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Biomedical subjects

W B Jennett

Publications and source records attributed to W B Jennett.

At least 19 recordsLinked to original sources
PubMed1988

Prognosis of the posttraumatic vegetative state.

Of 1373 patients who, following severe brain injury had been comatose for over 6 hours, 140 (10%) were in a vegetative state one month later. Fifty-nine regained consciousness but none of those aged over 40 became independent during the first year. Of those still in a vegetative state after 3 months, none became independent irrespective of age. Of all patients comatose for over 6 hours after severe brain injury, only 1% was in a vegetative state after one year. Certain scores for features such as age, pupillary reactions, eye-opening and eye movements indicate either a favourable prognosis, a fatal outcome or irreversible coma. It is only in some 10% of all patients in coma or in a vegetative state during the first two weeks after the accident that it is possible to predict with a high degree of probability (p greater than 0.95), an unfavourable outcome (death or irreversible coma) within one year. At no time after the onset of coma is it possible to predict or distinguish, with a fair degree of probability (e.g. p greater than 0.80), those patients who will remain in a vegetative state from those who will die.

Adult↗
PubMed1973

Raised intracranial pressure and cerebral blood flow. 2. Supratentorial and infratentorial mass lesions in primates.

Changes in cerebral blood flow with increasing intracranial pressure were studied in anaesthetized baboons during expansion of a subdural balloon in one of two different sites. With an infratentorial balloon, cerebral blood flow bore no clear relation to intracranial pressure, but was linearly related to cerebral perfusion pressure. Apart from an initial change in some animals, cerebrovascular resistance remained constant with increasing intracranial pressure, and autoregulation appeared to be lost from the outset. With a supratentorial balloon, cerebral blood flow remained constant as intracranial pressure was increased to levels around 60 mm Hg, corresponding to a cerebral perfusion pressure range of approximately 100 to 40 mmHg. Cerebrovascular resistance fell progressively, and autoregulation appeared to be effective during this phase. At higher intracranial pressure levels (lower cerebral perfusion pressure levels), autoregulation was lost and cerebral blood flow became directly dependent on cerebral perfusion pressure. The importance of the cause of the increase in intracranial pressure on the response of the cerebral circulation and the relevance of these findings to the clinical situation are discussed.

Animals↗
PubMed1972

Raised intracranial pressure and cerebral blood flow. I. Cisterna magna infusion in primates.

Changes in cerebral blood flow during incremental increases of intracranial pressure produced by infusion of fluid into the cisterna magna were studied in anaesthetized baboons. Cerebral blood flow remained constant at intracranial pressure levels up to approximately 50 mm Hg. At intracranial pressure levels between 50-96 mm Hg a marked increase in cerebral blood flow occurred, associated with the development of systemic hypertension and changes in cerebrovascular resistance. Further increases of intracranial pressure led to a progressive fall in cerebral blood flow. Prior section of the cervical cord prevented both the increase in cerebral blood flow and the systemic hypertension. Alteration of cerebral perfusion pressure by bleeding during the hyperaemia in a further group of animals suggested that autoregulation was at least partially preserved during this phase. After maximum hyperaemia had occurred, however, autoregulation appeared to be lost. The clinical implications of these findings are discussed.

Animals↗
PubMed1970

Relationship between volume flow and velocity in the cerebral circulation.

The relationship between the velocity of the cerebral circulation and the cerebral blood flow was explored at varying levels of PaCO(2), systemic arterial pressure, intracranial pressure, and perfusion pressure, using radioisotope techniques in baboons. Only at low flow rates did velocity increase with flow, and then non-linearly; at high rates velocity increased progressively less. Changes in flow are reflected by changes in velocity in such restricted circumstances that mean circulation time is a very unreliable indication of cerebral blood flow.

Animals↗
PubMed1970

Limitations of circulation time in the diagnosis of intracranial disease.

The mode circulation time was measured using intravenously injected technetium 99(m) and a collimation system devised to discriminate between the right and left sides of the head. The results in 21 normal men were used as a basis of assessing the findings in 205 patients, made up of five diagnostic groups (ischaemia, haematoma, subarachnoid haemorrhage, intracranial tumour, and head injury). The average mode circulation time in the affected hemisphere for the three groups with vascular disease was increased, but even in these groups half the patients had a mode circulation time within 1 SD of normal mean; similar results were found for asymmetry between the hemispheres. In serial measurements in 45 patients no correlation was found between change in mode circulation time and the clinical state. That so many results are within the normal range limits the value of this method.

Blood Circulation Time↗
PubMed1970

Effects of hyperbaric oxygen on intracranial pressure and cerebral blood flow in experimental cerebral oedema.

Increased intracranial pressure was induced in anaesthetized dogs by application of liquid nitrogen to the dura mater. Intracranial pressure and cerebral blood flow were measured, together with arterial blood pressure and arterial and cerebral venous blood gases.Carbon dioxide was administered intermittently to test the responsiveness of the cerebral circulation, and hyperbaric oxygen was delivered at intervals in a walk-in hyperbaric chamber, pressurized to two atmospheres absolute.Hyperbaric oxygen caused a 30% reduction of intracranial pressure and a 19% reduction of cerebral blood flow in the absence of changes in arterial PCO(2) or blood pressure, but only as long as administration of carbon dioxide caused an increase in both intracranial pressure and cerebral blood flow. When carbon dioxide failed to influence intracranial pressure or cerebral blood flow then hyperbaric oxygen had no effect. This unresponsive state was reached at high levels of intracranial pressure.

Animals↗