By Christiaan Myburgh, MD, and Jake Gold, MD
EXECUTIVE SUMMARY
- Stroke in patients ages 18 to 50 years accounts for 10% to 15% of strokes occurring each year.
- Cervical artery dissection, cardioembolic sources, paradoxical embolization, and infectious vasculitis are more common causes of stroke in younger adults (18-50 years) compared to older adults (> 50 years).
- If the initial computed tomography (CT) scan in a patient suspected of having acute stroke does show signs of ischemia or hemorrhage, the next imaging studies should include an assessment of the vascular anatomy (CT angiography or magnetic resonance angiography) and studies to assess ischemic tissue potentially recoverable with reperfusion (CT perfusion or diffusion-weighted magnetic resonance imaging).
- Administration of intravenous alteplase (tPA) in a patient with a stroke mimic has a low risk (about 0.4%) of symptomatic intracranial hemorrhage.
Stroke in young adults, typically defined as occurring between 18 and 50 years of age, presents a set of unique diagnostic and management challenges to emergency physicians and other acute care providers. Although stroke once was considered primarily a disease of older adults, recent epidemiological data underscore a rising incidence in younger populations worldwide, accounting for roughly 10% to 15% of all stroke cases in adults.1,2 This emerging trend carries significant implications in terms of long-term disability, the economic burden of stroke, and the disruption of an individual’s social and occupational life during what often is the most productive period of adulthood.
Younger patients experiencing acute cerebrovascular events may not exhibit the classic risk factor profile seen in older counterparts: diabetes, hypertension, and hyperlipidemia. Instead, etiologies such as arterial dissections, cardiac abnormalities (including patent foramen ovale [PFO], dilated cardiomyopathy, and even rare entities like atrial myxoma), autoimmune or inflammatory vasculopathies (e.g., lupus, human immunodeficiency virus [HIV]-associated vasculitis), or inherited metabolic disorders (e.g., homocystinuria, Fabry disease) might predominate. Identifying these etiologies is critical because interventions may differ significantly from those typically employed for older stroke patients with atherosclerosis-driven cerebrovascular disease.
Although the pathophysiological mechanisms of ischemic stroke (tissue ischemia caused by occlusion of a cerebral vessel) and hemorrhagic stroke (vessel rupture leading to intracranial bleeding) are fundamentally similar across age groups, the underlying causes diverge considerably in younger adults. This article will define the scope of young adult stroke, discuss its epidemiology and pathophysiology, highlight the wide etiological spectrum, delve into clinical diagnostic steps, offer a practical framework for management, and conclude with a summary that emphasizes the persistent practice gap.
Young adult stroke remains underrecognized in many emergency settings. With the incidence of stroke in younger individuals no longer negligible, emergency clinicians must expand their differential diagnoses beyond “typical” risk factors and remain vigilant for rarer presentations. In doing so, they potentially can improve patient outcomes through early intervention, targeted therapies, and focused prevention strategies.
Definition of the Problem
Young adult stroke is defined here as a cerebrovascular accident (ischemic or hemorrhagic) occurring in individuals from 18 to 50 years of age.3 Although age cutoffs vary among studies, this range serves to highlight a demographic in which classic age-related atherosclerosis typically is less prominent. This definition, although partially arbitrary, is crucial for distinguishing this population from pediatric stroke (younger than 18 years of age) and from older stroke populations, generally 60-65 years of age and older, where long-standing hypertension, diabetes mellitus, and hyperlipidemia predominate.
Importantly, the stroke subtypes (ischemic vs. hemorrhagic) do not intrinsically differ in pathomechanism in younger patients. Instead, the relative contributions of each underlying cause shift. For instance, large-artery atherosclerosis (LAA) is less common in individuals younger than 50 years of age, whereas non-atherosclerotic causes such as arterial dissection occur more frequently.3 This demographic distinction serves as the basis for advocating a separate categorization of “young adult stroke.”
In many parts of the world, the burden of young adult stroke has been gradually recognized only in the past two or three decades. Historically, these cases were overshadowed by the large volume of stroke occurrences in older age groups. Today, advanced neuroimaging, greater awareness, and evolving risk factor profiles have sharpened our understanding of this younger cohort, prompting updated diagnostic and therapeutic paradigms.
Relevancy of the Problem to the Adult Population
Stroke constitutes a leading cause of adult disability and the second leading cause of death worldwide.4,5 When stroke occurs in a person younger than 50 years of age, the consequences can be devastating not only from a medical perspective but also from socioeconomic and psychological standpoints. Younger individuals often are in the midst of career development, parenting, or higher education. A stroke can abruptly interrupt these life stages, creating long-term burdens on patients, families, and healthcare systems. Multiple epidemiological studies show that the incidence in younger adults has not only remained significant but in some populations has increased over the past decade.1,2,6
Beyond the physical impairments, up to half of young stroke survivors experience some degree of cognitive impairment, and around a quarter may present with aphasia.7 This cognitive and communicative dysfunction can lead to isolation, depression, and the potential for chronic unemployment.8 Additional psychosocial problems, such as relationship strain, loss of independence, and financial difficulties, further complicate the recovery process. Considering that stroke survivors often live for many decades after the event, ensuring optimal management and secondary prevention strategies becomes paramount.
