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Biomedical subjects

M R Koenigsberger

Publications and source records attributed to M R Koenigsberger.

33 records · Page 2Linked to original sources
PubMed1977

Effect of intermittent phototherapy on bilirubin dynamics in Gunn rats.

To determine whether continuous phototherapy is necessary to control neonatal jaundice, groups of jaundiced (Gunn) rats were exposed to four blue light regimens: continuous light, 30 min light/30 min dark, 6 min light/6 min dark, and 6 min light/18 min dark. An exponential decrease in serum bilirubin concentration (SBC) was found with all regimens. A logarithmic dose response curve was obtained with a 50% light dose exhibiting 75% efficacy, and a 25% light dose exhibiting 59% efficacy compared to continuous phototherapy. The time constants of the decrease in serum bilirubin concentration also varied logarithmically with doses with continuous therapy having a time constant of 1.4 days, and 6 min light/18 min dark therapy having a time constant of 3 days.

Animals↗
PubMedDate not supplied

Cerebellar infarction in children.

We report 3 children with posterior circulation strokes. Cerebellar infarction is rare in children; therefore, it was not the clinical diagnosis suspected primarily in 2 of these patients. The diagnostic value and limitations of neuroimaging studies, including computed tomography and magnetic resonance imaging, in cerebellar infarction in children are discussed. Because 3 patients were examined in a 2 year period in one institution, this entity may be more prevalent than generally believed and should be considered in the differential diagnosis of posterior fossa lesions in children.

Adolescent↗
PubMedDate not supplied

[Complications of intracranial hemorrhage in full term newborns].

The incidence of various types of intracranial hemorrhage is different in full-term infants than those that occur in small premature infants. Consequently, the complications are for the most part different. The previous article described the types of hemorrhage occurring at term, as well as their signs and symptoms. This brief review will focus on the complications that may arise from these. Examples are given of superficially occurring hemorrhages and of those that arise deeper in the parenchyma of the brain. The actual bleed is the acute event that may become subacutely complicated by virtue of its position or by extension. This occurs as part of the natural process or as a result of injudicious intervention. There follow chronic complications: cerebral palsy, intellectual deficit and seizure disorder which remain for the patient's lifetime.

Cerebral Palsy↗
PubMedDate not supplied

[Advances in neonatal neurology: 1950-2000].

INTRODUCTION: There have been innumerable advances in medicine and its specialties in the last half century. Neonatal intensive care did not really begin until the 1960's, when adequate mechanical ventilation for newborns became generally available. DEVELOPMENT AND CONCLUSIONS: With the increased survival of very small prematures, even with a smaller individual morbidity, a larger total number of survivors is graduating these units. Will they be able to function in this increasingly more complicated world? Organizational, Diagnostic, and Therapeutic advances in Neonatology and Neonatal Neurology are reviewed. Then, advances in some of those neonatal entities that threaten the CNS are briefly reviewed. Congenital anomalies, metabolic disease, infection, intraventricular hemorrhage, hydrocephalus, periventricular leukomalacia, are touched upon. Finally, the entity of hypoxi-ischemic encephalopathy is reviewed, emphasizing that its morbidity has changed little through the years, and describing a new hypothermic approach to its management currently under way in a global cooperative study.

Brain↗
PubMedDate not supplied

[Neonatal myasthenic syndromes].

INTRODUCTION: In the newborn, myasthenia can present either as transient neonatal myasthenia or as a congenital syndrome. At present at least 8 syndromes involving neonatal neuromuscular junction (NMJ) malfunction have been described; one caused by the passage of transplacental antibodies from mother to child, while all but one of the rest are inherited. Inheritance in all but two syndromes is autosomal recessive. One is an autosomal dominantly inherited illness; in another the mode of inheritance is not clear. The deficit in function of the NMJ is presynaptic in 3 instances, at the junctional gap in 1, and postsynaptic in at least 3 other syndromes. DEVELOPMENT: We will review the clinical symptoms, as well as neurophysiologic and genetic testing available for diagnosis. We explain how, at least, in some of the syndromes, one can begin appropriate therapy based on clinical, neurophysiological and simple pharmacological testing. CONCLUSION: However, in many cases, it becomes necessary to refer the patient or a tissue sample, usually an intercostal nerve muscle preparation, to one of the very few centers in the world where in vitro neurophysiologic, microstructural and genetic procedures leading to a more precise diagnosis can be performed.

Acetylcholine↗
PubMedDate not supplied

[Cerebral palsy: prenatal risk factors].

Prenatal risk factors causing cerebral palsy (CP), here defined as a non-progressive motor abnormality of tone or posture, are much more numerous than once believed, when a great deal of brain injury was attributed to factors surrounding delivery. Scientific advances in genetics and biochemistry, as well as clinical technical advances in, for example, amniotic fluid examination or fetal neuroimaging, has permitted us to find a multiplicity of new etiologies causing neonatal encephalopathy, most of which were formerly attributed to perinatal hypoxia-ischemia. This article reviews an expanded list of etiologies, including asphyxia, which has been found to cause only 6-10% of CP in full term infants, and periventricular leukomalacia, which is associated with 30-50% of CP in premature births. We also review a few of the genetic causes of CP, which lead to metabolic encephalopathies in come cases, to congenital anomalies in others, and sometimes to both. We discuss maternal gestational or intrapartum infections which may affect the fetus by direct in utero contagion or by other less direct means. Inborn metabolic errors affecting the fetus, such as diabetes, are touched on, as are the effects of maternal medications or recreational drugs on the fetus. Finally, we briefly cite the curious phenomenon occurring in multiple births, namely the potential of CP in the surviving infant or infants were the others have died in utero.

Brain Injuries↗