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Introduction: Small primary intracerebral haemorrhages (PICHs) cause mild stroke symptoms and resolve rapidly on CT. Delays in imaging in stroke incidence studies may therefore have inadvertently led to an underestimate of the frequency of small PICHs. Objective: To determine whether the rate and timing of CT in community-based stroke incidence studies was adequate to determine accurately the proportion of strokes due to PICH. Methods: A systematic review of community-based stroke incidence studies that included details on pathological type of stroke, excluding subarachnoid haemorrhage. We extracted information on the proportions of patients scanned, the timing of scans, characteristics of patients that were less likely to be scanned, and the proportion of ischaemic, or haemorrhagic, or unknown strokes. Results: In the 25 studies identified, scanning methods were poorly documented. When mentioned, the median proportion of patients scanned was 63 % (95 % confidence intervals (CI) 60 to 85 %) and mostly performed outside the time for reliable distinction of PICH from ischaemic stroke (median 18.5 days, 95 % CI 7 to 30 days). Patients particularly likely to miss scanning were older, those not admitted to hospital or who died early after stroke. Conclusion: The scanning strategy documentation, the proportion of patients scanned and the timing of scanning in stroke incidence studies has been suboptimal. The frequency of a primary intracerebral haemorrhage, and its distribution in different age groups of patients or severities of stroke, has been underestimated. Future incidence studies should adopt more rigorous scanning policies and describe these policies more precisely.

Objectives Lacunar infarcts are thought to be mostly due to intracranial small vessel disease. Therefore, when a stroke patient with a relevant lacunar infarct does have severe ipsilateral internal carotid artery (ICA) or middle cerebral artery (MCA) disease, it is unclear whether the arterial disease is causative or coincidental. If causative, we would expect ICA/MCA disease to be more severe on the symptomatic side than on the asymptomatic side. Therefore, our aim was to compare the severity of ipsilateral with contralateral ICA and MCA disease in patients with lacunar ischaemic stroke. Methods We studied 259 inpatients and outpatients with a recent lacunar ischaemic stroke and no other prior stroke. We used carotid Duplex ultrasound and transcranial Doppler (TCD) ultrasound to identify ICA and MCA disease, and compared our results with previously published data. Results In our study, there was no difference between the severity of ipsilateral and contralateral ICA stenosis within individuals (median difference 0 %, Wilcoxon paired data p=0.24, comparing severity of ipsilateral and contralateral stenosis). The overall prevalence of severe ipsilateral stenosis was 5 %, and the prevalence of severe contralateral stenosis was 4 % (OR 1.6, 95 % CI 0.6, 4.8). There was no difference in the prevalence of ipsilateral and contralateral MCA disease. A systematic review of the other available studies strengthened this conclusion. Conclusion Carotid stenosis in patients with a lacunar ischaemic stroke may be coincidental. Further studies are required to elucidate the causes of lacunar stroke, and to evaluate the role of carotid endarterectomy.

Borderzone infarcts are usually regarded as being caused by low cerebral blood flow distal to a severely stenosed or occluded artery, particularly the internal carotid artery. To explore this hypothesis we have related borderzone infarction, defined by CT both in the classical way and by taking into account the variable extent of the territory of the blood supply of the cerebral arteries, to the severity of any disease of the symptomatic artery in 384 patients in the European Carotid Surgery Trial in whom a scan showing infarction was available. Although there was a tendency for borderzone infarction to occur more often distal to severe carotid disease, this was not significant, and many cases of borderzone infarcts occurred in patients with mild or moderate carotid disease. Therefore, the topography of infarction on CT cannot be used to imply a particular pathophysiology based on the severity of disease of the artery supplying that area of the brain. Severe carotid stenosis is neither sufficient nor necessary to produce borderzone infarction. However, it has to be emphasized that patients with carotid occlusion are not included in this study.

