Search PubMed⌕ Search

Biomedical subjects

C M Shaw

Publications and source records attributed to C M Shaw.

At least 55 records · Page 3Linked to original sources
PubMed1987

Human immunodeficiency virus (HIV) infection in brains with AIDS-related leukoencephalopathy.

In addition to central nervous system (CNS) opportunistic infections and neoplasms, patients with acquired immunodeficiency syndrome (AIDS) develop unexplained dementia and encephalopathy and degeneration of the white matter. We studied autopsied brains from 20 adult patients who expired from AIDS to determine the relationship of human immunodeficiency virus (HIV) infection to white matter lesions and to clinical findings. In four patients with dementia/encephalopathy and abnormalities of the white matter, there was evidence of HIV infection as shown by in situ hybridization. In contrast, the remaining 16 patients who had no evidence of white matter degeneration revealed no hybridization to the HIV probe. The cells infected with HIV included endothelial cells, perivascular macrophages/monocytes, and multinucleated giant cells and were found in or adjacent to white matter degeneration. These results demonstrate a correlation between HIV-infected cells and AIDS leukoencephalopathy and provide further evidence for HIV-related dementia/encephalopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Multiple sclerosis beginning in infancy.

The clinical and autopsy findings on a 6-year-old child presenting with 11 episodes of relapsing neurological symptoms since age 10 months are reported. The brain showed multiple and irregular demyelinative lesions in the cerebral and cerebellar white matter as well as in the tegmentum and base of the brain stem. This case reconfirms the existence of typical multiple sclerosis (MS) in childhood, beginning even in infancy. In addition, elevated Epstein-Barr virus antibody titers during the clinical course of this patient raise an interesting but still speculative etiological possibility for MS.

Antibodies, Viral↗
PubMed1986

Electrical correlates of brain injury resulting from severe hypotension and hemodilution in monkeys.

The effects of hypotension, hemodilution, and their combination on the relationship between concurrent brain electrical activity and resulting brain injury were studied in anesthetized monkeys. The authors compared changes in the electroencephalogram and somatosensory and auditory evoked potentials with eventual neuropathologic outcome. Our goals were: 1) to define the margin of safety for the monkey brain during hemodilution and hypotension under several simulated clinical conditions; and 2) to determine whether noninvasive measurements of brain electrical activity can predict ischemic brain cell damage. Forty-one monkeys were anesthetized with halothane (0.8 vol % inspired) and ventilated mechanically. Arterial hypotension was induced with trimethaphan (25 +/- 8 mmHg mean arterial blood pressure [MABP] for 30 min). Hemodilution was induced by replacing blood with lactated Ringer's solution (14 +/- 2% hematocrit for 1 h). Combined hemodilution and hypotension consisted of 30 min of hemodilution alone followed by superimposing hypotension for 30 min (16 +/- 3% hematocrit and 29 +/- 5 mmHg MABP). Ten monkeys died following severe hypotension alone or combined hemodilution and hypertension as a consequence of cardiac arrest or undetermined (possibly neurologic) causes. No histologic evidence of ischemic brain cell injury was found in surviving monkeys subjected to hemodilution or hypotension alone. Neuropathologic alterations in the cerebral cortex, cerebellum, hippocampus and globus pallidus as well as neurologic and behavioral deficits were found in seven of 16 surviving monkeys subjected to both hemodilution and hypotension. These findings resulted from combinations of hematocrit less than 20% and MABP below 40 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Histologic analysis of tissue response to bucrylate-pantopaque mixture.

A toxicologic-pathologic study of isobutyl-2-cyanoacrylate (Bucrylate) was carried out first in dogs and then in humans whose arteriovenous malformations were infused with this embolic agent. The canine specimens obtained at 7, 18, 28, and 147 days after embolization showed the development of a mild histiocytic giant cell reaction, which evolved to end-state sclerotic arteritis. The response was confined to the vessels and did not involve contiguous parenchymal tissues. Ten human specimens, obtained from 1 hr to 7 years after treatment, showed a similar bland reaction with no evidence of suppuration or premalignant changes.

Adolescent↗
PubMed1985

Iron pigment in the brain of a man with tardive dyskinesia.

