الفهرس يوجد فقط 14 صفحة متاحة للعرض العام
 |  | from | 195 |  |  |
| | | from | 195 | | |
المستخلص
The classic old definition of TIA was based on the assumption that Transient symptoms last less than 24 hours without permenant brain injury. However, later on, most TIAs (approximately 2/3) were found to last less than an hour and the probability that symptoms lasting longer than one hour will resolve within 24 hours is low (about 15%).
Accordingly, there was an emerging consensus to adopt a new definition of TIA based on the more objective foundation of the presence or absence of tissue injury rather than time interval. Several groups, including the TIA working group developed or had advanced proposals for a new tissue-based definition that can be indexed by imaging or other laboratory measures rather than an arbitrary time limit. Currently TIA is defined as “a brief episode of neurological dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than 1 hour, and without evidence of acute infarction”.
It is important to note that the new definition advanced for TIA is not dependent on a particular imaging technique. A variety of modalities may be used to identify tissue injury in Transient cerebral ischemic episodes, including not only CT, MRI and diffusion imaging techniques but also serum biomarkers such as neuron specific enolase and S100 protein. The key biological variable is end-organ injury, which can be identified by a variety of neuroimaging and laboratory means.
A redefinition of TIA may underscore the need for urgent action when a patient has symptoms of acute brain ischemia because the physician will ultimately start diagnostic evaluation for evidence of acute infarction.
The true incidence of TIA is not known because many TIAs are never diagnosed and some events diagnosed as TIA have other etiologies such as migraine or seizure. However, an estimated 200,000 to 500,000 TIAs occur annually in the United States and it may be provisionally estimated that currently in the United States, tissue-defined TIAs occur with an annual incidence of 43 per 100000. In Egypt, the prevalence and incidence rates of TIA were estimated to be 0.36 and 0.2 per 1000 respectively.
TIAs result from such a decrease in cerebrovascular blood flow, which disrupts neuronal function temporarily to the extent that clinical deficits can be detected. More commonly, TIAs result from one of three etiologic pathways: atherosclerosis leading to luminal narrowing of vessels and plaque ulceration; thromboembolism; or a cardioembolic event
Ischemic Stroke and TIA share similar risk factors, symptoms, evaluation and secondary prevention. Some clinical features of a TIA provide substantial prognostic information as regard the risk of recurrent Stroke afterward, and these include age over 60 years, symptom duration greater than 10 min, motor weakness, speech impairment, diabetes mellitus and hypertension. The overall incidence of an adverse vascular outcome within 90 days of a TIA is 25%. 10 % of the events are strokes; half of these occur in the first 2 days. Several scoring systems were tested to predict the risk of Stroke after TIA, including the 6-point ABCD score (7 days risk), the California score (90 days risk) and most recently the dubbed ABCD score (2 days risk) which is highly clinically relevant to determine whether the patient might be admitted or not.
The clinical diagnosis of TIA remains unreliable because of the wide range of symptoms, the number of differential diagnosis and the fact that the diagnosis is retrospective. On clinical basis, TIAs can be classified as probable or possible and other TIA mimics should be excluded.
Many of the available investigations are also not conclusive in the diagnosis of TIA, like the neurological examination. The recommended neuroimaging investigation for patients suspected to have a TIA is MRI with DWI which can exclude acute infarction. If MRI is not possible or is contraindicated, CT scan should be used, mainly to exclude subarachnoid hemorrhage, intracranial hemorrhage, subdural hematoma, tumors and other masses.
All TIA patients need a baseline ECG, CBC, KFTs, PT, aPTT, blood glucose level and TEE should be considered in patients without an identifiable cause of TIA or known cardiac disease, because it may detect conditions requiring anticoagulation.
To determine the etiology and risk factors of the TIA some more investigations are required including carotid duplex, TCD, MRA or spiral CT angiography and possibly angiography (continue to be the gold standard for complete evaluation of intracranial and extracranial vessels) to diagnose atherosclerosis, vessels flow and stenosis. Also, lipid profile, glycosylated haemoglobin for long standing diabetes should be considered. For hypercoagulable states, initial tests include, protein C, protein S, antinuclear antibody test, rapid plasma reagent test, and antiphospholipid antibody tests.
