Approach

A TIA should be suspected in a patient who presents with sudden-onset, focal neurologic deficit that resolves spontaneously and cannot be explained by another condition such as hypoglycemia.[43] Until the neurologic symptoms and signs have resolved completely, the event should be treated as a stroke, and investigations and management should proceed for this working diagnosis.[43] See Ischemic stroke and Hemorrhagic stroke.

Every patient presenting with acute focal neurologic deficit should receive a rapid history and physical exam, with emphasis on the neurologic exam. An expedited evaluation should occur to determine the necessary workup.

Laboratory testing including complete blood count (CBC), chemistry profile, and blood glucose can help to identify potential mimics of cerebral ischemia.

US guidelines recommend that patients with TIA should preferably undergo neuroimaging evaluation within 24 hours of symptom onset.[1] In patients suspected of having a stroke or TIA, computed tomography (CT) or magnetic resonance imaging (MRI) of the brain is recommended to confirm the diagnosis.[2][21]​​​ Typically patients undergo a noncontrast head CT, to exclude a brain hemorrhage and guide treatment.[2][44]​​

Patients with a suspected TIA benefit from early neurology consultation; preferably in the emergency department or via rapid follow-up within 1 week of the TIA.[13] Evidence suggests that the site at which initial evaluation is provided (e.g., outpatient assessment, hospital emergency department) is not as important as ensuring that the evaluation is completed rapidly, and that all appropriate secondary prevention measures are implemented.[45] Early neurology consultation has been associated with lower 90-day and 1-year mortality rates.[46]

Hospital admission is warranted if any of the following high-risk features are present:[13]

  • ABCD2 score ≥4

  • Subacute stroke on CT

  • Presumed symptomatic (>50%) extracranial or intracranial stenosis

  • Infarct on MRI

  • TIA within the past month

  • Acute cardiac issues including arrhythmias

  • Barriers to rapid outpatient follow-up or testing.

In addition, the decision to admit may be influenced by the lack of a reliable observer in the home setting to call emergency medical services in case of second cerebral ischemic event.[47]

Diagnostic steps

Patient presenting with acute neurologic deficit

  1. A focused history to establish time of onset and risk factors for cerebrovascular disease, and to evaluate probability of presence of a mimic of TIA, should be obtained.[44]

  2. A rapid physical exam with focus on the neurologic exam to determine severity of deficits should be performed.[44]

  3. Laboratory tests including CBC, chemistry profile, blood glucose, prothrombin time (PT), and partial thromboplastin time (PTT) should be done.[44]

  4. ECG should be performed.[21]

  5. For rapidly resolving or resolved neurologic deficits referring to a single vascular territory, in the absence of alternative diagnosis to explain symptoms, TIA is the likely diagnosis.

  6. Patients with significant ongoing neurologic deficits should be treated for stroke with consideration of thrombolysis. Therapy should not be delayed in the hope of spontaneous recovery.

  7. CT or MRI of the brain is recommended to confirm the diagnosis in patients suspected of having a stroke or TIA.[2][21]​​​ Typically patients undergo a noncontrast head CT, to exclude a brain hemorrhage and guide treatment with thrombolysis.[2][44]​​​ MRI of brain with diffusion images is preferred to identify ischemia and potentially to identify distribution of injury.[2][13]​​​ However, MRI may take more than 30 minutes to complete, and is not universally available. If MRI is not available, noncontrast CT of the head can be performed. Patients with resolved symptoms may not require a CT scan, and may receive an MRI of the brain, if available. CT and MRI data should be reviewed and interpreted by a physician with expertise in stroke imaging.[44]

  8. For patients with TIA, follow-up testing should include cardiac monitoring for arrhythmia and echocardiogram to evaluate for cardioembolism, which would be suggested by intracardiac thrombus, valvular vegetation, or atrial fibrillation.[21]

