Approach

The cause of symptoms in a patient with transient neurologic deficits should be established, and ischemic insult distinguished from one of the mimics of TIA. The next objective is to assess the patient for the risk of early recurrent events and determine whether hospitalization is needed or whether the workup can be done on an expedited outpatient basis. One of the most important interventions to begin immediately (after brain imaging has ruled out intracranial hemorrhage) is antithrombotic therapy. This should be started on the day of initial evaluation. To maximize the benefit of stroke risk reduction, early intervention for all modifiable risk factors is needed. Evidence suggests that rapid evaluation and treatment in well-designed systems of care, such as dedicated TIA clinics, can significantly reduce the risk of second strokes.[45][78] 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]

Therapies to prevent second ischemic events should be instituted immediately based on the most likely etiology.

  • Antiplatelet agents are primary therapy for atherosclerotic disease.

  • Anticoagulation is preferred for cardioembolic events.

Aggressive risk-factor modification should be initiated including:

  • Statin therapy[71]

  • Antihypertensive therapy

  • Lifestyle modification

  • Carotid endarterectomy or stenting.

Studies of neuroprotective agents for the treatment of ischemic stroke have not demonstrated efficacy.[79]

All patients should be counseled to seek care in an emergency department immediately, preferably via Emergency Medical Services, in case of new stroke symptoms.

Assessing risk of early stroke

Speed is critical, regardless of whether the workup and treatment is performed in the inpatient or outpatient setting. Guidelines recommend this occurs in the first 1-2 days after TIA or as soon as possible.[47]

TIA is recognized as a medical urgency/emergency due to the risk of subsequent disabling stroke. The risk of stroke in the first 3 months after TIA is 10.5%.[80] Half of these strokes occur in the first 2 days post TIA, which emphasizes the narrow window of time to initiate evaluation and secondary prevention measures.[80]

US guidelines recommend that hospitalization be considered for high-risk patients (ABCD2 score ≥4), subacute stroke on computed tomography, presumed symptomatic (>50%) extracranial or intracranial stenosis, infarct on magnetic resonance imaging, TIA within the past month, acute cardiac issues including arrhythmias, and barriers to rapid outpatient follow-up or testing.[13] In addition, the decision to admit may be influenced by the lack of reliable home support to observe and, if necessary, call emergency medical services for new stroke symptoms.[47] Patients with transient neurologic deficits who have abnormalities on the magnetic resonance diffusion-weighted imaging are at increased risk for early stroke.[81]

Imaging-based scores, such as ABCD2, ABCD3, and ABCD3-I, can be used to help predict risk of stroke after TIA. There is some evidence to suggest that the ABCD3-I score is the most effective.[57][58] The ABCD2, ABCD3, or ABCD3-I scores are not a substitute for individualized judgment, but can aid in decision-making.[57][75] 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]

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

Patients with small-vessel TIA

Antiplatelet therapy should be started in the first 24 hours after intracranial hemorrhage is ruled out.

For patients with noncardioembolic ischemic stroke or TIA, guidelines from the American Heart Association/American Stroke Association (AHA/ASA) recommend aspirin, clopidogrel, or aspirin/dipyridamole for secondary prevention of ischemic stroke.[21] In patients with high-risk TIA (ABCD2 score ≥4), guidelines from the AHA/ASA recommend that dual antiplatelet therapy should be initiated early (ideally within 12-24 hours of symptom onset and at least within 7 days of onset) and continued for 21 to 90 days, followed by single antiplatelet therapy, to reduce the risk of recurrent ischemic stroke.​[21][44]​​ Loading doses are recommended for dual antiplatelet therapy but not for monotherapy.[82][83][84] Switching between single antiplatelet agents after a TIA could be considered, but there is no evidence that this reduces future stroke risk.

