Search PubMed⌕ Search

Biomedical subjects

G Teasdale

Publications and source records attributed to G Teasdale.

At least 19 recordsLinked to original sources
PubMed2001

Head injury in the United Kingdom.

This paper reviews aspects of head injury management and research in the United Kingdom (UK). We discuss evidence about the scale and etiology of head injury in Britain and how this information has supported a triage-based approach, incorporating risk analysis. A Cohesive organization based upon nationally accepted, yet regionally flexible head injury management guidelines is important. Research in the United Kingdom has clarified the effect of head injury on the brain and how this can be reduced. This clarification follows from improved understanding of the neurobiology of injury, of secondary damage and recovery, and information gained from new techniques aimed at investigating events in patients. Outcome is an important perspective and we highlight the increasing focus upon recovery and the extent of disability after so called mild head injury. Although we retain a UK perspective, comparisons with aspects of European head injury emphasize the increasing importance of an international approach in the future.

Brain Injuries↗
PubMed2001

Defining acute mild head injury in adults: a proposal based on prognostic factors, diagnosis, and management.

The lack of a common, widely acceptable criterion for the definition of trivial, minor, or mild head injury has led to confusion and difficulty in comparing findings in published series. This review proposes that acute head-injured patients previously described as minor, mild, or trivial are defined as "mild head injury," and that further groups are recognized and classified as "low-risk mild head injury," "medium risk mild head injury," or "high-risk mild head injury." Low-risk mild injury patients are those with a Glasgow Coma Score (GCS) of 15 and without a history of loss of consciousness, amnesia, vomiting, or diffuse headache. The risk of intracranial hematoma requiring surgical evacuation is definitively less than 0.1:100. These patients can be sent home with written recommendations. Medium risk mild injury patients have a GCS of 15 and one or more of the following symptoms: loss of consciousness, amnesia, vomiting, or diffuse headache. The risk of intracranial hematoma requiring surgical evacuation is in the range of 1-3:100. Where there is one computed tomography (CT) scanner available in an area for 100,000 people or less, a CT scan should be obtained for such patients. If CT scanning is not so readily available, adults should have a skull x-ray and, if this shows a fracture, should be moved to the "high-risk" category and undergo CT scanning. High-risk mild head injury patients are those with an admission GCS of 14 or 15, with a skull fracture and/or neurological deficits. The risk of intracranial hematoma requiring surgical evacuation is in the range 6-10:100. If a CT scan is available for 500,000 people or less, this examination must be obtained. Patients with one of the following risk factors--coagulopathy, drug or alcohol consumption, previous neurosurgical procedures, pretrauma epilepsy, or age over 60 years--are included in the high-risk group independent of the clinical presentation.

Brain↗
PubMed2000

Calcium channel blockers for acute traumatic brain injury.

BACKGROUND: Acute traumatic brain injury is a major cause of death and disability. Calcium channel blockers have been used in an attempt to prevent cerebral vasospasm after injury, maintain blood flow to the brain and so prevent further damage. OBJECTIVES: To estimate the effects of calcium channel blockers in patients with acute traumatic brain injury and in a subgroup of brain injury patients with traumatic subarachnoid haemorrhage. SEARCH STRATEGY: Hand searching and electronic searching for randomized controlled trials available by October 1997. SELECTION CRITERIA: Randomized controlled trials in patients with all levels of severity of clinically diagnosed acute traumatic brain injury. DATA COLLECTION AND ANALYSIS: Two reviewers (JL and CG) independently assessed the identified studies for eligibility and extracted data from each study. Summary odds ratios were calculated using the Mantel-Haenszel method. MAIN RESULTS: Four RCTs were identified as eligible for inclusion in the systematic review. The effect of calcium channel blockers on the risk of death was reported in all RCTs. The pooled odds ratio for the four studies was 0.91 (95% confidence interval 0. 70 to 1.17). For the three RCTs that reported death and severe disability the pooled odds ratio was 0.85 (95% CI 0.68 to 1.07). In the two RCTs which reported the risk of death in a sub group of traumatic subarachnoid haemorrhage patients, the pooled odds ratio was 0.59 (95% CI 0.37 to 0.94). Three RCTs reported death and severe disability as an outcome in this subgroup, and the pooled odds ratio was 0.67 (95% CI 0.46 to 0.98). REVIEWER'S CONCLUSIONS: This systematic review of randomized controlled trials of calcium channel blockers in acute traumatic head injury patients shows that considerable uncertainty remains over their effects. The effect of nimodipine in a subgroup of brain injury patients with subarachnoid haemorrhage shows a beneficial effect, though the increase in adverse reactions suffered by the intervention group may mean that the drug is harmful for some patients.

