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Biomedical subjects

P M Bath

Publications and source records attributed to P M Bath.

At least 19 recordsLinked to original sources
PubMed2001

Tinzaparin in acute ischaemic stroke (TAIST): a randomised aspirin-controlled trial.

BACKGROUND: Low-molecular-weight heparins and heparinoids are superior to unfractionated heparin in the prevention and treatment of venous thromboembolism, but their safety and efficacy in acute ischaemic stroke are inadequately defined. METHODS: This randomised, double-blind, aspirin-controlled trial tested the safety and efficacy of treatment with high-dose tinzaparin (175 anti-Xa IU/kg daily; 487 patients), medium-dose tinzaparin (100 anti-Xa IU/kg daily; 508 patients), or aspirin (300 mg daily; 491 patients) started within 48 h of acute ischaemic stroke and given for up to 10 days. Primary intracerebral haemorrhage was excluded by computed tomography. Outcome was assessed, with treatment allocation concealed, by the modified Rankin scale at 6 months (independence [scores 0-2] vs dependence or death [scores 3-6]). FINDINGS: Of 1486 randomised patients, two did not receive treatment and 46 were lost to follow-up. The proportions independent at 6 months were similar in the groups assigned high-dose tinzaparin (194/468 [41.5%]), medium-dose tinzaparin (206/486 [42.4%]), or aspirin (205/482 [42.5%]). There was no difference in effect in any predefined subgroup, including patients with presumed cardioembolic stroke. Other outcome measures were similar between the treatment groups (disability, case-fatality, and neurological deterioration rates). During the in-hospital treatment period no patient assigned high-dose tinzaparin developed a symptomatic deep-vein thrombosis compared with nine assigned aspirin. Conversely, seven patients assigned high-dose tinzaparin developed symptomatic intracerebral haemorrhage compared with one in the aspirin group. INTERPRETATION: Treatment with tinzaparin, at high or medium dose, within 48 h of acute ischaemic stroke did not improve functional outcome compared with aspirin. Although high-dose tinzaparin was superior in preventing deep-vein thrombosis, it was associated with a higher rate of symptomatic intracranial haemorrhage.

Aged↗
PubMed2001

Neuroprotective effect of aminoguanidine on transient focal ischaemia in the rat brain.

Using serial magnetic resonance imaging we have evaluated the effectiveness of aminoguanidine (AG) as a neuroprotective agent in a rat model of transient middle cerebral artery occlusion (MCAO). Because aminoguanidine's neuroprotective properties have primarily been ascribed to its action as iNOS inhibitor, we also performed a biochemical analysis of nitric oxide metabolites and NOS isoforms in our model of ischaemia. Daily injections of AG (100 mg/kg) or saline, were started at 6 h after the occlusion and the effects of this treatment on lesion progression monitored by T(2)-weighted MRI at 6 (pre-treatment scan), 24 and 72 h. Measurements of lesion volumes showed that between 6 and 72 h post-MCAO, lesion growth was slower in AG-treated rats than in control rats. This difference was most pronounced between 24 and 72 h post-MCAO when AG halted the lesion volume expansion observed in control rats. Measurements of plasma NOx (nitrite plus nitrate) at 0, 24, 48 and 72 h after MCAO, showed that NO levels did not differ significantly between the AG- and saline-treated groups at any time-point. Moreover, NOS activity assays revealed that no iNOS activity was present in any of the brains tested and that constitutive neuronal NOS activity was similar across the two hemispheres between both groups. The absence of iNOS protein in the ischaemic and contralateral hemispheres at 48 and 72 h after MCAO (control group only) was confirmed by Western blot analysis. These results suggest that AG treatment reduces the rate of growth of ischaemic lesions, perhaps preserving the functioning of perifocal neurons. Our observations contradict suggestions that high levels of NO generated by iNOS are partially responsible for exacerbating the neuronal damage in the postischaemic phase of MCAO. Although this does not rule out a role for AG as a neuroprotective agent via its ability to inhibit iNOS, these findings indicate that neuroprotective actions of AG may also be mediated via other cellular targets.

Animals↗
PubMed2001

Further characterisation of a thromboembolic model of stroke in the rat.