  • Aspirin monotherapy: the use of low-dose aspirin after TIA or small stroke reduces risk of second stroke or death by 15% to 18%.[85][86][87] There does not appear to be a clear dose effect for aspirin; both low- and high-dose aspirin reduce the risk of a second ischemic event by 15%, but the latter is associated with more gastrointestinal upset.[87]

  • Aspirin/dipyridamole: one meta-analysis found that aspirin/dipyridamole was more effective than aspirin alone for the prevention of stroke in patients with minor stroke or TIA (relative risk [RR] 0.77, 95% CI 0.67 to 0.89; approximate absolute risk reduction 2.3%).[88] However, subsequent meta-analyses failed to demonstrate that aspirin/dipyridamole significantly reduced stroke recurrence compared with aspirin alone in patients with acute ischemic stroke or TIA (RR 0.64, 95% CI 0.37 to 1.10, P=0.11).[89][90] Dual therapy with aspirin/dipyridamole did not appear to increase the risk of major bleeding.[90] Dipyridamole is not recommended as monotherapy.

  • Clopidogrel monotherapy: compared with aspirin, clopidogrel significantly reduced the annual rate of a combined endpoint of stroke, myocardial infarction, and vascular death in patients at risk of ischemic events (5.83% vs. 5.32%, respectively; RR 0.91, 95% CI 0.84 to 0.97; P=0.043).[91] Risk of bleeding did not differ between treatment groups; diarrhea and rash were more commonly reported in the clopidogrel treatment arm.[91] Clopidogrel can rarely cause thrombotic thrombocytopenic purpura. Clopidogrel is the preferred agent for patients with aspirin allergy.

  • Aspirin plus clopidogrel: one meta-analysis found that dual antiplatelet therapy with clopidogrel plus aspirin (within 24 hours after high-risk TIA [ABCD2 ≥4] or minor ischemic stroke) reduced the absolute risk of subsequent stroke by 2% compared with aspirin alone.[92] All-cause mortality did not differ between treatment groups; clopidogrel plus aspirin was associated with a small absolute increased risk of moderate or severe extracranial bleeding (0.2%).[92] In a second meta-analysis, the risk of recurrent ischemic stroke in patients with TIA or acute ischemic stroke was significantly reduced with short-term (≤1 month; RR 0.53, 95% CI 0.37 to 0.78) and intermediate-term (≤3 months; RR 0.72, 95% CI 0.58 to 0.90) aspirin plus clopidogrel compared with aspirin alone.[93] Long-term combination treatment (>3 months) did not reduce the risk of recurrent ischemic stroke (RR 0.81, 95% CI 0.63 to 1.04).[93] Intermediate-term (RR 2.58, 95% CI 1.19 to 5.60) and long-term (RR 1.87, 95% CI 1.36 to 2.56) combined treatment significantly increased the risk of major bleeding, but short-term treatment did not (RR 1.82, 95% CI 0.91 to 3.62).[93]

  • Ticagrelor: the dual antiplatelet therapy regimen of ticagrelor plus aspirin is approved by the Food and Drug Administration (FDA) in the US to reduce the risk for stroke in patients with acute ischemic stroke with a National Institutes of Health Stroke Scale (NIHSS) score of ≤5 or high-risk TIA. The choice of adding ticagrelor or clopidogrel to aspirin should be based on patient factors (e.g., medication adherence, dose frequency).[21] In Europe, an application to the European Medicines Agency (EMA) to change the marketing authorization of ticagrelor to include the prevention of stroke in adults who have had a mild to moderate ischemic stroke or high-risk TIA was withdrawn in December 2021. Based on trial data and the company's response to their questions, the EMA expressed concern that the benefits of short-term treatment with ticagrelor plus aspirin in preventing stroke in these patients did not clearly outweigh the risks of fatal and nonfatal bleeding. The THALES trial of 11,016 patients (none of whom received thrombolysis or thrombectomy or required anticoagulation) demonstrated that compared with aspirin alone, dual treatment with ticagrelor plus aspirin reduced the risk of disabling stroke or death within 30 days (4.0% vs. 4.7%).[83] Severe bleeding was more frequent with ticagrelor plus aspirin than with aspirin alone (0.5% vs. 0.1%), including in those with intracranial hemorrhage (0.4% vs. 0.1%). For people with recent stroke with NIHSS score of <5, ticagrelor plus aspirin for 30 days was more effective in preventing recurrent ischemic stroke than aspirin alone.[83]

Anticoagulation is not superior to antiplatelet therapy for secondary prevention of vascular events after noncardioembolic stroke or TIA, and carries higher hemorrhage risk.[94]

Patients should also be started on statin and antihypertensive therapy if appropriate. Patients with significant (>50%) symptomatic ipsilateral carotid stenosis should be referred to a vascular surgeon for treatment.

