Transient ischemic attacks (TIA)

Defined associated a focal neurologic deficit of ischemic origin that lasts less than 24 hours.

In most episodes the symptoms last less than 4 hours and therefore the diagnosis is based on history rather than clinical findings.

New definition: A brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms (typically less than one hour) and without evidence of acute infarction.

These symptomatic focal cerebral ischemic events should be considered cerebral infarction come which May bev minor,  moderate, severe, or fatal and may or may not be detectable using modern imaging techniques.

Sometimes referred to a ministroke.Caused by inadequate cerebral blood flow.

Causes of TIA or minor ischemic stroke are similar to those of all ischemic strokes.

Many patients have previous cerebral infarcts demonstrated on MRI.

TIA’s and prior silent infarcts may contribute to vascular dementia.

Important marker for short and long-term vascular risk.

Harbinger for stroke with a 90 day stroke rate of approximately 11% and with recurrent TIA attack rate of approximately 13%.

Nearly half of 90 day stroke risk for TIA and minor stroke occurs within the first 48 hours after an event.

The risk is modifiable with intervention, such as aspirin or dual anti-platelet therapy with clopidogrel or ticagrelor-aspirin if it is initiated within 24 hours.

Without treatment the risk of a major stroke in the week after a TIA or minor stroke can be as high as 10%.

Without treatment, the risk of stroke is as high as 20% in three months, and most of this risk occurs within the first 10 days, particularly within the first two days.
Prompt clinical diagnosis and immediate preventive measures for TIA are associated with the decrease of up to 80% in the three month risk of stroke.
Some studies have shown that immediate treatment with antiplatelet agents and statins, and blood pressure control, reduce the risk by 70-80%, with the benefit attributed  mainly to aspirin, but the residual seven day risk of recurrent stroke is still 2-3%.

No other single antiplatelet drugs is superior to aspirin in the acute phase after TIA or minor stroke.

Approximately one fourth of ischemic strokes preceded by a transient ischemic attack, frequently only hours or days before the ischemic stroke.

The greatest risk for post-TIA stroke is within the first 48 hours, and the risk continues for 3 months.

Aside from the increased risk of ischemic stroke, patients with a TIA are at increased risk of a major adverse cardiovascular event-approximately 22% at one year.

In a population-based study from 1948-2017 the estimated TIA incidence was 1.19/ Thousand person years, and the risk of stroke was significantly greater after TIA compare with match participants who did not have a TIA, and risk of stroke after TIA was significantly lower in the most recent studies compared with earlier periods (Liootas V).

Half of individuals who have a TIA do not report the event.

Symptoms depend on the affected vascular territory.

Most common folcal neurologic signs are sudden onset of unilateral weakness and numbness or tingling in a limb.

Symptoms usually last for seconds or minutes and typically less than one hour.
Transient  symptoms can be motor, sensory, or visual, or they could involve a speech disturbance.
Other types of transient symptoms including: vertigo, diplopia, dizziness, unsteady gait, or amnesia can also occur with transit ischemic brain injury, however uncommonly the occurrence of these symptoms or signs in isolation is explained by ischemia.
Rarely transient neurologic symptoms may occur with migraine aura, peripheral vertigo, epilepsy, hypoglycemia, postural hypotension, and transient global amnesia.
Similarly, transient neurologic symptoms may occur with myasthenia, cervical arthrosis, peripheral nerve injury, multiple sclerosis, or hypokalemia, as well as cerebral edema myeloid angiopathy, subdural hematoma, or subarachnoid or brain hemorrhage.

TIA symptoms include: numbness of the face, hands, leg with or without weakness, paralysis, slurred speech, dizziness, double vision, hemianopia, blindness, confusion, headache, impaired balance, aphasia, and confusion.

Immediate MRI imaging is the current preferred test for patients with a suspected TIA: Its sensitivity in detecting brain ischemia is much higher than that of CT.
In up to 50% of patients with suspected TIA there is a bright spot on diffusion-weighted imaging indicating ischemia.
If diffusion-weighted imaging is negative and there is strong clinical suspicion of TIA, perfusion-weighted imaging may be performed during the same MRI examination.; in 30% of cases of focal perfusion deficit is identified in the brain corresponding to the symptoms.
Many ischemic events that were previously considered to be TIAs are now considered to be minor strokes on the basis of the presence of a bright spot or spots on diffusion weighted imaging.

MRI and CT of brain demonstrate 1/3 of TIAs caused infarcts.

When a TIA or minor ischemic stroke is considered evaluation includes an extra cranial and intracranial artery assessment with noninvasive imaging-carotid artery ultrasound, CT angiography, or magnetic resonance angiography of the cervical vessels and of intracranial vasculature to diagnose a proximal intracranial stenosis, occlusion, or both.

