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Dive into the research topics where Peter Sandercock is active.

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Featured researches published by Peter Sandercock.


Stroke | 1990

Are hypertension or cardiac embolism likely causes of lacunar infarction

J. Lodder; John Bamford; Peter Sandercock; L. N. Jones; Charles Warlow

We tested the hypothesis that hypertension is more common and cardiac embolism less common in patients with lacunar infarction than in patients with other types of cerebral infarction. We studied risk factor profiles in a series of 102 consecutive patients with a lacunar infarct and 202 consecutive patients with a carotid artery-distribution infarct involving the cortex registered in the Oxfordshire Community Stroke Project, a community-based study of first-ever stroke. The two groups did not differ in the prevalence of prestroke hypertension (defined in a number of ways) or in the prevalence of markers of sustained hypertension. The presence of atrial fibrillation and a history of myocardial infarction, particularly during the 6 weeks before the stroke, were significantly more common in the group with carotid-distribution infarcts involving the cortex. There was no significant difference in the prevalence of other accepted risk factors for ischemic stroke, including previous transient ischemic attack, cervical bruit, diabetes mellitus, peripheral vascular disease, or cigarette smoking. Our results suggest that hypertension is no more important in the development of lacunar infarction than it is in the development of other types of ischemic stroke that are presumed to be due to atherosclerotic thromboembolism in a major cerebral artery. Our data support the autopsy evidence that cardioembolic occlusion is an unusual cause of lacunar infarction.


BMJ | 1989

Predisposing factors for cerebral infarction: the Oxfordshire community stroke project.

Peter Sandercock; Charles Warlow; L N Jones; Ian R. Starkey

The frequency of known causative factors of cerebral infarction was studied in 244 cases of first ever stroke due to cerebral infarction proved by computed tomography or at necropsy who were registered in the first two years of a prospective community based study. Risk factors for cerebral infarction were present in 196 (80%) cases; hypertension in 126 (52%); ischaemic heart disease in 92 (38%); peripheral vascular disease in 60 (25%); a cardiac lesion that was a major potential source of embolism to the brain in 50 (20%); transient ischaemic attacks in 35 (14%); cervical arterial bruit in 33 (14%); and diabetes mellitus in 24 (10%). Thirty one patients (13%) were in atrial fibrillation. Of the 48 patients who were free of risk factors or a major potential cardiac source of embolism at the time of the stroke, 18 were found to have hypertension after the stroke and 10 to have non-atheromatous non-embolic conditions (migrainous cerebral infarction (three), arteritis (two), inflammatory bowel disease (one), arterial trauma (one), autoimmune disease (one), carcinoma of the thyroid (one), and major operation (one). In 20 patients no causative factors could be identified. In this unselected series of patients with first ever stroke due to cerebral infarction most of the strokes were presumed to be due to either atheromatous arterial disease or embolism from the heart, and only 4% (95% confidence interval 2 to 7%) were probably due to non-atheromatous non-embolic causes. This has implications for research into strokes and allocation of public health expenditure.


Stroke | 2001

Variations Between Countries in Outcome After Stroke in the International Stroke Trial (IST)

N U Weir; Peter Sandercock; Steff Lewis; D F Signorini; Charles Warlow

Background and Purpose— This study describes the large variations in outcome after stroke between countries that participated in the International Stroke Trial and seeks to define whether they could be explained by variations in case mix or by other factors. Methods— We analyzed data from the 15 116 patients recruited in Argentina, Australia, Italy, the Netherlands, Norway, Poland, Sweden, Switzerland, and the United Kingdom. We compared crude case fatality and the proportion of patients dead or dependent at 6 months; we used logistic regression to adjust for age, sex, atrial fibrillation, systolic blood pressure, level of consciousness, and number of neurological deficits. We used the frequency of prerandomization head CT scan and prescription of aspirin at discharge to indicate quality of care. Results— The differences in outcome (all treatment groups combined) between the “best” and “worst” countries were very large for death (171 cases per 1000 patients) and for death or dependency (375 cases per 1000 patients). The differences were somewhat smaller after adjustment for case mix (160 and 311 cases per 1000 patients, respectively). Process of care may have accounted for some but not all of the residual variation in outcome. Conclusions— Adjustment for case mix explained only some of the variation in outcome between countries. The residual differences in outcome were too large to be explained by variations in care and most likely reflect differences in unmeasured baseline factors. These findings demonstrate the need to achieve balance of treatment and control within each country in multinational randomized controlled stroke trials and the need for caution in the interpretation of nonrandomized comparisons of outcome after stroke between countries.


BMJ | 1985

Clinical diagnosis of intracranial haemorrhage using Guy's Hospital score.