In a global context, approximately 2 million younger individuals (ages 18-49 years) experience a stroke every year.1 The absolute numbers vary by region, with developing countries experiencing changes in lifestyle patterns that may predispose to increased stroke risk in younger people. Smoking, substance abuse, a high prevalence of untreated hypertension, and metabolic syndrome can accelerate cerebrovascular changes.
Epidemiology
The epidemiology of young adult stroke can be assessed by incidence and prevalence trends, mortality patterns, demographic risk factors, and geographical variation. An estimated 10% to 15% of all strokes occur in individuals aged 18 to 49 years, translating to about 2 million cases globally per year.1 Some registries indicate that these incidence rates are rising, although the degree of increase is not uniform across regions.2,6 One prospective study of embolic stroke of undetermined source (ESUS) in adults younger than 50 years of age found that recurrent stroke rates, although lower compared to older ESUS cohorts, remain a clinical challenge.9 More than half of recurrent ischemic strokes in that cohort still met ESUS criteria, highlighting the diagnostic complexity in young adults.
Certain studies also note disparities in stroke-related mortality and incidence when stratified by race, ethnicity, and sex. For instance, non-Hispanic Black populations experience a higher burden of stroke risk factors, particularly uncontrolled hypertension, which remains one of the most potent contributors to stroke.10 Conversely, in white populations, smoking is a stronger risk factor. Additionally, rural communities may see higher stroke-related mortality than urban counterparts, potentially linked to limited access to acute stroke care, fewer specialty-trained providers, and socioeconomic issues.2
In adults with congenital heart disease, stroke incidence between ages 18 and 64 years is significantly higher than in the general population, particularly at younger ages, with one in 11 men and one in 15 women affected. Key predictors of future ischemic stroke include heart failure, diabetes, and recent myocardial infarction.11
Large vessel occlusion (LVO) strokes represent a particular threat in younger adults, although the etiology often differs from the atherosclerotic LVO found in older patients. Treatments like mechanical thrombectomy (MT) have markedly improved outcomes for LVO strokes, and data show that young patients may respond better to endovascular therapy, with higher rates of recanalization and favorable functional outcomes compared to older adults.12,13
In hemorrhagic stroke, younger adults may be predisposed to causes such as ruptured arteriovenous malformations, cerebral aneurysms, and complications of sickle cell disease. Mortality patterns for hemorrhagic stroke also can vary by region and underlying risk factors.
Etiology
Perhaps the most critical aspect of evaluating a stroke in a younger patient is understanding the broad range of possible etiologies. While atherosclerosis remains a leading cause of stroke among older adults, younger individuals more frequently experience strokes from dissection, cardioembolism secondary to structural heart disease, infections, prothrombotic states, and metabolic disorders. This heterogeneity necessitates a thorough, and sometimes more time-intensive, etiologic workup. See Table 1 for a comparison of key clinical and etiologic features of stroke in young adults compared to older adults. The major etiological categories in young stroke are discussed in the following sections.
Table 1. Stroke in Young Adults vs. Older Adults: Key Clinical and Etiological Comparisons | ||
Category | Young Adults (18-50 Years of Age) | Older Adults (50+ Years of Age) |
Common Etiologies | Non-atherosclerotic arteriopathies (e.g., dissection, fibromuscular dysplasia), cardioembolic causes (e.g., dilated cardiomyopathy, PFO), hematologic disorders (e.g., sickle cell disease), vasculitis/infections, and substance abuse | Predominantly large-artery atherosclerosis, cardioembolism from atrial fibrillation or valvular disease, and small vessel disease (lipohyalinosis) |
Risk Factors | Smoking, modest hypertension prevalence, substance use, and genetic/metabolic factors (e.g., homocystinuria) | Hypertension, hyperlipidemia, diabetes, and atrial fibrillation predominate |
Clinical Presentation | Sudden focal deficits, often with atypical features like neck pain (dissection) or thunderclap headache (reversible vasoconstriction); many have fewer traditional risk factors | Classic acute neurologic deficits, usually in the context of extensive vascular risk factor profiles |
Stroke Mimics | More likely to be mistaken for migraine, seizures, or functional disorders in the emergency setting | Migraine, seizures, and metabolic issues remain possible, but clinicians quickly suspect stroke given the high baseline risk |
Neuroimaging Findings | Cervical artery dissections or uncommon vasculopathies; MRI may reveal small or distal infarcts related to less common causes | Evidence of large or small vessel atherosclerosis; lacunar infarcts in deep structures are frequently observed |
Outcomes and Prognosis | Better collateral circulation can favor successful reperfusion therapy; long-term impact is high if deficits persist, given extended lifespan | Comorbidities are more common, possibly worsening functional recovery; higher overall risk of complications and mortality |
Secondary Prevention | Focus on addressing specific rarer etiologies (e.g., PFO closure, immunosuppressive therapies, exchange transfusions), along with lifestyle modification | Emphasis on controlling hypertension, diabetes, and hyperlipidemia; anticoagulation for atrial fibrillation; lifestyle changes |
PFO: patent foramen ovale; MRI: magnetic resonance imaging Younger adults with stroke often have a broader range of etiologies beyond classic atherosclerosis, including dissections, inherited or metabolic disorders, and infections. They may respond well to acute reperfusion therapies but can face substantial long-term impact on quality of life due to the younger age at onset. Older adults typically exhibit higher rates of atherosclerosis and conditions like atrial fibrillation. They often have a stronger burden of conventional risk factors (hypertension, diabetes, hyperlipidemia) and may experience more frequent large-vessel or small-vessel (lacunar) infarcts due to chronic vascular changes. | ||
Arteriopathies
Craniocervical arterial dissection is consistently reported as one of the most frequent causes of ischemic stroke in young adults, accounting for approximately 10% to 25% of cases.2,14 Dissections often involve the extracranial carotid or vertebral arteries. Precipitating events may include blunt trauma, high-velocity neck manipulation, sudden coughing, or athletic injuries, although many dissections are spontaneous. Magnetic resonance angiography (MRA) or computed tomography angiography (CTA) frequently reveals a “flap” or aneurysmal outpouching.
