Transient Ischemic Attack

Article Author:
Kiran Panuganti
Article Author (Archived):
Prasanna Tadi
Article Editor:
Forshing Lui
Updated:
3/21/2019 12:28:11 AM
PubMed Link:
Transient Ischemic Attack

Introduction

A transient ischemic attack is a medical emergency. It is defined as a transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia, without acute infarction or tissue injury. The definition of a TIA has moved from time-based to tissue-based. A TIA typically lasts less than an hour, more often minutes. TIA can be considered as a serious warning for an impending ischemic stroke; the risk is highest in the first 48 hours following a transient ischemic attack. Differentiating transient ischemic attack from other mimicking conditions is important. Transient ischemic attacks are usually associated with a focal neurologic deficit and/or speech disturbance in a vascular territory due to underlying cerebrovascular disease. It is always sudden in onset. Evaluation of TIA should be done urgently with imaging and laboratory studies to decrease the risk of subsequent strokes. The subsequent risk of TIA or ischemic stroke can be stratified with a simple clinical measure. Immediate multimodality therapeutic interventions should be initiated. These will include aggressive treatment of blood pressure, high dose statin, antiplatelet therapy, blood sugar control, diet, and exercises. Specific underlying etiology needs to be managed accordingly. This treatment scheme may substantially reduce the risk of recurrent strokes or future TIA by at least 80%.[1][2][3]

Etiology

TIA subtypes, classified according to the pathophysiological mechanisms are similar to ischemic stroke subtypes. They include large artery atherothrombosis, cardiac embolism, small vessel (lacunar), cryptogenic, and uncommon subtypes such as vascular dissection, vasculitis etc. The common risk factors for all TIA include diabetes, hypertension, age, smoking, obesity, alcoholism, unhealthy diet, psychosocial stress, and lack of regular physical activity. A previous history of stroke or TIA will increase substantially the subsequent risk of recurrent stroke or TIA.[4][5] Among all risk factors, hypertension is the most important one for an individual as well as in a population.

Epidemiology

TIA incidence in a population is difficult to estimate due to other mimicking disorders, but TIA incidence in the United States could be around half a million per year, and estimates are about 1.1 per 1000 in the United States population. The estimated overall prevalence of TIA among adults in the United States is approximately 2%. It has been shown that previous stroke history increases the prevalence of TIA. Few studies have shown that the majority of people who presented with initial stroke had prior TIA symptoms.[4]

Pathophysiology

The pathophysiology of TIA depends on the subtype as follows. The common issue is the transient interruption of arterial blood flow to an area of the brain supplied by that particular artery.

  • Large artery atherothrombosis. This may be intracranial or extracranial atherothrombosis. The mechanism may be lack of blood flow distal to the site of arterial stenosis or an artery to artery embolism which is actually the more common mechanism.
  • Small vessel ischemic diseases. The underlying pathology is either lipohyalinosis or small vessel arteriolosclerois. The commonest risk factor is hypertension followed by diabetes and age.
  • Cardiac embolism. A clot in the cardiac chamber most commonly in the left atrium secondary to atrial fibrillation.
  • Cryptogenic. This is usually a cortical pattern of ischemia without any identifiable large artery atherothrombosis or cardiac source of emboli. More recently it is often referred to as ESUS (embolic stroke of unknown source).
  • Other uncommon causes such as arterial dissection or hypercoagulable states. 

History and Physical

TIA symptoms have often resolved by the time the patients presented to her doctor or emergency department. The history of present illness should include onset, duration, timing, complete neurological symptoms, their associated symptoms, and any aggravating or relieving factors. The clinician should also try to identify the associated risk factors such as coronary artery disease, smoking, drug abuse, obesity, diabetes mellitus, dyslipidemia, and hypertension, as well as personal or family history of hypercoagulability disorders, stroke, or TIA. The history should include etiological clues such as a history of atrial fibrillation, recent myocardial infarction to suggest a cardioembolic source, transient loss of vision like a curtain rising or descending will suggest an internal carotid artery problem. Presence of any cortical symptoms such as language disturbance or visual field loss will point to a cortical TIA rather than a lacunar syndrome. 