A 64-year-old man with bipolar affective disorder developed persistent tardive dyskinesia following an overdose of lithium and haloperidol. Two years later he died of unknown causes. Neuropathologic examination revealed extensive deposition of iron in basal ganglia and substantia nigra.

Basal Ganglia↗
PubMed1985

Health risks from increases in methylmercury exposure.

Our present knowledge of the human health effects of methylmercury exposure is derived from study of major outbreaks of human poisonings in Japan and Iraq and experimental studies on primates. Methylmercury readily passes through such physiological barriers as the blood-brain barrier, blood-testes barrier, and the placenta. Its major pathological effects are on the nervous and reproductive systems and the developing embryo/fetus. The neurotoxicity of methylmercury is well established in both humans and non-human primates. Lesions in the cerebral and cerebellar gray matter consist of necrosis and lysis of neurons, phagocytosis and gliosis. The changes are most prominent in the deep sulci and may have a vascular component. A late effect is cerebral atrophy. At high dose levels the liver, kidneys, and other organs may also have degenerative changes. Although not yet described in humans, a major effect of exposure of female primates is an adverse effect on pregnancy. Maternal female M. fascicularis blood mercury levels above 1 ppm are associated with a decreased pregnancy rate and increased abortion rate. To date our experimental data lack sufficient numbers to detect infrequent pregnancy effects below 1 ppm. Preliminary studies also reveal that methylmercury may also decrease the number and function (swim speed) of sperm. Both human and primate studies demonstrate deleterious effects of methylmercury on the developing embryo/fetus. Autopsies on human and primate infants reveal retarded brain development and the occurrence of a cerebral palsy-like behavior in the newborns, whereas the mother may be free of signs and symptoms of methylmercury toxicity. The fetal blood level of mercury is higher than the maternal level.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Myelin basic protein and its antibodies in the cerebrospinal fluid in experimental allergic encephalomyelitis, multiple sclerosis and other diseases.

Our studies have revealed no essential differences between EAE in monkeys and MS and other CNS diseases in humans. High concentrations of BP occur early, especially if no anti-BP antibodies are also present. Lower concentrations of BP follow and may be associated with the presence of anti-BP antibodies. In EAE these antibodies come from the relatively strong peripheral sensitization to BP and enter the CSF through a damaged blood-brain barrier; in MS they come from the relatively weak immunologic stimulation probably evoked by previous attacks of the disease. Proteolytic enzymes also enter the CSF and produce peptide fragments of BP whose differing antigenic compositions permit antibodies to some fragments to coexist with other fragments unrelated antigenically but detected as "BP" in vitro. Since oligoclonal immunoglobulins (IgG) occur more often in MS than in other diseases, one can expect to find BP, anti-BP antibodies and oligoclonal IgG more often in MS, but even the combination is not specific for MS. Consideration of the temporal and immunochemical relationships as well as of the differential diagnosis provides a basis for the understanding of the significance of BP, its antibodies and other immunoglobulins in the CSF.

Animals↗
PubMed1983

Computerized tomography as a diagnostic aid in acute hemorrhagic leukoencephalitis.

Computerized tomography (CT) in a pathologically proven case of acute hemorrhagic leukoencephalitis (AHL) showed a mass effect and increased absorption coefficient in the right hemisphere within 18 hours of the onset of neurological symptoms. The changes corresponded to the site of white matter edema, necrosis, and petechial hemorrhages demonstrated postmortem. The early changes of CT reflect the hyperacute nature of AHL and differ from those of herpes simplex encephalitis.

Acute Disease↗
PubMed1983

Prolactinomas as part of the multiple endocrine neoplastic syndrome type 1.

The pituitary tumors seen in the multiple endocrine neoplastic syndrome type 1 have generally been considered "nonfunctional." Fewer than 40 persons with hyperprolactinemia as part of the syndrome have been described. A family with the largest number of subjects (six) with prolactinomas in one generation reported to date is described. The variable aggressiveness of this disease, the difficulty in treatment because of multiple prolactinomas or hyperplasia or both, and a case of tumor shrinkage with bromocriptine therapy are also demonstrated in this unique family.

Adult↗
PubMed1983

Profound arterial hypotension in dogs: brain electrical activity and organ integrity.