Fibromuscular dysplasia (FMD) also can lead to arterial stenoses, dissections, or aneurysms, particularly in young women.3 Moyamoya disease (genetic) or moyamoya syndrome (secondary to conditions such as sickle cell disease, Down syndrome, or cranial irradiation) also can cause progressive stenosis of intracranial arteries. Ischemic stroke linked to focal cerebral arteriopathy commonly affects the lenticulostriate branches originating from the proximal segments of the middle cerebral artery and anterior cerebral artery, which supply the basal ganglia and internal capsule.15 Finally, reversible cerebral vasoconstriction syndrome (RCVS) typically presents with thunderclap headaches and multifocal arterial narrowing that can lead to ischemic or hemorrhagic events if not identified promptly.3
Cardiac Sources
Cardioembolic strokes may arise from a range of structural lesions. Atrial fibrillation remains an important consideration, especially in young adults older than 30 years of age.14 However, dilated cardiomyopathy, valvular lesions, atrial myxomas, and intracardiac thrombi in left ventricular dysfunction all are possibilities.
Paradoxical Emboli
Paradoxical emboli, which are defined as venous thrombi that cross through a shunt into arterial circulation, may arise from cardiac and extracardiac shunts. Intracardiac shunts of note are the PFO, atrial septal defect, ventricular septal defect, and truncus arteriosus. A significant source of attention in young stroke has been the PFO. Although it exists in about one-quarter of the general population, studies show that it can be present in nearly half of young adult stroke patients.3,16
The paradoxical embolism theory posits that venous thrombi can traverse the PFO and cause arterial infarctions, often in the absence of other evident risk factors. Alternative theories include in situ thrombosis of the PFO as well as arrhythmogenesis.9 Recent trials indicate potential benefit from PFO closure in carefully selected younger stroke patients with cryptogenic stroke and high-risk PFO anatomical features.16 Extracardiac shunts, such as persistent left superior vena cava and pulmonary arteriovenous malformations, as seen in hereditary hemorrhagic telangiectasia (HHT), can serve as a conduit for paradoxical emboli, resulting in young-onset ischemic events.17
Infection-Related Causes
Infective endocarditis, neurosyphilis, tuberculous meningitis, varicella zoster vasculitis, and HIV vasculopathy each can result in ischemic stroke or, less commonly, hemorrhagic stroke, in younger adults.3 Infective endocarditis from intravenous (IV) drug use may lead to septic emboli, while HIV infection can provoke both vasculitic and prothrombotic phenomena. Tuberculosis and syphilis can induce arteritis within the cerebral vessels, culminating in luminal compromise and infarction. Proper antimicrobial therapy and, when indicated, immunomodulatory treatment are essential for stabilizing these conditions.
Hematologic Disorders
Sickle cell disease causes cerebral infarctions through hemolysis, inflammation, endothelial dysfunction, and the formation of moyamoya collaterals.18 It also increases the risk for hemorrhage, especially in association with aneurysms.19 Other prothrombotic conditions (antiphospholipid syndrome, protein S deficiency, or polycythemia vera) also have been documented as relatively more frequent etiologies in younger patients.14,20 Polycythemia vera, although often recognized in older adults, occasionally can manifest in a young adult with an initial presentation of ischemic stroke.20
Metabolic Disorders
Inherited metabolic conditions, such as homocystinuria, Fabry disease, and mitochondrial disorders (e.g., mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes [MELAS]) can lead to early-onset strokes.3 Homocystinuria, for instance, can predispose to both arterial and venous thrombosis. Fabry disease arises from alpha-galactosidase A deficiency and is associated with small vessel disease, leading to infarcts in the posterior circulation. Prompt recognition and targeted therapies (e.g., enzyme replacement in Fabry disease) can significantly alter the clinical course.
Substance Abuse
Recreational drug use, especially cocaine and amphetamines, is implicated in up to 12% of young adult strokes.3 Cocaine can cause acute vasospasm, dissection, or arrhythmias, with crack-cocaine inhalation posing particularly high risk. Chronic intravenous drug use can predispose to infective endocarditis and potential septic emboli. Opioid use also may create a prothrombotic state or predispose to infective complications.
Other Rare Causes
Tumors (primary or metastatic) and marantic endocarditis in malignancy also can generate emboli. The previously mentioned etiologies underscore the importance of adopting a structured approach to evaluating suspected stroke in a young adult, emphasizing the potential for uncommon causes.