Guidelines issued by the National Stroke Association recommend evaluation within hours of the onset of TIA symptoms, preferably in an emergency department. If appropriate imaging studies are not immediately available in the emergency department or outpatient setting, the patient should be hospitalized for observation.
There is substantial variation worldwide in how patients are investigated and treated in the acute phase. whereas in some health-care systems TIA patients are admitted routinely with immediate emergency inpatient care, others provide outpatient clinical assessment discharging patients with suboptimal management.
Current NSA recommendations are separated into five major categories: initial management, evaluation, medical treatment, surgical treatment, and risk factor management separated into subtopics and ordered by level of evidence.
Hospitalization should be considered for patients with their first TIA within the past 24 to 48 hours, crescendo TIAs, symptoms lasting longer than 1 hour, >50% symptomatic internal carotid stenosis , a known cardiac source of embolus such as AF, a known hypercoagulabte state or an appropriate combination of the California score or ABCD score. This will facilitate possible early deployment of lytic therapy and other medical management if symptoms recur and to expedite institution of definitive secondary prevention.
Also, a local admissions policy should be developed by hospitals and a local written protocol should be available that set out indications for both initial screening (such as brain imaging, vascular imaging, cardiac assessment, and blood tests) and more specialized investigations (such as angiography, TEE or more specialized blood tests) that the clinical situation may merit. Oior2eisgjoasdfijgoiajsdgi
Patients with suspected TIA who are not admitted to the hospital should have rapid (within 12 hours) access for urgent assessment as MRI, EKG and CDUS. If they are not performed in the emergency department, initial assessment should be performed within 24 to 48 hours.
The first step in evaluating a patient with symptoms of TIA is to confirm the diagnosis. Patients who have had symptoms for fewer than 180 minutes with evidence of acute infarction on brain imaging might be candidates for treatment with tissue plasminogen activator (tPA). If a patient is not a candidate for tPA, antiplatelet therapy should be initiated as soon as it can be determined that there are no contraindications.
Daily long-term antiplatelet therapy should be prescribed immediately for the secondary prevention of Stroke and other vascular events in patients who have sustained a noncardioembolic TIA.
It is often difficult to determine the precise mechanism, the choice of a platelet inhibitor or anticoagulant drug may be difficult. Patients who have suffered an ischemic Stroke who have a high-risk source of cardiogenic embolism should generally be treated with anticoagulant drugs to prevent recurrence.
CEA is beneficial for symptomatic patients with recent (within 2-4 weeks) hemispheric, nondisabling, carotid artery ischemic events and ipsilateral 70 to 99% carotid artery stenosis. It may also be beneficial for symptomatic patients with retinal TIA.
Antihypertensive treatment and lifestyle modifications are recommended for hypertensive patients who have had a TIA and are beyond the hyperacute period, and because this benefit extends to patients with and without a history of hypertension, this recommendation should be considered for all ischemic Stroke and TIA patients. The optimal drug regimens are diuretics and the combination of diuretics and an ACEI, with target blood pressure of less than 140/90 mmHg or less than 130/80mm Hg for diabetics, regardless of its initial level.
Glucose control is recommended to near normoglycemic levels among diabetics with TIA or ischemic stroke. The goal for hemoglobin A1c should be 7%.
Patients with TIA or ischemic Stroke with elevated cholesterol, comorbid coronary artery disease, or evidence of an atherosclerotic origin should be managed with lifestyle modification, dietary guidelines and statins. The target goal for cholesterol lowering for those with CHD or symptomatic atherosclerotic disease is an LDL of <100 mg/dL and LDL of <70 mg/dL for very-high-risk persons with multiple risk factors.
Some other important management guide lines include lifestyle and behavioral modifications including Smoking cessation, reducing alcohol consumption, weight reduction with goal BMI between 18.5 and 24.9 kg/m2, exercising for at least 30 minutes of moderate intensity physical exercise most days may be considered to reduce the risk of recurrence, control risk factors and comorbid conditions that increase the likelihood of recurrent stroke.