ISCHEMIC STROKE
Transient ischemic attack (TIA)
Updated on 23/09/2024, published on 29/12/2023
- Transient Ischemic Attack (TIA) is a medical emergency
- despite its seemingly mild course, TIA is a serious predictor of subsequent ischemic stroke and death
- following TIA, the risk of recurrent stroke is 8% in the first week, 11.5% at 1 month, and 17.3% at 3 months [Coull, 2004]
- following TIA, the risk of recurrent stroke is 8% in the first week, 11.5% at 1 month, and 17.3% at 3 months [Coull, 2004]
- true incidence and prevalence of TIA are challenging to determine because of inconsistent criteria
- the reported crude annual incidence rate of TIA was 35.2 per 100 000 (95% CI, 30.6–40.3); TIAs are rare in young adults (<45 years) and relatively rare in individuals aged 45–64 years; the incidence then rises steeply, peaking in individuals aged ≥ 85 years [Degan, 2017]
- evaluation of TIA and initiation of multimodal therapeutic interventions should be urgent to reduce the risk of subsequent stroke
- especially TIA within 24 to 48 hours should be managed as stroke
TIA definition
- the former definition of TIA (sudden focal neurological deficit lasting < 24 hours of presumed vascular origin) has become obsolete
- ~ 30-50% of patients defined by such criteria have infarct lesions on DWI [Oppenheim, 2004]
- the likelihood of a DWI lesion increases with the duration of symptoms; DWI is positive in over 60% of TIAs lasting > 30 minutes [Inatomi, 2004]
Transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia, usually lasting < 1 hour, without acute infarction or tissue injury.
TIA or stroke?
- TIA – characterized by a short duration of symptoms (usually minutes) with complete resolution of symptoms and negative DWI
- stroke – indicated by an infarct lesion on imaging and/or persistent clinical symptoms lasting > 24 hours
- symptomatic stroke (defined by evidence of brain, spinal cord, or retinal injury)
- persistent symptoms (stroke is diagnosed even if imaging is negative; other etiologies must be ruled out)
- transient symptoms with positive DWI
- clinically asymptomatic stroke (incidental finding on imaging)
- symptomatic stroke (defined by evidence of brain, spinal cord, or retinal injury)
Etiology
- TIA subtypes, classified according to pathophysiological mechanisms, are similar to subtypes of ischemic stroke
- the common vascular risk factors for TIA are the same as those for stroke (e.g., diabetes, hypertension, age, smoking, an unhealthy diet and obesity, alcoholism, stress, and physical inactivity)
Clinical presentation
- TIA symptoms occur suddenly
- TIAs typically last only a few minutes, with complete resolution of symptoms and signs
- the signs and symptoms of a TIA are similar to those of a stroke:
- hemiparesis or quadruparesis
- hemihypesthesia
- speech disorders
- aphasia
- slurred speech (dysarthria)
- visual disturbances
- blindness in one or both eyes, visual field deficits
- double vision
- vestibular syndrome
- cerebellar syndrome (characterized by ataxia, dysmetria)
- global symptoms (lightheadedness, isolated delirium, syncope) and positive symptoms (scintillations) are not typically associated with TIA
Diagnostic evaluation
- TIAs very often occur hours or days before a stroke; serving as both a warning sign and an opportunity for stroke prevention
- prompt evaluation and identification of treatable conditions are essential
- evaluation by a specialist within 24 hours of symptom onset is recommended (ESO guidelines 2021)
- review in a TIA clinic or admission to a stroke unit are reasonable options (depending on local resources and patient preference)
- the main goals of TIA evaluation:
- confirm the vascular origin of the symptoms and exclude non-ischemic causes
- neurological examination is usually normal at the time of presentation, and thus, a detailed history of symptoms is essential (may help to diagnose TIA or even its etiology)
- uniform, repeated attacks indicate either pathology at the level of a peripheral branch or perforator or stroke mimics (such as migraine, etc.)
- determine the underlying mechanism for selecting optimal therapy
- exclude significant carotid stenosis and major cardioembolic sources (especially atrial fibrillation)
- palpitations, arrhythmias, and valvular defects, together with symptoms and signs from multiple territories, suggest a cardiac etiology (TOAST 2)
- exclude significant carotid stenosis and major cardioembolic sources (especially atrial fibrillation)
- confirm the vascular origin of the symptoms and exclude non-ischemic causes
Who should be hospitalized?