Pathophysiology
Stroke pathophysiology in younger adults parallels that in older populations with respect to the final common pathway of ischemia or hemorrhage. However, the interplay of precipitating factors reveals distinctive elements. Neuroinflammatory mechanisms, immune dysregulation, or hypercoagulability can be more relevant in younger stroke patients. For instance, autoimmune conditions like systemic lupus erythematosus (SLE) or antiphospholipid syndrome can trigger either in situ thrombosis or contribute to vasculitis.
After traumatic brain injury (TBI), early stroke risk is driven primarily by coagulation abnormalities, vascular injuries, microvascular damage, ischemia, and increased intracranial pressure. Long-term post-TBI stroke mechanisms remain unclear but may involve vascular wall damage, amyloid angiopathy, and lifestyle factors like substance misuse and inactivity. Further research is needed to understand the prolonged stroke risk after TBI.21
Another realm of interest is the role of cancer-associated hypercoagulability in certain young adult cancers such as lymphoma or germ cell tumors.3 Tumors can induce a paraneoplastic hypercoagulable state, and some malignancies can cause marantic endocarditis (non-bacterial thrombotic endocarditis), whereby sterile vegetations form on valve leaflets and can dislodge.
Neuroinflammation has emerged as an important contributor to both the acute and chronic phases of stroke injury. Immune cells (e.g., microglia, macrophages) and inflammatory mediators (cytokines, adhesion molecules) become activated during ischemic injury, shaping tissue recovery, infarct expansion, and reperfusion injury.5 This general concept applies across the age spectrum, but in younger patients, infection-driven or autoimmune-driven inflammatory cascades can be especially significant in the genesis of stroke.
Hemodynamic factors also differ in younger adults, who typically have fewer atherosclerotic plaques in major vessels. Instead, mechanical disruptions like dissection or microangiopathic lesions from inherited disorders take center stage. Dissection leads to an intimal tear and the formation of a false lumen, enabling embolic fragments to break off and block downstream cerebral arteries. In conditions like sickle cell disease, chronic hemolysis and repeated vaso-occlusive events progressively damage the endothelium, generating an environment prone to infarcts and hemorrhages.19
Lastly, the concept of “cryptogenic stroke” takes on new complexity in young patients. Approximately 30% to 40% of ischemic strokes remain unclassified after initial evaluation; in younger populations, the cryptogenic subset frequently includes ESUS and potential paradoxical embolism through a PFO or pulmonary shunt.3,9 Identifying a definitive mechanism in these patients often hinges on advanced imaging of the heart and large vessels, as well as extended cardiac rhythm monitoring to detect intermittent arrhythmias.
Clinical Features
Young adults with stroke can present with a wide variety of clinical manifestations. While classic sudden-onset neurological deficits such as hemiparesis, hemisensory loss, aphasia, or facial droop remain common, practitioners also must consider “atypical” signs that may stem from rarer etiologies. A significant finding in one systematic review was that around half of all young stroke patients show cognitive impairment and roughly one-quarter present with aphasia.7 Because younger individuals might not fit the high-risk profile typically associated with stroke, clinicians risk missing these early neurological signs or attributing them to more benign causes.
Key historical clues may include headache at onset, possibly reflecting a vascular dissection or RCVS, or a history of trauma (even minor) that suggests arterial dissection. The presence of thunderclap headache — rapidly peaking in seconds — should raise suspicion for subarachnoid hemorrhage or RCVS. In hemorrhagic stroke, signs of increased intracranial pressure (severe headache, vomiting, depressed consciousness) may appear, although subtle presentations remain possible, especially for smaller bleeds. Infectious vasculitides may present with systemic symptoms such as fever, rash, night sweats, or weight loss, which could point toward an underlying infection like tuberculosis or HIV.3,9
Examination of younger patients should include careful cardiovascular assessment (potential murmurs indicating valvular disease or myxoma), scrutiny for cutaneous markers of connective tissue disorders (e.g., Ehlers-Danlos), or stigmata of intravenous drug use. Blood pressure might be normal or only moderately elevated, underscoring the potential for nonhypertensive mechanisms. A thorough neurological exam, inclusive of cranial nerve testing and a detailed search for focal deficits, is imperative. Cortical signs, such as gaze preference, neglect, aphasia, or visual field deficits, may suggest an embolic or large vessel territory infarct, while lacunar syndromes (pure motor hemiparesis, pure sensory stroke) point toward small vessel pathology.
In situations where the presentation is less typical — such as fluctuating neurological deficits, headache preceding focal deficits, or bilateral signs — clinicians should consider rarer etiologies. Recurrent transient ischemic attacks (TIAs) in a single vascular territory may signal focal cerebral arteriopathy, whereas new-onset seizures or confusion could mask an underlying stroke.22 Early neuroimaging, including magnetic resonance imaging (MRI) with diffusion-weighted imaging, frequently helps distinguish acute stroke from stroke mimics (including migraine with aura, complex partial seizures, or functional neurological disorder).
