transient ischemic attack transient ischemic attack a transient ischemic attack (tia), commonly known as a mini-stroke, is a minor stroke whose noticeable symptoms usually end in less than an hour. tia causes the same symptoms associated with strokes, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, or confusion. transient ischemic attackother namesmini-strokes, mild strokespecialtyneurology, vascular surgeryprognosissurvival rate ~ 91% (to hospital discharge) 67.2% (five years) all forms of stroke, including 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 (cbf). the primary difference between a major stroke and the tia's minor stroke is how much tissue death (infarction) 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 silent stroke, also known as silent cerebral infarct (sci), 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 (painless, temporary loss of vision) one-sided facial droop one-sided motor weakness diplopia (double vision) 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 (aphasia) difficulty with articulation of speech (dysarthria) unsteady gait difficulties with swallowing (dysphagia) numbness or weakness generally occur on the opposite side of the body from the affected hemisphere of the brain. 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 (see "diagnosis" section below). tia versus 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 (such as isolated bilateral blindness or bilateral positive visual phenomena), 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. tias used to be defined as ischemic events in the brain that last less than 24 hours, but 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 contraction leads to a 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 (elevated blood pressure), diabetes, hyperlipidemia, level of carotid artery stenosis (asymptomatic or symptomatic) 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 infarct 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 (including a neurological 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 (onset, duration, and resolution), 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 (aha/asa) 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. laboratory workup 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 a patient's risk factors for ischemic events. all patients should receive a complete blood count with platelet count, blood glucose, basic metabolic panel, prothrombin time/international normalized ratio, and activated partial thromboplastin time as part of their initial workup. these tests help with screening for bleeding or hypercoagulable conditions. other lab tests, such as a full hypercoagulable state workup or serum drug screening, should be considered based on the clinical situation and factors, such as age of the patient and family history. a fasting lipid panel is also appropriate to thoroughly evaluate the patient's risk for atherosclerotic disease and ischemic events in the future. other lab tests may be indicated based on the history and presentation; such as obtaining 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. cardiac rhythm monitoring an electrocardiogram is necessary to rule out abnormal heart rhythms, such as atrial fibrillation, that can predispose patients to clot formation and embolic events. hospitalized patients should be placed on heart rhythm telemetry, which is a continuous form of monitoring that can detect abnormal heart rhythms. prolonged heart rhythm monitoring (such as with a holter monitor or implantable heart monitoring) can be considered to rule out arrhythmias like paroxysmal atrial fibrillation that may lead to clot formation and tias, however this should be considered if other causes of tia have not been found. imaging according to guidelines from the american heart association and american stroke association stroke council, patients with tia should have head imaging "within 24 hours of symptom onset, preferably with magnetic resonance imaging, including diffusion sequences". 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. 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. vessels in the head and neck may also be evaluated to look for atherosclerotic lesions that may benefit from interventions, such as carotid endarterectomy. the vasculature can be evaluated through the following imaging modalities: magnetic resonance angiography (mra), ct angiography (cta), and carotid ultrasonography/transcranial doppler ultrasonography. carotid ultrasonography 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, and confirm with cta). confirming a diagnosis of carotid artery stenosis is important because the treatment for this condition, carotid endarterectomy, can pose significant risk to the patient, including heart attacks and strokes after the procedure. for this reason, the u.s. preventive services task force (uspstf) "recommends against screening for asymptomatic carotid artery stenosis in the general adult population". this recommendation is for asymptomatic patients, so it does not necessarily apply to patients with tias as these may in fact be a symptom of underlying carotid artery disease (see "causes and pathogenesis" above). therefore, patients who have had a tia may opt to have a discussion with their clinician about the risks and benefits of screening for carotid artery stenosis, including the risks of surgical treatment of this condition. cardiac imaging can be performed if head and neck imaging do not reveal a vascular cause for the patient's tia (such as atherosclerosis of the carotid artery or other major vessels of the head and neck). echocardiography can be performed to identify patent foramen ovale (pfo), valvular stenosis, and atherosclerosis of the aortic arch that could be sources of clots causing tias, with transesophageal echocardiography being more sensitive than transthoracic echocardiography in identifying these lesions. differential diagnosis diagnosis findings brain tumor severe unilateral headache with nausea and vomiting central nervous system infection (e.g., meningitis, encephalitis) fever, headache, confusion, neck stiffness, nausea, vomiting, photophobia, change in mental status falls/trauma headache, confusion, bruising hypoglycemia confusion, weakness, diaphoresis migraines severe headaches with or without photophobia, younger age multiple sclerosis diplopia, limb weakness, paresthesia, urinary retention, optic neuritis seizure disorder confusion with or without loss of consciousness, urinary incontinence, tongue biting, tonic-clonic movements subarachnoid hemorrhage