Neuroscience Clerkship

TRANSIENT ISCHEMIC ATTACKS

Transient ischemic attacks (TIAs) are brief episodes of acute cerebral ischemia with neurological deficits referable to a vascular distribution with subsequent rapid complete resolution.

There should be no evidence of neurological injury on physical exam or imaging studies.  The deficits usually resolve in 5-20 minutes, although the traditional definition of TIA allows for up to 24 hours for symptoms to resolve.  Nevertheless, many so called “TIAs” in the past were actually strokes that older MRI and CT imaging techniques were not capable of detecting early on.  It is important not to wait for TIA symptoms to resolve, as many TIAs are actually strokes in progress, and some patients may be eligible for thrombolytic treatment with TPA with the potential for reversing the stroke.

A resolved TIA should be taken as an alarm that a stroke could occur in the near future.  After having a TIA, the subsequent risk of stroke in the next year is about 10%, and about 20% of these strokes occur within a month.  Depending upon the etiology of TIA, the risk of future stroke can be as much as 15% in the first year, such as in the case of symptomatic carotid stenosis.  Thus, any patient presenting with symptoms of a TIA warrants an immediate and thorough workup, as many strokes can be prevented by medical or surgical intervention.  Interestingly, the main cause of death in people who have TIA is from a myocardial infarction.  Therefore, it may be wise to give a thorough look into cardiac risk factors after TIA as well.

Symptoms suggestive of anterior (carotid) circulation TIA

Symptoms suggestive of posterior (vertebrobasilar) circulation TIA

Symptoms not acceptable by themselves as evidence of TIA

Table adopted from Bradley, Daroff et.al.  Neurology in Clinical Practice, Fourth Edition, Vol II, 1202

Etiology of TIA:

Large Vessel:

-Secondary to stenosis of internal carotid, vertebrals or large arteries originating from the Circle of Willis such as the anterior cerebral (ACA) or middle cerebral (MCA) arteries.

- Usually recurrent, with stereotyped neurological deficits due to ischemia in the same vascular distribution each event. 

- May be triggered by hypoperfusion across a stenotic vessel, intrinsic thrombosis, or emboli from an ulcerated plaque.

Embolic:

-  May be secondary to cardiac embolus, aortic arch atheroma, or rarely from clot traversing from the venous to arterial circulation (i.e., right to left shunt).

-  Clinical presentation is usually a neurological deficit maximal at onset.

Small Penetrating Vessel (lacunar):

-  Secondary to intrinsic lipohyalinosis or micro-atheroma in a small penetrating artery in the subcortex.

-  Deficits may wax and wane, and have repetitive stereotyped symptoms.

-  Neurological deficits may fit with a lacunar syndrome such as pure motor hemiparesis, pure hemi-sensory loss, or clumsy-hand dysarthria

-  No cortical findings such as aphasia, visual field loss, gaze preference, or neglect syndrome are present.

Other Determined Causes:

-Vasculopathy, vasospasm, watershed hypoperfusion, or hypercoagulable state.

Undetermined cause (crytogenic):

- This classification is used when no clear cause of TIA/stroke is found after an extensive workup

Differential Diagnosis of TIA

- Transient migrainous attack

- Seizures

- Hypoglycemia

- Space-occupying lesions (symptoms from pressure or seizures)

- Syncope

- Labyrinthine disorders (e.g., Meniere’s disease)

- Transient global amnesia

- Psychogenic

Initial baseline workup and imaging for most patients:

- CBC, coags, lytes, BUN, Cr, UA, lipid panel, ECG, CXR

- Uncontrasted CT head to detect possible hemorrhage.

- Uncontrasted MRI brain with diffusion weighted imaging

- Uncontrasted MRA of the intracranial and extracranial circulation

Further workup depends on initial findings

and may include:

- Cardiac telemetry monitoring

- Transthoracic or transesophageal echocardiography (TTE or TEE)

- Carotid duplex ultrasonography

- Angiography

- Hypercoagulable laboratory testing

Treatment:  depends on etiology
 

Symptomatic High Grade Carotid Stenosis

Surgical intervention for symptomatic carotid stenosis has been shown to reduce the risk of recurrent stroke in the North American Symptomatic Carotid Endarterectomy Trial (NASCET). The stenosis must be > 70% and the surgical morbidity of the procedure must be < 3%. Endovascular techniques are an alternative, but there is little data comparing the two.
 

Small Vessel Disease

Modification of stroke risk factors is essential, such as hypertensive management and smoking cessation.

Anti-platelets such as aspirin or clopidogrel are generally used.

Cardiac Embolus

There is evidence based medicine to show that recurrent TIA and stroke is reduced with anticoagulation (heparin and warfarin therapy).

Cyptogenic Embolus

In patients who have a TIA or stroke suggestive of an embolus, they may be placed on IV heparin until the full workup is complete. However, if no source is found, this is evidence-based medicine that antiplatelets and anticoagulation are of equal efficacy in this situation.

Hypercoaguable States
 

In the absence of contraindications, patients are treated with anticoagulation. 

Inoperable Carotid Stenosis and Posterior Circulation Stenosis

Patients are generally treated with antiplatelets. Selected cases may warrant endovascular stenting, but future research is needed to determine the proper use of these techiques.