  9. Echocardiography has highest yield when TIA etiology is not evident after the initial evaluation and vascular imaging, or when there is suspicion for a cardioembolic risk factor based on history, ECG, or exam.[21] Transthoracic echocardiography (TTE) is preferred over transesophageal echocardiography (TEE) for the detection of left ventricular (LV) thrombus, but TOE is superior to TTE in detecting left atrial thrombus, aortic atheroma, prosthetic valve abnormalities, native valve abnormalities, atrial septal abnormalities, and cardiac tumors.[21]

  10. In patients with ischemic stroke or TIA in whom patent foramen ovale (PFO) closure is contemplated, transcranial Doppler with embolus detection might be reasonable to screen for right-to-left shunt.[21] Transcranial Doppler compares favorably with TTE for detecting right-to-left shunting, which is usually the result of PFO.[21] Transcranial Doppler can also be used to identify arterial occlusion of the major arterial branches of the circle of Willis. Spatial resolution is limited compared with CT and MR angiography.

  11. In patients with symptomatic anterior circulation cerebral infarction or TIA who are candidates for revascularization, noninvasive cervical carotid imaging with carotid ultrasonography, CT angiography (CTA), or MR angiography (MRA) is recommended to screen for stenosis of, or plaques within, the intracranial, carotid, or aortic vessels.[2][21]​​​ Since MRI is relatively rapid, noninvasive and does not required intravenous contrast, MRA may be preferable to CTA in patients with renal impairment, x-ray contrast allergy, or repeat presentations.[2]​ However, noncontrast MRA of the neck tends to overestimate the degree of carotid stenosis when compared with contrast-enhanced MRA, particularly in cases of high-grade stenosis.[2][48]​​ High-resolution imaging of the intracranial large arteries and imaging of the extracranial vertebrobasilar arterial system can also be used to identify atherosclerotic disease, dissection, moyamoya disease, or other etiologically relevant vasculopathies.[21] Transcranial Doppler is performed in rare cases as a complementary test to further evaluate for intracranial stenosis in the absence of CT/MRI.[2][49]​​

  12. A fasting lipid profile is recommended for patients to evaluate for treatable atherosclerotic risk factors.[21]

  13. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) should be ordered if central nervous system vasculitis is suspected, but this is not routine in many centers.[21]

  14. A hypercoagulability panel (acquired or inherited) may be considered for unexplained TIA in a young patient with self-history or family history of unprovoked thrombosis, prior miscarriages, or coexistence of systemic signs and symptoms suggestive of hypercoagulability.[21]

[Figure caption and citation for the preceding image starts]: Diagnostic algorithm for transient ischemic attackAdapted from an algorithm supplied by the previous contributor, Dr Ethan Cumbler [Citation ends].com.bmj.content.model.Caption@4f475cdb

History and physical examination

TIA is fundamentally a clinical diagnosis. Therefore, an accurate history, informed by the patient/caregiver's report of focal neurologic deficit, is key. TIA symptoms are typically brief and the majority will resolve within the first hour. Persistent symptoms at presentation should be treated as stroke, and therapy should not be delayed in the hope of spontaneous recovery.[43] TIAs are more common in middle age and in older people.[1] Symptoms in a young patient increase the possibility of alternative diagnosis or a less common etiology for ischemia, such as congenital heart disease, extracranial arterial dissections, drug use, hypercoagulability, or paradoxical emboli.

TIAs generally present with loss of power or sensation ("negative symptoms").[50] Unilateral weakness or sensory deficits as a result of ischemia in the carotid or middle cerebral artery territories are common.[7] Aphasia can be seen if the area of ischemia includes language centers. Occlusion of the posterior cerebral artery may give homonymous hemianopsia, whereas thrombus in the retinal artery leads to classic amaurosis fugax or monocular visual loss.[51] Posterior circulation ischemia may lead to symptoms of vertigo, incoordination, cranial nerve deficits, ataxia, or syncope.[7] Lacunar symptoms tend to give isolated sensory or isolated motor deficits but also a number of less common symptom complexes.[9]

