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Biomedical subjects

A B Sterman

Publications and source records attributed to A B Sterman.

At least 19 recordsLinked to original sources
PubMed1988

Acute stroke therapy trials: problems in patient accrual.

Temple University Hospital participated in a multicenter acute stroke trial but enrolled only one patient out of 192 screened over 2 years; other centers had similar difficulty in patient recruitment. We analyzed our screening data to determine which enrollment criteria created difficulties in recruitment and whether the problem was attributable to any single criterion or to combinations of criteria. Six individual criteria were frequent causes for exclusion; however, greater than 80% of the patients were excluded for multiple reasons. Consequently, modifying or eliminating any single criterion did not appreciably increase patient accrual. Only 17 of 210 possible pairs of criteria occurred with statistically significant frequency (p less than 0.05), and these were most likely random associations. Therefore, only by minimizing the number and stringency of enrollment criteria will patient accrual be at a level that allows the study to be completed in a timely manner with a fiscally reasonable number of centers.

Acute Disease↗
PubMed1986

Focal neurologic symptoms in panic attacks.

Among 350 referrals to a neurology service, 19 (5%) had panic attacks manifesting as focal neurologic symptoms. Diagnostic clues included multiple symptoms, normal results on neurologic examination, personal stress, dietary extremes, age 20-50 years, and symptom reproduction by hyperventilation. Focal neurologic symptoms should not exclude a diagnosis of panic attack.

Adolescent↗
PubMed1985

Cell body responses to axonal injury: traumatic axotomy versus toxic neuropathy.

To compare the evolution of cell body responses to two different types of axonal injuries--sciatic nerve crush (axotomy) and chronic 2,5-hexanedione-induced neuropathy--we studied rat lumbar dorsal root ganglion neurons with light microscopy and morphometry. Compared with control neurons, axotomized cells showed early (1 day) increases in the frequencies of two responses, nuclear eccentricity and Nissl body displacement, and later (4 day) increases in average satellite cell nuclei and decreases in perikaryal diameters. In toxin-induced axonal degeneration, there were similar patterns of defined alterations, although the evolution progressed over weeks and the response magnitudes were smaller. We conclude that the two experimental conditions show basic morphologic similarities, implying cell body reorganization in toxic axonopathy may be a response to axonal dysfunction or degeneration.

Animals↗
PubMed1985

Toxic neuropathy.

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Acrylamide↗
PubMed1985

Disseminated abnormalities of cardiovascular autonomic functions in multiple sclerosis.

To determine whether patients with MS had abnormalities of autonomic cardiovascular functions, we evaluated 22 MS patients and 20 control subjects with a battery of six standardized tests. The two groups differed on three tests: heart rate and blood pressure responses to standing, and the cold-face test. One-half of the MS patients had abnormalities on two or more tests, but individual patients showed diverse abnormality patterns. Abnormalities of neural cardiovascular regulation are frequent in MS patients and show a heterogeneous pattern, consistent with scattered plaques.

Adult↗
PubMed1984

Hexacarbon neuropathy: cell body changes are early, dynamic, and specific.

To study the evolution of cell body alterations during toxic neuropathy we exposed rats to the prototype neurotoxin 2,5-hexanedione and examined perikarya of lumbar dorsal root ganglia with electron microscopy and stereology at three stages of neuropathy. Compared to unintoxicated controls, neurons from rats with incipient (four weeks) and intermediate (six to seven weeks) neuropathy showed dispersion of Nissl substance and significant decreases (p less than 0.001) in the volume fractions of Nissl bodies, but not of mitochondria or Golgi apparatus. However, at advanced (twelve to fourteen weeks) stages the volume fraction of Nissl bodies had increased and no longer differed from that of controls; distinct chromatolysis-like changes also became prominent. To evaluate the specificity of this remodeling we compared current morphometric results to data from rats exposed to acrylamide monomer and found significant differences (p less than 0.001) in the volume fractions of Nissl bodies and mitochondria. We conclude: (1) in axonopathy, cell body remodeling occurs early and advances as a dynamic, evolving process, and (2) distinct differences in the patterns of cell body changes can distinguish the neuropathies studied, implying distinct cell body functions.

Animals↗
PubMed1984

Motoneuron axosomatic synapses are altered in axonopathy.