Additional evaluations should include electrocardiography, cardiac rhythm monitoring, and laboratory tests of C reactive protein, and erythrocytes sedimentation rate in patients with headaches with transit mono ocular blindness suggested of giant cell arteritis.

If the origin of the TIA is unclear after initial brain imaging and ECG further evaluation may include: prolonged cardiac monitoring.
Transthoracic and transesophageal echocardiography to detect cardiac structural abnormalities such as patient foramen ovale, atrial thrombus and valvular disease or atherosclerosis of the aortic arch may identify a source of cerebral embolism.

In a recent study of 1707 patients with emergency department presentation for TIA, 5.3% had a stroke within 2 days and 10.5% had a stroke within 90 days.

5% of patients who have a TIA will have an ischemic stroke within seven days.

The risk of stroke within three months after a TIA is approximately 10-20%, and is 24-29% over the following five years.

After a first episode of TIA or stroke aspirin or clopidogrel are the treatments of choice.

Clopidogrel may be preferred over aspirin when aspirin intolerance is present.

For patients who develop recurrent TIA while on aspirin extended release dipyridamole combined with aspirin or clopidogrel alone.

Treatment for TIA reduces the risk of early recurrent stroke by 80%.

A loading dose of aspirin 300 mg orally should be administered as soon as possible after TIA symptoms.

Aspirin should be continued for a dose of 75 to 100 mg per day for 90 days.

For patients developing TIA or stoke on clopidogrel, extended release dipyridamole and aspirin is an option.

Dual antiplatelet agents are more affective than monotherapy.

Anticoagulant treatment is not superior to aspirin in patients with non-cardio embolic TIA or stroke.

Of those related to severe carotid stenosis, 12-13% will experience a stroke within the first year after symptoms begin and 30-35%, before the end of 5 years.

An international multicenter registry study observed a substantial reduction in 30-day and 90-day stroke risk after a TIA presentation in patients on statins, if they had evidence of carotid stenosis, but not otherwise (Merwick A et al.).

Statins reduce stroke risk when initiated months after transient ischemic attack (TIA)/stroke.

Statins reduce early vascular events in acute coronary syndromes.

In acute symptomatic carotid stenosis, statin pretreatment was associated with reduced stroke risk supporting the hypothesis that statins started acutely after TIA symptom onset may also be beneficial to prevent early stroke.

Aggressive secondary prevention measures after an ischemic stroke or a TIA can substantially reduce the risk of recurrent ischemic stroke.

In the setting of ischemic stroke for TIA using high intensity lipid lowering therapy to achieve specific LDL target of less than 70 mg/dL that may reduce future events.

Secondary prevention for recurrent strokes and cardiovascular events include: blood pressure reduction, glycemic control in patients with diabetes, statin therapy with intensive lipid lowering in patients with evidence of atherosclerosis, and LDL level of greater than 100 mg/dL, smoking cessation, antiplatelet therapy with aspirin, and anticoagulation in patients with atrial fibrillation.

The ABCD scale calculated on the basis of age, blood pressure, presence of clinical weakness with speech disturbance, duration of symptoms, and the presence or absence of diabetes is used to project the risk of stroke.
ABCD scores range from 0 to 7 with higher scores indicating a greater risk of stroke.
ABCD-one score includes  findings of diffusion weighted imaging of the brain and improves risk reduction over ABCD score alone.
The ABCD scoring has not been found to be clinically relevant since patients with low and high scores frequently have similar stroke incidence.
Aspirin in non-embolic ischemic stroke is the most effective treatment to reduce the risk of recurrent stroke during the first 90 days, and is the only antiplatelet treatment shown to reduce the risk of recurrent disabling ischemic stroke during that time.
Beyond three months the efficacy of aspirin is less clear.
All patients should receive aspirin immediately after a TIA unless aspirin is contraindicated.

Dual antiplatelet therapy is indicated for high-risk patients with increased risk of bleeding versus decreased stroke incidence.

In patients  with TIA long-term treatment involves blood pressure management, lipid lowering therapy and control of diabetes, smoking cessation and lifestyle changes.

There are decreases in the risk of stroke and overall cardiovascular events with high dose statins.
 Carotid  or stenting should be considered  in patients  in whom underlying cause of the TIA is ipsilateral internal carotid artery stenosis of 50% or more.

Stenting intracranial stenosis is not usually recommended.

Among patients with mild ischemic stroke or high risk TIA of presumed atherosclerotic cause, combined clopidogrel and aspirin therapy initiated within 72 hours after stroke onset lead to a lower risk of new stroke at 90 days than aspirin therapy alone, but was associated with a low but higher risk of moderate to severe bleeding. (INSPIRES investigators).


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