Transient ischemic attack
A transient ischemic attack, commonly known as a mini-stroke, is a temporary stroke with noticeable symptoms that end within 24 hours. A TIA causes the same symptoms associated with a stroke, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language or slurred speech.
All forms of stroke, including a TIA, result from a disruption in blood flow to the central nervous system. A TIA is caused by a temporary disruption in blood flow to the brain, or cerebral blood flow. The primary difference between a major stroke and a TIA's minor stroke is how much tissue death can be detected afterwards through medical imaging. While a TIA must by definition be associated with symptoms, strokes can also be asymptomatic or silent. In a silent stroke, also known as a silent cerebral infarct, there is permanent infarction detectable on imaging, but there are no immediately observable symptoms. The same person can have major strokes, minor strokes, and silent strokes, in any order.
The occurrence of a TIA is a risk factor for having a major stroke, and many people with TIA have a major stroke within 48 hours of the TIA. All forms of stroke are associated with increased risk of death or disability. Recognition that a TIA has occurred is an opportunity to start treatment, including medications and lifestyle changes, to prevent future strokes.
Signs and symptoms
Signs and symptoms of TIA are widely variable and can mimic other neurologic conditions, making the clinical context and physical exam crucial in ruling in or out the diagnosis. The most common presenting symptoms of TIA are focal neurologic deficits, which can include, but are not limited to:- Amaurosis fugax
- One-sided facial droop
- One-sided motor weakness
- Diplopia
- Problems with balance and spatial orientation or dizziness
- Visual field deficits, such as homonymous hemianopsia or monocular blindness
- Sensory deficits in one or more limbs and of the face
- Loss of ability to understand or express speech
- Difficulty with articulation of speech
- Unsteady gait
- Difficulties with swallowing
A detailed neurologic exam, including a thorough cranial nerve exam, is important to identify these findings and to differentiate them from mimickers of TIA. Symptoms such as unilateral weakness, amaurosis fugax, and double vision have higher odds of representing TIA compared to memory loss, headache, and blurred vision. Below is a table of symptoms at presentation, and what percentage of the time they are seen in TIAs versus conditions that mimic TIA. In general, focal deficits make TIA more likely, but the absence of focal findings do not exclude the diagnosis, and further evaluation may be warranted if clinical suspicion for TIA is high.
TIA vis-à-vis mimics
| Symptoms | % TIA mimics | % TIAs |
| Unilateral paresis | 29.1 | 58 |
| Memory loss/cognitive impairment | 18 to 26 | 2 to 12 |
| Headache | 14.6 to 23 | 2 to 36 |
| Blurred vision | 21.8 | 5.2 |
| Dysarthria | 12.7 | 20.6 |
| Hemianopsia | 3.6 | 3.6 |
| Transient monocular blindness | 0 | 6 |
| Diplopia | 0 | 4.8 |
Non-focal symptoms such as amnesia, confusion, incoordination of limbs, unusual cortical visual symptoms, headaches and transient loss of consciousness are usually not associated with TIA, however patient assessment is still needed. Public awareness on the need to seek a medical assessment for these non-focal symptoms is also low, and can result in a delay by patients to seek treatment
Symptoms of TIAs can last on the order of minutes to one–two hours, but occasionally may last for a longer period of time. TIA is defined as ischemic events in the brain that last less than 24 hours. Given the variation in duration of symptoms, this definition holds less significance. A pooled study of 808 patients with TIAs from 10 hospitals showed that 60% lasted less than one hour, 71% lasted less than two hours, and 14% lasted greater than six hours. Importantly, patients with symptoms that last more than one hour are more likely to have permanent neurologic damage, making prompt diagnosis and treatment important to maximize recovery.
Cause
The most common underlying pathology leading to TIA and stroke is a cardiac condition called atrial fibrillation, where poor coordination of heart contraction may lead to the formation of a clot in the atrial chamber that can become dislodged and travel to a cerebral artery. Unlike in stroke, the blood flow can become restored prior to infarction which leads to the resolution of neurologic symptoms. Another common culprit of TIA is an atherosclerotic plaque located in the common carotid artery, typically by the bifurcation between the internal and external carotids, that becomes an embolism to the brain vasculature similar to the clot in the prior example. A portion of the plaque can become dislodged and lead to embolic pathology in the cerebral vessels.In-situ thrombosis, an obstruction that forms directly in the cerebral vasculature unlike the remote embolism previously mentioned, is another vascular occurrence with possible presentation as TIA. Also, carotid stenosis secondary to atherosclerosis narrowing the diameter of the lumen and thus limiting blood flow is another common cause of TIA. Individuals with carotid stenosis may present with TIA symptoms, thus labeled symptomatic, while others may not experience symptoms and be asymptomatic.
Risk factors
Risk factors associated with TIA are categorized as modifiable or non-modifiable. Non-modifiable risk factors include age greater than 55, sex, family history, genetics, and race/ethnicity. Modifiable risk factors include cigarette smoking, hypertension, diabetes, hyperlipidemia, level of carotid artery stenosis and activity level. The modifiable risk factors are commonly targeted in treatment options to attempt to minimize risk of TIA and stroke.Pathogenesis
There are three major mechanisms of ischemia in the brain: embolism traveling to the brain, in situ thrombotic occlusion in the intracranial vessels supplying the parenchyma of the brain, and stenosis of vessels leading to poor perfusion secondary to flow-limiting diameter. Globally, the vessel most commonly affected is the middle cerebral artery. Embolisms can originate from multiple parts of the body.Common mechanisms of stroke and TIA:
| Stroke mechanism | Frequency | Pattern of infarcts | Number of infarcts |
| In situ thrombotic occlusion | Uncommon | Large subcortical; Sometimes with borderzone; Rarely, whole territory; Sometimes enlarging | Single |
| Artery to artery embolism | Common | Small cortical and subcortical | Multiple |
| Impaired clearance of emboli | Common | Small, scattered, alongside the borderzone region | Multiple |
| Branch occlusive disease | Common | Small subcortical, lacune-like | Single |
| Hemodynamic | Uncommon | Borderzone; may be without lesion | Multiple; None |
Diagnosis
The initial clinical evaluation of a suspected TIA involves obtaining a history and physical exam. History taking includes defining the symptoms and looking for mimicking symptoms as described above. Bystanders can be very helpful in describing the symptoms and giving details about when they started and how long they lasted. The time course, precipitating events, and risk factors are particularly important.The definition, and therefore the diagnosis, has changed over time. TIA was classically based on duration of neurological symptoms. The current widely accepted definition is called "tissue-based" because it is based on imaging, not time. The American Heart Association and the American Stroke Association now define TIA as a brief episode of neurological dysfunction with a vascular cause, with clinical symptoms typically lasting less than one hour, and without evidence of significant infarction on imaging.