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Biomedical subjects

J B Bodensteiner

Publications and source records attributed to J B Bodensteiner.

At least 37 records · Page 2Linked to original sources
PubMed1997

The plantar response in normal newborn infants.

The neonatal plantar response has been reported as extensor in 90% of newborns and flexor in 93% of newborns, leading to uncertainty about its reliability and significance. To determine the normal neonatal plantar response we examined 349 healthy newborn infants, > 32 weeks gestation within 24 hours of birth. A supramaximal noxious stimulus was applied in a standardized manner to the lateral plantar surface of each foot. The plantar response was extensor in 90%, equivocal in 7%, and flexor in 3%. With proper physiologic technique, the normal neonatal plantar response is extensor.

Foot↗
PubMed1997

Macrocerebellum: neuroimaging and clinical features of a newly recognized condition.

Other than hamartomatous enlargement of the cerebellum as in Lhermitte-Duclos syndrome, diffuse enlargement of the cerebellum is not clearly described. We report four patients (ages 9 months to 2 years) with diffusely enlarged cerebelli as identified by measurement of the cerebellum and comparison to age appropriate normal values. The cerebellar measurements were determined in absolute numbers and expressed as ratios of cerebellum to whole brain and supratentorial brain. The clinical features of these four children (3 boys, 1 girl) consistently include global developmental delay, tone abnormalities, preserved reflexes, delayed or abnormal maturation of the visual system (oculomotor apraxia), and deficient or delayed myelination of cerebral white matter. The etiology of the macrocerebellum is unknown but we propose that the cerebellum is responding to the elaboration of growth factors intended to augment the slow development of cerebral structures. Regardless of the etiology, the finding of a macrocerebellum appears to allow the clinician to predict the clinical features of the patient and probably represents a marker for disturbed cerebral development.

Brain↗
PubMed1997

Dementia pugilistica and cavum septi pellucidi: born to box?

Described nearly 70 years ago as the 'punch drunk' syndrome, dementia pugilistica has recently received increasing attention in both the medical and lay press. The association between the finding of cavum septi pellucidi and dementia in old boxers was first described by Ferguson and Mawdsley in 1965. Since then it has commonly been listed as one of the features of this condition. We review the significance and the epidemiology of cavum septi pellucidi and present an alternative explantation for the association between this developmental anomaly of the brain and dementia pugilistica.

Aged↗
PubMed1996

Hypoplasia of the cerebellar vermis in neurogenetic syndromes.

There are conflicting reports on the relationship between cerebellar vermal lobule hypoplasia and autism. Using quantitative magnetic resonance image analysis, we measured the cerebellar vermis in 125 normal individuals with a broad age range and 102 patients with a variety of neurogenetic abnormalities. We conclude that hypoplasia of cerebellar vermal lobules VI and VII is a nonspecific finding that even occurs in several conditions with-out autistic behavior. This suggests that it is not a specific neuroanantomical marker for autism, nor is cerebellar dysgenesis likely to be solely responsible for clinical autistic behaviors.

Abnormalities, Multiple↗
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

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

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↗
PubMed1995

Longitudinal head growth in developmentally normal preterm infants.

OBJECTIVE: To determine growth in head circumference from birth to 18 months of age in normal infants with low birth weight. METHODS: Healthy, appropriate-for-gestational-age, singleton, white infants weighing less than or equal to 2500 g at birth and with normal development at 18 months of age were included in this study. Serial measurements of head circumference (corrected for gestational age) from 450 eligible infants were compared with reference data for head circumference. RESULTS: Longitudinal measurements of head circumference for infants weighing more than 1000 g at birth were similar to reference data for term infants. Head measurements for infants weighing less than or equal to 1000 g at birth were notably smaller than the measurements in the reference data. A cubic spline curve drawn through the head circumference measurements between birth and age 18 months (corrected for gestational age) for infants weighing less than or equal to 1000 g at birth was significantly (P < .001) below the curve for infants weighing more than 1000 g at birth. At age 18 months, the mean difference in head circumference between the group weighing less than or equal to 1000 g at birth and the weights in the reference data was 1.6 cm (P < .01). (Data were analyzed with Wilcoxon's signed rank test.) CONCLUSIONS: These data show that head circumference grids are appropriate for observing head growth in infants with a birth weight more than 1000 g. However, head circumference growth for normal infants with birth weight less than or equal to 1000 g does not "catch up" with that of larger premature infants or term infants.

