ISCHEMIC STROKE
Transient ischemic attack (TIA)
Created 23/03/2021, last revision 07/07/2023
- 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 subjects aged 45–64 years; then the incidence steeply increases, peaking in subjects aged ≥ 85 years [Degan, 2017]
- evaluation of TIA and initiation of multimodal therapeutic interventions should be urgent to reduce the risk of subsequent stroke
- particularly TIAs within 24-48 h should be managed as a stroke
TIA definition
- the former definition of TIA (sudden focal neurological deficit lasting < 24h of presumed vascular origin) has become obsolete
- about 30-50% of such defined TIA patients have infarct lesions on DWI [Oppenheim, 2004]
- the likelihood of a DWI lesion increases with symptoms duration; DWI is positive in over 60% of TIA cases lasting > 30 minutes [Inatomi, 2004]
New TIA definition [Albers, 2002]
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.
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 – short duration of symptoms (usually minutes, 24h maximum) with complete resolution of symptoms and negative DWI
- stroke – infarct lesion on imaging and/or persistent clinical symptoms lasting > 24h
- symptomatic stroke (evidence of brain, spinal cord, or retinal injury)
- persistent symptoms (stroke is diagnosed even in case of negative imaging; other etiology must be ruled out)
- transient symptoms with positive DWI
- clinically asymptomatic stroke (incidental finding on imaging)
- symptomatic stroke (evidence of brain, spinal cord, or retinal injury)
Etiology
- TIA subtypes, classified according to the pathophysiological mechanisms, are similar to subtypes of ischemic stroke
- the common vascular risk factors are the same as for stroke (e.g., diabetes, hypertension, age, smoking, unhealthy diet and obesity, alcoholism, stress, and physical inactivity)
Clinical presentation
- TIA symptoms are sudden in onset
- TIAs usually last 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, quadruparesis
- hemihypesthesia
- speech disorders
- aphasia
- slurred speech (dysarthria)
- vision disturbances
- blindness in one or both eyes, visual field deficit
- double vision
- vestibular syndrome
- cerebellar syndrome (ataxia, dysmetria)
- global symptoms (lightheadedness, isolated delirium, syncope) and positive symptoms (scintillations) are not typical for TIA
Diagnostic evaluation
- TIAs very often occur hours or days before a stroke; they can thus serve as both a warning of a future stroke and an opportunity to prevent it
- prompt evaluation and identification of potentially 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 a TIA evaluation:
- to prove the vascular origin of the symptoms and to exclude a nonischemic origin
- neurologic examiantion is usually negative at the time of presentation, so the history of symptoms must be carefully discussed (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 (migraine, etc.)
- determine the underlying mechanism to select the optimal therapy
- exclude significant carotid stenosis and major cardioembolic source
- palpitations, arrhythmias, and valvular defects, together with symptoms and signs from various territories, suggest cardiac etiology (TOAST 2)
- to prove the vascular origin of the symptoms and to exclude a nonischemic origin
Who should be hospitalized?
- high-risk patients should be hospitalized or managed via a specialized TIA clinic
- it is not yet known which is the best healthcare setting to treat TIA
- it is not yet known which is the best healthcare setting to treat TIA
- indication for admission to the hospital depends on the following:
- time 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 not to use prediction tools alone to identify high-risk patients and to make triage and treatment decisions (ESO guidelines 2021)
- a low ABCD2 score should not be a reason to delay diagnostic evaluation and treatment (those with an ABCD2 score ≤ 3 still include a significant number of individual patients at high risk of recurrent stroke who require early evaluation and treatment)
- it would be optimal to hospitalize all patients with TIA within 24-48 h, which would ensure rapid diagnostic evaluation and initiation of therapy
- novel score ABCD3-I was published, which further improves the detection of high-risk patients [Song, 2013]
- the items repeated TIA (Dual TIA) and imaging (I-Imaging – DWI, ICA stenosis > 50%) were added – all scored 2 points
- 14 points are the maximum
Acute evaluation of TIA patient
- focused history
- onset, duration, timing, symptoms specification, any aggravating or relieving factors
- risk factors, 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)
- 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 24h or CT+CTP if DWI cannot be performed) (ESO 2021) (AHA/ASA 2013 I/B)
- DWI has a greater sensitivity than CT for detecting small infarcts
- vascular examination – neurosonology or CTA/MRA (urgent in recent TIA) ( AHA/ASA guidelines 2013 I/A)
- ESO guidelines 2021 suggest using MRA/CTA for confirmation of 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
- urine drug screening in selected cases
- complete blood count (CBC) + coagulation tests + ESR
- 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 a future stroke or recurrent TIA (by 80%) – EXPRESS trial
- the same-day assessment and initiation of standard risk-modification measures following TIA decreased the 90-day risk of stroke from 10.3 to 2.1% compared with delayed (or routine) outpatient evaluation and treatment
- early treatment did not increase the risk of intracerebral hemorrhage or other bleeding
Antithrombotic therapy
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Surgery and endovascular procedures
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Vascular risk factors management and others
- start aggressive blood pressure treatment (⇒ BP < 130/80 mm Hg, ACE-I are preferred) → acute blood pressure management
- treat dyslipidemia
- manage other vascular risk factors
- consider specific treatment of some particular underlying etiologies (vasculitis, etc.)
- even TIA patients can develop post-traumatic stress disorder (PTSD) with depression or anxiety (Kiphuth, 2014]
- train adaptive coping skills and carefully explain the realistic risk of stroke associated with TIA
- use anxiolytics or antidepressants if necessary
- train adaptive coping skills and carefully explain the realistic risk of stroke associated with TIA
