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Biomedical subjects

J Moossy

Publications and source records attributed to J Moossy.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1983

Factors in predicting outcome from operation in patients with prolactin-secreting pituitary adenomas.

Forty female patients with pituitary adenomas were studied retrospectively to determine whether factors could be identified that would help predict outcome from operation. Twenty-five patients had a normal prolactin level (less than or equal to 30 ng/ml) during the early postoperative period (less than or equal to 3 months) and 15 patients had persistent disease (prolactin greater than 30 ng/ml). Nine of the 25 patients who initially had normal prolactin levels during the early postoperative period were found to have elevated prolactin levels during the late postoperative period (greater than 3 months). As has been shown previously, tumor size and preoperative prolactin levels were important factors in predicting surgical outcome. Patients with smaller (Hardy Grades I and II) tumors had significantly better outcome than those with larger (Hardy Grades III and IV) tumors. Patients with successful surgical outcomes had significantly lower preoperative prolactin values (204 ng/ml) than those with operative failures (524 ng/ml). In addition to the known factors, the patient's age at the time of operation, the length of amenorrhea, and the patient's growth hormone response to insulin hypoglycemia were newly identified as factors that helped predict surgical outcome. Patients who were less than or equal to 26 years of age and who had had amenorrhea for less than or equal to 6 years at the time of operation had significantly better surgical outcomes. Patients with normal growth hormone responses to stimulation testing had significantly better surgical outcomes than those with a blunted preoperative growth hormone response. The data suggest that prolactin-secreting pituitary tumors may cause a progressive disorder for which operative cure may be obtained only early in the disease.

Adenoma↗
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↗
PubMed1982

Delayed deterioration in the syndrome of temporal lobe contusion: evaluation by computed tomography (CT).

The clinical and computed tomographic (CT) features of three consecutive cases of temporal lobe contusion emphasize the presentation and frequent subsequent progressive neurological deterioration. The initial presentation was one of lethargy and combativeness with little or no focal neurological deficits. Thereafter all patients developed progressive neurological deterioration with decreasing levels of consciousness and lateralizing signs. Computed tomography (CT) which aided in making the initial diagnosis was repeated following clinical deterioration. Worsening in the patient's clinical condition correlated positively with changes within the contusion as visualized by CT.

Adult↗
PubMed1982

Malfunctioning ventriculoperitoneal shunts. Clinical and pathological features.

The authors report the clinical and pathological findings in 201 procedures to revise malfunctioning ventriculoperitoneal shunts in 114 patients. The revised shunts were predominantly Raimondi three-piece systems. Collection of fluid along the shunt track is emphasized as an early clinical feature of shunt malfunction. In some cases, there are few clinical signs of shunt infection, and the first indication of it may be shunt malfunction. Ventricular catheter obstruction was caused by tissue from the region in addition to choroid plexus. Inflammation was frequently found around both ventricular and peritoneal catheters. Foreign bodies (cotton fiber, hair, and talc) and granulomatous inflammation were often present at both ends. Tissues obstructing the peritoneal catheter included embolic neoplastic cells, choroid plexus, and leptomeninges. There was also more necrotic debris at the peritoneal end. To prevent shunt malfunction, attention should be directed to: 1) optimal placement of ventricular catheters inside the lateral ventricle; 2) prevention of infection; 3) avoidance of contamination by cotton fibers, hair, or talc; and 4) improvements in the biocompatibility of the implanted materials.

Adolescent↗
PubMed1980

Augmentation of postischemic brain damage by severe intermittent hypertension.

The neurological recovery and histological changes were studied in monkeys after intermittent postischemic arterial hypertension after 16 min of global brain ischemia. Ischemia was produced with a high pressure (1500 mm Hg) neck tourniquet and systemic arterial hypotension. Intensive care and life support, including monitoring of physiological variables, were provided for 7 days. Postischemia all monkeys were immobilized; ventilation was controlled and mean arterial pressure was maintained between 85--115 mm Hg for the first 48 hours. Immediately postischemia in four monkeys, intermittent arterial hypertension (i.e., 150--190 mm Hg) was induced by norepinephrine infusion for 3--5 min. Hypertensive episodes were repeated at 15, 30, 60, and 120 min postischemia, once every hour for the first 24 hours and once every 2 hours between 24 and 48 hours. Thereafter, the monkeys were allowed to breathe spontaneously. Four control monkeys were similarly treated except that arterial hypertension was not induced. Neurological recovery was evaluated by EEG, intracranial pressure, neurological deficit scoring, and histological examination of the brain after killing on day 7 postischemia. The neurological deficit score (100 % = brain death; 50% = vegetative state; 0% = normal) in control monkeys on day 7 was 17.8 +/- 1.8 (SEM) % compared to 46.3 +/- 6.5% (p less than 0.05) in the hypertension group. EEG recovery was delayed and the postischemic increase in intracranial pressure was prolonged in the hypertension group. Histological damage scores in the brain correlated with neurological deficit scores. Severe intermittent hypertension has a deleterious effect on neurological recovery after global brain ischemia.

Animals↗
PubMed1980

Effect of postcirculatory-arrest life-support on neurological recovery in monkeys.