Patients with cardioembolic TIA

Anticoagulation therapy is superior to antiplatelet therapy for prevention of cardioembolic strokes and should be started within the first 2 weeks.[95][96]

  • In patients with nonvalvular atrial fibrillation and stroke or TIA, oral anticoagulation (e.g., apixaban, dabigatran, edoxaban, rivaroxaban, or warfarin) is recommended to reduce the risk of recurrent stroke, regardless of whether the atrial fibrillation pattern is paroxysmal, persistent, or permanent.[21]

  • Direct-acting oral anticoagulants (DOACs), such as apixaban, dabigatran, edoxaban, or rivaroxaban, are recommended over a vitamin K antagonist, e.g., warfarin, in patients with stroke or TIA and atrial fibrillation who do not have moderate to severe mitral stenosis or a mechanical heart valve.[21] Large randomized trials have shown DOACs to clinically reduce the risk of thrombotic stroke with less bleeding risk compared with vitamin K antagonists.[21][97][98] DOACs have the significant advantage of fast onset, predictable dosing requirements, and eliminating the need for monitoring.[99] Disadvantages include higher drug cost and inability to reliably monitor anticoagulant effect using prothrombin time (PT), international normalized ratio (INR), or partial thromboplastin time (PTT).

  • Patients with valvular atrial fibrillation (i.e., moderate to severe mitral stenosis or mechanical heart valves) should be treated with warfarin. Range INR for patients on warfarin should be 2.0 to 3.0.[21] Mitral mechanical prosthetic valves require a higher INR goal of 3.0.[21] Antiplatelet therapy continues to be recommended over warfarin in patients with ischemic stroke or TIA and native aortic or nonrheumatic mitral valve disease (e.g., mitral annular calcification or mitral valve prolapse) who do not have atrial fibrillation or another indication for anticoagulation.[21]

  • Dabigatran is contraindicated in people with mechanical heart valves. Apixaban, edoxaban, and rivaroxaban have not been studied in patients with prosthetic heart valves and are not recommended in these patients.

  • Aspirin, or aspirin plus clopidogrel, should be used only if anticoagulation is contraindicated.[100] Aspirin is inferior to anticoagulation therapy in stroke prevention for patients with atrial fibrillation, but may be the only option for a patient with a contraindication to anticoagulants.[101]

Left atrial appendage closure with a mechanical device that occludes the left atrial appendage may be an option for patients who have a contraindication to lifelong anticoagulation, but who can tolerate 45 days of anticoagulation.[21]

A validated scoring system should be used to assess the bleeding risk of the patient; if high, the patient should be followed up more closely. See New-onset atrial fibrillation.

Patent foramen ovale (PFO)

Isolated PFO likely warrants antiplatelet therapy alone. Guidelines from the American Academy of Neurology state that evidence is insufficient to establish whether anticoagulation is equivalent or superior to antiplatelet therapy for patients with PFO.[102] Patients with cryptogenic stroke can remain on antiplatelet treatment while decisions are made about PFO closure.[35] The AHA recommends that closure of a PFO should be considered for patients with a nonlacunar stroke, particularly for those ages 18-60 years found to have high-risk features such as an atrial septal aneurysm and larger shunt size.[21] Evidence specific to TIA is scarce, as patients with TIA have been excluded from most PFO closure trials.[103] The Society for Cardiovascular Angiography and Interventions recommends against PFO closure in patients with TIA without prior PFO-associated stroke, but states that closure could be considered in patients with recurrent, high-probability TIAs who place a high value on the uncertain benefits of closure and low value on potential procedural risks.[104]

When to consider combination therapy

Combination therapy (anticoagulant and antiplatelet therapy) is recommended in patients with a mechanical mitral valve and a history of ischemic stroke or TIA before valve replacement to reduce the risk of thrombosis and recurrent stroke or TIA.[21] Routine combination therapy is not recommended for cardioembolic TIAs due to atrial fibrillation or rheumatic valve disease.[21][105] One meta-analysis found no incremental benefit of combination therapy over anticoagulation alone.[106]

