INTRODUCTION — Although more common in older adults, stroke also occurs in neonates, infants, children, and young adults, resulting in significant morbidity and mortality.
An overview of the epidemiology, risk factors, etiology, clinical presentation, and differential diagnosis of arterial ischemic stroke in children ≥1 month of age and adults <50 years of age is provided here.
Other aspects of ischemic stroke in children and young adults are reviewed elsewhere. (See "Ischemic stroke in children: Clinical presentation, evaluation, and diagnosis" and "Ischemic stroke in children: Management and prognosis" and "Stroke in the newborn: Classification, manifestations, and diagnosis" and "Cerebral venous thrombosis: Etiology, clinical features, and diagnosis".)
EPIDEMIOLOGY — Stroke occurrence increases exponentially with age (figure 1) [1].
●Infants and children – Annual incidence rates of arterial ischemic stroke in infants and children range from 0.6 to 7.9/100,000 children per year [2-5].
Several studies have found that pediatric ischemic stroke is more common in boys than in girls [6-8]. As an example, among 1187 children in a multinational pediatric stroke registry, boys accounted 540 of 925 cases (58 percent) of arterial ischemic stroke (n = 925) and 170 of 262 cases (65 percent) of cerebral sinovenous thrombosis cases [8]. The explanation for the apparent male predominance is unknown.
●Young adults – In adults <45 years old, the incidence of ischemic stroke worldwide ranges from 8 to 100/100,000 people per year [9,10]. In the United States, the incidence of ischemic stroke in young Black adults is higher than in young White adults [11], and young Black adults are more likely to have multiple atherosclerotic risk factors (hypertension, obesity, diabetes, and smoking) compared with young White adults [12].
The reported incidence of ischemic stroke in young adults has increased since the 1980s; potential reasons include improved stroke diagnostic methods with neuroimaging, increased prevalence of risk factors, and increased use of illicit drugs [13-16]. (See 'Substance use' below.)
ETIOLOGIES AND RISK FACTORS
Differences among age groups — The etiologies and risk factors for arterial ischemic stroke in children and young adults differ from those typical in older adults. In children and young adults, congenital and acquired heart problems, hematologic conditions, vasculopathies, metabolic disorders, and drug ingestion are more common compared with older adults (table 1). These are discussed individually below. While some etiologies are mainly descriptive (eg, vasculopathy) and some pathogenic (eg, infection), there is often overlap among them (eg, infection may cause arteriopathy).
In older adults, hypertension, smoking, diabetes, and hypercholesterolemia are more common. These risk factors are also present in some young adults [17-20] and rarely in children [20,21].
Etiologies and risk factors in children — The most common etiologies and risk factors for ischemic stroke in children include cardiac abnormalities, vascular lesions (eg, focal cerebral arteriopathy), hematologic abnormalities, infection, head and neck trauma, and genetic conditions [21-25]. The incidence of these factors varies greatly depending on the population being studied.
Data on pediatric stroke come from several population-based or referral-based cohorts, as well as smaller case series. None were conducted with standardized evaluations in all patients, so the true incidence of risk factors cannot be inferred. In a multicenter report that evaluated over 600 children (age 29 days to 18 years) with arterial ischemic stroke identified from the referral-based cohort of the International Pediatric Stroke Study (IPSS), the most frequent conditions associated with arterial ischemic stroke were arteriopathy, cardiac disorders, and infection, seen in 53, 31, and 24 percent, respectively [23,24].
Etiologies and risk factors in young adults — In young adults with stroke, data on causes and risk factors come from a few single center or population-based cohorts. Conditions associated with ischemic stroke include vasculopathy (such as arterial dissection), cardiac defects, recent pregnancy, other hypercoagulable states, smoking, illicit drug use, premature atherosclerosis, hypertension, low physical activity, high body mass index in adolescents, metabolic disorders, and possibly migraine [1,19,26-31]. Rare cases of focal cerebral arteriopathy have also been reported [32].
One of the largest cohorts consisted of 1008 consecutive patients (15 to 49 years of age) with first-ever ischemic stroke from Finland [1]. Overall, the most frequent risk factors were dyslipidemia, smoking, and hypertension, found in 60, 44, and 39 percent, respectively. The most common etiologies were cardioembolism and cervicocephalic arterial dissection in 20 and 15 percent respectively; the proportions of small vessel disease and large artery atherosclerosis (14 and 8 percent) increased beginning at age 30 to 35, while the frequency of undetermined etiology (33 percent) decreased with age (figure 2). As noted previously, stroke occurrence increased exponentially with age (figure 1).
