Transient Ischemic Attack

Article Author:
Kiran Panuganti
Article Editor:
Scott Dulebohn
Updated:
2/17/2019 9:23:02 AM
PubMed Link:
Transient Ischemic Attack

Introduction

A transient ischemic attack can be considered as a prodrome for stroke. It is a transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia, without acute infarction. The definition of a TIA has changed from to tissue-based from time-based. TIA is one of the major risk factors for Ischemic stroke; the risk is highest in the first 48 hours following a transient ischemic attack. Differentiating transient ischemic attack with other mimicking conditions is important. Transient ischemic attacks are usually associated with a focal neurologic deficit and speech disturbance and are sudden in onset. Evaluation of TIA should be done urgently with imaging and laboratory studies to decrease the burden of future strokes. Modifiable risk factors should be identified and treated. Immediate therapeutic interventions should be initiated. This may substantially reduce the risk of recurrent strokes or future TIA.[1][2][3]

Etiology

Usually, transient ischemic attacks are caused by three main mechanisms: low-flow TIAs, embolic TIAs, and lacunar TIAs. Several risk factors are cause them. These factors include diabetes, hypertension, age, smoking, obesity, alcoholism, unhealthy diet, psychosocial stress, and regular physical activity. A previous history of stroke, especially posterior circulation ischemic stroke, can also cause recurrent TIAs.[4][5]

ABCD score is used for predicting future stroke risk. The newer, ABCD2 score was derived from providing a more robust prediction standard. The ABCD2 score includes factors such as 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 point), 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.

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

Four pathologic processes give rise to low-flow or embolic TIA. These can produce sudden, devastating stroke if not recognized and treated:

  1. Internal carotid artery stenosis due to atherothrombotic lesions which are greater than 70%
  2. TIA due to lesions of the distal vertebral artery, vertebrobasilar junction, and proximal basilar artery; these are from low-flow or emboli arising from intracranial atherothrombotic disease
  3. Emboli at the top of the basilar artery or the middle cerebral artery stem that come from either arterial, aortic, or cardiac source
  4. Dissection at the origin of the petrous portion of the internal carotid artery or at the C1-2 level of the vertebral artery as it enters the foramen transversarium.

History and Physical

TIA symptoms can often resolve on initial presentation. A 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.

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. Other nonspecific findings like dizziness and vertigo can occur.

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
  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 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 in the outpatient setting is reasonable, 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]

Treatment / Management

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. Management of TIAs should focus on treating underlying etiologies.[8][9][10]

Antiplatelets agents are the treatment of choice for TIA. Per stroke guidelines, aspirin, Plavix and extended-release dipyridamole/aspirin (Aggrenox) are acceptable first-line agents. Revascularization is recommended for symptomatic cervical internal carotid artery stenosis, Fifty percent to 99% who have a life expectancy of at least 5 years are usually treated with carotid endarterectomy. Blood pressure reduction, antithrombotic therapy, statin therapy, and lifestyle modification should be initiated for selected patients. Oral anticoagulation should also be considered for patients with atrial fibrillation and 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

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 a multidisciplinary 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. [11][12](Level V)