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Transient Ischemic Attack

Pathophysiology

A transient ischemic attack is a temporary reduction in the perfusion of blood to a focal region of the brain (1,2,4). The result is a short lived disturbance of function (1,2,4). The onset of a TIA is quite rapid (5 minutes) and has a short duration (2 to 15 minutes usually, but may be up to 24 hours) (1,2,4). Embolization is an important cause of TIA (1,2). TIAs may be due to emboli to the brain or from the in situ thrombosis of an intracranial vessel (1,2). In many patients that develop TIA, a source of the emboli is readily apparent in the heart or from a major extracranial artery to the head (1,2,4). With TIA, the blood vessel that is occluded reopens and the neurological function is restored (1,2,4). Usually, a decrease in cerebral blood flow to zero causes the death of brain tissue within 4-10 minutes (1,). If the blood flow is restored prior to a significant amount of cell death occurring, then the patient will only experience transient symptoms, known as a TIA (1). Thus, no neurological deficit remains after a TIA (1). Thrombotic occlusion may also contribute to a TIA (1). This is when a thrombus forms inside an artery that is present in the brain, which will lead to an interruption of the blood supply to an area of the brain (1).

Signs and Symptoms/ Diagnosis

The symptoms of TIA vary among patients, but are usually consistent within an individual (1,2,4). The symptoms that manifest are dependent on the area of the brain that is affected by the ischemia (1,2,4). This may include numbness or weakness of the face, arm or leg (partial or complete), difficulty forming words to speak or understanding spoken words, dizziness, nausea, and sense of loss of balance and coordination (1,2,4). A CT or MRI scan is indicated within 24 hours of symptom onset (4). This is important to exclude the possibility of a small cerebral hemorrhage or a cerebral tumor that may be causing these symptoms (4). The results of a physical examination may be normal at the time of presentation; there may be no residual signs (1). During a TIA, consciousness is usually intact (3).

Prognosis

The natural history of the attacks is dependent on the patient (1,2,4). Some patients may have a major stroke after a few TIAs, whereas some may have frequent attacks for weeks or months without experiencing a stroke at all (1). The risk of having a stroke is high in the first 3 months of a TIA; more so in the first month and especially within the first 48 hours (1,5). The risk of stroke is 4.4% in the first month and 11.6% in the first year following the TIA (The major difference between a TIA and a stroke is that the stroke lasts at least 24 hours) (1,4,5). Without having any treatment, the risk of stroke is 12% in the first 90 days following a TIA, with half the risk in the first 48 hours (4). The risk of stroke over 5 years is estimated to be greater than 25% and the annual risk of MI is 2.4% (4).

Risk Factors

Non modifiable risk factors can include gender, ethnicity, heredity, and age. Ischemic stroke risk is higher in those that are greater than 55 years of age, in men and specifically in African Americans, Hispanics, and Asian Pacific Islanders (2,4). Patients who have a family history of stroke also have an increased risk of TIA (2,4). Modifiable risk factors include hypertension, which is the single most important risk factor (2,4). Trauma, cigarette smoking, cocaine use, heavy alcohol use, cerebral aneurysm, atrial fibrillation, physical inactivity, obesity, diet and oral contraceptive use with estrogen content greater than 50 mcg are all risk factors for TIA (2,4).

Place in Therapy

ASA is given as initial therapy for the prevention of stroke (3). The specific relative risk reduction of vascular events which include cardiac and cerebral effects is about 25% for high risk individuals (3). The protective effect is more modest in patients that have TIA or ischemic stroke as the relative risk reduction is approximately 15% for major vascular events (3). The recommended dose for stroke prevention is 50-325 mg/day (3). This medication is well tolerated; however it interacts with the garlic that AW is taking (7). The specific interaction is that garlic may enhance the toxic and adverse effects of salicylate (7).. The concomitant use of garlic, which has antiplatelet and anticoagulation properties with ASA should be avoided and therapy modification should be considered (7). If a patient experiences a TIA while on ASA, switching to clopidogrel or ASA with dipyridamole is recommended (3).