Peter Sandercock; C. M. C. Allen; R. N. Corston; M. J. G. Harrison; Charles Warlow

We tested the Guys Hospital stroke diagnostic score using the clinical data from two independent samples of patients with acute stroke. These were 228 patients from the Oxfordshire community stroke project and 130 referred to the National Hospital for Nervous Diseases in London. The diagnosis was confirmed by computed tomography or necropsy in each case. The optimum cut off point on the clinical score for the differentiation of intracranial haemorrhage from infarction was found to be the same for both the patients in our study and those from whose data the score was derived originally. Set at this level, the score achieved a sensitivity for the diagnosis of haemorrhage of 81% and 88% in the patients from Oxford and London, respectively. In those from Oxford infarction was diagnosed with a sensitivity of 78% with an overall predictive accuracy of 78% with an overall London the sensitivity for infarction was also 78% with an overall predictive accuracy of 82%. When it is essential to exclude intracerebral blood before starting treatment in the small proportion of patients with stroke who require anticoagulation the Guys Hospital score is not sufficiently accurate to replace computed tomography. The score is, however, the most accurate clinical means of differentiating haemorrhage from infarction as the cause of stroke. It is suggested that it should be used as a screening test in epidemiological studies and in large scale trials of low risk treatment for the secondary prevention of stroke when computed tomography in all cases is impracticable.


Angiology | 2012

Why the US Center for Medicare and Medicaid Services should not extend reimbursement indications for carotid artery angioplasty/stenting.

Anne L. Abbott; Mark A. Adelman; Andrei V. Alexandrov; Henry J. M. Barnett; Jonathan Beard; Peter R.F. Bell; Martin Björck; David Blacker; Clifford J. Buckley; Richard P. Cambria; Anthony J. Comerota; E.S. Connolly; Alun H. Davies; Hans-Henning Eckstein; Rishad Faruqi; Gustav Fraedrich; Peter Gloviczki; Graeme J. Hankey; Robert E. Harbaugh; Eitan Heldenberg; Steven J. Kittner; Timothy J. Kleinig; Dimitri P. Mikhailidis; Wesley S. Moore; Ross Naylor; Andrew N. Nicolaides; Kosmas I. Paraskevas; David M. Pelz; James W. Prichard; Grant Purdie

Why the US Center for Medicare and Medicaid Services Should Not Extend Reimbursement Indications for Carotid Artery Angioplasty/Stenting


BMJ | 1984

Effects of treatment for hypertension on cerebral haemorrhage and infarction.

Peter Sandercock; Charles Warlow; Lesley Jones

Surgeons attempting curative surgery for stomach cancer would not intentionally leave behind macroscopic disease. Histological evidence of resection line disease must therefore represent submucosal spread undetectable to the naked eye. The ability of a cancer to spread submucosally must represent a biological property of that cancer, which might be a sensitive predictor of subclinical distant metastases. The resection line disease therefore could be an expression rather than a determinant of the bad prognosis. This point might be clarified if the authors could show whether those patients with resection line disease were dying from an increased incidence of distant metastases or as a direct result of the mechanical problems from local recurrence. In the meantime, attempts to clear resection margins by resecting 6-12 cm of apparently normal tissue beyond the macroscopic edge of the cancer will inevitably increase the operative morbidity and mortality. Of course, I could be wrong but these considerations surely indicate the need for a randomised controlled trial comparing macroscopic resection of a stomach cancer versus a more radical approach aimed at producing margins free of microscopic disease. I would wager good money that the latter approach would increase the operative mortality and reduce complications from suture line recurrence but fail to influence mortality from distant metastases. MICHAL BAUm


Archive | 2014

Critical appraisal tools

Joanna Wardlaw; Miriam Brazzelli; Hector Miranda; Francesca M. Chappell; Paul McNamee; Graham Scotland; Zahid Quayyum; Duncan Martin; Kirsten Shuler; Peter Sandercock; Martin Dennis


Stroke: Practical Management, Third Edition | 2008

Is it a Vascular Event and Where is the Lesion?: Identifying and Interpreting the Symptoms and Signs of Cerebrovascular Disease

Charles Warlow; J. van Gijn; Martin Dennis; Joanna Wardlaw; J. Bamford; Graeme J. Hankey; Peter Sandercock; G. J. E. Rinkel; Peter Langhorne; C. Sudlow; Peter M. Rothwell


BMJ | 2011

Thrombolysis in elderly people. Observational data insufficient to change treatment.

Richard Lindley; Joanna Wardlaw; Peter Sandercock


Archive | 2014

Strengthening the Reporting of Observational studies in Epidemiology (STROBE) checklist

Joanna Wardlaw; Trevor Carpenter; Eleni Sakka; Grant Mair; Geoff Cohen; Kirsten Shuler; Jeb Palmer; Karen Innes; Peter Sandercock

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Joanna Wardlaw

Singapore General Hospital

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J. Bamford

Southampton General Hospital

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