Repetitive TMS has beneficial effects on motor recovery that can be translated to clinically meaningful improvement in disability in patients with post-stroke hemiparesis, with a well-sustained effect. The similarity of inhibitory and stimulatory rTMS in producing these effects supports the inter-hemispheric balance hypothesis and encourages further research into their use in long-term neurorehabilitation programmes of patients with stroke.

Background and Purpose-Early neurological deterioration (END) is a relatively common unfavorable course after anterior circulation ischemic stroke that can lead to worse clinical outcome. None of the END predictors identified so far is sufficiently reliable to be used in clinical practice and the mechanisms underlying END are not fully understood. We review the evidence from the literature for a role of hemodynamic and perfusion abnormalities, more specifically infarction of the oligemia, in END. Summary of Review-After an overview of the neuroimaging, including perfusion imaging, predictors of END, we review the putative mechanisms of END with a special focus on hemodynamic factors. The evidence relating perfusion abnormalities to END is addressed and potential hemodynamic mechanisms are suggested. Conclusions-Hemodynamic factors and perfusion abnormalities are likely to play a critical role in END. Infarction of the oligemic tissue surrounding the penumbra could be the putative culprit leading to END as a result of perfusion, but also physiological and biochemical abnormalities. Further studies addressing the role of the oligemia in END and developing measures to protect its progression to infarction are now needed. (Stroke. 2009;40:e443-e450.)

Background and Purpose-Nitroimidazole imaging is a promising contender for noninvasive in vivo mapping of brain hypoxia after stroke. However, there is a dearth of knowledge about the behavior of these compounds in the various pathophysiologic situations encountered in ischemic stroke. In this article we report the findings from a systematic review of the literature on the use of the nitroimidazoles to map hypoxia after stroke. Summary of Review-We describe the characteristics of nitroimidazoles as imaging tracers, their pharmacology, and results of both animal and clinical studies during and after focal cerebral ischemia. Findings in brain tumors are also presented to the extent that they enlighten results in stroke. Early results from application of kinetic modeling for quantitative measurement of tracer binding are briefly discussed. Conclusions-Based on this literature review, nitroimidazole hypoxia imaging agents are of considerable interest in stroke because they appear, both in animal models and in humans, to specifically detect the severely hypoxic viable tissue, but not the reperfused nor the necrotic tissue. To fully realize this potential in stroke, however, formal validation by concurrent measurement of tissue oxygen tension, together with development of novel ligands with faster distribution kinetics, faster clearance from normal tissue, and well-defined trapping mechanisms, are important goals for future investigations.

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.

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Background and Purpose-Watershed ischemia is a significant cause of stroke in severe carotid disease, but its pathophysiology is unsettled. Although hemodynamic compromise has long been regarded as the main mechanismparticularly with deep watershed infarction-there is some contradictory evidence from clinical and pathological studies for a role of microembolism, thought to result from plaque inflammation. However, no study so far has directly addressed these conflicting scenarios. Methods-In 16 consecutive patients with recent transient ischemic attack/minor stroke and ipsilateral 50% to 99% carotid stenosis, we prospectively obtained (1) plaque inflammation mapping with 18 F fluorodeoxyglucose positron emission tomography; (2) brain MRI and perfusion MR; and (3) transcranial Doppler detection of microembolic signals (MES). Patients were excluded if on dual antiplatelets or with a potential cardiac source of emboli or contralateral MES. Results-We found the expected significant relationship between (1) degree of stenosis and severity of distal hemodynamic impairment in the watershed areas; and (2) degree of in vivo plaque inflammation and rate of MES/hr. Deep watershed infarcts were present in 8 patients and MES in 8 (3 with both). There was no systematic association between the presence of deep watershed infarcts and either hemodynamic impairment or MES, but deep watershed infarcts were present only when either hemodynamic impairment or MES was present (Pϭ0.01). Conclusion-This pilot study supports the idea that in symptomatic carotid disease, deep watershed infarcts result either from hemodynamic impairment secondary to severe lumen stenosis or from microembolism secondary to plaque inflammation. There was no direct evidence that both mechanisms act in synergy. (Stroke. 2010;41:1410-1416.)Key Words: carotid stenosis Ⅲ CBF Ⅲ PET Ⅲ transcranial Doppler Ⅲ watershed infarcts C erebral events distal to atherosclerotic carotid disease are thought to be mostly embolic 1 and to originate from the unstable plaque as supported by a parallel time course of microembolic signals (MES) detected on transcranial Doppler (TCD). 2,3 Plaque inflammation, a key component of this process, 4 can now be assessed in vivo using 18 F fluorodeoxyglucose positron emission tomography. 5 Events distal to severe internal carotid artery (ICA) disease may also be due to hemodynamic impairment (HDI) 6 -8 and this is particularly relevant to the pathophysiology of watershed (WS) infarction, a significant cause of stroke in severe ICA disease. 9 Historically, HDI was regarded as the sole determinant of cortical WS (CWS) infarction owing to the latter's prevalence after severe systemic hypotension, and indeed HDI has been repeatedly demonstrated in association with CWS infarcts (reviewed by Momjian-Mayor and Baron 8 ). However, some pathological reports also support a role for microemboli in CWS infarcts, 8,10 and synergism between these 2 mechanisms has been proposed 11 although not directly evidenced so far.The second type of WS infarct foun...

Background-Cerebral

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