Physical examination should focus on identifying focal neurological deficits and speech disturbances which are the most common presenting symptoms in patients with TIA. Cranial nerve examination can yield findings of monocular blindness, disconjugate gaze, facial droop, hemianopia, diplopia, abnormal tongue movement, difficulty swallowing, and auditory dysfunction. Some of the motor findings include unilateral weakness in the upper or lower extremities, face, and tongue, increased tone, clonus, rigidity and also abnormal reflexes could occur with TIA. Cardiac examination and carotid auscultation for a carotid bruit are very important. Fundoscopy is important to look for any fundoscopic evidence of vascular changes as a result of hypertension or diabetes. It may also show a Hollenhurst plague which will indicate an underlying internal carotid artery disease.

Evaluation

The goals of evaluation of TIA are

  1. To prove the vascular origin of the symptoms either directly or indirectly. This means to find evidence of hypoperfusion and/or acute infarction or identify a presumptive source such as a large-vessel stenosis
  2. To exclude an alternative nonischemic origin
  3. To determine the underlying vascular mechanism, for example, large-vessel atherothrombotic, cardioembolic, small-vessel lacunar. This determination allows selecting the optimal therapy for secondary prevention of TIA pr stroke.
  4. To identify prognostic outcome categories.

The 2009 AHA/ASA guidelines include "neuroimaging within 24 hours of symptom onset and further recommend MRI and diffusion-weighted MR imaging as preferred modalities." A head CT preferably with CT angiogram is recommended if an MRI cannot be performed. Brain MRI with diffusion-weighted imaging has a greater sensitivity than CT for detecting small infarcts in patients with TIA. The practitioner should assess the patient's cervicocephalic vasculature for atherosclerotic lesions using carotid ultrasonography/transcranial Doppler ultrasonography, magnetic resonance angiography, or CT angiography. These lesions are treatable. In candidates for carotid endarterectomy, carotid imaging should be performed within 1 week of the onset of symptoms. Cardiac assessment should be done with ECG, Echocardiogram/TEE  to find a cardioembolic source and the presence of patent foramen ovale, valvular disease, cardiac thrombus, and atherosclerosis. Holter monitor or more prolonged cardiac rhythm monitor in the outpatient setting is reasonable for patients with cortical infarct without any clear source of emboli, primarily to evaluate for paroxysmal atrial fibrillation. Routine blood tests including complete blood count (CBC), PT/INR, CMP, FBS, lipid panel, urine drug screen, and ESR should be considered.[6][7][5].

National Stroke Association has established guidelines for TIA evaluation as follows in 2006:[8]

CBC = complete blood countCEA = carotid endarterectomyTCD = transcranial Doppler TEE = transesophageal echocardiogramTTE = transthoracic echocardiogram

ABCD2 score is very important for predicting subsequent risks of TIA or stroke. The ABCD2 score was derived from providing a more robust prediction standard. The ABCD2 score includes factors including age, blood pressure, clinical symptoms, duration, and diabetes.

  • Age: older than 60 years (1 point)
  • Bood pressure greater than or equal to 140/90 mmHg on first evaluation (1 point)
  • Clinical symptoms: focal weakness with the spell (2 points) or speech impairment without weakness (1 point)
  • Duration greater than 60 min (2 points), or 10 min to 59 min (1 point)
  • Diabetes mellitus (1 point).