Clopidogrel 75 mg daily is slightly more effective than ASA in the prevention of ischemic events, including stroke (3). The absolute difference in the annual rate of having an ischemic stroke, MI or vascular death between ASA and clopidogrel is 0.5% (3). There is a 8.7% relative risk reduction that is in favor of clopidogrel (3). Clopidogrel is therefore used as an alternative antiplatelet agent in patients that are allergic to or cannot tolerate ASA (3). It is significantly more expensive than ASA (3). When combined with low-dose ASA, clopidogrel did not reduce the rate of ischemic events, including stroke significantly in patients with recent TIA (3). This combination increased the risk of bleeding and intracranial hemorrhaging significantly (3). Thus this combination should not be used for long term secondary prevention of ischemic events in patients that have a history of TIA (3).

Although ticlopidine 250 mg twice daily is at least comparable to ASA in prevention all vascular events in high risk patients and may be slightly superior in preventing strokes, however, the risk of developing neutropenia (which requires frequent monitoring (q 2 weeks for 3 months) limits its use in routine stroke prevention (3).

The combination of dipyridamole SR plus low dose ASA (200/25 mg) twice daily reduces the relative risk of stroke by 23% (mostly ischemic strokes) when compared with ASA in patients that have cerebral ischemic symptoms (3). A RCT showed that the incidence of death, stroke, MI or major bleeding complications was significantly less in patients that have cerebral ischemic treated with the combination rather than ASA alone (13% vs 16% over a 3.5 year period) (3).

Oral anticoagulants can prevent cerebral and systemic emboli in patients that have acute MI, valvular and nonvalvular atrial fibration (3). Vitamin K antagonists, like warfarin is superior to clopidogrel plus ASA in preventing vascular events in patients with atrial fibriliation at high risk for stroke (3).

A systematic review that examined patients with or without a previous history of stroke, TIA or CAD, found that statin therapy significantly reduced the risk of stroke compared to placebo or no treatment after an average follow up of 4.3 years (3). Furthermore, a RCT compared atorvastatin 80 mg/d verus placebo in patients that had a history of stroke or TIA within a period of 1 to 6 months before admitted to the study, LDL cholesterol levels of 2.6-4.9 mmol/L and no known coronary heart disease (3). The atorvastatin treatment was associated with a reduced overall incidence of stroke and cardiovascular events despite a small increase in the incidence of hemorrhagic stroke compared to placebo (3).

References

  1. Aminoff MJ, Kerchner GA. Chapter 24. Nervous System Disorders. In: McPhee SJ, Papadakis MA, Rabow MW, eds. CURRENT Medical Diagnosis & Treatment 2012 [online]. New York: McGraw-Hill; 2011 [cited 2011 Oct 29]. Available from: http://www.accessmedicine.com/content.aspx?aID=12507.
  2. Prabhakaran S, Wijdicks EFM, Misulis KE, Ferri F. Transient Ischemic Attack. MD Consult [online]. Maryland Heights MO: Elsevier Inc. 2011 [cited 2011 Nov 6]. Available from: www.mdconsult.com
  3. Repchinsky C, editor-in-chief. Therapeutic Choices. 6th ed. Canadian Pharmacists Association; 2011. p.550.
  4. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill; 2007. p. 375.
  5. Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, Hatsukami TS, et al. AHA/ASA Scientific Statement: Definition and Evaluation of Transient Ischemic Attack. Stroke 2009; 40:2276-2293. doi:10.1161/STROKEAHA.108.192218
  6. Prabhakaran S, Wijdicks EFM, Misulis KE, Ferri F. Transient Ischemic Attack. MD Consult [online]. Maryland Heights MO: Elsevier Inc. 2011 [cited 2011 Nov 6]. Available from: www.mdconsult.com
  7. ASA. In: Drug Monographs [online]. McGraw-Hill’s Access Medicine; No date [cited 2011 Nov 6]. Available from: http://www.accessmedicine.com/

Disclaimer

This information is presented for informational purposes only and is not meant to be a substitute for advice provided by qualified health care professionals. You should contact your qualified health care provider if you have or suspect any health problems. This article is not intended to provide medical advice for its readers


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