We have used magnetic resonance imaging (MRI) techniques to characterise a rat model of thromboembolic stroke. The consequences of acute perfusion deficit associated with a middle cerebral artery occlusion (MCAo) by a newly formed thrombus was mapped by interrogation of the tissue oxygenation status using gradient echo methods and production of T2* maps. Final infarct size was subsequently assessed at 24-h post-ischaemia by histology with 2,3,5-triphenyltetrazolium chloride (TTC) staining. Animals displayed an infarct volume of 178.7+/-84.2 mm(3) (mean+/-S.D.) with a large coefficient of variation (47%) and range of values (85.6--265.5 mm(3)). This variability provided us with an opportunity to assess the relationships between early imaging observations and eventual infarct size. For a single cerebral slice, at the centre of the MCA territory, a relationship between the area of reduced T2* at 1 and 2 h post MCAo correlated highly with final lesion area (Spearman rank correlation, r=0.98, P<0.01, n=9). Lesion volumes in the thromboembolic MCAo model were compared with a 120-min occlusion, 22-h reperfusion protocol using an intraluminal thread MCAo approach. For the thromboembolic model, the total lesion volume was found to be smaller (178.7+/-84.2 vs. 243.3+/-50.1 mm(3), mean+/-S.D., Student's t-test P=0.046) and showed a greater variability (coefficient of variations: 47% vs. 21%). These data underline the relative variability of this embolic model and provide important preliminary information regarding the value of early changes in T2* in predicting eventual infarct size.

Animals↗
PubMed2001

Tirilazad for acute ischaemic stroke.

BACKGROUND: Tirilazad mesylate is neuroprotective in experimental models of ischaemic stroke suggesting it might be of benefit clinically. OBJECTIVES: To assess whether tirilazad mesylate is safe and effective at improving outcome in patients with acute ischaemic stroke. SEARCH STRATEGY: Trials of tirilazad were identified from searches of the Cochrane Stroke Group Specialised Trials Register (last searched: May 2001) and the Cochrane Controlled Trials Register (CENTRAL/CCTR). In addition, we contacted the Pharmacia & Upjohn company, the manufacturer of tirilazad, to identify unpublished studies and further information. SELECTION CRITERIA: Truly and quasi-randomised unconfounded placebo or open controlled trials of tirilazad administered within 24 hours onset of suspected or proven acute ischaemic stroke. DATA COLLECTION AND ANALYSIS: Data relating to early and end-of-trial case fatality, disability (Barthel Index and Glasgow Outcome Scale), phlebitis, and QTc were extracted by treatment group from published data and company reports. MAIN RESULTS: Six trials (four published, two unpublished) assessing tirilazad in 1757 patients with presumed acute ischaemic stroke were identified; all were double-blind and placebo-controlled in design. Tirilazad did not alter early case fatality (odds ratio, OR 1.11, 95% confidence intervals, 95% CI 0.79 to 1.56) or end-of-trial case fatality (OR 1.12, 95% CI 0.88 to 1.44). Tirilazad increased the odds of being dead or disabled by about one fifth, though the result was only just statistically significant; the odds ratios were similar whether the expanded Barthel Index or Glasgow Outcome Scale were used to assess outcome (OR 1.23, 95% CI 1.01 to 1.51; OR 1.23, 95% CI 1.01 to 1.50 respectively). Tirilazad significantly increased the rate of infusion site phlebitis (OR 2.81, 95% CI 2.14 to 3.69). Functional outcome (EBI) was significantly worse in prespecified subgroups of patients: females (OR 1.46, 95% CI 1.08 to 1.98) and subjects receiving low dose tirilazad (OR 1.31, 95% CI 1.03 to 1.67); a non-significant worse outcome was also seen in patients with mild-moderate stroke (OR 1.40, 95% CI 0.99 to 1.98). REVIEWER'S CONCLUSIONS: Tirilazad mesylate increased the combined end-point of 'death or disability' by about one-fifth, but did not alter case fatality, when given to patients with acute ischaemic stroke. Although further trials of tirilazad are now not warranted, analysis of individual patient data from the trials may help elucidate why tirilazad appears to worsen outcome in acute ischaemic stroke.

Humans↗
PubMed2001

Prothrombotic megakaryocyte and platelet changes in hypertension are reversed following treatment: a pilot study.