Low-dose heparin or low-molecular-weight heparin (LMWH) decreases early stroke recurrence after acute stroke, but increases risk of intracranial hemorrhage and is therefore not recommended.[44]​​[107]​ Bridging treatment (i.e., treatment after stroke onset until start of oral anticoagulation) using LMWH is not recommended by most guidelines since the level of supportive evidence is low. Some observational studies have suggested worse outcomes (e.g., early ischemic recurrence and hemorrhagic transformation) in patients treated with LMWH before oral anticoagulant therapy.[108][109]

Statin therapy in patients with TIA

Statin therapy provides benefit acutely after cerebrovascular ischemia. Statin treatment should not be started immediately. There is consensus that it is safe to start statins after 48 hours.[43] Statin treatment should be continued in people who are already receiving statins.[43] A large randomized trial among people with stroke or TIA within the previous 6 months found that high-dose atorvastatin reduced the absolute risk of second stroke over the ensuing 5 years by 2.2% compared with placebo.[110]

Guidelines recommend:[71]

  • High-intensity statin therapy for all patients ages ≤75 years with TIA.

  • Moderate-intensity or high-intensity statin therapy as being reasonable for patients ages >75 years with TIA, after evaluation of the potential for risk reduction, adverse effects, and drug-drug interactions, as well as patient frailty and patient preferences.

Intensity of statin therapy is defined as follows:[71]

  • High-intensity: daily dose typically lowers low-density lipoprotein (LDL) cholesterol by ≥50%.

  • Moderate-intensity: daily dose typically lowers LDL-cholesterol by 30% to 49%.

  • Low-intensity: daily dose typically lowers LDL-cholesterol by <30%.

In patients with ischemic stroke or TIA and atherosclerotic disease (intracranial, carotid, aortic, or coronary), lipid-lowering therapy with a statin, with or without ezetimibe, to a goal low-density lipoprotein cholesterol (LDL-cholesterol) of <70 mg/dL (<1.81 mmol/L) is recommended to reduce the risk of major cardiovascular events.[21][23]​ There is evidence that the rate of recurrent cardiovascular events or stroke is lower in patients whose LDL-cholesterol is controlled to <70 mg/dL (<1.81 mmol/L) compared with those with LDL-cholesterol between 90 mg/dL (2.33 mmol/L) and 110 mg/dL (2.85 mmol/L).[111]

Guidelines state that it may be reasonable to add ezetimibe for patients with clinical atherosclerotic cardiovascular disease (ASCVD) who still have LDL-cholesterol ≥70 mg/dL (≥1.8 mmol/L) on maximally tolerated statin therapy.[112] The BMJ: PCSK9 inhibitors and ezetimibe for the reduction of cardiovascular events: a clinical practice guideline with risk-stratified recommendations Opens in new window

Statin therapy has the strongest evidence base for reducing stroke risk, but niacin and fibrates (e.g., gemfibrozil) may also mildly lower LDL-cholesterol in patients with normal triglycerides. Statins may be useful in some patients with severe hypertriglyceridaemia.[71]

A robust evidence base supports the use of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors (e.g., evolocumab, alirocumab) in patients with ischemic stroke or TIA and atherosclerotic disease (intracranial, carotid, aortic, or coronary) who might not be eligible for other lipid‐lowering drugs, or those who cannot meet their lipid goals on more traditional therapies (e.g., statins or ezetimibe).[113][114] The BMJ: PCSK9 inhibitors and ezetimibe for the reduction of cardiovascular events: a clinical practice guideline with risk-stratified recommendations Opens in new window [ Cochrane Clinical Answers logo ] ​​​​​ PCSK9 inhibitors reduce LDL-cholesterol. Evolocumab and alirocumab have been approved by the FDA for the reduction of LDL-cholesterol in patients unable to reach LDL-cholesterol goals alone or in combination with other lipid-lowering therapies.[21][114]​ The AHA recommends evolocumab or alirocumab for very high-risk patients including those with a history of multiple major ASCVD events or one major ASCVD event and multiple high-risk conditions (e.g., age ≥65 years; heterozygous familial hypercholesterolemia; history of coronary artery bypass surgery or percutaneous coronary intervention outside of the major ASCVD events; diabetes; hypertension; chronic kidney disease; or current smoking).[21] Alirocumab significantly reduced LDL-cholesterol levels in patients with heterozygous familial hypercholesterolemia receiving statin therapy at the maximum tolerated dose.[115] In one multicenter, randomized, double-blind, placebo-controlled trial of patients who had a previous acute coronary syndrome and were receiving high-intensity statin therapy, the risk of recurrent ischemic cardiovascular events was lower among those who received alirocumab than in those who received placebo.[116]