The 2-day risk of stroke was 0% for scores of 0 or 1, 1.3% for 2 or 3, 4.1% for 4 or 5, and 8.1% for 6 or 7. Most stroke centers will admit patients with TIA to the hospital for expedited management and observation if the score is 4 or 5 or higher. For those patients who have a lower score, expedited evaluation and management is still warranted. This expedited approach has been proven to improve the outcome. [9]

Treatment / Management

The main aim of treatment of TIA is to decrease the risk of subsequent stroke or TIA. Early treatment after a TIA can significantly reduce the risk of early stroke. Post TIA, the risk of stroke within 3 months has been reported to be around 20%, with approximately 50% of these strokes occurring within the first 2 days after initial presentation. It is extremely important to evaluate the vessel status and look for atrial fibrillation when a patient comes with TIA. This will significantly reduce future strokes. Management of TIAs should focus on treating underlying etiologies.[10][11][12]

Studies in the new millennium already confirmed the importance of expedited evaluation and treatment plus the polytherapy approach. The EXPRESS study in the UK has shown the importance of early intervention versus regular treatment by reducing 80% of the stroke risk. [13] Hackam et al did a meta-analysis in 2007 showing that combination of diet, exercise, antiplatelet, statin and antihypertensive therapy may reduce the subsequent stroke by 80-90%.[14]

More recent studies in China (CHANCE trial) and the multinational POINTE trail also confirmed dual antiplatelet with aspirin and clopidogrel for 3 weeks to 1 month followed by a single antiplatelet agent is the best scheme for antiplatelet therapy. [15][16]

The other part of the treatment will depend on the underlying etiology of the TIA. Revascularization is recommended for symptomatic cervical internal carotid artery stenosis of 70% or higher. Carotid endarterectomy may have a slight benefit to risk ratio compared with endovascular intervention and stenting. Whether to operate on patients with 50-69% stenosis will depend more on the surgeon's complication rates given the vast improvement in the efficacy of aggressive medical therapy. SAPPRIS trial showed that endovascular Wingspan stenting of intracranial major arterial stenosis of 70-99% stenosis is not better than aggressive medical therapy alone. [17]

Oral anticoagulation is indicated for patients with atrial fibrillation or other sources of cardioembolic sources of TIA.

Staging

Risk Stratification Scores

To help physicians manage patients with a TIA, several risk stratification scores have been developed. One widely used score is the ABCD2 score:

A= Age more than 60 years / Score 1

B= SBP> 140 or DBP> 90 / Score 1

C= Clinical features:

Speech impairment without weakness / Score 1

Weakness with/without speech impairment / Score 2

D= Duration

More than 60 mins / Score 2

Between 10-59 mins / Score 1

D= Diabetes / Score 1

Patients with an ABCD2 score of 6-7 have an 8% risk of stroke within 48 hours

Patients with an ABCD2 score of less than 4 have a 1% risk of stroke within 48 hours

Even though scales are important in the evaluation of TIA, be aware that patients with critical carotid artery stenosis may some times present with a very low ABCD2 score.

Pearls and Other Issues

Differentiating other potential causes which mimic TIA is important since diagnosing and treating TIA early can potentially help in preventing a future stroke. Differential diagnosis of TIA includes but is not limited to vertigo, dizziness, seizures, headaches, bells palsy, drug withdrawal, dementia, electrolyte disorders, acute infections, syncope, and alcoholism.

Enhancing Healthcare Team Outcomes

Patients with a TIA often present to the emergency department or the primary caregiver. Because there is a real risk of a severe stroke, it is important that these patients are managed with an interprofessional team of healthcare workers. The triage nurse must be familiar with the symptoms of a TIA and when to call the neurologist. The early risk of stroke varies from 4-9% within 90 days and without treatment, the risk of a stroke within five years varies from 20-30%. At the same time, these patients also have the same risk factors for adverse cardiac events. Once a TIA has been diagnosed, the patient must be referred to a neurologist. At the same time, the patient should be educated about the importance of blood pressure control, discontinuing smoking and eating a healthy diet. Finally, the patient should be educated about the symptoms of a stroke and when to seek immediate medical assistance. [18][19](Level V)


References

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