpus callosum on neuroimaging had recurrent episodes of coma associated with profound spontaneous hypothermia. An evaluation, differential diagnosis and insights into the pathogenesis of this disorder are discussed.

Body Temperature Regulation↗
PubMed1996

Midazolam in the treatment of refractory neonatal seizures.

Midazolam, a potent short-acting benzodiazepine, is a safe and highly effective agent for the control of status epilepticus. Its efficacy in the control of neonatal seizures, however, has not been determined. Six neonates (aged 1-9 days; gestation, 30-41 weeks) developed seizures from a variety of causes. In each case, seizures persisted for > 12 h despite high-dose phenobarbital therapy with or without the addition of phenytoin. Midazolam was then administered by continuous intravenous infusion (0.1-0.4 mg/kg/h) for 1 to 3 days. Within 1 h of initiation of midazolam, seizures were controlled in all six neonates. Electroencephalographic seizures were abolished in four of six neonates; however, two neonates continued to have electrographic seizures (without clinical accompaniment) for a further 12 h. Blood pressure and pulse rate were not changed after the initiation of midazolam, and adverse reactions were not observed in any neonate. Because more than one third of all neonatal seizures are refractory to high-dose phenobarbital and phenytoin, midazolam administered by continuous intravenous infusion may be a valuable adjunctive therapy.

Anticonvulsants↗
PubMed1996

Vigabatrin in childhood epilepsy: comparable efficacy for generalized and partial seizures.

Thirty-one patients, aged 12.6 +/- 5.6 years, with refractory seizures for 8 +/- 4.3 years, were treated with adjunctive vigabatrin. Twenty-four percent had a > 50% reduction in seizure frequency (95% one-sided confidence interval). Generalized myoclonic, atonic, and tonic clonic and partial, with and without secondary generalization, seizures were all reduced at a mean dose of 70 +/- 38 mg/kg/day. Comparison of vigabatrin therapy duration, for partial and generalized seizure groups, utilizing Kaplan-Meier methodology showed similar survival times. Vigabatrin therapy was ineffective in the four children with tuberous sclerosis. Transient somnolence, ataxia and dizziness were the most frequent side effects. A severe aggressive agitation occurred in three patients, and necessitated discontinuation of vigabatrin in one patient. Vigabatrin was as effective in generalized as in partial seizures in this study. Clinical utility may be limited by unacceptable behavioral side effects in some patients.

Adolescent↗
PubMed1996

Size of the corpus callosum in cerebral palsy.

It has been suggested that the size of the corpus callosum may have diagnostic significance in cerebral palsy, although this relationship is incompletely defined. Ninety-one patients with cerebral palsy had been studied by magnetic resonance imaging in the 5-year period from 1990 to 1994. Fifty-seven of these 91 patients had a technically appropriate midsagittal magnetic resonance image for quantitative morphometric analysis. The ratio of the area of the corpus callosum to the area of the supratentorial brain was compared to published age- and gender-specific norms. Imaging findings were correlated with clinical history and cause of cerebral palsy. The corpus callosum was of normal size in 43 patients and more than 2 standard deviations below the mean in 14 patients. The causes for cerebral palsy included hypoxic ischemic encephalopathy (32), cerebral dysgenesis (8), and porencephalic strokes (6); the etiology could not be established in 11 patients. The size of the corpus callosum was highly correlated with the cause of cerebral palsy, such that all patients with cerebral dysgenesis had hypoplasia of the corpus callosum (one-sided z test, p < 0.0001). Conversely, the callosum was of normal size in 32 of 38 patients with hypoxic ischemic encephalopathy and porencephalic strokes. The presence of a hypoplastic corpus callosum is highly associated with cerebral dysgenesis as a cause for cerebral palsy.

Adolescent↗
PubMed1996

Parietal occipital edema in hypertensive encephalopathy: a pathogenic mechanism.

Eight patients with hypertensive encephalopathy from diverse etiologies developed cerebral edema in the vertebrobasilar distribution which resolved after blood pressure was lowered. Parietal occipital edema is a recognized feature of hypertensive encephalopathy. The explanation for this regional pathological variation in hypertensive encephalopathy remains undefined. Some evidence suggests that sympathetic innervation of the anterior cerebral vasculature may be protective, and conversely, the relative lack of sympathetic innervation in the vertebrobasilar vasculature may predispose the parietal occipital region to the development of cerebral edema in hypertensive encephalopathy.

Adolescent↗