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Background: Mapping high oxygen extraction fraction (OEF) in acute stroke is of considerable interest to depict the at-risk tissue. Being sensitive to deoxyhemoglobin, T2*-weighted MRI has been suggested as a potential marker of high OEF. Methods: We compared T2*-weighted images from pre-contrast arrival perfusion scans against quantitative positron emission tomography in 5 patients studied 7–21 h after onset of carotid territory stroke. OEF and T2* signal were obtained in the voxels with significantly high OEF. Results: All patients showed increased OEF. No significant relationship between OEF and T2*-weighted signal was found either within or between subjects. Conclusion: We found no indication that T2*-weighted MRI in the way implemented in this investigation was sensitive to high OEF in acute stroke. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Preventing death and limiting handicap from ischaemic stroke are major goals that can be achieved only if the pathophysiology of infarct expansion is properly understood. Primate studies showed that following occlusion of the middle cerebral artery (MCA)––the most frequent and prototypical stroke, local tissue fate depends on the severity of hypoperfusion and duration of occlusion, with a fraction of the MCA territory being initially in a ‘penumbral’ state. Physiological quantitative PET imaging has translated this knowledge in man and revealed the presence of considerable pathophysiological heterogeneity from patient to patient, largely unpredictable from elapsed time since onset or clinical deficit. While these observations underpinned key trials of thrombolysis, they also indicate that only patients who are likely to benefit should be exposed to its risks. Accordingly, imaging-based diagnosis is rapidly becoming an essential component of stroke assessment, replacing the clock by individually customized management. Diffusion- and perfusion-weighted MR (DWI-PWI) and CT-based perfusion imaging are increasingly being used to implement this, and are undergoing formal validation against PET. Beyond thrombolysis per se, knowledge of the individual pathophysiology also guides management of variables like blood pressure, blood glucose and oxygen saturation, which can otherwise precipitate the penumbra into the core, and the oligaemic tissue into the penumbra. We propose that future therapeutic trials use physiological imaging to select the patient category that best matches the drug's presumed mode of action, rather than lumping together patients with entirely different pathophysiological patterns in so-called ‘large trials’, which have all failed so far.British Journal of Pharmacology (2008) 153, S44–S54; doi:10.1038/sj.bjp.0707530; published online 26 November 2007 [ABSTRACT FROM AUTHOR]

Because it is the main determinant of clinical recovery, early reperfusion of the ischemic penumbra has become the mainstay of acute stroke therapy. Although early permanent recanalization can be associated with spectacular and complete recovery, some patients in fact exhibit delayed or incomplete recovery, even despite small infarcts on late structural imaging. This might result from tissue inflammation and selective neuronal death/damage, two probably inter-related cellular events well described in the animal literature, precluding full functional restoration in the salvaged penumbra. However, impact of these processes on recovery may be complex because of the interplay with ongoing plasticity and the possible promoting effect of inflammation on the latter. Preliminary results from imaging studies of inflammation and selective neuronal loss after middle cerebral artery territory stroke, using radioligands of the central benzodiazepine receptor and the activated microglia, respectively, reviewed here, suggest these phenomena also exist in man, although their relationship with acute-stage hypoperfusion and their impact on clinical recovery, if any, remain poorly understood. Furthermore, their inter-relationships in the salvaged penumbra have not been addressed. Better understanding of these potentially harmful processes might help to maximize benefits from thrombolysis, and could also have implications for patients who enjoy spontaneous recanalization. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Recent years have seen major advances in the imaging of cerebrovascular disease. Although quantitative positron emission tomography (PET) has continued to be the gold standard in acquiring functional imaging data, with recent developments continuing to bear fruit, it remains a complex, costly, and not readily available technique. The emphasis in this overview is in the development of the newer magnetic resonance (MR) techniques, such as diffusion-weighted (DWI) and perfusion-weighted imaging (PWI), which allow rapid assessment of the underlying pathophysiology in acute ischaemic stroke. This is of major importance in classifying patients according to pathophysiology rather than clinical and structural imaging data, which may be essential in deciding therapy such as thrombolysis (which has proven benefit within 3–6 h of clinical onset, but can also lead to harmful haemorrhagic transformation) and/or neuroprotection, as well as patient selection in clinical trials. In conjunction with magnetic resonance angiography (MRA), DWI-PWI has been shown to improve the diagnosis and clinical management of stroke. Other novel MR techniques which have yet to reach the clinician, such as spectroscopic imaging, diffusion tensor imaging (DTI) and blood oxygenation level-dependent functional MRI (BOLD-fMRI), are currently established research tools which provide data about infarct evolution, fibre disruption and the mechanisms of stroke recovery. Electrophysiological methods including transcranial magnetic stimulation (TMS) and magneto-encephalography (MEG) will not be addressed here. [ABSTRACT FROM AUTHOR]

We report the rare presentation of lacunar stroke syndrome secondary to single perforator mouth occlusion from radiation-induced middle cerebral artery (MCA) stem arteriopathy. A 30-year-old female had acute-onset right-sided ataxic hemiparesis and dysarthria. As a child, she had a medulloblastoma of the posterior fossa and had surgery followed by cranial radiotherapy. She had no significant vascular risk factors. Acute CT showed extensive bilateral basal ganglia and left thalamic calcification; DWI showed a left internal capsule lacunar infarct; and MRA and CTA showed a 50% stenosis of the proximal left MCA. [ABSTRACT FROM AUTHOR]

Current guidelines on thrombolysis post stroke with recombinant tissue plasminogen activator (rt-PA) exclude its use where time of onset is unknown, thus denying some patients potentially beneficial treatment. Contrast enhanced perfusion computed tomography (pCT) imaging can be used together with plain CT and information on clinical deficits to decide whether or not thrombolysis should be initiated even though the exact time of stroke onset is unknown. Based on the results of pCT and CT, rt-PA was administered to two patients with unknown time of stroke onset; one of the patients also underwent suction thrombectomy. Results in both cases were excellent. [ABSTRACT FROM AUTHOR]

This article focuses on tools to quantify secondary degeneration after stroke and monitor effects of intervention. Researchers monitored in two patients the time course of Wallerian degeneration (WD) of the pyramidal tract following striatocapsular stroke. Diffusion tensor imaging was obtained on three occasions from the subacute into the chronic stage. They found a progressive decrease of the fractional anisotropy (FA) with an increase in mean diffusivity (MD) in the pyramidal tract at the level of the cerebral peduncle, reflecting the changes expected in WD-a progressive disintegration of fibre structure. They found significant increases in MD from 1 month onward, without parallel changes in FA, presumably reflecting a progressive loss of neurons and glial cells.

The article focuses on the identification of patients at high risk of subsequent stroke to implement appropriate prevention. Although atherothrombotic occlusion of the internal carotid artery can cause a devastating stroke. In many instances it is a benign event, causing only transient ischaemic attacks, a minor stroke, or even no symptom at all. The presence of ophthalmic or leptomeningeal collaterals in a patient with no striatocapsular infarct accurately predicts increased oxygen extraction fraction, and in turn a high risk of subsequent ipsilateral stroke.

A letter to the editor is presented in response to the article about aortic plaque inflammation as a potential cause of stroke that was published in the previous issue of the periodical.