Seminars in Cerebrovascular Diseases and Stroke最新文献

Currently there are no “gold standards of care” in place for the treatment of intracerebral hemorrhage (ICH). Clinical trial data have indicated that the largest expansion of the hemorrhage volume occurs within the early hours after the onset of symptoms. This expansion of hematoma volume has been shown to be a critical factor in predicting mortality 30 days postictus. Thus, it is reasonable that minimizing hematoma growth, and any associated perihematomal edema, could potentially provide clinical benefit, reduce the degree of neurological damage, improve functional outcomes, and reduce mortality. Traditionally, surgical interventions were the only option for improving patient outcome or preventing mortality. There has been a great deal of debate surrounding the clinical benefit of surgery. The results of the International Surgical Trial in Intracerebral Hemorrhage conclusively demonstrated that there was no clear advantage gained by the early surgical evacuation of hematomas, as compared with conservative treatment. The results of a recently concluded clinical trial of ICH patients demonstrated that the early administration of the hemostatic agent, recombinant activated coagulation factor VIIa, within 4 hours of the onset of symptoms, reduced hematoma expansion as compared with placebo. In addition, the treatment of ICH patients with recombinant activated coagulation factor VIIa also demonstrated significant improvements in several neurological, functional, and disability scales. This review will summarize the current understanding, provide an overview of new treatment trends, and suggest potential strategies for future investigations into ICH.

Deep venous thrombosis and pulmonary emboli are common preventable causes of morbidity and mortality in patients with acute intracerebral hemorrhage (ICH). The frequency of venous thromboembolism (VTE) in patients with acute ICH ranges from 0.5 to 13% in scant reports. The dilemma in the prevention and treatment of these complications is to reduce the morbidity of VTE without increasing the risk of intracranial rebleeding. There is a paucity of information about this issue, and the applicability of the recommendations for patients with ischemic stroke to those with ICH is unclear. From the available literature, the recommendations for prevention of VTE in patients with ICH are early mobilization, adequate hydration, pneumatic compression stockings, and (in stable patients) low-dose subcutaneous heparins. Considering the treatment of VTE in patients with ICH, placement of an inferior vena caval filter is the most frequent expert recommendation. While existing data are sparse and not sufficient to recommend modifications to current options, the way is open for randomized trials to test early use of antithrombotic agents for VTE in acute ICH patients.

An elderly man with multiple hemorrhagic, presumed neoplastic lesions of the brain is described who could not undergo magnetic resonance imaging because of a pacemaker. On autopsy, metastatic melanoma was identified. In this report, we discuss the differential diagnosis of hemorrhagic metastases, the incidence and prognosis of metastatic melanoma to the brain, and the limited therapeutic options for metastatic melanoma.

Intracerebral hemorrhage (ICH) and some of its associated features are accompanied by increased levels of certain biochemical markers in serum. The amount of peri-hematoma edema formation is correlated with serum levels of glutamate, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and intercellular adhesion molecule-1 (ICAM-1). In addition, serum glutamate levels are associated with poor neurological outcome. The matrix metalloproteinases (MMPs) are elevated in serum in patients with ICH. The MMP-9 isoform is also correlated with the initial volume of peri-hematoma edema, its subsequent enlargement in the first 48 hours from ICH onset, and neurological worsening. Hematoma enlargement after ICH onset is correlated with high serum levels of IL-6, TNF-α, MMP-9, and cellular fibronectin (c-Fn). The risk of hemorrhagic complications after acute ischemic stroke treated with t-PA thrombolysis is increased in subjects with elevated baseline serum levels of MMP-9. The above observations suggest that the determination of a number of serum markers may become an important tool for the prediction of ICH outcome, as well as for the assessment of risk of bleeding after thrombolysis for acute ischemic stroke.

Carotid revascularization procedures for the prevention of acute ischemic stroke have a low but definite risk of intracerebral hemorrhage (ICH). After carotid endarterectomy (CEA) the risk is less than 1%, and accumulating data on the newer carotid angioplasty and stenting (CAS) procedure suggest a similar risk. A probably more common and underdiagnosed complication of CEA and CAS is the so-called “hyperperfusion” syndrome. A post-revascularization increase in cerebral blood flow (CBF) in the ipsilateral hemisphere is thought to underlie the pathophysiology of the syndrome. The increased unilateral hemispheric CBF leads to vasogenic edema due to re-perfusion of maximally dilated capillaries which have lost their autoregulatory capacity as a result of chronic ischemia. The clinical features of severe post-procedural hypertension followed by headache, focal neurological deficits, and seizures has an imaging correlate of unilateral hemispheric vasogenic edema in the absence of MRI features of infarction. In the absence of associated ICH, the symptoms often improve over a period of days after aggressive control of hypertension. The key to the prevention of the hyperperfusion syndrome and post-carotid revascularization ICH is close monitoring of peri-procedural blood pressure, and aggressive treatment of hypertension.