Diagnostic Studies
In an emergency setting, initial neuroimaging typically involves a noncontrast head computed tomography (CT) to discriminate between ischemic and hemorrhagic stroke. If hemorrhage is excluded, many centers proceed rapidly to vascular imaging, such as CT angiography (CTA) or magnetic resonance angiography (MRA), to identify or rule out large vessel occlusions, dissections, or other structural anomalies.23 Advanced imaging, such as CTA with CT perfusion (CTP) or MRA with diffusion-weighted MRI (DW-MRI), is valuable for identifying candidates for mechanical thrombectomy six to 24 hours after the last known well time.24 CTA and MRA yield high sensitivity (in the range of 87% to 100%) for detecting significant intracranial stenoses or occlusions compared to the gold standard of digital subtraction angiography.23 For posterior circulation strokes, CTA or MRA is even more crucial, given the higher risk of catastrophic deficits in basilar artery occlusion.25
Advanced MRI sequences, including DWI and fluid-attenuated inversion recovery (FLAIR), provide early detection of ischemic infarcts and potential clues about stroke timing. The WAKE-UP trial demonstrated that patients with DWI-positive but FLAIR-negative patterns could safely receive intravenous alteplase (tPA) even when the time of onset was unknown, expanding treatment windows.26 This approach may be especially pertinent in young adults who awaken with stroke symptoms or in cases where the exact onset is not witnessed.
Cardiac evaluation is essential in young patients with cryptogenic stroke. Transthoracic echocardiogram (TTE) with bubble study often is the first step to detect PFO, valvular lesions, or intracardiac thrombi. In younger patients with cryptogenic-appearing strokes or suspicion of an embolic source, a transesophageal echocardiogram (TEE) can reveal pathologies that TTE might miss, such as atrial septal aneurysms, small intracardiac masses, or aortic arch atheromas.3 According to one reference, TEE findings in young stroke patients can alter management in about 17% of cases.3
Laboratory investigations begin with a fingerstick glucose test, complete blood count (CBC), prothrombin time/international normalized ratio (PT/INR), activated partial thromboplastin time (aPTT), troponin, and basic metabolic panel. These tests aim to exclude hypoglycemia or other metabolic causes that can mimic stroke. In potential hypercoagulable states or suspected vasculitis, the workup expands to include inflammatory markers (erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]), rheumatologic panels (antinuclear antibody [ANA], anti-double-stranded deoxyribonucleic acid [anti-dsDNA], antiphospholipid antibodies), and, if indicated, infectious testing (HIV, syphilis, tuberculosis [TB]).3,9 Toxicology screening may be indicated in a younger patient with possible substance use. If the clinical presentation suggests sickle cell disease complications or polycythemia vera, specialized testing (hemoglobin electrophoresis, JAK2 mutation analysis) is warranted.20
Because so many etiologies exist, the clinician must systematically direct testing based on initial clinical clues. For instance, in suspected dissection, vascular imaging of the cervical arteries (e.g., CTA of the neck) is essential. In suspected vasculitis (especially if the patient has associated headache, seizures, or systemic symptoms), MR angiography or conventional angiography might show beading or alternating stenoses and aneurysms. Lumbar puncture could be indicated if central nervous system (CNS) infection or inflammatory disease remains high on the differential.
Differential Diagnosis
The differential diagnosis for acute neurological deficits in young adults includes a broad array of conditions beyond ischemic or hemorrhagic stroke. Stroke mimics, such as seizures (with postictal paralysis), complex migraines, encephalitis, or demyelinating disease (multiple sclerosis), can present similarly. Metabolic derangements — hypoglycemia, hyperglycemia with ketoacidosis, hypercalcemia, hepatic or uremic encephalopathy — also might manifest with focal or global neurological signs.3 While time is of the essence in stroke management, a comprehensive but rapid assessment is critical to avoid the misapplication of thrombolysis in non-stroke conditions.
In some cases, intravenous (IV) alteplase may be administered to a patient who ultimately proves to have a stroke mimic. However, current data indicate that hemorrhagic risk is relatively small (about 0.4% risk of symptomatic intracranial hemorrhage) when administering IV tPA to patients who turn out to have a mimic.3 This risk may be considered acceptable given the high stakes of missing or delaying treatment in patients with a genuine ischemic stroke.
Additionally, intracranial tumors such as gliomas, meningiomas, or metastases sometimes can mimic stroke presentations if they cause acute neurological deficits through hemorrhage, edema, or seizures. Demyelinating lesions in multiple sclerosis can present with localized weakness or vision loss that might simulate a stroke. Finally, functional neurological disorders or factitious disorders occasionally can mimic the acute onset of unilateral weakness, yet these typically lack supportive findings on imaging or exam patterns consistent with organic disease.
Management
Management principles for young adult stroke broadly align with guidelines for all adult stroke patients but require careful consideration of etiologic subtleties. Emergency stabilization follows standard protocols: Ensure a patent airway, provide supplemental oxygen to maintain saturation above 94%, secure intravenous access, and address hyperglycemia or hypoglycemia.27 Blood pressure (BP) management also is crucial, particularly for those who may receive thrombolysis. Current guidelines recommend reducing BP to below 185/110 mmHg prior to IV alteplase administration.27
For assessing LVO in confirmed ischemic stroke patients in the emergency department, the National Institutes of Health Stroke Scale (NIHSS) score is recommended as the most effective predictive tool. A threshold of ≥ 10 offers the best balance between sensitivity (73%) and specificity (74%), while a lower threshold of ≥ 6 increases sensitivity to 87% but reduces specificity to 52%, leading to more false positives and still missing some LVO cases.28
Acute Reperfusion Therapies
Intravenous alteplase remains the mainstay for eligible patients presenting within 4.5 hours of ischemic stroke onset.29-31 The greatest benefits are seen with earlier administration in patients with moderately severe ischemic stroke. The PRISMS RCT assessed IV alteplase in patients with mild acute ischemic stroke (NIHSS score 0–5) whose deficits did not impact daily living or work. The study found no benefit from treatment within three hours of symptom onset.32 See Table 2 for a non-exhaustive list of tPA contraindications.