Headache can occur after TIA but is not common and suggests alternative etiology for neurologic deficit such as complex migraine, giant cell arteritis (temporal arteritis), or intracranial bleed.[50] Seizures prior to deficit make partial seizure or post-seizure (Todd's) paralysis a more likely diagnosis than TIA.[50]

Key risk factors include atrial fibrillation, valvular disease, carotid stenosis, intracranial stenosis, congestive heart failure, hypertension, hyperlipidemia, diabetes, cigarette smoking, alcohol abuse, and advanced age.​[19][20][21]​​[26][27]​​​[28][31][52][53]​​ Presence of hypertension, diabetes, hyperlipidemia, or chronic renal disease increases the probability of atherosclerotic disease as a risk factor for TIA.[21] Presence of family history of stroke at a young age suggests a potential heritable risk factor such as familial hyperlipidemia or hypercoagulability.[21] Personal history of miscarriage or thromboembolic events may also suggest inherited or acquired thrombophilia.[21]

Patients will often have increased blood pressure (BP) on presentation as BP rises acutely after a cerebral ischemic event. The presence of a carotid bruit is not sensitive or specific for significant stenosis.

It is useful to consider four questions when assessing whether a TIA has occurred:

  • Are the symptoms focal?

  • Are the symptoms negative (i.e., a deficit) rather than positive (i.e., paresthesias, visual scotoma)?

  • Did the symptoms have a sudden onset?

  • Were the symptoms at maximum intensity shortly after onset?

A rapid complete neurologic exam is critical for any patient who presents with acute focal deficits. Pre-hospital screening exams such as the Cincinnati, Los Angeles, or ROSIER tools can be used to quickly assess the possibility of stroke/TIA, but lack specificity.[54][55][56] Cincinnati prehospital stroke scale Opens in new window [ Cochrane Clinical Answers logo ]

The National Institute of Health Stroke Scale (NIHSS) is the preferred method of quantifying the degree of deficits from stroke. The NIHSS will be abnormal during the occurrence of symptoms, but by definition will revert to the pre-TIA score after the symptoms have resolved. ABCD2, ABCD3, or ABCD3-I scores have been used to predict the risk of stroke after TIA; there is some evidence to suggest that the ABCD3-I score (which incorporates imaging of the brain and carotid arteries) is the most effective.[57][58] Evidence shows that risk prediction scores used in isolation are poor at discriminating low and high risk of stroke after TIA.[58][59]​​ This has led some national guidelines outside the US, e.g., the National Institute for Health and Care Excellence (NICE) in the UK, to recommend that all people with suspected TIA are considered as potentially high risk for stroke, with specialist assessment and investigation within 24 hours of symptom onset.[43]

[ NIH Stroke Score Opens in new window ]

[ ABCD2 Score to Predict Stroke Risk after TIA Opens in new window ]

Laboratory studies

These are performed primarily to exclude metabolic or other systemic illness that may mimic cerebral ischemia. Focused laboratory evaluation including a chemistry profile, serum glucose, fasting lipid profile, and CBC is recommended.[13][21]​​

Every patient with TIA or stroke should be screened for diabetes mellitus by measuring fasting plasma glucose or hemoglobin A1c, or with an oral glucose tolerance test.[21]

Other testing should be dictated by clinical suspicion for alternative etiology. PT, international normalized ratio, and activated PTT can be ordered if the neurologic deficit persists at time of presentation, there is reason to suspect abnormal coagulation (such as liver disease or use of anticoagulant therapy), and thrombolytic therapy for stroke is being considered. Completing these tests in high-risk patients for early second ischemic events could speed future thrombolysis decisions. ESR and CRP may be helpful if other clues suggest temporal arteritis.[21]

A hypercoagulability blood panel may be indicated in unexplained TIA in a young patient with self-history or family history of unprovoked thrombosis, prior miscarriages, or coexistence of systemic signs and symptoms suggestive of hypercoagulability.[21] Rare associations, such as underlying malignancy, may be considered as potential underlying etiologies of thrombophilia.

