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Biomedical subjects

H G Sullivan

Publications and source records attributed to H G Sullivan.

28 records · Page 2Linked to original sources
PubMed1977

Significance of intracranial hypertension in severe head injury.

Measurements of intracranial pressure (ICP) were begun within hours of injury in 160 patients with severe brain trauma, and continued in the intensive care unit. Some degree of increased ICP (greater than 10 mm Hg) was present on admission in most cases (82%), and in all but two of the 62 patients with intracranial mass lesions requiring surgical decompression; ICP was over 20 mm Hg on admission in 44% of cases, and over 40 mm Hg in 10%. In patients with mass lesions only very high ICP (greater than 40 mm Hg) on admission was significantly associated with a poor neurological picture and outcome from injury, while in patients with diffuse brain injury any increase in ICP above 10 mm Hg was associated with a poorer neurological status and a worse outcome. Despite intensive measures aimed at prevention of intracranial hypertension, ICP rose over 20 mm Hg during the monitoring period in 64 of the 160 patients (40%). Postoperative increases in ICP over 20 mm Hg (mean) were seen in 52% of the patients who had had intracranial masses evacuated, and could not be controlled by therapy in half of these cases. Even in patients without mass lesions, ICP rose above 20 mm Hg in a third of the cases, despite artificial ventilation and steroid therapy. Of the 48 patients who died, severe intracranial hypertension was the primary cause of death in nearly half and even moderately increased ICP (greater than 20 mm Hg) was associated with higher morbidity in patients with mass lesions and those with diffuse brain injury. Measurement of ICP should be included in management of patients with severe head injury.

Brain Injuries↗
PubMed1977

The physiological basis of intracranial pressure change with progressive epidural brain compression. An experimental evaluation in cats.

Sequential cerebrospinal fluid (CSF) pressure-volume studies were carried out in seven cats during the expansion at a constant rate of an epidural balloon. The same studies were performed in three control cats. Beginning after 20 minutes of inflation and continuing to the point of pupillary dilatation there was a progressive increase in the pressure-volume index (volume required to change intracranial pressure (ICP) by tenfold). During the course of balloon inflation, there was also a progressive increase in CSF elastance (instantaneous ICP change per unit change in CSE volume). At the point of pupillary dilatation there was a marked, abrupt increase in the pressure-volume index and an equally dramatic decrease in CSF elastance. The CSF outflow resistance increased to a variable extent during balloon inflation. The plot of the CSF pressure versus balloon volume (the mass lesion pressure-volume curve) was of the classical configuration with an initial relatively flat segment and a final steep segment. A hypothesis is presented that interprets the shape of the mass lesion pressure-volume curve in terms of changes occurring in the elastic properties of the tissues surrounding the CSF space and the volume of the CSF space. It is proposed that this hypothesis will explain most of the commonly observed variations in CSF pressure. Confusion regarding the ICP-volume relationships has arisen because of lack of specificity regarding which anatomical spaces are being perturbed.

Animals↗
PubMed1976

Fluid-percussion model of mechanical brain injury in the cat.

Mechanical brain injury was produced in 36 cats with a fluid-percussion model in which brain damage or dysfunction is produced by a single, brief, hydraulically-induced pressure transient that is conducted through the brain. Fluid-percussion injury induce elastic deformation of the brain resembling the brain deformation known to occur following head impact. Physiological responses and pahtological changes following injury were expressed as a function of peak pressure. Macroscopic central nervous system lesions concentrated at the pontomesencephalic junction, cervicomedullary junction, and in the cerebellar tonsils were consistently observed at and above 2.6 atmospheres (atm). At higher levels of injury (greater than or equal to 3.2 atm) there was extensive basal subarachnoid hemorrhage. At very high levels of injury (greater than 4.0 atm) hemorrhagic contusions were noted at the cerebral hemisphere impact site. A spectrum of neuronal alterations was identified in the damaged areas. Computer analysis showed correlation of electroencephalographic (EEG) changes with the neuropathological changes, since EEG recovery became severely impaired above 2.6 atm. No EEG changes were noted below 1.5 atm. From 1.5 to 2.2 atm there was a physiological response to injury but no significant changes were seen on neuropathological examination. This range of injury should permit further studies of the more subtle changes following mechanical brain injury without intraparenchymal hemorrhage or subarachnoid hemorrhage. The fluid-percussion model relates brain deformation following mechanical loading to a single pressure transient that is easily measured and controlled. Further quantitative investigation into the pathobiology of mechanical brain injury following graded brain deformation is thus made possible.

Animals↗
PubMed1975

Embolic posterior cerebral artery occlusion secondary to spondylitic vertebral artery compression. Case report.

The authors report a case of isolated homonymous hemianopsia secondary to embolic occlusion of the posterior cerebral artery. The cause of embolism was demonstrated to be spondylitic vertebral artery compression. The importance of arteriography is emphasized since the clinical syndrome may be nonspecific and myelographic or plain x-ray changes may be minimal. Surgical therapy is also discussed.

Adult↗
PubMedDate not supplied

Inhalation regional cerebral blood flow: the use of tidal CO2 data to find radionuclide activity associated with exhaled alveolar gas.

When calculating cerebral blood flow by the inhalation regional cerebral blood flow technique, radionuclide activity associated with exhaled alveolar gas is used to represent the arterial input function for each brain region. In this study, tidal CO2 data are used to identify respiratory gas samples that contain alveolar gas. Traditional methods identify alveolar gas samples by searching for maxima and minima in the raw air curve. The raw air curve is determined by sequentially counting radionuclide activity in respiratory gases sampled at the mouth. Traditional methods sometimes erroneously identify and use maxima or minima that do not represent alveolar gas. The use of CO2 data is advantageous since the range of CO2 during exhalation can identify those exhalations that approach the functional reserve capacity and hence represent alveolar gas. The arterial input function is represented by counting intervals from the raw air curve which coincide with exhalation of alveolar gas as identified by CO2 data. This approach for representing the arterial input function is fully automatic, accurate, and reproducible.

Brain↗
PubMedDate not supplied

Analysis of inhalation rCBF data.

Relative to other approaches that have been recommended, fitting all head data, solving for a time shift, and including an air passage artifact term in the model significantly improved the estimate of gray matter blood flow by the inhalation technique. A robust algorithm, which incorporates these features, has been developed. Formulas which facilitate implementation of this algorithm are reported. An artifact from large scalp arteries was not significant and does not need to be included in the model.

Administration, Inhalation↗