Table 2. Contraindications to tPA for Acute Ischemic Stroke | |
Category | Contraindications |
Absolute |
|
Relative |
|
aPTT: activated partial thromboplastin time; INR: international normalized ratio; PT: prothrombin time; CT: computed tomography Adapted from: Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines. Stroke. 2019;50(12):e344-e418 | |
Mechanical thrombectomy with stent retrievers has revolutionized the treatment of LVOs in the anterior circulation. Numerous trials (MR CLEAN, ESCAPE, SWIFT PRIME, EXTEND-IA, REVASCAT, and THRACE) have confirmed that endovascular therapy significantly improves functional outcomes if performed within about six hours, with subsequent trials (DAWN, DEFUSE 3) extending the window up to 24 hours in selected patients with salvageable brain tissue.33-39 A pooled analysis of five randomized trials comparing endovascular treatment with medical therapy alone showed that the odds of improved 90-day disability outcomes (measured by modified Rankin Scale [mRS] scores) decreased as the time from symptom onset to arterial puncture increased, highlighting the importance of early intervention.40
Younger adults, by virtue of having better collateral circulation and fewer comorbidities, often demonstrate excellent recanalization and neurological recovery.12,13
For posterior circulation strokes, particularly basilar artery occlusion, mechanical thrombectomy may similarly confer a benefit, although the evidence base is less robust.25
For patients initially seen at hospitals without mechanical thrombectomy capability, “bridging IV tPA is” recommended if the patient arrives within the standard time windows, unless specific contraindications exist, before transfer to a center capable of endovascular therapy. The risk-benefit ratio of thrombolytics in younger patients remains favorable overall.
Special Considerations in Etiology
Management can diverge significantly based on the underlying cause. In cases of arterial dissection, practitioners may use antiplatelet agents or anticoagulation, although evidence on the superiority of one regimen over the other remains limited. Infectious causes, such as infective endocarditis or HIV vasculopathy, require targeted antimicrobial or antiretroviral therapy along with stroke therapies. For example, in bacterial endocarditis, urgent antibiotic treatment is mandatory to curb ongoing septic embolization.
In vasculitis (primary or secondary), high-dose corticosteroids or immunosuppressants (e.g., cyclophosphamide) may be indicated, usually in coordination with rheumatology or infectious disease specialists.3,41 In sickle cell disease, exchange transfusion to lower hemoglobin S percentage can mitigate ongoing vascular damage.19 For catastrophic presentations like malignant middle cerebral artery (MCA) infarction, decompressive hemicraniectomy within 48 hours has proven to be lifesaving and to improve functional outcomes in patients younger than 60 years of age.42-44
Complication Prevention and Supportive Care
Medical complications are common after a stroke, affecting 25% to 85% of hospitalized patients, and can hinder recovery and lead to worse outcomes.45 Common post-stroke complications include urinary tract infections (UTIs), fever, pneumonia, and deep vein thrombosis (DVT). Risk reduction measures include venous thromboembolism prophylaxis, thigh-high intermittent pneumatic compression devices, dysphagia screening to prevent pneumonia, and minimizing indwelling catheter use to prevent UTIs.46-48 Evidence shows that stroke unit care, with organized inpatient stroke services, significantly reduces mortality and improves functional outcomes.49
Young stroke patients, while presumably healthier overall, still risk adverse events like malignant cerebral edema (particularly with large hemispheric strokes) or acute obstructive hydrocephalus in cerebellar infarctions. Early neurosurgical evaluation can be lifesaving in these scenarios.
The PROPHY-VAP trial, conducted across nine intensive care units (ICUs) in France, studied the effects of a single dose of ceftriaxone (2 g) vs. placebo in comatose adult patients requiring mechanical ventilation after acute brain injury. Ceftriaxone significantly reduced early ventilator-associated pneumonia (VAP) incidence (14% vs. 32%; hazard ratio [HR], 0.60; P = 0.030) without adverse effects or microbiological impact. The findings support including a single early dose of ceftriaxone in VAP prevention protocols for brain-injured, mechanically ventilated patients.50
BP after revascularization is another area of focus. While it is essential to maintain adequate perfusion, excessively high BP can increase hemorrhagic transformation risk, whereas overly aggressive lowering of BP could jeopardize cerebral perfusion in the penumbra.51,52 Currently, a general consensus is to keep BP below 180/105 mmHg for at least the first 24 hours post-thrombectomy, although some centers aim for even lower thresholds. Findings from the BEST-II trial suggest that aggressive blood pressure control (systolic < 140 mmHg or < 160 mmHg) has a low likelihood of significant benefit vs. more permissive goals (systolic < 180 mmHg).52
Glycemic management has undergone scrutiny as well. Intensive insulin protocols do not necessarily improve outcomes and may lead to hypoglycemic events.53 Current guidance typically recommends maintaining glucose between 140 mg/dL and 180 mg/dL, a moderate strategy aligned with the American Heart Association/American Stroke Association (AHA/ASA) guidelines.27,53
Because head positioning can affect cerebral perfusion pressures, a logical assumption would be that prone positioning potentially would improve outcomes in acute ischemic stroke. However, a recent meta-analysis suggests that the lying-flat position is not more effective than the sitting-up position in terms of 90-day mRS score in patients with suspected acute stroke.54
Secondary Prevention
Long-term secondary prevention measures differ by etiology. Patients with confirmed cardioembolic sources such as atrial fibrillation generally are treated with anticoagulants (either warfarin or direct oral anticoagulants). Those with PFO-mediated strokes may benefit from closure if certain anatomical criteria are fulfilled, in addition to antiplatelet therapy.16 In suspected dissection, a variable duration of antiplatelet or anticoagulant therapy typically is recommended, although high-level evidence is lacking.