Imaging

Testing should be individualized.

  • Head CT scan has poor ability to rule out ischemia in TIA or early stroke.[13][60] However, CT has nearly 100% sensitivity in ruling out hemorrhage.

  • MRI diffusion imaging will demonstrate restricted diffusion in areas of ischemia, and approximately half of all patients with a clinical diagnosis of TIA will have abnormal findings.[4] The probability of abnormal imaging findings rises with the duration of clinical symptoms, and one quarter to one half of patients with clinical resolution of symptoms in <24 hours will have permanent infarction on follow-up imaging, thus suggesting these were actually strokes.[61][62] Although TIAs may have normal neuroimaging, MRI with diffusion may be helpful in confirming cerebral ischemia or risk stratification for early second events.[2]​ In some cases, areas with infarcts in multiple arterial distributions are seen, which may suggest embolic etiology not suspected by clinical exam. Small posterior fossa ischemic strokes can be missed with diffusion-weighted MRI up to 48 hours after symptom onset.[63] If diffusion-weighted imaging is negative and there is a strong clinical suspicion of TIA, perfusion-weighted imaging may be performed during the same MRI examination; in 30% of cases, a focal perfusion deficit is identified in the brain area corresponding to the symptoms.[2][3][64][65]

  • In patients suspected of having had a TIA, if the initial head imaging (CT or MRI) does not demonstrate a symptomatic cerebral infarct, follow-up MRI is reasonable to predict risk of early stroke and to support the diagnosis.[21]

  • Carotid Doppler ultrasound is a commonly employed screening test for stenosis, but is not useful in posterior circulation TIAs. Intracranial vasculature is not visualized with carotid Doppler.[2]

  • In patients with symptomatic anterior circulation cerebral infarction or TIA who are candidates for revascularization, noninvasive cervical carotid imaging with carotid ultrasonography, CT angiography, or MR angiography is recommended to screen for stenosis of, or plaques within, the intracranial, carotid, or aortic vessels.[13][21]​​ High-resolution imaging of the intracranial large arteries and imaging of the extracranial vertebrobasilar arterial system can also be effective in identifying atherosclerotic disease, dissection, moyamoya, or other etiologically relevant vasculopathies.[21]

  • Transcranial Doppler is less commonly used to further evaluate intracranial stenosis suggested on other imaging modalities.[2]

Physiological studies

Telemetry/Holter monitor studies should be performed in all patients with a TIA to evaluate for atrial fibrillation and other arrhythmias.[21] Extended cardiac monitoring will identify new atrial fibrillation/flutter in significantly more patients than ECG/short-term telemetry monitoring and is an appropriate consideration for patients with unexplained TIA.[21][66][67] An echocardiogram may be done in the TIA evaluation to look for intracardiac thrombus or valvular disease.[21] TTE is preferred over TEE for the detection of LV thrombus, but TEE is superior to TTE in detecting left atrial thrombus, aortic atheroma, prosthetic valve abnormalities, native valve abnormalities, atrial septal abnormalities, and cardiac tumors.[21] Bubble studies can establish if there are intracardiac shunts for selected patients such as those with TIA under the age of 65 years without risk factors, and patients with cryptogenic TIA or neurologic deficits occurring with Valsalva.[47] Transcranial Doppler with bubble study may help quantify the magnitude of a right-to-left shunt and can be performed simultaneously with a TTE bubble study.[68]

Venepuncture and phlebotomy: animated demonstration
Venepuncture and phlebotomy: animated demonstration

How to take a venous blood sample from the antecubital fossa using a vacuum needle.

How to perform an ECG: animated demonstration
How to perform an ECG: animated demonstration

How to record an ECG. Demonstrates placement of chest and limb electrodes.

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