Traditional Medicine vs Modern Medicine

Essential update: A short course of aspirin plus clopidogrel cuts stroke risk. The study enrolled 5170 patients in China who were aged 40 years or older and who had sustained a TIA or minor stroke.[3] Within 24 hours after symptom onset, the patients were randomly assigned to 1 of 2 groups: (1) aspirin (1-day loading dose of 75-300 mg, followed by 75 mg/day) plus placebo or (2) the same aspirin regimen plus clopidogrel (loading dose of 300 mg followed by 75 mg/day). Signs and symptoms A TIA may last only minutes, and symptoms often resolve before the patient presents to a clinician. Thus, historical questions should be addressed not just to the patient but also to family members, witnesses, and emergency medical services (EMS) personnel regarding changes in any of the following: Behavior Speech Gait Memory Movement Initial vital signs should include the following: Temperature Blood pressure Heart rate and rhythm Respiratory rate and pattern Oxygen saturation The examiner should assess the patient’s overall health and appearance, making an assessment of the following: Attentiveness Ability to interact with the examiner Language and memory skills Overall hydration status Development The goals of the physical examination are to uncover any neurologic deficits, to evaluate for underlying cardiovascular risk factors, and to seek any potential thrombotic or embolic source of the event. Ideally, any neurologic deficits should be recorded with the aid of a formal and reproducible stroke scale, such as the National Institutes of Health Stroke Scale (NIHSS). A neurologic examination is the foundation of the TIA evaluation and should focus in particular on the neurovascular distribution suggested by the patient’s symptoms. Subsets of the neurologic examination include the following: Cranial nerve testing Determination of somatic motor strength Somatic sensory testing Speech and language testing Assessment of the cerebellar system (be sure to watch the patient walk) See Presentation for more detail. Diagnosis Ruling out metabolic or drug-induced etiologies for symptoms consistent with a TIA is important. The following tests are considered on an emergency basis: A fingerstick blood glucose for hypoglycemia Complete blood count Serum electrolyte levels Coagulation studies 12-lead electrocardiogram (ECG) with rhythm strip The following tests typically are helpful and often can be performed on an urgent basis: Erythrocyte sedimentation rate Cardiac enzymes Lipid profile Additional laboratory tests, ordered as needed and on the basis of the history, include the following: Screening for hypercoagulable states (particularly in younger patients with no known vascular risk factors)[4] Syphilis serology Antiphospholipid antibodies Toxicology screens Hemoglobin electrophoresis Serum protein electrophoresis Cerebrospinal fluid examination Imaging of the brain should be performed within 24 hours of symptom onset, as follows[4, 5] : Magnetic resonance imaging (MRI) with diffusion-weighted imaging (preferred) Noncontrast computed tomography (CT; ordered if MRI is not available) The cerebral vasculature should be imaged urgently, preferably at the same time as the brain. Vascular imaging for TIA includes the following: Carotid Doppler ultrasonography of the neck CT angiography (CTA) Magnetic resonance angiography (MRA) See Workup for more detail. Management The following should be done urgently in patients with TIA[4, 2, 6, 7] : Evaluation Risk stratification (eg, with the California or ABCD score[4] ) Initiation of stroke prevention therapy For patients with a recent (≤1 week) TIA, guidelines recommend a timely hospital referral with hospitalization for the following: Crescendo TIAs Duration of symptoms longer than 1 hour Symptomatic internal carotid stenosis greater than 50% Known cardiac source of embolus (eg, atrial fibrillation) Known hypercoagulable state Appropriate combination of the California score or ABCD score (category 4)[7] In view of the high short-term risk of stroke after TIA, antithrombotic therapy should be initiated as soon as intracranial hemorrhage has been ruled out. For noncardioembolic TIA, the following antiplatelet agents are all reasonable first-line options for initial therapy: Aspirin (50-325 mg/day) Aspirin plus extended-release dipyridamole Clopidogrel Stroke prevention medication typically recommended for cardioembolic TIA is as follows: For patients with atrial fibrillation after TIA, long-term anticoagulation with warfarin (target international normalized ratio [INR], 2-3); aspirin 325 mg/day for those unable to take oral anticoagulants In acute myocardial infarction (MI) with left ventricular thrombus, oral anticoagulation with warfarin (target INR, 2-3; concurrent aspirin up to 162 mg/day for ischemic coronary artery disease [CAD]) In dilated cardiomyopathy, oral anticoagulation with warfarin (target INR, 2-3) or antiplatelet therapy In rheumatic mitral valve disease, oral anticoagulation with warfarin (target INR, 2-3) For patients with TIA due to 50-99% stenosis of a major intracranial artery, the following is recommended: Aspirin 50-325 mg/day rather than warfarin Maintenance of blood pressure below 140/90 mm Hg and total cholesterol below 200 mg/dL Angioplasty or stent placement is investigational and of unknown utility Initial assessment is aimed at excluding emergency conditions that can mimic a TIA, which include the following: Hypoglycemia Seizure Tumor or mass lesion Migraine with aura Peripheral nerve/root disorder Demyelinating disease Vestibular dysfunction Intracranial hemorrhage Electrolyte derangements Thus, a fingerstick blood glucose test should be performed to check for hypoglycemia, and blood should be drawn for laboratory studies. The following tests are considered on an emergency basis: serum chemistry profile, including creatinine; coagulation studies; and complete blood count (CBC).