Birth Weight↗
PubMed1995

Acute confusional migraine: variant of transient global amnesia.

Acute confusional migraine in children and transient global amnesia in adults share a number of similar clinical manifestations. Acute confusional migraine in 6 children (mean age: 11.7 years; range: 7.5-17 years) was characterized by transient episodes of amnesia and acute confusion lasting 1-12 hours. Episodes were preceded by headache and vomiting in 4 patients. In 2 patients acute confusional migraine was the initial symptom. A history of preceding trivial head injury was reported in 3 patients and migraine in 4. Urine and serum drug screens were negative. Cerebral imaging studies and interictal electroencephalograms were normal. Ictal electroencephalograms in 3 patients revealed diffuse or bioccipital delta wave slowing. Recurrent episodes of acute confusional migraine occurred in 2 children during 1-3 years of follow-up. The clinical manifestations of acute confusional migraine in this series of children are similar to those reported in transient global amnesia. The similarity of the clinical manifestations of acute confusional migraine in children and transient global amnesia in adults suggests that these disorders may share a common pathophysiology.

Acute Disease↗
PubMed1995

Progressive neurologic impairment from an arteriovenous malformation vascular steal.

Approximately 15% of all cerebral arteriovenous malformations (AVMs) present with progressive neurologic deficits, the pathogenic mechanism of which has not been established. One suggestion is that AVMs by expanding over time compress normal surrounding cerebral parenchyma and thereby cause progressive neurologic impairment. Alternatively, a vascular steal results in progressive ischemia of normal cerebral tissue. Because the area occupied by the AVM and the area of observed blood flow reductions in all reported patients have overlapped, delineating the relative contribution of local compression from that of vascular steal has not been possible. We present a 7-month-old girl and a 7-year-old boy with AVMs restricted to the diencephalon who had progressive cognitive impairment and dystrophic cerebral hemispheral calcification (in the 7-month-old girl) indicating diffuse cerebral cortical involvement remote from the AVM. These patients provide evidence for vascular steal, and not local compression, as the primary mechanism underlying a progressive neurologic course associated with some AVMs.

Brain Ischemia↗
PubMed1995

Effect of carbamazepine and valproate on bone mineral density.

OBJECTIVE: To examine the effect of carbamazepine and valproate monotherapy on bone mineral density in children. METHODS: Axial (second, third, and fourth lumbar vertebrae) and appendicular (distal third of radius) bone mineral density was measured by dual-energy x-ray absorptiometry in 27 healthy children and 26 children with uncomplicated idiopathic epilepsy treated with either carbamazepine (n = 13) or valproate (n = 13) for more than 18 months. Control subjects and patients were similar with respect to age, race (all white), and geographic area, and had no dietary restrictions, neurologic impairment, or physical handicaps. RESULTS: Subjects were seizure-free for more than 6 months on a regimen of carbamazepine or valproate therapy, and had mean serum trough levels of 6.88 +/- 2 micrograms/ml and 72.04 +/- 45.6 micrograms/ml, respectively. Dietary calcium intake was similar in control and treated groups. After correction for gender and age, children treated with valproate had a 14% (p = 0.003) and 10% (p = 0.005) reduction in bone mineral density at the axial and appendicular sites, respectively. The reduction in bone mineral density increased with the duration of valproate therapy. Carbamazepine did not significantly reduce bone mineral density. CONCLUSION: Valproate montherapy, but not carbamazepine therapy, significantly reduces axial and appendicular bone mineral density in children with idiopathic epilepsy and may increase their risk of osteoporotic fractures.

Absorptiometry, Photon↗
PubMed1995

Critical illness neuromuscular disease in children manifested as ventilatory dependence.

Four children with prolonged dependency on a ventilator were found to have reversible quadriparesis, muscle wasting, and hyporeflexia after 8 to 20 days of assisted ventilation for life-threatening sepsis or respiratory failure. Critical illness neuromuscular disease, which was recently recognized as a distinct clinical syndrome in adults, may also be manifested in children by prolonged ventilatory dependency.

Adolescent↗