Brain Injuries↗
PubMed1998

Early 1H magnetic resonance spectroscopy of acute head injury: four cases.

In an attempt to examine in vivo the early metabolic consequences of severe acute head injury, 1H MRS was performed in four patients from 8 to 25 h (mean 15 h) following trauma. In three of these patients, decompressive surgery was performed 4-5 h prior to the MRS. High levels of lactate (area of lactate peak >50% of the mean areas of the NAA, choline-containing, and creatine-containing compound peaks) were found at 8 h posttrauma in the one patient who was not operated on and at 10 h posttrauma in one of the patients who underwent surgery. In the other two postoperative patients, at 18 and 25 h after trauma, lactate levels were found to be low (lactate peak <20% of the mean area of the other three peaks). In the one patient who had a follow-up at 6 days and who had the largest initial lactate levels, these remained high. These findings suggest that high levels of lactate may not be an inevitable consequence of severe head injury and that similar MRS studies should be performed on each individual patient before therapies to reduce lactate are considered. There appeared to be no correlation between the relative amounts of lactate and outcome.

Acute Disease↗
PubMed1997

Early changes in peritumorous oedema and contralateral white matter after dexamethasone: a study using proton magnetic resonance spectroscopy.

AIMS: To study the mechanism of action of steroids in patients with peritumorous oedema. METHODS: To investigate early cerebral metabolic changes proton magnetic resonance spectroscopy (1H-MRS) was used before and 11 to 14 hours after treatment with dexamethasone (12 mg oral loading and 4 mg four times daily maintenance). Nine patients (two men, seven women, mean age 54) with pronounced oedema associated with various intracranial tumours (two astrocytomas, three meningiomas, two glioblastoma, and two metastases) were examined using MRI and MRS. SE1500/135 volume selected MRS (mean volume 21 ml) were performed on an oedematous region and a contralateral region. All spectra were acquired with and without water suppression. Metabolite peak area ratios were determined. RESULTS: Regions of oedema had significantly (P < 0.01) higher unsuppressed water than the contralateral regions, as expected. There was no change at this early time point after dexamethasone. The ratio of the area of choline containing compounds to that creatine and phosphocreatine compounds was determined after which the serial ratios of these before and after were calculated (a serial ratio of 1.0 would indicate no change in the choline to creatine ratios after steroid administration). The mean serial ratios for the area of oedema were 1.02 (SEM 0.08) and 1.10 (0.08) for the contralateral volume of interest, indicating no significant changes. However, significant changes (P < 0.02) were found in the N-acetyl-aspartate (NAA)/choline serial ratios (0.86 (0.06) in the area of oedema, 1.20 (0.10) in contralateral brain) and the NAA/creatine serial ratios (0.86 (0.08) for the oedema, 1.25 (0.11) in contralateral brain). CONCLUSIONS: Such rapid changes may be explained either by relatively large alterations in the relaxation characteristics of NAA or, more controversially, by actual changes in the amounts of NAA. It is proposed that steroids act primarily by causing early metabolic changes that are later expressed in improvements in intracranial volume relations.

Antineoplastic Agents, Hormonal↗
PubMed1996

Changes in local microvascular permeability and in the effect of intervention with 21-aminosteroid (Tirilazad) in a new experimental model of focal cortical injury in the rat.

In a new, reproducible model of rodent focal cortical injury, we have shown that in the absence of early traumatic disruption of the microvasculature and subsequent hemorrhage, delayed perivascular protein leakage and polymorphonuclear leukocyte infiltration of the injured cortex occur. In this study we employed a sensitive quantitative autoradiographic technique (using alpha-aminoisobutyric acid as a tracer) to investigate the focal changes in microvascular permeability with time and to determine the effects of administration of a 21-aminosteroid (Tirilazad) initiated 5 min after induction of the cortical injury. At all time points studied, there was a significant increase in perilesional blood-brain barrier permeability in lesioned animals treated with vehicle, compared to shamoperated animals, with the most marked increase in blood-brain barrier permeability at 4 h postinjury (mean Ki +/- SE = 19.2 +/- 2.4/1000 min with cortical injury, 1.5 +/- 0.3/1000 min in shams) (mean volume +/- SE = 15.48 +/- 0.7 mm3). In animals with cortical injury treated with Tirilazad (10 mg/kg), there was a significant reduction in microvascular permeability at the site of injury (Ki = 3.1 +/- 0.5, p < 0.001) and a significant reduction in volume of increased permeability (4.86 +/- 0.7 mm3, p < 0.01) at 4 h postinjury. In this model of cortical injury, a delayed increase in microvascular permeability occurs, which is significantly attenuated by postinjury treatment with Tirilazad.