Lifestyle modifications remain fundamental. Smoking cessation stands out as imperative, given that tobacco use is a powerful risk factor for arterial disease. Moderation or avoidance of substances like cocaine can prevent recurrent events, and controlling traditional risk factors such as dyslipidemia, hypertension, and diabetes is universally advised.3,10 For those with rare metabolic disorders, specialized interventions (e.g., enzyme replacement therapy for Fabry disease) can reduce the risk of future events. Genetic counseling may be offered to patients with strongly inherited conditions.
In U.S. adults receiving hypertension treatment in outpatient settings, maintaining tight blood pressure control (< 130 mmHg) was linked to a 42% lower stroke incidence compared to standard control (130 mmHg to 139 mmHg).55
Interdisciplinary Collaboration
Management of young adult stroke frequently necessitates close coordination between emergency medicine, neurology, neurosurgery, cardiology, infectious disease, hematology, and rehabilitative services. A thorough evaluation that identifies rare etiologies can prevent recurrent strokes, thereby improving long-term prognosis. Communication with primary care providers and outpatient specialists is critical to ensure continuity of care, since these patients often have ongoing risk factors that must be monitored and addressed after discharge.
Additional Aspects
Potential Complications, Controversies, and Pitfalls
Young adult stroke, due to its varied etiologies, carries unique risks. Patients with malignant MCA stroke face higher mortality due to risks of cerebral edema, increased intracranial pressure, and herniation. Decompressive hemicraniectomy may be a surgical treatment option.56 Malignant cerebral edema can cause a rapid decline, particularly in large MCA infarctions.42-44 Posterior fossa strokes demand vigilant observation for swelling leading to obstructive hydrocephalus. Neuroimaging helps identify these complications early, and emergent decompression can be lifesaving.
Another area of controversy is the approach to PFO closure. While recent trials have shown benefit in certain younger patients, many factors need to be weighed, including the presence of high-risk anatomical features (e.g., large shunt or atrial septal aneurysm), concurrent vascular risk factors, and patient preferences.16 A uniform recommendation for closure does not exist, highlighting the importance of individualized decision-making based on imaging findings and thorough cardiac evaluation.
With respect to intravenous thrombolysis, caution is warranted in subpopulations like those with vasculitis. Although neither is considered a strict contraindication, the risk of hemorrhagic complications may be elevated.41,57 Clinicians must balance the time-sensitive benefit of tPA in salvaging brain tissue against these added risks, often consulting with hematology or neurology.
Subclinical cerebrovascular disease, including lacunes, white matter hyperintensities (WMHs), perivascular spaces (PVS), and cerebral microbleeds (CMBs), is highly prevalent in adults older than age 60 years, affecting more than 70%. It increases the risk of dementia, stroke, poor stroke outcomes, gait instability, late-life depression, and death. In young adults with ischemic stroke, subclinical vascular lesions affect about 20%, but while associated with thrombotic recurrence, they do not enhance outcome prediction beyond established clinical predictors.58
CMBs are observed in 15% to 27% of patients receiving IV alteplase.59 Two meta-analyses found that baseline CMBs were associated with a higher risk of symptomatic intracerebral hemorrhage (sICH) after alteplase, whereas two other meta-analyses and one multicenter study did not confirm this association.60-62 Currently, there is no direct evidence suggesting that IV alteplase provides no benefit or causes harm in eligible patients with CMBs.27 Therefore, withholding alteplase solely due to the presence of CMBs risks excluding patients who potentially could benefit from treatment.
The gravest risk associated with thrombolytic administration is the risk of symptomatic intracranial bleeding, which is reported to be between 5% to 10% in the setting of acute ischemic stroke. Management of symptomatic intracranial bleeding after IV alteplase is briefly outlined in Table 3.