Intracerebral hemorrhage (ICH) has been traditionally imaged with computerized tomography (CT), which allows an immediate distinction between ICH and ischemia as the mechanism of an acute stroke. In recent years, the refining of several techniques of magnetic resonance (MR) imaging has allowed a more precise characterization of the anatomy of ICH, its associated events (such as surrounding edema), and its time-course. The latter has been facilitated by an understanding of the various biochemical changes that take place in and around the hematoma, and which correlate with the temporal course of the evolution of the ICH. In addition, the measurement of the susceptibility effect by MR imaging has permitted the identification of small asymptomatic microhemorrhages, which are potentially important predictors of ICH recurrence, as well as risk factors for ICH due to anticoagulant and thrombolytic treatment.

Intraventricular hemorrhage (IVH) as a primary event or as a complication of intracerebral hemorrhage (ICH) carries a poor prognosis. The effects of IVH on brain function are mediated via complicating hydrocephalus (with increased intracranial pressure and decreased cerebral perfusion pressure), presence of blood clots in the ventricular system, and carrying of blood degradation products into the CSF pathways, all of which contribute to morbidity and mortality. The management of IVH has been traditionally based on draining the blood from the ventricular system (and reducing hydrocephalus) via external ventricular drainage techniques. Their inadequate results (due to frequent obstruction of the draining system by clot) and tendency to complications (mainly infection) has led to the search of alternative treatments. A promosing approach has been the addition of intraventricular instillation of thrombolytics to the external ventricular drainage, in an attempt at accelerating blood clot lysis and removal. This approach has shown initial encouraging results, with adequate drainage of intraventricular clots without an increase in intracranial bleeding. The procedure is currently being tested in a prospective randomized clinical trial.

A 53-year-old woman with a prosthetic heart valve developed a left occipital intracerebral hemorrhage (ICH) while on treatment with warfarin for thromboembolism prophylaxis. The international normalized ratio was 5.8. She presented with left occipital headache, right homonymous hemianopia, and fluent aphasia. The ICH expanded in the initial hours after onset but subsequently stabilized after treatment with vitamin K₁, fresh frozen plasma, and recombinant activated factor VII. Her hospital course was stable, and the clinical deficits gradually resolved (aphasia) or improved (right homonymous hemianopia) after hospital discharge. She had the warfarin treatment restarted after 8 days from ICH onset, without subsequent complications. The available data and recommendations on the issue of restarting warfarin anticoagulation after an episode of intracranial bleeding are reviewed.

Intracerebral hemorrhage (ICH) accounts for approximately 10% of strokes. Its causes include hypertension and cerebral amyloid angiopathy in the middle-aged and elderly, respectively, while vascular malformations predominate in the younger than 45 years old population. Recurrence of ICH is not as low as it was traditionally thought, and overall it is about 4.5% for an aggregate of several studies with different lengths of follow-up. Most of these recurrences occur over a 1-2 year period after the initial episode of ICH, but late recurrence (over several years) is not uncommon, leading to cumulative frequencies of recurrence of up to 25-55% after 7-8 years of follow-up in some series. The main risk factors for recurrence are age, poorly controlled hypertension, lobar location (probably due to cerebral amyloid angiopathy), presence of asymptomatic microhemorrhages, and carrying the ϵ2 and ϵ4 alleles of the apolipoprotein E gene. The initial location of ICH (ganglionic vs. lobar) is generally predictive of the same topography for the recurrent event. Recurrent ICH is associated with high mortality, in the order of 70%.

Intracerebral hemorrhage (ICH) has an incidence of 10-20/100,000. Its most important risk factors are age, gender, race (more common in African-American, Hispanic, and Asian populations), hypertension, excessive alcohol use, and smoking. The latter two underline the importance of prevention via modification of behavior, while the value of treatment of hypertension is highlighted by clinical trial data (Perindopril Protection Against Recurrent Stroke Study [PROGRESS]) indicative of substantial risk reduction (50% relative risk reduction) by relatively modest lowering of blood pressure (by 9/4 mmHg). The importance of genetic factors for ICH has been recently documented, with endoglin gene insertions and Factor XIII polymorphisms being associated with a significant increase in the risk of ICH. The prognosis of ICH is dependent on age, level of consciousness, hematoma volume, and intraventricular extension of hemorrhage, which are all predictors of mortality. The risk of ICH recurrence is about 2%/year overall, but with an increase to 4-5%/year if the localization is lobar. Predictors of ICH recurrence include age > 65, carrying the ϵ2 and ϵ4 alleles of the apolipoprotein E gene, the presence of asymptomatic microhemorrhages and leukoaraiosis. The functional outcome of ICH is poor, with only 12% of survivors being independent at 30 days.