Estrogen-containing contraceptive use is associated with stroke, but some studies with formulations containing low-dose estradiol have not confirmed this association. (See "Combined estrogen-progestin contraception: Side effects and health concerns", section on 'Cardiovascular effects'.)
Arteriopathy — Abnormalities of the cerebral vasculature, whether inherited or acquired, predispose to arterial ischemic stroke in the young. Arteriopathy is defined as the imaging appearance of an in-situ arterial abnormality (ie, stenosis, irregularity, occlusion, banding, pseudoaneurysm, dissection flap) that is not attributable to an exogenous thrombus (eg, cardioembolism) and is not considered a normal developmental variant [33].
Arteriopathies can be divided into noninflammatory and inflammatory etiologies [34,35]. A report from the IPSS of 2127 children (age 1 month to 18 years) with arterial ischemic stroke identified arteriopathy in 725 (34 percent) [36]. In the 725 cases with arteriopathy, the following subtypes were reported:
●Craniocervical dissection, 27 percent
●Moyamoya disease, 24 percent
●Focal cerebral arteriopathy, inflammatory subtype (FCA-i), 15 percent
●Diffuse cerebral vasculitis, 15 percent
●Other arteriopathy, 19 percent
In the IPSS, variables associated with arteriopathy compared with no arteriopathy included age between six to nine years, headache, multiple infarctions, sickle cell anemia, and head or neck trauma [36].
Childhood arteriopathy subtypes can be challenging to distinguish, particularly in the acute setting. However, typical clinical characteristics and imaging features can aid in classification [37]. Intracranial arterial wall imaging is useful in identifying inflammatory versus non-inflammatory etiologies. (See "Ischemic stroke in children: Clinical presentation, evaluation, and diagnosis", section on 'Arterial wall imaging'.)
Focal cerebral arteriopathy — Focal cerebral arteriopathy of childhood (FCA) is the term originally used by the IPSS to describe an unexplained, nonatherosclerotic, unilateral focal arterial stenosis in a child with arterial ischemic stroke [23]. The term FCA now defines a specific angiographic appearance of unifocal and unilateral stenosis or irregularity of one of the large intracranial arteries of the anterior circulation (distal internal carotid artery and/or its proximal branches) [37]. Some investigators recognize two subtypes:
FCA-dissection type (FCA-d) — FCA-d includes intracranial but not extracranial dissection of the anterior circulation. In children, intracranial dissection can be difficult to distinguish from FCA-i based upon radiographic imaging features alone, as demonstrated by post-mortem cases [37,38].
FCA-inflammatory type (FCA-i) — FCA-i includes cases others have labeled transient cerebral arteriopathy (TCA) and is thought to represent a focal vasculitis in most cases. In the IPSS, single infarctions and hemiparesis were clinical presentations associated with FCA-i [36].
Possible causes of FCA-i are inflammation and vasculitis due to infection (eg, antecedent varicella infection) or autoimmune disease [35,39-43] (see 'Infection' below). Other possible causes of FCA include thromboembolic arterial occlusion or stenosis followed by variable recanalization, arterial spasm, and prothrombotic factors [39,40].
TCA was originally defined as a monophasic transient arteriopathy characterized, on serial vascular imaging, by a nonprogressive unilateral focal or segmental stenosis or occlusion of the distal internal carotid and/or initial segments of the large intracranial arteries [34].
A segmental banding pattern (image 1) is considered a pathognomonic feature of FCA-i (TCA), but is only present in approximately one-quarter of cases [37]. A report of cases labeled TCA found that the stenosis may worsen in the first three months after stroke, sometimes associated with new neurologic symptoms, but stabilizes and can even improve by six months after initial presentation [44]. While the term "transient" in TCA implies complete resolution, some patients are left with some degree of residual arterial stenosis [34,45].
Ischemic stroke associated with FCA often occurs in the distribution of the lenticulostriate branches that arise from the proximal segments of the middle cerebral artery and anterior cerebral artery, supplying the basal ganglia and internal capsule [44,45]. In a subset of cases, this finding is associated with antecedent varicella infection [39,45,46]; other viral infections may underlie the pathophysiology in idiopathic cases.
Moyamoya — Moyamoya syndrome is characterized by progressive stenosis of the internal carotid arteries and formation of collateral vessels that give a "puff of smoke" appearance on angiography. Moyamoya disease occurs mainly in Japanese and other Asian populations and may have a genetic basis. In the IPSS, seizures and recurrent strokes were associated with moyamoya [36].
