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Biomedical subjects

G F Molinari

Publications and source records attributed to G F Molinari.

16 recordsLinked to original sources
PubMed1992

Cognitive dysfunction in a patient with long-term occupational exposure to ethylene oxide. Role of ethylene oxide as a causal factor.

This case illustrates a comprehensive approach to assessing causality in a woman with apparent cognitive dysfunction, as measured by neuropsychological testing, and a 10-year history of occupational exposure to ethylene oxide. The analysis included a multidisciplinary examination of the patient, which took place several years after the termination of her exposure. In addition, all of the patient's prior medical and psychiatric records were reviewed, as were the records of her employer to ascertain her exposure history. Our evaluation revealed a pattern of neuropsychological findings not consistent with nervous system damage secondary to an organic effect of ethylene oxide. A more likely causal hypothesis is adopted: the patient's apparent cognitive dysfunction had a psychiatric etiology. This case also illustrates the potential impact of a patient's involvement in legal proceedings related to claims of neurocognitive dysfunction.

Adult↗
PubMed1978

Comparison of ketamine and pentobarbital anesthesia in the Mongolian gerbil.

The clinical course of pentobarbital and ketamine anesthesia are compared following a single injection of each and as anesthesia for carotid ligation in the Mongolian gerbil. Induction time to pinprick insensitivity was found to be the same for each agent; however, ketamine allowed earlier emergence and, moreover, observation of peripheral motor activity during the operative procedure.

Anesthesia↗
PubMed1977

Sedative drug surveys in coma: how reliable are they?

Routine blood tests of comatose patients for drugs that depress the CNS are highly desirable, but techniques of analysis are not well standardized and the results do not correlate well with clinical condition. Determining the role of sedative drugs in coma requires a high degree of suspicion and sound clinical judgment.

Adolescent↗
PubMed1976

Respirator brain. Report of a survey and review of current concepts.

Because of renewed public and scientific interest in the concept of brain death and its diagnostic criteria, an opinion survey was undertaken, polling the membership of the American Association of Neuropathologists, regarding the definition, gross and microscopical features, and pathogenesis of the syndrome popularly designated the "respirator brain." Of the 191 respondents who completed the questionnaire, 174 (91%) indicated that the term respirator brain is properly used to describe a specific pathological entity, and 160 (84%) considered the characteristics of respirator brain to be distinct from those of late fixation. Of the 174 respondents who accepted the designation, 148 (85%) regarded a history of respiratory dependency as essential, and a vast majority (95%) agreed that extensive tissue necrosis occurs with little inflammatory cell reaction; other criteria were more controversial. Microscopical changes that suggest a pathogenetic mechanism attracted a number of informative, limiting, or qualifying remarks. Nonetheless, 54% thought that impaired cerebral blood flow contributed to pathogenesis.

Brain↗
PubMed1975

Barbiturate attenuation of the clinical course and pathologic lesions in a primate stroke model.

To evaluate the potential for clinical application, the reputed protective action of barbiturates in cerebral ischemia was tested in a controlled study after segmental middle cerebral artery occlusion in primates. Surviving treated animals promptly recovered consciousness, locomotion, and feeding behavior despite persistent hemiplegia, while control animals ran an indolent course, with slow recovery of poor quality. Cerebral lesions in treated animals were confined to the deep hemispheric structures, while control specimens showed larger deep lesions confluent with extensive areas of cortical infarction. These results are less dramatic than those reported by others, but the protective effect observed in fields of collateral circulation deserves further exploration as an adjunct to medical and surgical management.

Animals↗
PubMed1975

Criteria of cerebral death.

This critical survey of the current means of determining cerebral death has indicated certain shortcomings in each of the sets of criteria currently in use. It is apparent that criteria applied at a point in time and based upon a single organ system-clinical history and findings, EEG examinations or cerebral blood flow determinations - will fall short of absolute accuracy. The clinical examinations alone have an accuracy approximating 90%, the EEG findings have greater accuracy but a much smaller scope. Cerebral blood flow studies, short of four-vessel angiography, achieve about the same accuracy, but their scope is not yet determined. The combination of all three may prove to be optimal.

Brain Death↗
PubMed1975

Clinicopathological validation of a primate stroke model.

A method recently developed in our laboratory has been evaluated for clinical and pathological reliability and validity. Intracarotid injection of a silicone polymer molded into an elastic cylinder regularly caused segmental occlusion of the middle cerebral artery in sedated but conscious rhesus monleys. Clinical changes were quantitatively monitored continuously from onset through acute and chronic phases and precise correlations made with postmortem vascular and parenchymal pathology. Minor anatomical variations in the size and branching patterns of the middle cerebral artery in this primate species paralleled those in man. Uniformity in patterns of the acute natural history and specificity in clinical pathological correlations substantiate the utility of this stroke model for tests of therapeutic efficacy.

Anesthesia, General↗
PubMedDate not supplied

Primate model of cerebral hematoma.

Using specific anesthetic agents, permanent segmental occlusion of the proximal middle cerebral artery (MCA) causes ischemic infarction limited to the putamen and other deep hemispheral structures in primates. Using this model, 25 rhesus monkeys were subjected to acute arterial hypertension before, during and up to 5 days after onset of MCA occlusion in order to reevaluate the possible role of the ischemic process in pathogenesis of cerebral hemorrhage. Norepinephrine infusion induced prompt rapid rise in mean arterial pressure (MAP) and intracranial pressure (ICP) limited to the duration of infusion. This procedure produced acute ischemic lesions which were totally bland but topographically more extensive than untreated controls; in chronic lesions, however, deep nuclear masses showed hemorrhagic infarction. Animals given 5% CO2 air had slowly progressive elevation in ICP and MAP. Acute specimens showed intact, widely-dilan hypercarbia was induced 5 days after MCA occlusion, animals developed intracerebral hematoma involving putamen, external capsule and claustrum, occasionally dissecting through to ipsilateral ventricle. In acute cerebral ischemia, elevated MAP produced only quantiative changes in lesion size. In the vasoproliferative stages of mature infarction, MAP elevation induced by a cerebral vasoconstrictor caused hemorrhagic infarctions while cerebral vasodilation caused intracerebral hematomas.

Angiotensin II↗
PubMedDate not supplied

Modification of cerebral ischemic damage by anesthetics.

The yield of infarcted hemispheres following unilateral carotid ligation in gerbils under ketamine anesthesia substantially exceeded that occurring under pentobarbital anesthesia. In addition to increasing the gerbil stroke model's efficiency, ketamine provided a shorter recovery period, thus allowing earlier observation of clinical signs of brain injury. These results support the contention that anesthetic agents may modify the response of central neuronal tissues to acute ischemia.

Anesthetics↗