You suffered a mini-stroke ...what to do now? You were told you apparently had a mini-stroke (in medical terminology a transient ischemic attack or TIA). I explain below what is a TIA, how different…

[Dr Alain L Fymat]

You suffered a mini-stroke ...what to do now?

You were told you apparently had a mini-stroke (in medical terminology a transient ischemic attack or TIA). I explain below what is a TIA, how different is it from a stroke, what are its signs, symptoms and risks, why a thorough and competent neurologic exam is necessary, what are the possible causes, how is a diagnosis to be arrived at, and what are your treatment options. I will also discuss the medications usually prescribed in North America for this condition and also offer some recommendations.

What is a TIA? A TIA is defined as:

• A brief episode of neurological dysfunction,
• with a vascular cause, that is loss of blood flow (ischemia) in the brain (also perhaps the spinal cord or the retina),
• with clinical symptoms typically lasting on the order of minutes to 1-2 hours but, occasionally, may last longer (a study from 10 hospitals showed that 60% lasted less than 1 hour, 71% lasted less than 2 hours, and 14% lasted greater than 6 hours), and
• without evidence of tissue death (infarction) on imaging testing.

Of course, symptoms that last more than one hour are more likely to have permanent neurologic damage, making prompt diagnosis and treatment important to maximize recovery. In a full-blown (not transient) stroke, where the loss of cerebral blood flow lasts longer (it can persist beyond 7 days), the damage is extensive and accompanied by tissue death.

QUESTION # 1: How long did my episode last?

What are the signs and symptoms? Both a TIA and a stroke present the same symptoms (although not all symptoms may be present). I have listed them below for you to identify what you actually felt during that episode (my acronym: GANCSD5):

• Weakness or numbness on one side of the body, occurring generally on the opposite side of the body from the affected hemisphere of the brain.
• Sudden dimming or temporary loss of vision or double vision (diplopia) or other visual field deficits.
• One-sided facial droop.
• Sensory deficits in one or more limbs or of the face.
• One-sided motor weakness (difficulty walking, awkward gait).
• Problems with balance and spatial orientation or dizziness.
• Difficulty understanding or expressing speech (aphasia).
• Slurred speech or difficulty with articulation of speech (dysarthria). 
• Difficulties with swallowing (dysphagia).
• Confusion.

QUESTION # 2: Which of these symptoms did you notice?

What are the risk factors? They are categorized as either non-modifiable or modifiable. Thus:

• Non-modifiable risk factors: They include age (greater than 55), sex (more men than women are affected), family history, genetics, and race/ethnicity.
• Modifiable risk factors: They include cigarette smoking, hypertension (elevated blood pressure), diabetes, hyperlipidemia, level of carotid artery stenosis, and activity level.

Only the modifiable risk factors are commonly targeted in treatment options to attempt to minimize a further risk of TIA.

QUESTION # 3: What modifiable risk factors were identified in your case? In particular, did you have an echocardiography of your carotid arteries to ascertain they are clear? If not, I strongly recommend you arrange to have one done promptly.

A thorough and competent neurologic exam is needed - Because the above symptoms are widely variable and can mimic other neurologic conditions, and because of the several risk factors, a thorough and competent clinical exam is important in ruling-in or -out the initial diagnosis. This should consist of a detailed neurologic exam, including a thorough cranial nerve exam to ascertain it was indeed a TIA and not another neurologic condition it mimics.

QUESTION # 4: Do you believe you were administered such an exam?

What are the possible causes? There are 4 possible causes (my acronym: FETS):

• Atrial fibrillation (or Afib): This is the most common cause. It is a poor coordination of the heart's contraction. It leads to the formation of a clot in the atrial chamber that can become dislodged and travel to a cerebral artery. If the blood flow is restored prior to infarction, the problem is resolved. Note: Afib increases stroke risk by five times.

• Remote embolism: This is also common. An atherosclerotic plaque located in the common carotid artery or a portion of it can become dislodged and relocate in the cerebral vessels.

• In-situ thrombosis: Unlike the remote embolism, this obstruction is formed directly in the cerebral vasculature.