Secondary moyamoya syndrome is seen in association with neurofibromatosis, trisomy 21, Williams syndrome, sickle cell disease, congenital dwarfism, and as a sequela of cranial irradiation. In children, moyamoya typically presents with recurrent transient ischemic attacks (TIAs) or ischemic strokes, while intracranial hemorrhage is more common in young adults. (See "Moyamoya disease and moyamoya syndrome: Etiology, clinical features, and diagnosis".)
Extracranial dissection — Extracranial arterial dissection of the carotid and vertebral arteries is a common vascular abnormality in some young adult series [17,30,47-49], and is a cause of stroke in children as well [3,6,21,50]. While definite or probable trauma is identified in some patients, spontaneous dissection also occurs. Connective tissue disorders such as vascular Ehlers-Danlos syndrome and Marfan syndrome can predispose to dissection. (See "Cerebral and cervical artery dissection: Clinical features and diagnosis".)
Intracranial dissection, termed FCA-d in childhood stroke, is discussed above. (See 'FCA-dissection type (FCA-d)' above.)
In the IPSS, head and neck trauma were associated with both intracranial and extracranial dissection. Headache was associated with intracranial dissection, while male sex and posterior circulation involvement were associated with extracranial dissection [36].
Diffuse vasculitis — Vasculitis (inflammatory changes in the cerebral vessels) can be primary or secondary. In the IPSS, bilateral infarctions and acute systemic findings were associated with vasculitis [36].
Primary vasculitides associated with stroke include:
●Takayasu arteritis (see "Clinical features and diagnosis of Takayasu arteritis")
●Giant cell arteritis (see "Clinical manifestations of giant cell arteritis")
●Polyarteritis nodosa (see "Clinical manifestations and diagnosis of polyarteritis nodosa in adults")
●Kawasaki disease (see "Kawasaki disease: Clinical features and diagnosis")
●Primary angiitis of the central nervous system (see "Primary angiitis of the central nervous system in adults")
Adenosine deaminase 2 (ADA2) deficiency, caused by CECR1 pathogenic variants, is a cause of early childhood stroke that may mimic polyarteritis nodosa [51-53]. Variable clinical features of this condition include intermittent fevers, proteinuria, hypertension, peripheral neuropathy, humoral immunodeficiency, and skin disease (eg, livedo reticularis, hand nodules).
Secondary vasculitides due to collagen vascular diseases such as lupus or infections are also associated with stroke:
●Systemic lupus erythematosus (see "Childhood-onset systemic lupus erythematosus (SLE): Clinical manifestations and diagnosis" and "Clinical manifestations and diagnosis of systemic lupus erythematosus in adults")
●Bacterial meningitis (see "Bacterial meningitis in children: Neurologic complications", section on 'Cerebrovascular complications' and "Clinical features and diagnosis of acute bacterial meningitis in adults")
●HIV [54,55] (see "Pediatric HIV infection: Classification, clinical manifestations, and outcome", section on 'Other')
●Varicella [46] (see "Clinical features of varicella-zoster virus infection: Chickenpox")
●Syphilis (see "Neurosyphilis")
●Central nervous system tuberculosis (see "Central nervous system tuberculosis: An overview")
Monogenic arteriopathies
●Arterial tortuosity syndrome, caused by pathogenic variants in SLC2A10 [56].
●CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy), caused by pathogenic variants in the NOTCH3 gene, which leads to progressive degeneration of smooth muscle cells in the vessel wall. The underlying vascular lesion in CADASIL is a nonatherosclerotic angiopathy involving small arteries and capillaries, primarily in the brain. Patients with CADASIL may present with migraine, TIA, or ischemic stroke in late childhood or early adulthood. (See "Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)".)
●CARASAL (cathepsin A–related arteriopathy with strokes and leukoencephalopathy), caused by pathogenic variants in the CTSA gene [57,58].
●CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy), due to pathogenic variants of the HTRA1 gene [59].
Other vascular abnormalities — Other abnormalities of vessel structure have been associated with ischemic stroke, including the following:
●Fibromuscular dysplasia, a nonatherosclerotic, noninflammatory arteriopathy that predominantly affects females [60].
●PHACE (syndrome of posterior fossa brain malformations, hemangiomas, arterial anomalies, coarctation of the aorta and cardiac defects, and eye abnormalities) [61]; children with PHACE syndrome may develop progressive narrowing of the cerebral arteries, which increases the risk for arterial ischemic stroke. (See "PHACE syndrome".)