Table 3. Management of Symptomatic Intracranial Bleeding After IV Thrombolytics | |
Step | Action |
1. Stop alteplase infusion | Discontinue alteplase/tenecteplase immediately. |
2. Perform urgent laboratory tests | Obtain CBC, PT (INR), aPTT, fibrinogen level, and type/cross-match. |
3. Imaging | Perform an emergent non-contrast head CT. |
4. Administer cryoprecipitate | Infuse 0.15 IU/kg (max 10 U) over 10-30 minutes; repeat if fibrinogen is < 150 mg/dL. |
5. Consider antifibrinolytics |
OR
|
6. Routine ICH care | Consult neurosurgery, consider osmotherapy, manage blood pressure (BP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), mean arterial pressure (MAP), temperature, and glucose levels. |
CBC: complete blood count; PT: prothrombin time; INR: international normalized ratio; aPTT: activated partial thromboplastin time; CT: computed tomography; IV: intravenous; ICH: intracranial hemorrhage Adapted from: Yaghi S, Eisenberger A, Willey JZ. Symptomatic intracerebral hemorrhage in acute ischemic stroke after thrombolysis with intravenous recombinant tissue plasminogen activator: A review of natural history and treatment. JAMA Neurol. 2014;71(9):1181-1185. | |
Medicolegal Considerations
Failure to diagnose stroke promptly in younger patients who do not present with a conventional risk profile can lead to significant morbidity and mortality. Proper documentation of the initial clinical exam, the justification for imaging decisions, and consultations with neurology or appropriate specialists can mitigate medicolegal risk. Delaying treatment by attributing symptoms to migraine, intoxication, or anxiety can have grave consequences if the patient is indeed experiencing an acute stroke.
Cost Considerations
Diagnostic thoroughness in young adult stroke — comprising advanced imaging (CTA, CTP, MRI/MRA), extended cardiac evaluations (including TEE), and additional laboratory work — can be expensive. However, from a health economics perspective, the cost of missing treatable etiologies (e.g., a resectable atrial myxoma, a curable infection, or a correctable PFO) far outweighs the short-term expense of a comprehensive evaluation. Effective acute care and secondary prevention measures ultimately can reduce long-term disability, translating to cost savings for healthcare systems and society at large.
Ethical Concerns and Patient Advocacy
Decisions surrounding interventions like mechanical thrombectomy, decompressive hemicraniectomy, or PFO closure can raise ethical questions, especially if prognoses are uncertain and complications significant. Therefore, shared decision-making with the patient and family is paramount. The younger demographic often has a strong desire to return to full function, which may influence a more aggressive therapeutic stance. Clinicians must balance these aspirations with realistic assessments of potential risks and benefits.
Disposition
Hospital admission is recommended for most young stroke patients. Even if the neurological deficits are mild, an inpatient stay allows for completion of the workup, close monitoring for complications, and initiation of secondary prevention measures. Data strongly indicate that specialized stroke unit care improves survival and functional independence, regardless of age or stroke severity.49,63 Such units incorporate early mobilization, dysphagia screening, prophylaxis against venous thromboembolism, and coordinated multidisciplinary rehabilitation.
For large territory infarctions or posterior fossa strokes, ICU-level monitoring is critical to detect and manage elevated intracranial pressure, malignant edema, or other acute complications. Early neurosurgical involvement is essential if emergent decompressive hemicraniectomy (for large MCA strokes) or posterior fossa decompression (for large cerebellar strokes) appears warranted. These interventions can be lifesaving for younger patients and may improve long-term outcomes.42-44
Before discharge, many young adult stroke survivors will need a carefully designed rehabilitation program addressing mobility, communication, cognition, and psychosocial challenges. Once stable, these individuals should be transitioned to outpatient follow-up with neurologists, possibly cardiologists (for cardioembolic or structural heart sources), hematologists (for prothrombotic conditions), or other relevant specialists. Early coordination with occupational, physical, and speech therapy can optimize the potential for meaningful recovery and a return to daily activities.
Summary
Stroke in young adults constitutes a heterogeneous and increasingly recognized clinical entity. While many core principles of acute stroke management — rapid neuroimaging, intravenous thrombolysis if indicated, and potential endovascular therapy — remain the same, awareness of unique etiologies and risk factors is paramount. Cervical artery dissection, cardioembolic sources (including PFO and atrial myxomas), infectious vasculitis, hematologic disorders (such as sickle cell disease or polycythemia vera), and metabolic conditions are key considerations. Early collaborative management involving emergency physicians, neurologists, neurosurgeons, cardiologists, infectious disease specialists, and hematologists can significantly affect outcomes.
Practice Gap
There is a persistent practice gap in recognizing and thoroughly investigating stroke in younger patients, who may not present with classic vascular risk factors. Failure to consider rarer etiologies or to perform advanced imaging and specialized tests can lead to misdiagnosis, delay in appropriate interventions, and preventable morbidity. Thus, one of the central aims for emergency medicine and acute neurology teams is to maintain high vigilance for stroke in young adults, expedite diagnostic evaluations, and tailor management plans that address both standard and uncommon causes. By closing this gap, healthcare professionals can enhance functional outcomes, minimize disability, and potentially save lives over the often-extended lifespan that remains for these younger stroke survivors.
Christiaan Myburgh, MD, is Associate Program Director, Baycare Emergency Medicine, St. Joseph’s Hospital, Tampa, FL.
Jake Gold, MD, is Faculty, Emergency Medicine Residency Program, BayCare Health System/St. Joseph’s Hospital EM Physician, Excelis Medical Associates, Tampa, FL.
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Although stroke once was considered primarily a disease of older adults, recent epidemiological data underscore a rising incidence in younger populations worldwide. This article will define the scope of young adult stroke, discuss its epidemiology and pathophysiology, highlight the wide etiological spectrum, delve into clinical diagnostic steps, offer a practical framework for management, and conclude with a summary that emphasizes the persistent practice gap.
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