In patients with severe hypertriglyceridemia (i.e., fasting triglycerides ≥500 mg/dL [≥5.7 mmol/L]), it is reasonable to identify and address causes of hypertriglyceridemia. If triglycerides are persistently elevated or increasing, it is recommended to further reduce triglycerides to lower the risk of ASCVD events. This may be achieved via a very low-fat diet, avoidance of refined carbohydrates and alcohol, and consumption of omega-3 fatty acids; fibrate therapy can be used if necessary to prevent acute pancreatitis.[21]

In patients with TIA and hyperlipidemia, adherence to changes in lifestyle and the effects of LDL-cholesterol-lowering medication should be assessed by measurement of fasting lipids and appropriate safety indicators 4 to 12 weeks after statin initiation or 4 to 12 weeks after any adjustment in dose, and every 3 to 12 months thereafter, based on individual need.[21]

Antihypertensive therapy in patients with TIA

Control of chronic blood pressure (BP) results in a 30% to 40% risk reduction in stroke.[21]​ Diuretics, angiotensin-II receptor antagonists, and ACE inhibitors effectively reduce stroke risk, but the optimal agent or combination has not been determined.[21] [ Cochrane Clinical Answers logo ] Long-term BP reduction to secondary prevention goals is clearly beneficial for stroke prevention.[39]

BP reduction appears to reduce second stroke rates without a threshold for benefit.

Patients with previously treated hypertension should be restarted on antihypertensive treatment after the first few days of the index event.[39] Patients not previously treated for hypertension who experience a TIA and have an established BP ≥140/90 mmHg should be prescribed antihypertensive treatment a few days after the index event, preferably in partnership with a primary care physician.[13][39]​​

Caution is advised in lowering BP in patients with severe carotid stenosis to prevent cerebral hypoperfusion prior to carotid revascularization.[117]

AHA/ASA guidelines recommend an office BP goal of <130/80 mmHg for most patients to reduce the risk of recurrent stroke and vascular events.[21] The American Academy of Neurology recommends a long-term BP target of <140/90 mmHg in patients with symptomatic intracranial atherosclerotic arterial stenosis.[23]

Drug regimens should be individualized to take into account patient comorbidities, agent pharmacologic class, and patient preference.[21][23][39]

Lifestyle modifications including salt restriction, weight loss, healthy diet, exercise, and limited alcohol consumption are considered reasonable interventions for most people with above-normal BP.[39]​​

TIA with stenosis of a major intracranial artery

In patients with stroke or TIA (within 30 days) attributable to severe stenosis (70% to 99%) of a major intracranial artery (i.e., in the distribution of the intracranial carotid, intradural vertebral, basilar, and anterior/middle/posterior cerebral arteries), the addition of clopidogrel to aspirin for up to 90 days is reasonable to further reduce recurrent stroke risk in patients who have low risk of hemorrhagic transformation.[21][23]

The dual antiplatelet therapy regimen of ticagrelor plus aspirin is approved by the FDA in the US to reduce the risk for stroke in patients with acute ischemic stroke with NIHSS score of ≤5 or high-risk TIA. The choice of adding ticagrelor or clopidogrel to aspirin should be based on patient factors (e.g., medication adherence and dose frequency).[21]

In patients with minor stroke or high-risk TIA within 24 hours and concomitant ipsilateral >30% stenosis of a major intracranial artery, the addition of ticagrelor to aspirin for up to 30 days might be considered to further reduce recurrent stroke risk.[21]

In Europe, an application to the EMA to change the marketing authorization of ticagrelor to include the prevention of stroke in adults who have had a mild to moderate ischemic stroke or high-risk TIA was withdrawn in December 2021. Based on trial data and the company's response to their questions, the EMA expressed concern that the benefits of short-term treatment with ticagrelor plus aspirin in preventing stroke in these patients did not clearly outweigh the risks of fatal and nonfatal bleeding.