This study was designed to answer two questions: 1) are synapses on motoneuron cell bodies affected during toxic neuropathy and 2) what is the nature and extent of the changes? We describe synaptic alterations on motoneuron cell bodies during intoxication with 2,5-hexanedione, a prototype neurotoxin known to induce axonal degeneration. Ultrastructural study of lumbar motoneurons from experimental and control rats revealed an array of pathologic changes including: partial and, less frequently, complete detachment of synaptic boutons; synaptic degeneration in a minority of boutons; and involvement of both microglia and astrocytes. Quantitatively, there was a significant decrease in the percent of neuronal membrane contacted by both F and S boutons and a significant increase in F boutons displaying degeneration. These results suggest that some neurotoxin-induced diseases of axons are associated with alterations of synaptic complexes that may have important implications for neuronal functioning.

Animals↗
PubMed1983

Subacute toxic delirium following nitrous oxide abuse.

Nitrous oxide (N2O) abuse has been associated with myeloneuropathy, but significant mental status changes rarely have been described. We treated a patient in whom a subacute delirium developed after heavy N2O abuse; symptoms slowly cleared over three weeks after removal of the neurotoxin.

Acute Disease↗
PubMed1983

Does pyruvate prevent acrylamide neurotoxicity? Implications for disease pathogenesis.

We used the prototype environmental neurotoxin, acrylamide monomer, to evaluate the hypothesis that neurotoxin-induced nerve fiber degeneration results from inactivation of axonal glycolytic enzymes. Treating intoxicated rats with sodium pyruvate, we hypothesized, would bypass the putative neurotoxin-induced blockade in glycolysis, thus ameliorating neurobehavioral and morphologic measures of neurotoxicity. After establishing that pyruvate itself did not affect behavior, we examined its effects on acrylamide-intoxicated animals. Pyruvate treatment had a significant effect on only one of eight neurobehavioral measures, though others showed similar trends. A morphologic observation of lumbar dorsal root ganglion cell bodies and peripheral nerves failed to show an effect of pyruvate. Those results suggested that inactivation of glycolytic enzymes alone is not a sufficient explanation of pathogenesis.

Acrylamides↗
PubMed1983

Does neurotoxic conditioning accelerate nerve regeneration?

The prototype environmental neurotoxin, 2,5-hexanedione (2,5-HD), induces changes in somata of sensory ganglia that are morphologically similar to chromatolysis: this study assessed the functional significance of neuronal alterations. Experimental rats were exposed 6 weeks to 2,5-HD, and after 1 week without treatment were then subjected to experimental crush of the sciatic nerve (paired controls were unintoxicated). Nerve regeneration was assayed by the pinch test 4 to 13 days after crush. These preliminary results did not show an accelerated rate of axonal outgrowth; however, there was a small but significant (P less than 0.05) decrease in the initial delay.

Animals↗
PubMed1983

Altered sensory ganglia in acrylamide neuropathy. Quantitative evidence of neuronal reorganization.

To learn more about the nerve cell body in neurotoxin-induced degeneration of axons, Sprague-Dawley rats were intoxicated with 50 mg/kg/day of the prototype neurotoxin acrylamide monomer. The lumbar dorsal root ganglia were studied in those rats with progressive disease (controls were not intoxicated). Qualitative changes in cytological organization included nuclear eccentricity, reduction in the size of Nissl bodies or displacement to a peripheral mantle, and marked enlargement of mitochondria. Quantitatively, there were statistically significant increases in these alterations, occurring early during disease and progressing over time. A stereological analysis showed a significant increase in the volume density of mitochondria, a significant decrease in Nissl bodies, but no change in the Golgi apparatus. The data suggest that cell body alterations may represent a progressive, orderly reorganization, supporting the concept that the cell body functions in determining the fate of intoxicated neurons.

Acrylamides↗
PubMed1983

Autonomic-cardiovascular dysfunction accompanies sensory-motor impairment during acrylamide intoxication.

