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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A thrombolytic agent, recombinant tissue plasminogen activator (rt-PA), was recently approved in Japan for use on patients within 3 hrs of the onset of cerebral infarction. In order to salvage cerebral tissue after an ischemic insult, it is crucial to detect the ischemic lesion before it becomes irreversible and to detect the core and penumbra areas of the lesion for guidance in selecting the suitable therapy. In this symposium we discuss the detection of ischemic lesions using plain CT, perfusion CT, and MRI. In the section on plain CT, we present a typical case with early CT signs. In the section on perfusion CT, we report on the feasibility and limitation of the technique for the diagnosis of acute cerebral infarction. In the section on MRI, we study the usefulness of DWI for the early and highly reliable detection of ischemic stroke.
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PMID:[Early detection of ischemic lesions in the super-acute phase of ischemic cerebrovascular diseases by imaging]. 1743 94

Ultrasound harmonic imaging of perfusion after ultrasound contrast agent (UCA) bolus injection (BHI) can detect cerebral perfusion deficits. In a pilot study, we evaluated the ability of time-intensity curve (TIC) measurements to differentiate between normal and hypoperfused brain areas in acute ischemic stroke. Ten patients with symptoms of acute middle cerebral artery infarction were investigated (SONOS 5500, Harmonic Imaging 1.6/3.8 MHz, diencephalic plane, 10 cm investigation depth, SonoVue 2.4 mL bolus). Peak signal increase (PSI), time-to-peak intensity (TPI) and area under the curve (AUC) were calculated for 60 regions-of-interest (ROIs) in each patient. Reference methods: Perfusion- and diffusion-weighted MRI (PWI/DWI) within 4 h before/after BHI (PWI threshold: 4 s). Receiver operating characteristics (ROC) analysis defined cut-off values for each TIC variable to distinguish between normal and affected brain areas as defined by PWI/DWI. In five patients, PWI showed a perfusion delay >4 s; seven patients had a DWI lesion. In three patients, both PWI and DWI findings showed pathology; one patient had a normal MRI of the insonation plane. Cut-off values for PWI delay: PSI: 5.53% (sensitivity .98, specificity .89); TPI: 4.04 s (sensitivity .74, specificity .69) and AUC: .63 (sensitivity .94, specificity .58). Referred to the mean value in unaffected brain areas the relative thresholds were 17.6%, 109.5% and 16.1%, respectively. Regarding DWI, only for PSI, a significant cut-off value was defined: 10.86%, sensitivity .84, specificity .60 (34.6% of mean). In conclusion, these thresholds distinguish between normal and affected brain areas in acute ischemic stroke.
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PMID:Ultrasound perfusion imaging: determination of thresholds for the identification of critically disturbed perfusion in acute ischemic stroke--a pilot study. 1744 70

The use of blood biomarkers is getting increasingly popular in the field of cerebrovascular diseases, since biomarkers might aid physicians in several steps of stroke evaluation. We will discuss whether stroke diagnosis might be possible using some specific brain biomarkers and if this approach will permit rapid referral of stroke patients to hospitals with acute treatments such as tissue plasminogen activator (t-PA) available. Although thrombolytic therapy in acute stroke is effective since it accelerates clot lyses and earlier restoration of blood flow, up to 40-50% of treated patients do not recanalize or do it too late, and between 6 and 15% suffer hemorrhagic transformations with high death rates. In the context of the neurovascular unit, t-PA may degrade extracellular matrix integrity and increase risks of neurovascular cell death, blood-brain barrier leakage, edema and hemorrhage. In humans, biomarkers such as matrix metalloproteinase-9 (MMP-9) or fibronectin, which might be used to select patients at higher risk of hemorrhagic transformation, and high plasminogen activator inhibitor-1 (PAI-1) interfering with tPA-induced recanalization, thus predicting clot-lyses resistance and poor outcome, have been recently identified. Moreover, high levels of MMP-9 and MMP-13 are involved in DWI lesion growth in spite of thrombolytic therapy suggesting its ultra-early role in brain injury. Other biomarkers such as C-reactive protein may accurately predict stroke mortality following reperfusion therapies. Finally, we will also show that genetic background of stroke patients may condition plasma levels of some of these biomarkers and influence therapeutic response in t-PA-treated patients.
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PMID:Stroke biomarkers: can they help us to guide stroke thrombolysis? 1722 Sep 57

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.
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PMID:Lacunar stroke attributable to radiation-induced intracranial arteriopathy. 1766 19

We reported a 66-year-old man who complained of headache, vertigo, vomiting and chest oppression sensation. He could not walk veering to right and spontaneous contrarateral horizontal nystagmus was noted. A MRI DWI showed scattered multiple small high signals within the territory of left medial branch of posterior inferior cerebellar artery. Cerebellar infarcts specifically affected the tonsil and nodulus, which has tight connections with vestibular labyrinth and vestibular nuclei. Digital subtraction angiography exhibited tapered occlusion on the V4 segment of the right vertebral artery. Stroke mechanism of artery to artery embolism from occlusive site was presumed. As small multiple infarcts were limited within the cerebellar tonsil and nodulus, repeated CT or MRI T2 weighted image did not showed obvious findings. It is worth noting for differential diagnosis that small cerebellar infarcts only detected by diffusion MRI can produce strong vertigo, nausea and chest oppression.
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PMID:[A patient with small cerebellar infarcts at tonsil and nodulus who complained of vertigo, vomiting and chest oppression]. 1788 47