To determine whether non-invasive measurement of brain electrical activity can predict ischemic brain damage, we recorded the electroencephalogram (EEG) and somatosensory- (SEP) and auditory- (AEP) evoked potentials before, during, and after trimethaphan-induced profound arterial hypotension in dogs. The authors set out to compare the change in electrical activity with the degree of brain damage, as determined by microscopic examination. Dogs were anesthetized with halothane (1.4 vol % inspired), maintained horizontal (head at the level of the heart), and ventilated mechanically (FIO2 0.50); deviations from normal acid-base status were corrected. Twenty animals received a 1.5-mg/kg intravenous bolus of trimethaphan. Three animals were resistant to the drug. The remaining animals had profound hypotension [mean arterial blood pressure (MABP) at some steady level between 12 and 25 mmHg] for 1 h. Eight of these animals died during or soon after the hypotensive period as a consequence of cardiac arrest (three), intestinal bleeding (three) or unknown causes (two). In all survivors, EEG intensity and the amplitude of the SEP decreased during hypotension; both variables recovered with restoration of MABP. All nine animals surviving hypotension had no apparent neurologic or behavioral deficit nor any histologic evidence of ischemic brain cell injury. We were thus unable to find a MABP threshold for brain with minimal brain injury. Our findings suggest, under the conditions of our experiments, a great margin of tolerance for profound hypotension by the brain in this species. Other organ systems--the heart, gastrointestinal tract, and liver--proved to be more susceptible to ischemic damage. Eight of the nine surviving animals had elevations in serum alanine transaminase (SGPT), aspartate transaminase (SGOT), and alkaline phosphatase. Animals with the greatest increases in these enzymes showed centrilobular hepatocyte degeneration.

Animals↗
PubMed1982

Pathogenic mechanisms of heterotopic neural tissue associated with anencephaly.

Central nervous tissue was found in both the lung and the abdominal surface of the diaphragm in an anencephalic baby with gastroschisis. These findings support the hypothesis that the heterotopic neural tissue in anencephalic babies is due to transamniotic implantation. It thus appears that the pathogenic mechanism of the heterotopic neural tissue in the lung is aspiration.

Anencephaly↗
PubMed1982

Immediate and delayed neurotoxicity after mechlorethamine preparation for bone marrow transplantation.

Twenty-four patients, including two with aplastic anemia and 22 with malignancy, underwent marrow transplantation after preparation with mechlorethamine, 0.3 to 2.0 mg/kg body weight. Fourteen of the 21 neurologically evaluable recipients developed immediate neurotoxicity a median of 4 days after treatment (range, 0 to 34 days). Confusion and disorientation were observed in six patients, headache in six, hallucinations n four, lethargy in four, tremors in three, paraplegia in one, seizure in one, and vertigo in one. Whereas acute symptoms cleared in 11 patients, three remained symptomatic until death. Twelve evaluable patients survived more than 60 days; all six with previous acute toxicity subsequently developed delayed onset of new neurologic findings (personality change, confusion, seizure, diplopia, or dementia) a median of 169 days (range, 70 to 248 days) after treatment. Cerebrospinal fluid analysis was usually normal but cerebral computed tomographic scans showed ventricular enlargement and electroencephalograms showed diffuse slowing. Postmortem histologic examination of brain showed neuronal degenerative changes with increased vascularity, gliosis, and perivascular fibrosis. Neurotoxicity appeared to increase with age and mechlorethamine dose and was commoner in patients given additional procarbazine or cyclophosphamide.

Adolescent↗
PubMed1981

Bleeding patterns from ruptured intracranial aneurysms: an autopsy series of 205 patients.

The autopsy records from 205 patients who died from ruptured intracranial aneurysms were reviewed. Special emphasis was placed on the cause of death and the time after rupture that death occurred. One hundred and sixty-eight patients (82%) died within one week of their last aneurysmal rupture. Eighty-eight died within one week of their initial rupture. Massive subarachnoid hemorrhage was the cause of death in 53% and localized hematomas in 14%. Eighty patients died within one week following a subsequent rupture. Intracranial hematoma was the cause of death in 87%, with 31% harboring a localized mass potentially amenable to surgical therapy.

Adolescent↗