Platelets are formed from, and their function determined by, bone marrow megakaryocytes (MK). Previous studies have found that hypertension is associated with accentuated platelet function and that some antihypertensive drug classes have antiplatelet activity. We measured MK ploidy (DNA content), size, granularity, and expression of the adhesion molecule glycoprotein (GP) IIIa, using flow cytometry and measures of platelet function, in 12 untreated hypertensive patients and 14 normotensive subjects. Eight hypertensive patients were then treated with losartan (50 mg daily), an angiotensin receptor antagonist that lowers blood pressure, and MK and platelet parameters re-measured after 6 weeks. Hypertensive patients had, as compared with matched normotensive subjects: increased MK ploidy (mean +/- SD) 22.9 +/- 2.2 N versus 20.8 +/- 1.6 N (2P = 0.009); increased platelet size, 10.67 +/- 1.03fl versus 9.26 +/- 0.72fl (2P < 0.001); increased platelet expression of GP IIIa, 108.6 +/- 22.5 versus 92.0 +/- 12.3 (2P = 0.036); and reduced platelet count, (207 +/- 52) x 10(9)/l versus (257 +/- 55) x 10(9)/l (2P = 0.026). Losartan significantly reduced MK ploidy, 22.6 +/- 2.2 N versus 21.4 +/- 1.9 N (2P = 0.006); MK size, 607 +/- 22 versus 579 +/- 16 (2P = 0.003); and lengthened cutaneous bleeding time, 424 +/- 86s versus 563 +/- 164s (2P = 0.011), in hypertensive patients. Losartan did not alter MK granularity or GP IIIa expression, or platelet count, size, mass, GP IIIa expression, or aggregation. The data suggest that platelet changes in hypertension may be secondary to changes in MKs, and that anti-hypertensive treatment can alter MKs and the function of platelets they produce. Since antihypertensive therapy reduces the risk of stroke and myocardial infarction, MKs are a novel therapeutic target for the prevention of vascular events.

Adult↗
PubMed2001

The effect of transdermal glyceryl trinitrate, a nitric oxide donor, on blood pressure and platelet function in acute stroke.

BACKGROUND AND PURPOSE: Hypertension is a common medical complication in acute stroke and is associated with a poor outcome. However, no large trials have assessed the effect of lowering blood pressure (BP) on outcome, and it remains unclear how BP should be managed in acute stroke. We assessed, in a double-blind randomised controlled trial, whether the nitric oxide (NO) donor glyceryl trinitrate (GTN, a known systemic and cerebral vasodilator), would lower BP and alter platelet function. METHODS: Thirty-seven patients with recent (< 5 days) ischaemic or haemorrhagic stroke were randomised by minimisation to 12 days of daily treatment with transdermal GTN or matching placebo patches. Twenty-four-hour ambulatory BP was measured before and during GTN treatment at days 0, 1 and 8. Platelet aggregation and expression of adhesion molecules were assessed at the same time points. Functional outcome (Rankin scale) and case fatality were assessed at 3 months. Analysis was by intention-to-treat. RESULTS: GTN significantly lowered BP by 13.0/5.2 mm Hg at day 1 and 9.3/5.0 mm Hg at day 8. The lesser reduction at day 8 than day 1 suggests that tolerance to GTN was developing. Non-significant falls of 0.9/0.6 and 3.8/0.0 mm Hg occurred at days 1 and 8, respectively, in the placebo group. GTN had no effect on heart rate, or platelet aggregation or expression of platelet adhesion molecules, including glycoproteins Ia, Ib, IIIa and P-selectin. Additionally, GTN did not alter case fatality or dependency, although the study was not powered for these outcomes. CONCLUSIONS: Transdermal GTN, an NO donor, lowered BP by 5-8%, a clinically significant and relevant, but not excessive, degree in patients with acute stroke. However, GTN had no effect on platelet aggregation or expression of adhesion molecules. Since NO donors increase cerebral blood flow in patients with acute ischaemic stroke, GTN may be an appropriate drug for testing the effect of lowering BP on functional outcome.

Administration, Cutaneous↗
PubMed2001

Quadriceps muscle weakness following acute hemiplegic stroke.