We incorporated diffusion-weighted magnetic resonance imaging (MRI) (DWI) and perfusion-weighted MRI (PWI) to evaluate the efficacy of thrombolysis in experimental embolic stroke using a plasminogen activator, reteplase. Reteplase (rPA) is an unglycosylated plasminogen activator with enhanced fibrinolytic potency. Right internal carotid arteries of 34 rabbits were embolized using aged heterologous thrombi. Baseline DWI and PWI scans 0.5 hours after embolization confirmed successful embolization among 32. Intravenous treatment with rPA (n=11; 1 mg/kg bolus), recombinant tissue plasminogen activator (rt-PA) (n=11; 6 mg/kg bolus over 1 hour), or placebo (n=10) commenced 1 hour after stroke induction. MRIs were performed at 1.75, 3, and 5 hours after embolization. Six hours after embolization, brains were harvested and examined for hemorrhage. Posttreatment areas of diffusion abnormality and perfusion delay were graded using both a semiquantitative scale and percent areas expressed as a ratio of the baseline values. Improved perfusion was seen among the rt-PA, and rPA-treated groups compared with placebo, using a semiquantitative scale (P<.01 rt-PA v controls, P<.05, rPA v controls). DWI scans, however, were not improved with thrombolysis. Cerebral hemorrhage was not increased with thrombolytic treatment, although the incidence of wound site hemorrhage was higher with either rPA or rt-PA. One fatal systemic hemorrhage was observed in each of the thrombolytic-treated groups. Cerebral perfusion was equally improved with either rt-PA or rPA without causing excess cerebral hemorrhage. An advantage of rPA is single-bolus dosing rather than continuous infusion. Use of rPA for stroke treatment should be further explored.
J Stroke Cerebrovasc Dis
PMID:Thrombolysis with reteplase, an unglycosylated plasminogen activator variant, in experimental embolic stroke. 1789 78

Diffusion-weighted and perfusion-weighted magnetic resonance imaging (DWI, PWI) are useful in detecting early cerebral ischemic lesions. Intra-arterial thrombolysis is an effective treatment for some patients with acute thromboembolic occlusion. We evaluated the efficacy of acute thrombolytic therapy by using DWI and PWI in 3 patients who presented with internal carotid artery or middle cerebral artery occlusion. On the initial magnetic resonance imaging scans, the abnormal areas shown by PWI were bigger than those shown by DWI. All patients received thrombolytic therapy within 6 hours after stroke onset. In 1 patient, the hyperintensity area detected by initial DWI scanning diminished after thrombolysis. DWI and PWI may be useful to monitor the effectiveness of intra-arterial thrombolysis.
J Stroke Cerebrovasc Dis
PMID:Diffusion-weighted and perfusion-weighted magnetic resonance imaging to monitor acute intra-arterial thrombolysis. 1789 7

During the acute phase shortly after the onset of an ischemic stroke, tissue in the penumbra surrounding an infarct receives sufficient blood flow to survive, but not enough to function. As time passes, neurons in this penumbra die. Imaging techniques have given valuable information about the length of time that brain cells can survive under these ischemic conditions. 15O positron-emission tomography (PET) scanning gives information about perfusion of tissue, its oxygen consumption, and its oxygen extraction fraction. Tissue in the penumbra has a reduced blood flow, near normal oxygen consumption, but markedly raised oxygen extraction fraction. With the use of a set of rigorous criteria, PET scanning has provided evidence that, in a fraction of the patients, a penumbra of viable, potentially salvageable neurons exists for at least 7 hours, and possibly for as long as 16 hours, after the onset of ischemic stroke, whereas in others the infarct reaches its maximal extent only a few hours after clinical onset. Recent developments in magnetic resonance imaging (MRI) technology, especially diffusion-weighted and perfusion-weighted imaging (DWI and PWI), also have enabled potentially salvageable penumbral tissue to be identified in patients who have suffered ischemic strokes. The typical signature of salvageable tissue is that it has a PWI-DWI mismatch. This type of MRI evidence shows that there may be salvageable tissue as late as 24 hours after the onset of symptoms.
J Stroke Cerebrovasc Dis 2000 Nov
PMID:For how long is brain tissue salvageable? Imaging-based evidence. 1789 15

Recent developments in neuroimaging have changed the diagnostic aspect of acute stroke and improved our understanding of stroke pathophysiology. Both diffusion weighted MR imaging and CT are capable of detecting the infarcted volume damaged by cytotoxic edema. However, within six hours of stroke onset, DWI has both higher sensitivity and specificity than CT. Perfusion weighted MR imaging and perfusion CT can identify the tissue at risk surrounding the core of the infarct. CT and MR-angiography contribute important information concerning the intra and extracerebral arteries.
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PMID:[Imaging of the pathophysiology in acute stroke]. 1795 55

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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PMID:Pathophysiology of ischaemic stroke: insights from imaging, and implications for therapy and drug discovery. 1803 22


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