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Biomedical subjects

B O Berg

Publications and source records attributed to B O Berg.

At least 37 records · Page 2Linked to original sources
PubMed1985

Brain-stem auditory evoked potentials in children with brain-stem or cerebellar dysfunction.

Brain-stem auditory evoked potentials (BAEPs) were recorded in 23 children who had signs of brain-stem or cerebellar dysfunction. In patients with brain-stem gliomas, BAEPs were abnormal in all except one, in whom involvement of the brain-stem auditory pathway was limited to the midbrain tectum. The BAEPs were normal in neuronal ceroid lipofuscinosis, but abnormal bilaterally in inheritable leukoencephalopathies. All patients with Leigh's encephalopathy had BAEP abnormalities; in two, abnormalities occurred before the appearance of lesions on computed tomographic scan. Patients with Friedreich's ataxia and giant axonal dystrophy had abnormal BAEPs, but the test was normal in a child with similar neurologic findings with vitamin E deficiency. Patients with diffuse metabolic encephalopathies had variable findings. Thus, BAEP abnormalities are nonspecific for various disease processes but are frequently seen in neoplastic and neurodegenerative diseases, with primary white matter or extensive brain-stem involvement.

Adolescent↗
PubMed1985

beta-Adrenergic treatment of hyperkalemic periodic paralysis.

In a patient with hyperkalemic periodic paralysis, metaproterenol prevented muscular weakness and hyperkalemia in periods of rest after exercise. During a severe attack, the drug rapidly corrected hyperkalemia and seemed to enhance the return of strength. The action of metaproterenol may involve a beta-adrenergic-mediated increase of potassium transport via the sodium-potassium pump.

Adolescent↗
PubMed1985

Unusual neurocutaneous syndromes.

During the last several decades, the number of these rare heterogeneous disorders described as neurocutaneous syndromes has significantly increased. The criteria for inclusion have become more general, although most of the disorders have dysplastic features, many do not have a tendency for tumor formation. Further, not all of these disorders are heritable and some are reported in only one or two families. Nonetheless, there is some merit for the clinician, geneticist, and embryologist to consider these anomalies of embryologic development on some common ground. Knowledge of these syndromes is important to correctly establish the diagnosis and prognosis. In cases of the heritable disorders, genetic counseling is essential. Finally, these disorders are of theoretic importance to all biologists, as the exchange of information will be essential to ultimately unravel the reasons for their cause.

Arteriovenous Malformations↗
PubMed1984

Pyruvate carboxylase activity in subacute necrotizing encephalopathy (Leigh's disease).

Leigh's disease is a heterogeneous group of disorders, in which clinical and biochemical features suggest abnormal pyruvate metabolism. In two patients with Leigh's disease, diagnosed according to rigorous clinical, radiographic, and histologic criteria, we tested the hypothesis that pyruvate carboxylase deficiency might be the primary etiology. Pyruvate carboxylase specific activities in extracts of cultured skin fibroblasts from both patients were in the normal range. These results, together with other evidence, suggest that isolated pyruvate carboxylase deficiency does not cause the Leigh's disease phenotype.

Brain Diseases↗
PubMed1982

Progressive hemifacial atrophy: report of three cases, including one observed over 43 years, and computed tomographic findings.

Three cases of progressive hemifacial atrophy were studied. In two patients, abnormalities were noted on the computed tomographic (CT) brain scan, whereas a third patient, with widespread cutaneous and neurologic involvement, had a normal CT scan. Patient 1, first described 44 years ago, had a neurologic disorder with features that have previously been associated with progressive hemifacial atrophy, but that have appeared years after the hemifacial atrophy ceased progression.

Adolescent↗
PubMed1981

Ataxic hemiparesis from a midbrain mass.

A 10-year-old boy with leukemia developed ipsilateral corticospinal and cerebellar signs: the ataxic hemiparesis syndrome. Computed tomography revealed a mass lesion in the contralateral rostral midbrain. Previous reports of this syndrome placed the lesion in the basis pontis. The anatomical substrate of the ataxic hemiparesis syndrome includes the basis pontis, rostral midbrain, and possibly other areas within the central nervous system.

Brain Neoplasms↗
PubMed1979

Progressive rubella panencephalitis: immunovirological studies and results of isoprinosine therapy.

Two patients with progressive rubella panencephalitis, one with and one without stigmata of congenital rubella, were treated for 9 months with isoprinosine and showed continued clinical deterioration. Immunoviorological studies performed before, during and after treatment were unaffected by drug therapy. The virus was recovered on one occasion from the lymphocytes of one of these cases. Neither patient showed any major defects in cellular or humoral immunity. However, the lymphocytes of the patient with stigmata of congenital rubella failed to respond to rubella virus in vitro and had a heat stable, non-dialysable serum inhibitor of in vitro protein A stimulated proliferative responses. Both patients' serum interfered with the production of interferon by normal donor lymphocytes following stimulation with rubella and varicella virus antigen. Increasing serum titres of interferon which did not appear to be lymphoid or immune-specific in origin were found in these two cases.

Adolescent↗
PubMed1976

Progressive rubella panencephalitis.

A patient with progressive rubella panencephalitis developed initial symptoms of neurologic deterioration 12 years after childhood German measles. Progressive rubella panencephalitis should be considered in adolescents with progressive dementia attended by pyradmidal and cerebellar dysfunction.

Adult↗
PubMed1975

Cerebellular calcification in tuberous sclerosis.

A rarely observed pattern of cerebellar calcification was noted in the skull roentgenograms of a child with tuberous sclerosis in the absence of cerebellar dysfunction. The computerized tomographic brain scan was useful in defining the extent of the cerebellar lesion and in detecting two additional foci of calcification that were not detected by standard roentgenographic methods.

Brain↗