OBJECTIVE: To determine whether quadriceps muscle weakness develops on the side ipsilateral to the brain lesion in the first week following acute ischaemic hemiplegic stroke. DESIGN: A prospective study of muscle strength. SETTING: Acute stroke unit (ASU) in a teaching hospital. SUBJECTS: Ten patients admitted within 48 hours of stroke onset, and 10 healthy age-matched controls. INTERVENTIONS: Repeat nonvolitional measurements of quadriceps muscle strength of the unaffected limb in patients and the right leg in normal subjects using magnetic femoral nerve stimulation (MS), prospectively one week apart. In addition the level of voluntary activation was assessed during a maximum voluntary contraction (MVC) manoeuvre. The Trunk Control Test (TCT) was measured in the patients. RESULTS: The median (95% confidence interval, (CI)) baseline quadriceps twitch tension (Tw Q) and MVC in the control group were 9.4 kg (6.1-12.5 kg) and 37.2 kg (23.8-54.6 kg), and in the stroke group were 7.6 kg (4.4-9.9 kg) and 12.15 kg (7.9-30.8 kg). The median (95% CI) change in Tw Q and MVC respectively between baseline and one week later were 1.75% (-9.8 to 8%) and 5.45% (-15.1 to 22.7%) (NS) in the control group and -16.2% (-6 to -25.9%) and -30.45% (0 to -78.6%) (p < 0.01) in the stroke patients. There was a significant correlation between the percentage fall in Tw Q and both change in TCT (rs = 0.83, p < 0.01) and percentage change in body weight (rs = 0.83, p < 0.01). CONCLUSION: In the first week after acute hemiplegic stroke, weakness develops in the unaffected leg.

Aged↗
PubMed2000

Pentoxifylline, propentofylline and pentifylline for acute ischaemic stroke.

BACKGROUND: Methylxanthine derivatives are vasodilators. They also inhibit platelet aggregation and thromboxane A2 synthesis, decrease the release of free radicals and may be neuroprotective. OBJECTIVES: The objective of this review was to assess the effect of intravenous or oral methylxanthines (pentoxifylline, propentofylline, or pentifylline) in patients with acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register, Medline (from 1965), Embase (from 1981), ISI (from 1981) and the Ottawa stroke trials registry. We contacted drug companies. SELECTION CRITERIA: Randomised trials comparing pentoxifylline, propentofylline or pentifylline with placebo or control in patients with definite or presumed acute ischaemic stroke. Trials were included if treatment was started within one week of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the inclusion criteria. Trial quality was assessed. MAIN RESULTS: Five trials were included. Four trials tested pentoxifylline in 763 people, and one tested propentofylline in 30 people. No trials of pentifylline were found. Early death (within four weeks) occurred in 34 of 408 patients given a methylxanthine drug compared with 49 of 385 given placebo (odds ratio 0.64, 95% confidence interval 0.41 to 1.02). This non-significant trend to less deaths was due mainly to one pentoxifylline trial that found a highly significant reduction in early deaths. Two trials reported early death or disability and found a non-significant reduction (odds ratio 0.49, 95% confidence interval 0.20 to 1.20). Late death (beyond four weeks) was reported in the propentofylline trial involving 30 patients, with no difference between treatment and placebo (odds ratio 0.70, 95% confidence interval 0.13 to 3.68). Data for neurological impairment and disability were not in a form suitable for analysis. Data on quality of life, stroke recurrence, thromboembolism and bleeding were not reported. REVIEWER'S CONCLUSIONS: There is not enough evidence to assess the effectiveness and safety of methylxanthines after acute ischaemic stroke.

Brain Ischemia↗
PubMed2000

Prostacyclin and analogues for acute ischaemic stroke.

BACKGROUND: Prostacyclin is an agent with a number of effects on platelets, blood vessels and nerve cells which might improve outcome after acute ischaemic stroke. OBJECTIVES: The objective of this review was to assess the effect of prostacyclin or analogues on survival in people with acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register (last searched: March 1999), Medline (from 1965), Embase (from 1980) and ISI (from 1981). We contacted drug companies. SELECTION CRITERIA: Randomised trials comparing prostacyclin or analogues with placebo or control. Trials where people were entered within one week of stroke onset were included. DATA COLLECTION AND ANALYSIS: Trial quality was assessed. MAIN RESULTS: Five trials involving 191 people were included. Six early deaths (within four weeks) occurred with prostacyclin and nine with placebo (odds ratio of 0.63, 95% confidence interval 0.22 to 1.85). One trial of 32 patients reported late deaths (by 10 to 18 months) in 50% of patients in each group. REVIEWER'S CONCLUSIONS: Too few patients have been studied in randomised trials to allow conclusions to be drawn about the effect of prostacyclin treatment on survival of people with acute stroke.

Brain Ischemia↗
PubMed2000

Theophylline, aminophylline, caffeine and analogues for acute ischaemic stroke.