[4, 8] (See Workup.) Causes in children TIA etiologies in children, which can differ from those in adults, include the following: Congenital heart disease with cerebral thromboembolism (most common) Drug abuse (eg, cocaine) Clotting disorders Central nervous system infection Neurofibromatosis Vasculitis Idiopathic progressive arteriopathy of childhood (moyamoya) Fibromuscular dysplasia Marfan disease Tuberous sclerosis Tumor Sickle cell disease Focal arteriopathies Pharmacologic Therapy In view of the high short-term risk of stroke after TIA, antithrombotic therapy should be initiated as soon as intracranial hemorrhage has been ruled out. The guidelines developed by the AHA and the American Stroke Association (ASA) for the prevention of stroke in patients with stroke or TIA, issued in 2006[45] and updated in 2010,[46] are summarized below. Noncardioembolic transient ischemic attack Antiplatelet agents, rather than oral anticoagulants, are recommended as initial therapy. Aspirin 50-325 mg/day, a combination of aspirin and extended-release dipyridamole, and clopidogrel are all reasonable first-line options (class I recommendation). The AHA/ASA guidelines do not recommend clopidogrel plus aspirin for patients with a hemorrhagic contraindication to warfarin, because this combination carries a risk of bleeding similar to that of warfarin. The efficacy of adding clopidogrel to aspirin is being evaluated in the ongoing POINT (Platelet-Oriented Inhibition in New TIA and minor ischemic stroke) trial. Cardioembolic transient ischemic attack In patients who have atrial fibrillation in association with a TIA, long-term anticoagulation with warfarin to a target international normalized ratio (INR) of 2-3 is typically recommended. Aspirin 325 mg/day is recommended for patients unable to take oral anticoagulants. The 2010 AHA/ASA guidelines also state that bridging therapy with subcutaneous low-molecular-weight heparin (LMWH) is reasonable for patients with atrial fibrillation who require temporary interruption of oral anticoagulation but are at high risk for stroke.[46] In acute myocardial infarction (MI) with left ventricular thrombus, oral anticoagulation with warfarin (target INR, 2-3) is reasonable. Aspirin up to 162 mg/day should be used concurrently for ischemic coronary artery disease (CAD). In dilated cardiomyopathy, either oral anticoagulation with warfarin (target INR, 2-3) or antiplatelet therapy may be considered. In rheumatic mitral valve disease, oral anticoagulation with warfarin (target INR, 2-3) is reasonable. Antiplatelet agents would not normally be added to warfarin unless patients experience recurrent embolism despite a therapeutic INR. The benefit of warfarin after stroke or TIA in patients with sinus rhythm and cardiomyopathy characterized by systolic dysfunction has not been established.[46] In mitral valve prolapse, long-term antiplatelet therapy is reasonable. In mitral annular calcification, antiplatelet therapy can be considered. Patients with mitral regurgitation can be considered for warfarin or antiplatelet therapy. In aortic valve disease, antiplatelet therapy may be considered. For patients with mechanical prosthetic valves, oral anticoagulation with warfarin (target INR, 2.5-3.5) is recommended. For those who experience TIAs despite therapeutic INR, aspirin 75-100 mg/day can be added to the regimen. Patients with bioprosthetic valves and no other source of thromboembolism who experience TIAs can be considered for oral anticoagulation with warfarin (target INR, 2-3). Transient ischemic attack (TIA) is a brief episode of neurologic dysfunction resulting from focal temporary cerebral ischemia not associated with cerebral infarction. TIA was originally defined clinically by the temporary nature (<24 hours) of the associated neurologic symptoms. However, the arbitrary nature of the 24-hour time limit and lack of specific pathophysiologic meaning hampered the clinical and research utility of the term "TIA." Recognition of these problems led to a change to a tissue-based definition of TIA. The change was driven by advances in neuroimaging that enabled very early identification of ischemic brain injury. Texans coach Gary Kubiak was released from a Houston hospital Tuesday after suffering what the team said was a mini-stroke during Sunday night’s loss to Indianapolis. The team said the 52-year-old Kubiak suffered a transient ischemic attack at halftime.