●Hereditary hemorrhagic telangiectasia (HHT), an autosomal dominant vascular disorder with a wide spectrum of clinical manifestations. Patients with HHT may develop pulmonary arteriovenous malformations (AVMs) and various types of cerebrovascular malformations. Ischemic stroke in HHT occurs primarily from paradoxical embolism through a pulmonary AVM [62]. (See "Clinical manifestations and diagnosis of hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)".)
●Radiation-induced vasculopathies; presumed small or large vessel vasculopathies in childhood cancer survivors exposed to cranial or cervical radiation [63-65].
●Rotational vertebral artery syndrome (also called bow hunter syndrome), characterized by symptoms of brainstem or cerebellar ischemia due to compression of the V3 segment of the vertebral artery by bony elements of the spine (typically at C1-C2) that occurs with physiologic head rotation and is more common in boys [22,66-70]. Repeated trauma to the artery leads to the development of pseudoaneurysm and dissection, and in some cases to recurrent posterior circulation arterial ischemic stroke.
●RCVS (reversible cerebral vasoconstriction syndrome), which represents a group of conditions characterized by reversible narrowing and dilatation of the cerebral arteries. (See "Reversible cerebral vasoconstriction syndrome".)
●RVCL-S (retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations), also known as HERNS (hereditary endotheliopathy, retinopathy, nephropathy, and stroke), due to heterozygous pathogenic variants in TREX1 gene. (See "Retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S)".)
●Smooth muscle dysfunction syndrome, caused by pathogenic variants in ACTA2 and other genetic abnormalities, and characterized by neurovascular abnormalities (an abnormally straight course of the internal carotid and intracranial arteries, dilation of the proximal internal carotid arteries, and occlusive disease of the terminal internal carotid arteries), aortic disease, pulmonary hypertension, congenital mydriasis and pupillary abnormalities, and presentation in infancy with a patent ductus arteriosus [71-73].
●Vasospasm resulting from subarachnoid hemorrhage. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Vasospasm and delayed cerebral ischemia'.)
Cardiac — Congenital and acquired heart disease is a risk factor for cardioembolic stroke, especially in the perioperative period or following catheterization or extracorporeal membrane oxygenation (ECMO) [24,74-81]. Potential mechanisms of ischemic stroke associated with congenital heart disease include the following [75,79]:
●Paradoxical embolism
●Hyperviscosity (eg, from polycythemia and compensatory erythrocytosis)
●Increased risk of infective endocarditis and septic embolism
●Propensity to thrombosis (figure 3)
●Dilation of cardiac chambers with intracardiac thrombus formation
●Arrhythmias
Congenital heart disease remains a stroke risk factor for years after palliative and corrective surgeries. Compared with the general population, the risk of ischemic stroke in young adults (ages 18 to 55 years) with congenital heart disease is 9 to 12 times higher [76], and the risk of stroke in children with congenital heart disease is approximately 19 times higher [82].
Acquired heart disease (eg, myocarditis, endocarditis, cardiomyopathy, and prosthetic valve placement) is also a risk factor for arterial ischemic stroke [81,83,84]. (See "Clinical manifestations and diagnosis of myocarditis in children" and "Infective endocarditis in children".)
The role of common cardiac abnormalities such as PFO and mitral valve prolapse is reviewed separately. (See "Atrial septal abnormalities (PFO, ASD, and ASA) and risk of cerebral emboli in adults" and "Mitral valve prolapse: Overview of complications and their management".)
Infection — There is evidence certain infectious agents may act as direct causes of stroke, while systemic infections may act as nonspecific stroke triggers [85].
●Direct causes of stroke – Examples of infections that may cause stroke directly (table 2) include a number of bacterial infections (eg, neurosyphilis, tuberculous meningitis), parasitic infections (eg, Chagas disease, neurocysticercosis, cerebral malaria), fungal infections (cryptococcal meningitis and vasculitis), and viral infections (HIV vasculopathy, herpes simplex virus vasculitis, and varicella-zoster virus vasculitis) [85,86].