In patients with TIA caused by 50% to 69% stenosis of a major intracranial artery, aspirin is recommended in preference to warfarin to reduce the risk of recurrent ischemic stroke and vascular death.[21]

Percutaneous angioplasty and stenting for prevention of stroke in moderate (50% to 69%) symptomatic intracranial stenosis, or as initial treatment of stroke in severe (70% to 99%) symptomatic intracranial stenosis, is not recommended. For patients with stroke due to intracranial stenosis of the anterior circulation, direct and indirect extracranial to intracranial (EC/IC) bypass are not recommended.[23]

Patients with extracranial carotid stenosis

In patients with a TIA or nondisabling stroke within the past 6 months and ipsilateral severe (70% to 99%) carotid artery stenosis, carotid endarterectomy is recommended to reduce the risk of future stroke, provided that perioperative morbidity and mortality risk is estimated to be <6%.[21][118]​ Referral for carotid endarterectomy is appropriate as long as the patient is neurologically stable, with surgery within 2 weeks of the event preferred.[21][32]​​[43]​​

In patients with symptomatic carotid stenosis (i.e., TIA or nondisabling stroke), carotid artery stenting is preferred over carotid endarterectomy if the degree of stenosis is between 50% and 69% by digital subtraction angiography. This is appropriate only if perioperative risk of morbidity and mortality is <6%.

In patients with recent TIA or ischemic stroke and ipsilateral moderate (50% to 69%) carotid stenosis as documented by catheter-based imaging or noninvasive imaging, carotid endarterectomy is recommended to reduce the risk of future stroke, depending on patient-specific factors such as age, sex, and comorbidities, if the perioperative morbidity and mortality risk is estimated to be <6%.[21]

Endovascular treatment of intracranial stenosis has not been demonstrated to be better than aggressive medical therapy.[21][119][120]

Optimization of glycemic control in patients with TIA

In diabetic patients with TIA, existing guidelines for glucose control should be followed. A goal hemoglobin A1c (HbA1c) of <7% is recommended for most patients.[21]

Lifestyle modification in patients with TIA

  • Patients with TIA who smoke are strongly advised to stop smoking. Counseling with or without drug therapy (nicotine replacement, bupropion, or varenicline) is recommended to assist in stopping smoking to reduce risk of recurrent stroke.[21] Avoidance of environmental (passive) tobacco smoke is also recommended.[21]

  • Patients with TIA who drink >2 alcoholic drinks a day (men) or >1 alcoholic drink a day (women) should be counseled to eliminate or reduce their consumption of alcohol to reduce stroke risk.[21]

  • In patients who are overweight or obese, weight loss is recommended.[21] In patients who are obese, referral to an intensive, multicomponent, behavioral lifestyle-modification program is recommended to achieve sustained weight loss.[21]

  • In patients with stroke or TIA who are able and willing to increase physical activity, engaging in an exercise class that includes counseling to change physical activity behavior can be beneficial for reducing cardiometabolic risk factors and increasing leisure time physical activity participation.[21] All patients who have had ischemic stroke or TIA who are capable of physical exercise should be strongly advised to participate in at least moderate intensity aerobic activity for a minimum of 10 minutes 4 times a week or vigorous-intensity aerobic activity for a minimum of 20 minutes twice a week.[21] When this is not possible, the patient's physical goals should be customized to their exercise tolerance, stage of recovery, environment, available social support, physical activity preferences, and specific impairments, activity limitations, and participation restrictions. For those who sit for long periods of uninterrupted time during the day, it may be reasonable to break up sedentary time with intervals as short as 3 minutes of standing or light exercise every 30 minutes for their cardiovascular health.[21]

  • It is reasonable to counsel individuals to follow a Mediterranean-type diet, typically with emphasis on monounsaturated fat, plant-based foods, and fish consumption, with either high extra virgin olive oil or nut supplementation, in preference to a low-fat diet, to reduce risk of recurrent stroke.[21] For patients with stroke and hypertension who are not currently restricting their dietary sodium intake, it is reasonable to recommend that individuals reduce their sodium intake by at least 1 g/day (2.5 g/day salt) to reduce the risk of cardiovascular disease events (including stroke).[21] Adherence to the MIND (Mediterranean-DASH Intervention for Neurodegenerative Delay) dietary pattern may be helpful for secondary prevention.[121]

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