Analysis of Variance↗
PubMed1995

Neurosurgical management of cerebellar haematoma and infarct.

The clinical features, treatment, and outcome were reviewed for 48 patients with a haematoma and 71 patients with an infarct in the posterior fossa in order to develop a rational plan of management. Clinical features alone were insufficient to make a diagnosis in about half of the series. Patients with a haematoma were referred more quickly to the neurosurgical unit, were more often in coma, and more often had CT evidence of brain stem compression and acute hydrocephalus. Ultimately, 75% of the patients with a haematoma required an operation. By contrast, most patients with an infarct were managed successfully conservatively. Early surgical management in both cerebellar haemorrhage and infarct (either external ventricular drainage or evacuation of the lesion), associated with early presentation and CT signs of brain stem compression and acute hydrocephalus, led to a good outcome in most patients. Of the patients with cerebellar haematoma initially treated by external drainage, over half subsequently required craniectomy and evacuation of the lesion; but, in some cases, this failed to reverse the deterioration. In patients with a cerebellar infarct, external drainage was more often successful. The guidelines, findings, and recommendations for future management of patients with posterior fossa stroke are discussed.

Adult↗
PubMed1994

Focal brain injury: histological evidence of delayed inflammatory response in a new rodent model of focal cortical injury.

Cortical contusions are one of the most common characteristics in head injury and are regarded by many as the hallmark of significant injury. No experimental study has clarified the roles of mechanical forces, haemorrhage and ischaemia in the process of progressive acute brain damage and later neurobehavioural dysfunction. We have devised a new, simple reproducible rodent model of focal cortical injury which employs a 'pure' mechanical/physical force applied through the intact dura. Using this model we have investigated the time course and pattern of changes in neurons, glia and microvasculature. With the exception of haemorrhage, this model closely reproduces the light- and electron microscopy features of human contusion. In the absence of perivascular haemorrhage we have demonstrated delayed perivascular protein leakage and polymorphonuclear-leukocyte infiltration of the damaged cortex. We postulate that a component of the delayed blood brain barrier breakdown demonstrated in human focal head injury (which may contribute to swelling and brain damage) is due to an acute inflammatory response, the magnitude of which is dependent on the amount of tissue injury.

Acute-Phase Reaction↗
PubMed1992

Computed tomographic and magnetic resonance imaging classification of head injury.

Neuroimaging with CT and MRI is a basis for decision making in individual head-injured patients and also provides a classification of patients according to severity of damage, patterns of injury, pathophysiologic mechanisms and prognosis. Such classifications can be based on the intracranial lesions identified: subdural, extradural, and intracerebral hematomas, contusions, and shearing lesions, or indirect indications of raised intracranial pressure and brain swelling: shift, obliteration of the third ventricle and basal cisterns, and signs of ischemia. The appropriate classification for early diagnosis and acute decision making may differ from the assessment of severity of damage, prognosis and late sequelae. Parallel systems of classification, suitable for these purposes, are proposed.

Brain Edema↗
PubMed1992

A randomized trial of nimodipine in severe head injury: HIT I. British/Finnish Co-operative Head Injury Trial Group.

We studied the efficacy of nimodipine in severely head-injured patients in a randomized study. Of 176 patients who received nimodipine, 2 mg/h iv for 2 day, 53% had a favorable outcome (moderate or good recovery). Of 175 control patients, 49% had a favorable outcome. This difference was not statistically significant but does not exclude the possibility that a study of a larger number of patients could show a clinically useful benefit.

Adult↗
PubMed1991

Pituitary apoplexy and its effect on vision.

A series of 15 patients with a clinical diagnosis of pituitary apoplexy is reviewed. Clinical features are highlighted, with stress on the defects of visual function and ocular motility, and the associated endocrine abnormalities are described. Potential diagnostic errors and their significance are considered. The incidence of this complication in a large series of pituitary adenoma patients is measured, and the radiological and pathological findings are recorded. The results of treatment by surgery and/or radiotherapy and/or bromocriptine are assessed, particularly in relation to visual consequences, and compared with previous reports in the literature, which are reviewed.

Adult↗