Stroke in children and young adults may occur in association with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (coronavirus disease 2019 [COVID-19]). Potential risk factors and mechanisms include established stroke risk factors and those related to COVID-19 (eg, hypercoagulability and proinflammatory state, endothelial dysfunction, and/or cardiogenic embolism). In a survey of international centers that treat pediatric stroke, 23 of 7231 (0.3 percent) children hospitalized with SARS-CoV-2 infection had an arterial ischemic stroke; in 22 of the arterial ischemic stroke cases with sufficient data, SARS-CoV-2 was considered the main stroke risk factor in 6, a possible contributory factor in 13, and an incidental factor in 3 [87]. The relationship between COVID-19 and stroke is reviewed in detail elsewhere. (See "COVID-19: Neurologic complications and management of neurologic conditions", section on 'Cerebrovascular disease'.)
●Stroke triggers – Clinical and subclinical childhood infections have been implicated as a trigger for stroke across etiologies, including arteriopathy, cardioembolic, and idiopathic ischemic stroke in children. In an international, multicenter study, infection in the week prior to stroke onset (for 355 cases of children with arterial ischemic stroke) or the week prior to interview date (for 354 stroke-free controls) was significantly more common among cases compared with controls (18 versus 3 percent) [88]. In addition, cases were more likely to have missed some or all of the routinely recommended childhood vaccines (8 versus 1 percent). In multivariable logistic regression analysis, independent risk factors for childhood arterial ischemic stroke included recent infection within one week of stroke (odds ratio [OR] 6.3, 95% CI 3.3-12) and under-vaccination (OR 8.2, 95% CI 2.5-26).
In a subsequent report from the same group, serologic evidence of an acute herpesvirus infection was associated with a twofold increase in the odds of arterial ischemic stroke compared with controls (OR 2.2, 95% CI 1.2-4.0) [89]. Among the subset of 187 stroke cases with both acute and convalescent blood samples, serologic evidence of acute herpesvirus infection was present in 45 percent. Most of these infections were asymptomatic.
Infections with parvovirus B19 [90] and varicella-zoster virus [91] have also been implicated as triggers in childhood stroke.
Hematologic
Sickle cell disease — Sickle cell disease is a common cause of stroke in children, with a rate approximately 200 times higher than that seen in children without sickle cell disease [22]. The rate is highest in hemoglobin SS and hemoglobin S-beta thalassemia. This issue is discussed in detail elsewhere. (See "Prevention of stroke (initial or recurrent) in sickle cell disease", section on 'Incidence'.)
Prothrombotic disorders
●Children – Numerous other inherited or acquired prothrombotic disorders have been associated with pediatric stroke in case series, case-control studies, and prospective cohorts [21,92-96]. These include:
•Anemia (particularly iron deficiency)
•Antiphospholipid syndrome
•Abnormal activated protein C resistance (usually related to the Factor V Leiden)
•Protein C deficiency
•Protein S deficiency
•Antithrombin deficiency
•Prothrombin G20210A
•Elevated lipoprotein(a)
•Elevated homocysteine
The strongest evidence supporting an association of prothrombotic conditions with pediatric stroke comes from a meta-analysis of 22 observational studies that included 1526 children with arterial ischemic stroke, 238 with cerebral venous sinus thrombosis, and 2799 control subjects [97]. Odds ratios (ORs) for arterial ischemic stroke were as follows:
•Two or more genetic thrombophilias, OR 18.6 (95% CI 6.5-54.1)
•Protein C deficiency, OR 11.0 (95% CI 5.1-23.6)
•Antiphospholipid antibodies/lupus anticoagulant, OR 7.0 (95% CI 3.7-13.1)
•Elevated lipoprotein(a), OR 6.5 (95% CI 4.5-9.6)
•Factor V Leiden, OR 3.7 (95% CI 2.8-4.9)
•Antithrombin deficiency, OR 3.3 (95% CI 0.7-15.5)
•Prothrombin G20210A, OR 2.6 (95% CI 1.7-4.1)
•MTHFR TT genotype, OR 1.6 (95% CI 1.2-2.1)
•Protein S deficiency, OR 1.5 (95% CI 0.3-6.9)
The association with arterial ischemic stroke was statistically significant for all of the above traits except antithrombin deficiency and protein S deficiency [97]. The strength of these findings is limited by the observational methodology of the included studies, the uncertain quality of the control group, and the potential for confounding from transient acquired abnormalities of some thrombophilic factors [97,98].
●Young adults – In young adults, several of these prothrombotic factors are associated with venous thromboembolism but not clearly with arterial ischemic stroke [99]. Because of the small size of many of the studies reporting associated prothrombotic abnormalities in patients with stroke and the high frequency of some of these abnormalities in the general population, the precise contribution of these prothrombotic states to stroke pathophysiology remains unclear. Nevertheless, there are data suggesting that antiphospholipid antibodies [100], and possibly factor V Leiden [101], contribute to stroke risk in young adults.