BACKGROUND: Theophylline causes potent cerebral vasoconstriction which decreases blood flow in the non-ischaemic areas of the brain and increases collateral blood flow surrounding the ischaemic region. OBJECTIVES: The objective of this review was to assess the effect of theophylline and its analogues (aminophylline and caffeine) in people with confirmed or presumed acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register (last searched: March 1999), Medline (from 1965), Embase (from 1980), and ISI (from 1981). We contacted drug companies. SELECTION CRITERIA: Randomised trials of theophylline or an analogue compound compared with placebo or control in people with confirmed or presumed acute ischaemic stroke. Trials were included if treatment was started within one week of stroke onset. DATA COLLECTION AND ANALYSIS: Three reviewers applied the inclusion criteria, assessed trial quality and extracted data. MAIN RESULTS: Two trials involving 119 patients were included. Trial quality was good. Both of the trials tested aminophylline. Analysis was by intention-to-treat where possible. No difference was shown in early death (within four weeks) between aminophylline and placebo (odds ratio 1.12, 95% confidence interval 0.49 to 2.56). There was no significant difference for early mortality and deterioration (odds ratio 0.87, 95% confidence interval 0.41 to 1.88). Death or disability was not reduced by treatment based on 73 patients in one trial (odds ratio 0.64, 95% confidence interval 0.24 to 1.68). Data for late mortality and disability were not in a form suitable for analysis. No data on quality of life were available. REVIEWER'S CONCLUSIONS: There is not enough evidence to assess whether theophylline or its analogues reduce mortality or morbidity, or are safe, in people with acute ischaemic stroke.

Aminophylline↗
PubMed2000

Interventions for dysphagia in acute stroke.

BACKGROUND: It is unclear how dysphagic patients should be fed and treated after acute stroke. OBJECTIVES: The objective of this review was to assess the effect of different management strategies for dysphagic stroke patients, in particular how and when to feed, whether to supplement nutritional intake, and how and whether to treat dysphagia. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register, Medline, Embase, ISI, and existing review articles. We contacted researchers in the field and equipment manufacturers. Date of the most recent searches: March 1999. SELECTION CRITERIA: Unconfounded truly or quasi randomised controlled trials in dysphagic patients with acute/subacute (within 3 months) stroke. DATA COLLECTION AND ANALYSIS: Three reviewers independently applied the trial inclusion criteria. Two reviewers assessed trial quality and extracted the data. MAIN RESULTS: Percutaneous endoscopic gastrostomy (PEG) versus nasogastric tube (NGT) feeding: two trials (49 patients) suggest that PEG reduces end-of-trial case fatality (Peto Odds Ratio, OR 0.28, 95% CI 0.09 to 0.89) and treatment failures (OR 0.10, 95% CI 0.02 to 0.52), and improves nutritional status, assessed as weight (Weighted Men Difference, WMD +4.1 kg, 95% CI -4.3 to +12.5), mid-arm circumference (WMD +2.2 cm, 95% CI -0.5 to +4.9) or serum albumin (WMD + 7.0 g/l, 95% CI +4.9 to +9.1) as compared with NGT feeding; two larger studies are ongoing. Timing of feeding: no completed trials; one large study is ongoing. Swallowing therapy for dysphagia: two trials (85 patients) suggest that formal swallowing therapy does not significantly reduce end-of-trial dysphagia rates (OR 0.55, 95% CI 0.18 to 1.66). Drug therapy for dysphagia: one trial (17 patients); nifedipine did not alter end-of-trial case fatality or the frequency of dysphagia. Nutritional supplementation: one trial (42 patients) found a non-significant trend to a lower case fatality, and significantly increased energy and protein intake; one large trial is ongoing and data is awaited from two other studies. Fluid supplementation: one trial (20 patients) found that supplementation did not alter the time to resolution of dysphagia. REVIEWER'S CONCLUSIONS: Too few studies have been performed, and these have involved too few patients. PEG feeding may improve outcome and nutrition as compared with NGT feeding. Further research is required to assess how and when patients are fed, and the effect of swallowing or drug therapy on dysphagia.

Deglutition Disorders↗
PubMed2000

Nitric oxide donors (nitrates), L-arginine, or nitric oxide synthase inhibitors for acute ischaemic stroke.

