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Biomedical subjects

M Ahdab-Barmada

Publications and source records attributed to M Ahdab-Barmada.

25 records · Page 2Linked to original sources
PubMed1986

Neurophysiological and anatomical correlations in neonatal nonketotic hyperglycinemia.

Electroencephalographic (EEG) and brainstem auditory evoked response (BAER) findings have not been previously described and correlated with the pathological findings in an autopsied case of neonatal nonketotic hyperglycinemia (NKH). A 38 week gestation male infant presented within two hours of age with stimulus-evoked myoclonus and seizures in the context of progressive coma. Electrographic studies demonstrated cortical myoclonus and electrical seizures exquisitely localized to the midline region as well as a suppression-burst background disturbance. These vertex spike discharges were elicited after tactile stimulation. Prolonged intra-axial latencies for waves III and V were recorded on the BAER on the second day of life. Spongy leukodystrophy was noted on gross and microscopic examination of the brain involving all myelinated tracts especially in the reticular activating system, cerebellar peduncles and optic tracts. Neuropathological confirmation of brainstem involvement emphasizes the role of the nonspecific diffuse somatosensory projection system in the generation of myoclonus and stimulus-evoked seizures in the comatose patient with NKH.

Brain Diseases↗
PubMed1986

Hyperoxia produces neuronal necrosis in the rat.

Widespread cerebral neuronal necrosis occurred in newborn Sprague-Dawley rats submitted to three hours of pure oxygen (100% O2) at normal atmospheric pressure. Neuronal necrosis (NN) was most severe in the immediate newborn period and less marked with advanced maturation. It was minimal and different in its morphological characteristics in rats 10, 15 and 20 days old, and in adults breathing pure oxygen at normal atmospheric pressure for three hours. In the newborn rat, hyperoxemic NN was different in topography and cytopathology from that induced by hypoxia in the same animals. Hyperoxemic NN was similar to the NN described in human premature infants submitted to episodic hyperoxemia. Neuronal damage with karyorrhexis was most prominent in the subiculum of the hippocampus, thalamus, reticular nuclei of the brain stem and the granular cells of the cerebellum. Ultrastructural studies demonstrated nuclear and cytoplasmic membrane damage in neurons and the cellular accumulation of electron-dense lipid droplets. The pathogenesis of NN produced by hyperoxia in the human premature newborn infant may be related to lipid peroxidation of cell membranes such as that induced by oxygen-free radicals in other experimental and in vitro studies, when the anti-oxidant cellular defenses (mainly enzymes such as superoxide dismutase) are overwhelmed.

Animals↗
PubMed1984

The neuropathology of kernicterus in the premature neonate: diagnostic problems.

Yellow staining of central nervous system (CNS) nuclei occurs in the brains of some neonates, despite low levels of serum bilirubin. Two conditions appear to be important in the evolution of this form of kernicterus: prematurity and asphyxia. In a seven year retrospective study of a large neonatal autopsy population, 102 cases had kernicterus as indicated by selective macroscopic yellow staining and microscopic damage within specific CNS nuclei. Neuropathological study disclosed minor variations and numerous similarities in the manifestations of kernicterus in the asphyctic premature neonate with low levels of serum bilirubin, as compared to kernicterus in the full-term neonate with high levels of serum bilirubin. Acidosis, hypoxia, hyperoxia, hypothermia and sepsis have been considered significant risk factors, but recent comparative clinical studies have not defined predictive indices. Analysis of this disorder is difficult because of the concurrence of other complications of asphyxia and its pathological correlates in premature infants. Diagnostic difficulties are also compounded by variations in the definitions of kernicterus as used by different investigators.

Asphyxia Neonatorum↗
PubMed1984

Connatal brain tumors in patients with tuberous sclerosis.

Two neonates with tuberous sclerosis and giant cell astrocytomas diagnosed soon after birth are described. During attempted surgical resection of their tumors, both infants developed refractory intraoperative cardiac arrhythmias and died. At autopsy, both patients had multiple cardiac rhabdomyomas. Subependymal giant cell astrocytomas rarely present in the neonate, but genetic implications and associated cardiac hamartomas warrant special consideration of these connatal tumors. Surgical considerations suggest that an operative approach to these tumors should be delayed beyond the neonatal period.

Astrocytoma↗
PubMed1982

Hydrocephalus in weanling mice induced by a temperature-sensitive mutant of vesicular stomatitis virus.

Hydrocephalus developed in weanling Swiss-Webster mice after intracerebral (IC) inoculation of a naturally selected temperature-sensitive (ts) mutant of vesicular stomatitis virus (VSV). This spontaneous ts mutant was isolated from a persistent infection (pi) of mouse L cells with VSV, and named VSV-tspi 364 (complementation Group I). High doses of the mutant virus induced hydrocephalus in 87% of the mice. Infected mice were clinically asymptomatic, except for a few with transient hind-limb paralysis and proximal muscle weakness. After inoculation, mice were killed every other day for the first two weeks, and weekly thereafter for two months. Virological studies showed replication in the brain in the first nine days post-inoculation (DPI). Neutralizing antibody titers increased rapidly after 15 DPI, and elevated titers were measured at 30 DPI. Pathologically, there was patchy ependymal cell necrosis in the aqueduct and lateral ventricles, as early as the second DPI. Mild meningoencephalitis and severe ependymal cell necrosis with focal aqueductal stenosis were present iun the first two weeks of infection. Hydrocephalus began as early as 10 DPI and became severe at 28 DPI. This represents the first animal model for hydrocephalus following IC inoculation of a spontaneous ts mutant of a rhabdovirus. In our study, inoculation of mice with wild-type VSV and with other spontaneous and chemical ts mutants of VSV IC as well as with tspi 364 by other routes did not cause hydrocephalus.

Animals↗
PubMed1980

Pontosubicular necrosis and hyperoxemia.

Pontosubicular necrosis (PSN) is confined to a short perinatal developmental period and is apparently related to asphyxia at birth. Neuronal necrosis with karyorrhexis and proliferative changes in astrocytes are most prominent in the pontine gray matter and subiculum of the hippocampus. We have observed a striking association of PSN in neonates with high arterial blood oxygen (PO2) levels during the first week of life. All autopsies performed on neonates in 1977 at Magee-Womens Hospital (University Health Center of Pittsburgh) were reviewed, and all 64 neonates who survived long enough to have multiple PO2 determinations were studied. All had severe hypoxia, respiratory distress, and/or apnea. Twenty-seven (group I) did not have PO2 levels higher than 150 torr whereas 37 (group II) had PO2 levels higher than 150 torr for a sustained period. PSN was not seen in group I; it was prominent in group II. PSN was most severe between the gestational ages of 26 to 36 weeks. Hyperoxemia may decrease cerebral blood flow selectively at this critical phase of development or there may be a greater sensitivity to the toxic action of high blood oxygen levels in the presence of acidosis and hypoxia. A combination of these factors seems most probable.

Cerebrovascular Circulation↗