• Carotid stenosis secondary to atherosclerosis: This is a narrowing of the diameter of the blood vessel thus limiting blood flow.

QUESTION # 5: Were you told which of the above may have been the cause(s) of your TIA? Note, again, the issue of the carotid artery.

What should be done to reach a correct diagnosis? There are 10 elements (my acronym: ELBES-LIIEI) although not all may be required:

• Initial clinical evaluation: obtaining a history and a physical exam (including a neurological exam). Here, the time course (onset, duration, and resolution), precipitating events, and risk factors are particularly important.

• Laboratory work-up: Laboratory tests should focus on ruling-out metabolic conditions that may mimic TIA (e.g. hypoglycemia causing altered mental status), in addition to further evaluating the risk factors for ischemic events. This includes:

• Complete blood count (acronym: PGMPT) with

  • Platelet count.

  • Blood glucose.

  • Basic metabolic panel. 

  • Prothrombin time/international normalized ratio,.

  • Activated partial thromboplastin time.  

• These tests help with screening for bleeding or hypercoagulable conditions.

Electrocardiogram: Necessary to rule-out abnormal heart rhythms, such as atrial fibrillation (one of the four causes listed above).

Full hypercoagulable state work-up or serum drug screening: Should be considered based on the clinical situation and factors, such as age and family history.

Fasting lipid panel: Appropriate to thoroughly evaluate the risk for atherosclerotic disease and ischemic events in the future.

Inflammatory markers (erythrocyte sedimentation rate and C-reactive protein): To evaluate for giant cell arteritis (which can mimic a TIA) in those presenting with headaches and monocular blindness.

Imaging: Head imaging within 24 hours of symptom onset, preferably with magnetic resonance imaging, including diffusion sequences. Diffusion sequences can help further localize the area of ischemia and can serve as prognostic indicators. Presence of ischemic lesions on diffusion-weighted imaging has been correlated with a higher risk of stroke after a TIA.MRI is a better imaging modality for TIA than computed tomography (CT), as it is better able to pick up both new and old ischemic lesions than CT. CT, however, is more widely available and can be used particularly to rule-out intracranial hemorrhage.

Carotid endarterectomy (surgery): The vasculature can be evaluated through the following imaging modalities: 

• Magnetic resonance angiography (MRA), 

• CT angiography (CTA), and 

• Carotid ultrasonography/transcranial doppler ultrasonography: This is often used to screen for carotid artery stenosis, as it is more readily available, is noninvasive, and does not expose the person being evaluated to radiation.

• However, all of the above imaging methods have variable sensitivities and specificities, making it important to supplement one of the imaging methods with another to help confirm the diagnosis (for example: screen for the disease with ultrasonography but confirm with CTA). Confirming a diagnosis of carotid artery stenosis is important because the treatment for this condition, carotid endarterectomy, can pose significant risk, including heart attacks and strokes after the procedure.

QUESTION # 6: You may opt to have a discussion with your clinician about the risks and benefits of screening for carotid artery stenosis, including the risks of surgical treatment of this condition, if needed.

• Cardiac imaging: It can be performed if head and neck imaging do not reveal a vascular cause for the TIA (such as atherosclerosis of the carotid artery or other major vessels of the head and neck). Echocardiography can be performed.

QUESTION # 7: Which of the above two tests were done?

What are the treatment options? By definition, TIAs are transient, self-resolving, and do not cause permanent impairment. However, they are associated with an increased risk of subsequent ischemic strokes, which can be permanently disabling. Therefore, management centers around the prevention of future ischemic strokes and addressing any modifiable risk factors. The optimal regimen depends on the underlying cause of the TIA. Measures include:

• Lifestyle modifications: Unfortunately, they have not been shown to reduce the risk of stroke after TIA. Nonetheless, keep in mind the DESS principle (Diet such as a Mediterranean diet or the MIND diet, Exercise, Stress, and Sleep). A Mediterranean diet is rich in fruits, vegetables, and whole grains, and is limited in red meats and sweets. Vitamin supplementation has not been found to be useful. However, it is recommended to:

  • Avoid smoking.

  • Cutting down on fats: to help reduce the amount of plaque buildup.