- high-risk patients should either be hospitalized or managed via a specialized TIA clinic
- the best healthcare setting for treating TIA is still a subject of ongoing research
- the decision to hospitalize the patient depends on several factors:
- time elapsed since the last TIA
- rapid availability of necessary diagnostic tests on an outpatient basis
- ABCD2 score + clinical judgment + imaging findings (ideally CT+CTA or DWI+MRA, neurosonology)
- recent ESO guidelines suggest that predictive tools should not be used alone to identify high-risk patients and to make decisions about triage and treatment (ESO guidelines 2021)
- a low ABCD2 score should not be a reason to delay diagnostic evaluation and treatment (as individuals with an ABCD2 score ≤ 3 can still be at significant risk of recurrent stroke and require early evaluation and treatment
- ideally, all patients with TIA should be hospitalized within 24-48 hours to ensure rapid diagnostic evaluation and initiation of therapy
- novel ABCD3-I score further improves the detection of high-risk patients [Song, 2013]
- this score includes the elements of repeated TIA (Dual TIA) and imaging findings (I-Imaging – DWI, ICA stenosis > 50%) – each scored with 2 points, with a maximum score of 14 points
Acute evaluation of TIA patient
- focused history
- onset, duration, timing, symptom specification, any aggravating or relieving factors
- risk factors and comorbidities (CAD or PAD, smoking, drug abuse, obesity, diabetes, dyslipidemia, and hypertension)
- clinical examination
- assess neurological deficits, including speech disturbances, visual field defects, etc. (→ NIHSS)
- perform a cardiac examination
- carotid auscultation to detect carotid bruit
- assess neurological deficits, including speech disturbances, visual field defects, etc. (→ NIHSS)
- brain imaging (preferred modality is DWI within 24 hours or CT+CTP if DWI cannot be performed) (ESO 2021) (AHA/ASA 2013 I/B)
- DWI is more sensitive than CT for detecting small infarcts
- vascular examination – neurosonology or CTA/MRA (urgent in recent TIA cases) ( AHA/ASA guidelines 2013 I/A)
- ESO guidelines 2021 suggest MRA/CTA for confirming large artery stenosis ≥ 50% detected by ultrasound to guide further management
- strength of MRA compared to ultrasound and CTA is its relative insensitivity to arterial calcifications
- blood tests
- complete blood count (CBC) + coagulation tests + ESR
- basic metabolic panel
- lipid panel
- diabetes screening tests
- urine drug screening in selected cases
- complete blood count (CBC) + coagulation tests + ESR
- electrocardiogram (ECG)
- standard ECG (AFib?)
- continue with Holter ECG or prolonged ECG monitoring for at least three weeks (loop recorder)
- prolonged cardiac rhythm monitoring is reasonable, especially in patients with cortical infarcts with no clear source, to exclude paroxysmal AFib
- standard ECG (AFib?)
- TTE (transthoracic echocardiogram) + TEE (transesophageal echocardiogram)
- search for PFO, valvular disorder, and other intracardial abnormities
- assess aortic plaques
- EEG in DDx of stroke mimics
Differential diagnosis
- differentiate TIA from stroke mimics (on-vascular conditions presenting with symptoms similar to those of stroke)
Therapy and prevention
- immediately start multimodal therapeutic intervention
- treatment may substantially reduce the risk of recurrent stroke or TIA (by 80%) – EXPRESS trial
- same-day assessment and initiation of standard risk-modification measures following a TIA decreased the 90-day risk of stroke from 10.3 to 2.1%, compared with delayed (or routine) outpatient evaluation and treatment
- importantly, early treatment did not increase the risk of intracerebral hemorrhage or other bleeding
Antithrombotic therapy
- antiplatelet drugs (aspirin, clopidogrel, ticagrelor)
- for patients with an ABCD2 score ≥ 4 prefer short-term (21 days) dual antiplatelet therapy (ASA + clopidogrel), subsequently followed by monotherapy (ESO guidelines 2021)
- DAPT with ASA + ticagrelor may be considered as an alternative regimen in patients for whom clopidogrel and aspirin are not an option. This is particularly recommended for those with an ABCD2 score of ≥ 6 or symptomatic intracranial or extracranial arterial stenosis (≥ 50%), according to the THALES trial criteria used to define high-risk TIA
- use monotherapy for low-risk TIA or in cases where the TIA diagnosis is uncertain
- anticoagulation is indicated for patients with AFib or other major sources of cardioembolism)
Surgery and endovascular procedures
- carotid endarterectomy (CEA) should be performed within 2-14 days if significant carotid stenosis is detected
- ultra-early preventive CEA (performed <2 days from symptom onset) appears to be associated with a higher perioperative risk of stroke
- a slight delay may allow the onset of antiplatelet and statin therapy effects, leading to the stabilization of carotid plaque ⇒ ↓ risks associated with CEA [Kennedy, 2012]
- carotid angioplasty with stenting (CAS) – an alternative to CEA
- intracranial stenoses should be treated with the best medical therapy
- as the SAMMPRIS trial showed that endovascular stenting is not superior to aggressive medical therapy alone
Vascular risk factors management and others
- start aggressive blood pressure treatment (⇒ target BP < 130/80 mm Hg, with ACE inhibitors being the preferred medication) → acute blood pressure management
- treat dyslipidemia and manage other vascular risk factors
- consider specific treatment of certain underlying etiologies (vasculitis, etc.)
- even TIA patients can develop post-traumatic stress disorder (PTSD) with depression or anxiety (Kiphuth, 2014]
- teach patients adaptive coping skills and carefully explain the realistic risk of stroke associated with TIA
- use anxiolytics or antidepressants if necessary
- teach patients adaptive coping skills and carefully explain the realistic risk of stroke associated with TIA
FAQs
- TIA is defined as a transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia, usually lasting < 1 hour, without acute infarction or tissue injury
- the symptoms of a TIA are similar to those of a stroke and may include sudden hemiparesis or quadruparesis, hemihypesthesia, speech disorders (aphasia, dysarthria), visual disturbances, vestibular and cerebellar symptoms, etc.
- a TIA is diagnosed based on medical history, a neurological exam (symptoms must resolve within 24 hours), and negative brain imaging (CT/MRI shows no signs of relevant permanent brain damage)
- the symptoms of a TIA are temporary and do not cause permanent brain damage, while a stroke causes permanent damage to the brain
- managing risk factors such as hypertension, diabetes, and high cholesterol, along with a healthy lifestyle ( a healthy diet, regular exercise, quitting smoking), can significantly reduce the risk of TIA