The aim of the study reported here was to test the validity of a simple clinical classification of acute ischaemic stroke (Oxfordshire Community Stroke Project, OCSP) in predicting the site and size of cerebral infarction on computed tomography (CT). Consecutive patients admitted to hospital with acute ischaemic stroke were prospectively identified and classified into one of four clinical syndromes according to the OCSP classification, blind to the result of CT. The CT brain scans were classified blind to the clinical features into those demonstrating: small, medium or large cortical infarcts; small or large subcortical infarcts in the anterior circulation territory; and posterior cerebral circulation territory infarcts. A total of 108 patients were included. A recent infarct was seen on the CT scan in 91 patients (84%), and the clinical classification correctly predicted the site and size of the cerebral infarct in 80 of these (88%; 95% confidence interval 77-92%). The positive predictive value was best for large cortical infarcts (0.94) and worst for small subcortical infarcts (0.63). The OCSP clinical classification is a reasonably valid way of predicting the site and size of cerebral infarction on CT and can, therefore, be used very early after stroke onset before the infarct appears on the scan.

Anticardiolipin antibodies (aCL), one of a group of antiphospholipid antibodies which include the lupus anticoagulant (LA), may occur in association with systemic lupus erythematosus (SLE) and are less commonly detected in other diseases. We retrospectively reviewed the clinical and immunological features of 39 consecutive patients with abnormal aCL identified by one laboratory, to examine the spectrum of neurological disease in those patients without SLE. Fourteen patients in this category are described, 6 of whom did not have evidence of LA. All but 1 presented with neurological symptoms. Stroke and migraine dominated the clinical presentation, but many patients had features to suggest the presence of a hypercoagulable state. This study lends support to the concept of a primary antiphospholipid syndrome.

A total of 323 cases of first-ever stroke were registered in the first 2 years of the Oxfordshire Community Stroke Project. Of these patients, 244 (76%) had a stroke due to cerebral infarction. There was a past history of migraine headaches in 56 (17%) of the 323 cases of stroke and in 44 (18%) of the 244 cases of cerebral infarction. A past history of migraine headaches was no commoner in patients with stroke due to cerebral infarction than in those with stroke due to intracranial haemorrhage. One hundred and seventy-three (71%) patients with cerebral infarction had at least one risk factor for ischaemic stroke; the frequency of such risk factors was similar in patients with and without a history of migraine. In 7 (3%) of the 244 patients the cerebral infarction was presumed to be "migrainous"; however, only 3 of these 7 (1.2% of the 24) were free of risk factors for ischaemic stroke. If all 7 cases were considered migrainous, the incidence rate of first migrainous cerebral infarction was 3.36 per 100,000 per year (95% confidence limits 0.87-5.86). If only the 3 patients who were free of risk factors were included, the incidence was 1.44 per 100,000 per year (95% confidence limits 0-3.07).

In a group of 75 patients under the age of 45 years with stroke, ischaemic cerebral infarction was diagnosed in 60 patients and primary intracerebral haemorrhage in 15. Trauma was found to be the commonest identifiable predisposing factor to cerebral infarction, being present in 13 cases (22%). Migraine was the second most commonly identified predisposing factor while atheroma and hypertension were infrequent. Such a high frequency of preceding trauma has not previously been described, perhaps because it is not generally appreciated that the delay between the traumatic event and subsequent stroke may be considerable. The diagnostic management of young stroke patients is considered with particular reference to the indications for specialized cardiac and neuroradiological investigations.

Rupture of a mycotic aneurysm often occurs before the diagnosis of bacterial endocarditis is made or whilst the patient is being treated with antibiotics. It is recognised that cerebral embolism continues to occur after adequate antibiotic treatment, but the late rupture of a mycotic aneurysm seems to be very unusual. We report such a case where rupture of a peripherally sited aneurysm, demonstrated angiographically and pathologically, occurred 6 months after bacteriologically adequate treatment of streptococcal bacterial endocarditis.