  • Eating a healthy diet: including plenty of fruits and vegetables.

  • Limiting sodium: in the diet, thereby reducing blood pressure.

  • Exercising (cardio) regularly.

  • Moderating intake of alcohol, stimulants, sympathomimetics, etc.

  • Maintaining a healthy weight.

  • In addition, it is important to control any underlying medical conditions that may increase the risk of stroke or TIA, including:

    • Hypertension.

    • High cholesterol.

    • Diabetes mellitus.

    • Atrial fibrillation.

• Antiplatelet medications: Aspirin and Plavix/clopidogrel are both recommended for secondary prevention of stroke after high-risk TIA. The clopidogrel can generally be stopped after 10 to 21 days. After a TIA or a minor stroke, aspirin therapy has been shown to reduce the short-term risk of recurrent stroke by 60-70%, and the long-term risk of stroke by 13%. However, a study conducted by Dr. Robert Hart, Professor of Neurology at McMaster University in Hamilton, Ontario, Canada has shown that plavix adds little if anything to aspirin alone in reducing the risk of a further incident.
• Anticoagulants: If the TIA is due to either Afib or a blood clot originating from the heart (causes # 1 and #3). Anticoagulant therapy can decrease the relative risk of ischemic stroke in those with atrial fibrillation by 67%.Warfarin is a common anticoagulant used, but direct acting oral anticoagulants (DOACs), such as apixaban, are equally effective while also conferring a lower risk of bleeding.
• Combined anticoagulants and antiplatelet therapy: Generally, anticoagulants and antiplatelets are not used in combination, as they result in increased bleeding risk without a decrease in stroke risk. However, the combination may be warranted only if the patient has symptomatic coronary artery disease in addition to atrial fibrillation (Causes #1 and #4).
• Blood pressure control: About 70% of patients with recent ischemic stroke are found to have hypertension, usually defined as systolic blood pressure (SBP) > 140 mmHg, or diastolic blood pressure (DBP) > 90 mmHg. Until the first half of the 2010s, blood pressure goals have generally been SBP < 140 mmHg and DBP < 90 mmHg. However, newer studies suggest that a goal of SBP <120 and a DBP<80 mmHg may confer even greater benefit. The optimal treatment regimen for blood pressure control depends on the individual and is often achieved using:

  • Diuretics.

  • Niacin.

  • A combination of diuretics and angiotensin converter enzyme (ACE) inhibitors.

  • Beta-blockers.

  • Calcium channel blockers.

• Cholesterol control: While its role in stroke prevention is currently unclear, statin therapy has been shown to reduce all-cause mortality and may be recommended after TIA.
• Diabetes control: Diabetes mellitus increases the risk of ischemic stroke by 1.5-3.7 times, and may account for at least 8% of first ischemic strokes. There is little evidence that intensive glucose control can decrease the risk of stroke or death. However, metformin, pioglitazone, and semaglutide may reduce stroke risk.

QUESTION # 8: What treatment options were you offered and are they congruent with the above indications.

• What is the prognosis for a stroke occurring after a TIA? The risk can be predicted using the so-called ABCD² score (available to cardiologists). One limitation of the ABCD² score is that it does not reliably predict the level of carotid artery stenosis, which is a major cause of stroke in TIA patients.

QUESTION # 9: Please see your cardiologist to assess your future risk.

• What are the medications usually prescribed? In addition to medications for pre-existing conditions, they usually include:
• 1/ Aspirin (baby dose 81 mg).
• 2/ Plavix/clopidrogel: An antiplatelet.
• 3/ Atorvastatin/Lipitor: Only because of the TIA. Cholesterol levels should be regularly monitored as the statin may have to be changed. (There are 9 of them and combinations thereof - see my previous blog on statins.)
• 4/ Amlodipine: A calcium channel blocker used to treat hypertension. It may have a nasty side effect (swelling of ankles). If that is the case, the dose may be reduced to 2.5 mg. If not resolved, the medication may have to be changed. There are plenty of them.
• Note: Atorvastatin + Amlodipine also come in a single tablet.

QUESTION # 10: Do the medications prescribed conform to the above indications?