Recovery of cerebral autoregulation during the first three months after acute ischaemic stroke

Recovery of cerebral autoregulation during the first three months after acute ischaemic stroke - A longitudinal study using transcranial Doppler ultrasonography by Dr Joseph Shiu Kwong Kwan Cerebral autoregulation (CA) is a mechanism that maintains a constant cerebral blood flow over wide ranges of blood pressure (BP). CA is impaired after stroke and changes in cerebral blood flow may become passive to changes in BP. Manipulation of BP after stroke may worsen regional cerebral blood flow with possible clinical implications. However, little is known about the recovery of CA soon after stroke. In this study, we used transcranial Doppler (TCD) to examine the recovery of CA after ischaemic stroke. We studied ten stroke patients and eleven controls. Each patient was examined within seven days, at six weeks, and at three months. For each examination, cerebral blood flow velocity (CBFV) and BP were continuously recorded by bilateral TCD and Finapres, respectively. We examined the relationship between spontaneous oscillations of BP and CBFV, and between induced BP oscillations (by rhythmic handgrip) and CBFV, using cross-spectral transfer function analysis (calculation of phase, gain, and coherence). We demonstrated that, using rhythmic handgrip, CA changes over the first three months after stroke, although no difference was found between patients and controls. Moreover, these changes appear to affect the hemisphere contralateral to the ischaemia, which suggests that disturbances in cerebral haemodynamics after stroke may be global in nature. We also found that the competence of CA was dependent on the frequency of BP oscillations. This indicates that CA behaves as a high-pass filter system, even after ischaemic stroke. The combination of TCD and rhythmic handgrip appear to be a useful non-invasive method of assessing CA after stroke. This technique may become a useful clinical tool in the future.</p

Cerebral microbleeds and stroke risk after ischaemic stroke or transient ischaemic attack:a pooled analysis of individual patient data from cohort studies

BACKGROUND Cerebral microbleeds are a neuroimaging biomarker of stroke risk. A crucial clinical question is whether cerebral microbleeds indicate patients with recent ischaemic stroke or transient ischaemic attack in whom the rate of future intracranial haemorrhage is likely to exceed that of recurrent ischaemic stroke when treated with antithrombotic drugs. We therefore aimed to establish whether a large burden of cerebral microbleeds or particular anatomical patterns of cerebral microbleeds can identify ischaemic stroke or transient ischaemic attack patients at higher absolute risk of intracranial haemorrhage than ischaemic stroke. METHODS We did a pooled analysis of individual patient data from cohort studies in adults with recent ischaemic stroke or transient ischaemic attack. Cohorts were eligible for inclusion if they prospectively recruited adult participants with ischaemic stroke or transient ischaemic attack; included at least 50 participants; collected data on stroke events over at least 3 months follow-up; used an appropriate MRI sequence that is sensitive to magnetic susceptibility; and documented the number and anatomical distribution of cerebral microbleeds reliably using consensus criteria and validated scales. Our prespecified primary outcomes were a composite of any symptomatic intracranial haemorrhage or ischaemic stroke, symptomatic intracranial haemorrhage, and symptomatic ischaemic stroke. We registered this study with the PROSPERO international prospective register of systematic reviews, number CRD42016036602. FINDINGS Between Jan 1, 1996, and Dec 1, 2018, we identified 344 studies. After exclusions for ineligibility or declined requests for inclusion, 20 322 patients from 38 cohorts (over 35 225 patient-years of follow-up; median 1·34 years [IQR 0·19-2·44]) were included in our analyses. The adjusted hazard ratio [aHR] comparing patients with cerebral microbleeds to those without was 1·35 (95% CI 1·20-1·50) for the composite outcome of intracranial haemorrhage and ischaemic stroke; 2·45 (1·82-3·29) for intracranial haemorrhage and 1·23 (1·08-1·40) for ischaemic stroke. The aHR increased with increasing cerebral microbleed burden for intracranial haemorrhage but this effect was less marked for ischaemic stroke (for five or more cerebral microbleeds, aHR 4·55 [95% CI 3·08-6·72] for intracranial haemorrhage vs 1·47 [1·19-1·80] for ischaemic stroke; for ten or more cerebral microbleeds, aHR 5·52 [3·36-9·05] vs 1·43 [1·07-1·91]; and for ≥20 cerebral microbleeds, aHR 8·61 [4·69-15·81] vs 1·86 [1·23-1·82]). However, irrespective of cerebral microbleed anatomical distribution or burden, the rate of ischaemic stroke exceeded that of intracranial haemorrhage (for ten or more cerebral microbleeds, 64 ischaemic strokes [95% CI 48-84] per 1000 patient-years vs 27 intracranial haemorrhages [17-41] per 1000 patient-years; and for ≥20 cerebral microbleeds, 73 ischaemic strokes [46-108] per 1000 patient-years vs 39 intracranial haemorrhages [21-67] per 1000 patient-years). INTERPRETATION In patients with recent ischaemic stroke or transient ischaemic attack, cerebral microbleeds are associated with a greater relative hazard (aHR) for subsequent intracranial haemorrhage than for ischaemic stroke, but the absolute risk of ischaemic stroke is higher than that of intracranial haemorrhage, regardless of cerebral microbleed presence, antomical distribution, or burden. FUNDING British Heart Foundation and UK Stroke Association