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TIA and ischemic stroke

Severe iron-deficiency anemia causes non-specific neurological symptoms, which are presumably hypoxic in origin, including poor concentration, malaise, giddiness, fatigue and weakness. Occasionally, TIAs and ischemic strokes seem to be provoked by profound anemia in association with severe extracranial occlusive arterial disease or thrombocytosis (Akins et al. 1996 Keung and Owen 2004). [Pg.76]

The causes of spontaneous intracerebral hemorrhage are sometimes, but not always, different from those of TIA and ischemic stroke. Spontaneous intracranial hemorrhage may be classified as ... [Pg.91]

In a recent systematic review and meta-analysis of studies of the risk of myocardial infarction and vascular death after TIA and ischemic stroke (Touze et al. 2005), cohort studies including over 100 patients with TIA or ischemic stroke and reporting risks of myocardial infarction or non-stroke vascular death over at least one year of follow-up published between 1980 and 2005 were identified. The analysis included 39 studies reporting outcomes in 65 996 patients. The ranges of annual risks reported in individual studies were 0.4% to 3.8% for non-stroke vascular death, 0.5% to 4.7% for total myocardial infarction, 0.4% to 3.2% for non-fatal myocardial infarction and 0.2% to 3.7% for fatal myocardial infarction. The annual risks obtained through meta-regression were 2.1% (95% Cl, 1.9-2.4) for non-stroke vascular death (29 studies), 2.2% (95% Cl, 1.7-2.7) for total myocardial infarction (22 studies), 0.9% (95% Cl, 0.7-1.2) for non-fatal myocardial infarction (16 studies), and 1.1% (95% Cl, 0.8-1.5) for fatal myocardial infarction (19 studies) (Touze et al. 2005) (Fig. 17.2). [Pg.217]

Antiplatelet therapy reduces the risk of recurrent vascular events after TIA and ischemic stroke, although few trials have distinguished between different etiological subtypes (Antithrombotic Trialists Collaboration 2002). Most trial data concern aspirin, but other antiplatelet agents such as clopidogrel (CAPRIE Steering Committee 1996) or extended-release dipyridamole (Sivenius et al. 1991) have also been shown to be effective although mechanisms of action may differ (Table 24.2). [Pg.285]

Table 24.1. Major trials and meta-analyses contributing to the evidence base for medical treatment in secondary prevention after TIA and ischemic stroke... Table 24.1. Major trials and meta-analyses contributing to the evidence base for medical treatment in secondary prevention after TIA and ischemic stroke...
A similar trade-off between diagnostic accuracy and risk is necessary when imaging the carotid bifurcation in patients with TIA or ischemic stroke. Performing intra-arterial catheter angiography in everyone is clearly unacceptable because of the risks and cost. Fewer than 20% of patients will have an operable carotid stenosis even if only those with cortical rather than lacunar events are selected (Hankey and Warlow 1991 Hankey et al. 1991 Mead et oL 1999). Coirfining angiography to patients with a carotid bifurcation bruit will miss some patients with severe stenosis and still subject too many with mild or moderate stenosis to the risks. Nor will a combination of a cervical bruit with various clinical features do much better (Mead et al. 1999). [Pg.161]

Apart from patients with symptomatic carotid stenosis and endarterectomy, to date, only the Fast Assessment of Stroke and Transient Ischemic Attack to Prevent Early Recurrence (FASTER) trial has addressed the difference between specific treatments administered early for patients with TIA and minor stroke (Kennedy et al. 2007). [Pg.246]

Dipyridamole ESPS II Aspirin and modified-release dipyridamole versus placebo in a 2x2 factorial design started within three months of TIA or ischemic stroke... [Pg.286]

Aortic arch atheroma is now increasingly diagnosed by transesophageal echocardiography in patients with TIAs or ischemic stroke, but so far there are no surgical, or indeed medical, treatment options over and above controlling vascular risk factors and antiplatelet drugs. One trial of medical treatment has been started, the Aortic Arch Related Cerebral Hazard (ARCH) trial (MacLeod et al. 2004). [Pg.310]

Although only a minority of patients with TIA or ischemic stroke are potential candidates for carotid endarterectomy (CEA) or stenting, the decision to opt for interventional treatment rather than medical treatment alone can be difficult and is, therefore, given detailed consideration in this Ch. Most of the discussion relates to CEA because far more data are available on the risks and benefits of surgery than for stenting. However, most of the issues discussed are applicable to both procedures. [Pg.312]

The REACH system in southern Georgia (United States) and the TEMPiS system in Germany reported decreased latency to rt-PA delivery on a larger scale. REACH system investigators reported 194 acute stroke consultations dehvered via telemedicine. The time from symptom onset to rt-PA delivery decreased from 143 minutes in the first 10 patients treated to 111 minutes in last 20 patients of 30 patients treated with rt-PA, 23% were treated in 90 minutes or less and 60% were treated within 2 hours without any incidence of post-treatment symptomatic intracerebral hemorrhage. In 2004, the second year of the TEMPiS system, 115 patients in telemedicine-networked community hospitals and 110 patients in stroke centers received rt-PA for acute ischemic stroke or TIA. Patients treated at networked community... [Pg.223]

Elevated blood pressure is common after ischemic stroke, and its treatment is associated with a decreased risk of stroke recurrence. The Joint National Committee and AHA/ASA guidelines recommend an angiotensin-converting enzyme inhibitor and a diuretic for reduction of blood pressure in patients with stroke or TIA after the acute period (first 7 days). Angiotensin II receptor blockers have also been shown to reduce the risk of stroke and should be considered in patients unable to tolerate angiotensinconverting enzyme inhibitors after acute ischemic stroke. [Pg.173]

The National Cholesterol Education Program considers ischemic stroke or TIA to be a coronary risk equivalent and recommends the use of statins in... [Pg.173]

Bashein. G., et al, Preoperative Aspirin Therapy and Reoperation for Bleeding After Coronary Artery Bypass Surgery, Arch. Intern. Med., 114, 835-9 (J991). Dutch TIA Trial Study Group A Comparison of Two Doses of Aspirin (30 mg vs. 283 mg a day) in Patients. After a Transient Ischemic Attack or Minor Ischemic Stroke, N. Eng. J. Med., 1261 (May 1, 1992). [Pg.153]

Transient ischemic attack (TIA) is a clinical syndrome characterized by focal neurological symptoms presumed to be of vascular origin that last less than 24 h. Despite the transient nature of symptoms, the cerebrovascular thread is not over yet following a TIA. The mechanism that has given rise to the transient spell may also cause more severe ischemic syndromes if not properly treated. About 10% of patients with TIA suffer from stroke within the ensuing 3 months, 50% of which occur within the first 2 days (Johnston et al. 2003). Accurate and prompt recognition of ischemia as the cause of neurological symptoms is imperative to prevent subsequent strokes. This is, however, a complicated task... [Pg.185]

In order to understand the clinical management of transient ischemic attacks (TIAs) and stroke, to plan clinical services or to design randomized controlled trials, and to measure the overall impact of treatments, it is important to understand the epidemiology of stroke. [Pg.1]


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Causes of TIA and ischemic stroke

Ischemic

Ischemic stroke

Stroke and

TIA and ischemic stroke syndrome

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