We investigated the effects of acrylamide monomer on autonomic-cardiovascular functions and simple sensory-motor behaviors. Rats were intoxicated by ip injections of acrylamide at a dose of 50 mg/kg/day for 10 days; control animals received an equivalent volume of saline. Heart rate (HR) and systolic arterial blood pressure (BP) were measured using the method of indirect tail plethysmography. Intoxicated animals showed fluctuating but significant increases in HR and BP after the first dose of acrylamide, during the course of the intoxication, and two days after the last dose. Deficits in sensory-motor behaviors appeared after the first dose of acrylamide and progressed steadily throughout the exposure period, remaining two days after the last dose. More complex sensory-motor behaviors were affected earliest; hindlimb functions were affected before forelimb functions, characteristic of dying-back axonopathy. These results demonstrate that acrylamide alters common measures of autonomic-cardiovascular functioning in addition to simple sensory-motor behaviors.

Acrylamides↗
PubMed1982

Cell body remodeling during dying-back axonopathy: DRG changes during advanced disease.

Although the neuronal cell body functions critically in maintaining and repairing the axon, little attention has been focused on the soma during neurotoxin-induced dying-back of the axon. To help elucidate changes in the perikarya during axonal dying-back, this study employed the hexacarbon model of axonal neuropathy in a setting designed to maximize the chances of detecting structural alterations. A spectrum of cell body modifications occurred in the fifth lumbar dorsal root ganglia (DRG) of rats chronically exposed to 2,5-hexanedione. These included distinctive cytoplasmic remodeling, a perineuronal cell reaction, and evidence of neuronal death with neuronophagia. These findings suggest the importance of the cell body in the pathogenesis of neurotoxin-induced axonal degeneration and imply that complex soma-axon interactions may help determine the fate of intoxicated neurons.

Animals↗
PubMed1982

Acrylamide induces early morphologic reorganization of the neuronal cell body.

Rats were intoxicated with acrylamide monomer at 50 mg per kilogram per day; lumbar dorsal root ganglia and distal sural and tibial nerves were studied morphologically. At the sixth day of intoxication, large and small neuronal cell bodies showed a spectrum of remodeling changes that included nuclear eccentricity, cytoplasmic reorganization with an outer mantle of Nissl and an inner perinuclear zone of pigmented bodies, and increased perineuronal cells. Distal axons showed little degeneration at this time. These findings suggest that the cell body plays an important role in the pathogenesis of dying-back neurotoxic disease, and that there may be direct toxic affect on the perikaryon itself.

Acrylamide↗
PubMed1981

The pathogenesis of primary internodal demyelination produced by acetyl ethyl tetramethyl tetralin: evidence for preserved Schwann cell somal function.

The pathogenesis of primary internodal PNS demyelination produced by acetyl ethyl tetramethyl tetralin (AETT) has been studied using subchronically intoxicated rats with intact sciatic nerves (right side), and with focally traumatized nerves (left side) undergoing myelin breakdown and repair. Sixteen Sprague-Dawley rats were given approximately 50 mg/kg/d of AETT, dissolved in ethanol and placed in food. Six age-matched control animals received daily an equivalent amount of food treated with the same volume of alcohol. After six weeks and prior to the onset of demyelination, AETT treatment had increased the number of visible Schmidt-Lanterman incisures per internode of large-diameter fibers in tibial nerves. By ten weeks, the same group of fibers had begun to develop juxtanodal and internodal myelin bubbles. Subsequently, intramyelinic phagocytes of hematogenous derivation removed entire internodes of edematous myelin. Schwann cell response to injury was studied in control and AETT-intoxicated animals which had undergone left hindlimb surgery 1 to 2 days after beginning toxin treatment: (a) a perineurial window was placed in the peroneal nerve to induce focal demyelination and remyelination, (b) the tibial nerve was transected between ligatures to study Wallerian degeneration of the distal stump, and (c) the sural nerve was focally crushed to induce axonal regeneration and myelination. Qualitatively similar responses to nerve injury were seen 1 to 16 weeks later in AETT-treated and control animals. These results are compatible with the view that AETT damages myelin directly, that Schwann cell somal functions are not seriously affected by AETT, and that Schmidt-Lanterman incisures undergo changes prior to demyelination, which may represent a physiological response of the Schwann cell to toxic attack on its myelin sheath. Taken in concern, these observations challenge the long-held view that primary internodal demyelination is necessarily indicative of metabolic dysfunction of the Schwann cell soma.

Animals↗