The existence of treatable postischemic (PI) changes which influence neurological outcome has been documented by this group before. A global brain ischemia model without cardiac arrest was developed in monkeys. It includes high-pressure neck tourniquet inflation plus hypotension for a reproducible ischemic insult; survival with reproducible neurological deficit (ND) under continuous PI life-support for 7 days with control of extracranial variables; and new ND and histopathological damage scoring systems. Hypoxemia, hypercarbia, hypotension, uremia, sepsis, and other extracranial complications PI in 50 unsatisfactory experiments led to immediate worsening in ND and brain death (ND = 100%) in most of these monkeys. In contrast, all monkeys with the same initial insult, with life-support according to protocol, survived with a 7 day ND of 60% or less. In 46 experiments of seven treatment groups, after 16 or 18 min ischemia, life support was according to protocol for 7 days. The control 1 protocol (spontaneous breathing when feasible) resulted in a mean 7-day ND score of 53% (including quadriplegia). Immobilization with pancuronium and controlled ventilation ameliorate deficit to an ND score of 19% (P less than 0.05) (including quadriparesis); this became control 2 protocol. Immobilization resulted in less neuronal damage in the neocortex. Severe repetitive hypertension worsened ND to 46%, versus 19% in controls (P less than 0.05). In separate series, neither heparinization over 72 hours PI, nor hemodilution to hematocrit 25% with dextran 40, changed final ND significantly from that of their control groups. Histopathological damage scores correlated with ND scores.

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↗
PubMed1979

Cerebral infarcts with arterial occlusion in neonates.

Among 592 infants examined at autopsy during a four-year period, 32 (5.4%) had cerebral infarcts. Excluded were cases of traumatic hemorrhages and softening, periventricular leukomalacia, venous lesions, and any mass, including encephaloceles, with arterial distortion and infarction. Histological abnormalities were similar to those of infarcts in adults. Relatively advanced histopathological changes in some infants living only a few hours indicated that some infarctions may have occured in utero. The most common cause of arterial occlusion was embolization, with sepsis and disseminated intravascular coagulation playing a major role. The brains of term neonates were more frequently involved than those of premature infants. Multiple small infarcts occurred more often in premature infants. In most cases autonomic dysfunction with prolonged apnea, episodic seizures, and metabolic acidosis were the major associated clinical features, rather than focal neurological deficits. Similar cerebral infarcts in infants who survive with less severe systemic complications may lead to porencephaly, hemiplegia, mental and motor retardation, and recurrent seizures.

Brain↗
PubMed1979

Further studies on the effects of lesions in the rostral hypothalamus on gonadotropin secretion in the female rhesus monkey (Macaca mulatta).

Bilateral radiofrequency lesions were stereotaxically placed in the rostral hypothalamus of four adult female rhesus monkeys. These lesions resulted in extensive destruction of the ventromedial preoptic-anterior hypothalamic area (POA-AHA) and included the suprachiasmatic nucleus as well as, with the exception of one animal, the organum vasculosum of the lamina terminalis. In three of these four animals, gonadotropin surges similar to those observed before surgery were elicited in response to either a spontaneous increment in serum estrogen concentration or an estradiol benzoate injection. This stimulatory action of estradiol on LH and FSH release was not demonstratable in the remaining lesioned animal, but estradiol benzoate injections also failed to elicit a gonadotropin discharge in one of a series of five normal control animals. These findings fail to support the view that destruction of the ventromedial POA-AHA in this species compromises the ability of the hypothalamicohypophysial apparatus to respond to the positive feedback action of estradiol. The diurnal variation in serum cortisol concentration was not interrupted by placement of the lesions in the ventromedial POA-AHA.

Animals↗
PubMed1979

Anencephaly and heterotopic central nervous tissue in lungs.

Heterotopic nodules of moderately well-differentiated central nervous tissue were seen in the lung of a full-term anencephalic baby who survived a few hours after birth. The pathogenesis of this rare condition remains obscure. None of the three hypotheses previously offered to explain this condition can be accepted or rejected on the basis of the recorded evidence.

Adrenal Insufficiency↗
PubMed1978

The arcuate nucleus and the control of gonadotropin and prolactin secretion in the female rhesus monkey (Macaca mulatta).

Attempts were made to destroy selectively the arcuate nucleus with radiofrequency current in adult female rhesus monkeys as a first step in identifying the areas of the mediobasal hypothalamus (MBH) that are responsible for the neural control of gonadotropin secretion in this species. Extensive or complete destruction of the arcuate region was produced in three animals and in two of these the lesion was confined primarily to the arcuate region and the dorsal aspect of the posterior median eminence. These lesions resulted in the cessation of LH and FSH secretion and blocked the positive feedback action of estradiol on gonadotropin release but did not appear to influence grossly basal thyroid and adrenocortical function, or to abolish GH discharge in response to insulin hypoglycemia. Adenohypophysial infarcts were not observed and exogenous LHRH and TRH induced marked discharges of the appropriate anterior pituitary hormones. In two additional animals with large hypothalamic lesions, destruction of the arcuate region was incomplete. In this group only partial inhibition of gonadotropin secretion was observed. LH and FSH secretion did not appear to be influenced in one animal bearing a large MBH lesion that entirely spared the arcuate region. Although serum prolactin remained at pre-lesion control levels after placement of the two relatively discrete lesions confined to the arcuate region, unambiguous increases in the secretion of this hormone were observed when the area of destruction encompassed tissue anterior and/or dorsal to the arcuate region. These observations suggest that the arcuate region is the primary structure mediating the hypothalamic control of gonadotropin secretion in the rhesus monkey. They also suggest that, in this species, the regions of the MBH involved with the regulation of gonadotropin release and those which control prolactin secretion are anatomically distinct.

Animals↗