Prothrombotic medications such as L-asparaginase and oral contraceptives are also associated with stroke. (See "Combined estrogen-progestin contraception: Side effects and health concerns", section on 'Cardiovascular effects'.)
Metabolic disorders — Several metabolic conditions are associated with arterial ischemic stroke, generally through effects on the vessel wall.
●Fabry disease, an X-linked lysosomal disease due to deficiency of alpha-galactosidase A, may result in vessel narrowing and infarction in affected young adult males and carrier females. (See "Fabry disease: Neurologic manifestations".)
●Homocystinuria is a rare condition associated with stroke in which elevated plasma homocysteine results from a deficiency of cystathionine beta-synthase. Thromboembolism has been implicated as the stroke mechanism in a small case series and case reports [102-104].
●Menkes disease, a rare X-linked condition resulting in impaired copper transport, is associated with cerebral vessel tortuosity and stroke [105].
●Deficiency of adenosine deaminase 2 (ADA2) is a rare disorder characterized by recurrent fever, vasculopathy, childhood stroke, and mild immunodeficiency [52]. Common manifestations include ischemic or hemorrhagic stroke in small vessel distributions, livedoid rash, and hepatosplenomegaly. The condition is caused by loss-of-function pathogenic variants in the CECR1 gene that encodes adenosine deaminase 2. Inheritance is autosomal recessive.
Mitochondrial disorders — Some mitochondrial disorders are associated with metabolic stroke. This category includes mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) and disorders caused by pathogenic variants in the POLG gene (ie, POLG-related disorders). (See "Mitochondrial myopathies: Clinical features and diagnosis", section on 'MELAS' and "Ischemic stroke in children: Clinical presentation, evaluation, and diagnosis", section on 'Rare causes of stroke'.)
Substance use — Use of sympathomimetic drugs, such as cocaine and methamphetamine, can cause stroke due to hypertension, vasospasm, or vasculitis [106-108]. Other substances linked to stroke by epidemiologic data include heroin, other opiates, marijuana, synthetic cannabinoids ("spice"), and gamma hydroxybutyrate [109-112]. (See "Substance use disorder in adolescents: Epidemiology, clinical features, assessment, and diagnosis" and "Substance use disorder in adolescents: Treatment overview".)
Substance use among young adults may be increasing over time since the 1990s. One report from the Greater Cincinnati Northern Kentucky Stroke Study found that substance use, documented by toxicology screening in young adults with stroke, increased from 4.4 percent of cases in 1993/1994 to 28.8 percent of cases in 2015 [113].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in children".)
SUMMARY
●The etiologies and risk factors for arterial ischemic stroke in children and young adults differ from those typical in older adults, although hypertension, smoking, diabetes, and hypercholesterolemia are found in some young adults and rarely in children. Conditions commonly associated with arterial ischemic stroke in children and young adults (table 1) include congenital and acquired cardiac lesions, arteriopathies, hematologic abnormalities, infection, head and neck trauma, and genetic conditions. (See 'Etiologies and risk factors' above.)
●Arterial dissection is the most common vascular abnormality in some young adult series. Additional risk factors in young adults include recent pregnancy, drug use, premature atherosclerosis, and possibly migraine. (See 'Etiologies and risk factors in young adults' above.)
●Arteriopathies are the most common cause of stroke in children. Abnormalities of the cerebral vasculature that predispose to arterial ischemic stroke include arterial dissection, focal (or transient) cerebral arteriopathy of childhood, fibromuscular dysplasia, moyamoya syndrome, and vasculitis. (See 'Arteriopathy' above.)
●Congenital and acquired heart disease is an established risk factor for stroke in children and young adults. (See 'Cardiac' above.)
●Acute clinical and subclinical infections may act as a trigger for stroke in children who have other risk factors such as cardiac disease, sickle cell disease, or arteriopathies. (See 'Infection' above.)
●Sickle cell disease and several inherited or acquired prothrombotic disorders have been associated with stroke in children and young adults. (See 'Hematologic' above.)
●Metabolic conditions associated with arterial ischemic stroke, generally through effects on the vessel wall, include Fabry disease, homocystinuria, and Menkes disease. (See 'Metabolic disorders' above.)
●Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) and other rare mitochondrial disorders are associated with metabolic stroke. (See 'Mitochondrial disorders' above.)
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