BACKGROUND: Nitric oxide has several effects that may be beneficial in ischaemic stroke and useful in the management of hypertension in acute stroke. Some forms of nitric oxide synthase inhibition may also be beneficial. However, high concentrations of nitric oxide are likely to be toxic to brain tissue. OBJECTIVES: The objective of this review was to assess the effects of nitric oxide donors, L-arginine, or nitric oxide synthase-inhibitors in people with acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register (July 1997), Medline (for trials from 1965), Embase (from 1980) and ISI (from 1981). We contacted drug companies and researchers in the field. SELECTION CRITERIA: Randomised and quasi-randomised trials comparing nitric oxide donors, L-arginine, or nitric oxide synthase-inhibitors in patients within one week of onset of confirmed ischaemic stroke. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the inclusion criteria. MAIN RESULTS: No completed trials were found. One small placebo-controlled trial of glyceryl trinitrate patches is underway. REVIEWER'S CONCLUSIONS: There is currently no evidence from randomised trials on the effects of nitric oxide donors, L-arginine, or nitric oxide synthase-inhibitors in patients with acute ischaemic stroke.

Arginine↗
PubMed2000

Hypertension in patients presenting with stroke.

Hypertension is a major risk factor for stroke disease. There is now some international agreement on what constitutes hypertension, and at what level of blood pressure treatment is required. Large randomised controlled trials demonstrate the benefit of reducing blood pressure for the primary and secondary prevention of stroke disease. Studies have also demonstrated the benefit of particular classes of antihypertensive agents in certain patient groups. Research is beginning to elucidate the problems of hypertension in the acute phase of ischaemic stroke and the therapeutic strategies that may be helpful. Given the significant impact of stroke disease on all health services, it remains an important priority to determine the best management of hypertension in stroke.

Antihypertensive Agents↗
PubMed2000

Low-molecular-weight heparins and heparinoids in acute ischemic stroke : a meta-analysis of randomized controlled trials.

BACKGROUND AND PURPOSE: Low-molecular-weight heparins and heparinoids (LMWHs) are superior to unfractionated heparin in the prevention and treatment of venous thromboembolism and acute coronary syndromes. We performed a systematic review of randomized controlled trials (RCTs) to examine the safety and efficacy of LMWH in acute ischemic stroke. METHODS: Randomized, controlled, and nonconfounded trials of LMWH in acute ischemic stroke were identified from the Cochrane Library (version 2, 1999), previous systematic reviews, and a review of publication quality relating to acute stroke trials. The authors each independently extracted data by treatment group and assessed trial quality using Cochrane Collaboration criteria. RESULTS: Eleven completed RCTs involving 3048 patients were identified; data were available from 10 of these. Four trials explicitly excluded patients with presumed cardioembolic stroke. Treatment with LMWH was associated with significant reductions in prospectively identified deep vein thrombosis (OR 0.27, 95% CI 0.08 to 0.96) and symptomatic pulmonary embolism (OR 0.34, 95% CI 0.17 to 0.69) and with increased major extracranial hemorrhage (OR 2.17, 95% 1.10 to 4.28). Nonsignificant increases in end-of-treatment (OR 1.20, 95% CI 0.86 to 1.69) and end-of-trial (OR 1.05, 95% CI 0.83 to 1.32) case fatality and symptomatic intracranial hemorrhage (OR 1.77, 95% CI 0. 95 to 3.31) were observed. End-of-trial death and disability was nonsignificantly reduced (OR 0.87, 95% CI 0.72 to 1.06). CONCLUSIONS: ++LMWHs reduce venous thromboembolic events in patients with acute ischemic stroke and increase the risk of extracranial bleeding. A nonsignificant reduction in combined death and disability and nonsignificant increases in case fatality and symptomatic intracranial hemorrhage were also observed. On the basis of the current evidence, LMWH should not be used in the routine management of patients with ischemic stroke.

Acute Disease↗
PubMed2000

Optimising homeostasis.

There is a wealth of experimental and clinical information showing that hypertension, hyperglycaemia, hyperthermia and intracranial hypertension are each independent indicators of a poor prognosis after stroke, but there is an astonishing lack of evidence from randomised controlled trials to tell us how to manage these problems, bearing in mind their frequency in stroke patients. The therapeutic options will, in most cases, not involve patented drugs, and financial support for running the necessary randomised controlled trials will have to come from government or charity sponsors rather than from the pharmaceutical industry. It is vital that academic researchers now devise studies of appropriate design and size to answer these important questions. In the absence of randomised data, severe hyperglycaemia and pyrexia should be treated, whilst acute hypertension is probably best left untreated unless very severe or complicated by other medical conditions. The management of cerebral oedema remains an enigma.

Fever↗