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Cerebral infarction

Cerebral infarction, commonly referred to as an ischemic stroke, is a type of stroke that occurs when blood flow to a portion of the brain is obstructed, depriving brain cells of essential oxygen and nutrients, which leads to rapid cell death and potential permanent damage.^[1] This condition accounts for approximately 87% of all strokes in the United States as of 2022, making it the most prevalent form of cerebrovascular accident.^[1] It is typically caused by either thrombotic occlusion, where a blood clot forms within a cerebral artery due to atherosclerosis, or embolic occlusion, where a clot or debris travels from elsewhere in the body, such as the heart, to block a brain vessel.^[1]^[2] The underlying pathophysiology involves a critical reduction in cerebral blood flow, below 10-12 mL per 100 grams of brain tissue per minute, which triggers ischemic penumbra—a salvageable area surrounding the core infarct—before progressing to full infarction if not addressed promptly.^[1] Common risk factors include advanced age (over 55), hypertension, diabetes, smoking, atrial fibrillation, and obesity, with non-Hispanic Black individuals facing nearly twice the risk of a first stroke compared to other groups.^[2]^[1] Symptoms manifest suddenly and vary by the affected brain region but often include unilateral weakness or numbness (hemiparesis), facial droop, speech difficulties (aphasia or dysarthria), vision loss, and severe headache, assessed via tools like the National Institutes of Health Stroke Scale (NIHSS).^[2]^[1] Diagnosis begins with an urgent clinical evaluation and non-contrast computed tomography (CT) scan within 20 minutes to rule out hemorrhage, followed by magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) for confirmation of infarction.^[1]^[3] Treatment focuses on rapid reperfusion: intravenous thrombolysis with tissue plasminogen activator (tPA, such as alteplase) administered within 4.5 hours of symptom onset, or mechanical thrombectomy using a stent retriever for large vessel occlusions, ideally within 6 to 24 hours depending on eligibility.^[1]^[3] Post-acute management includes blood pressure control (target <180/105 mmHg after tPA), antiplatelet therapy, and rehabilitation to mitigate long-term disability, which affects up to 795,000 Americans annually as of 2022 and contributes to one in six cardiovascular deaths worldwide as of 2022.^[1]^[3]

Overview

Definition and epidemiology

Cerebral infarction, also known as ischemic stroke, is defined as the death of brain or retinal cells attributable to prolonged ischemia, resulting from an interruption in blood supply that leads to tissue necrosis in the cerebrum due to insufficient arterial or venous flow.^[4]^[5] This condition is distinguished from hemorrhagic stroke, which involves vessel rupture and bleeding rather than occlusion or reduced perfusion. Clinically, it manifests as focal neurological deficits persisting for more than 24 hours, caused by an acute vascular event affecting the central nervous system, excluding trauma or other non-ischemic origins.^[6] Globally, cerebral infarction accounts for the majority of strokes, with approximately 7.8 million incident cases annually, representing about 65% of the 11.9 million total incident strokes reported in 2021.^[7]^[8] The age-standardized incidence rate stands at 92 per 100,000 population, though absolute numbers have risen by nearly 88% since 1990 due to population growth and aging. Regional variations are stark, with over 83% of incident strokes, including ischemic types, occurring in low- and middle-income countries (LMICs), where southeast Asia and east Asia report the highest rates driven by limited preventive care.^[7]^[8] Demographic trends show an increasing burden among younger adults, with incidence in the 15-39 age group rising globally, particularly in lower sociodemographic index regions, attributed to lifestyle factors such as obesity and hypertension—the leading modifiable risk factor.^[9]^[10] Mortality from cerebral infarction reaches 3.6 million deaths per year, comprising roughly half of the 7.3 million total stroke-related deaths worldwide, making it the second leading cause of death overall.^[7]^[8] The condition imposes a substantial healthcare burden, contributing 70.4 million disability-adjusted life years (DALYs) lost annually—about 44% of total stroke DALYs and ranking third among non-communicable diseases—with 89% of stroke-related DALYs borne by LMICs due to inadequate rehabilitation access.^[7]^[8] These figures underscore the escalating global impact, with prevalence affecting 69.9 million individuals living with sequelae.^[7]

Historical context

The understanding of cerebral infarction, historically encompassed under the broader term "apoplexy" or "stroke," evolved from ancient supernatural interpretations to a scientifically grounded recognition of vascular pathology. In ancient times, conditions resembling cerebral infarction were described as sudden calamities, with Hippocrates (circa 460–370 BCE) providing the earliest systematic account in the Hippocratic Corpus, terming it "apoplexy" to denote a violent seizure causing loss of sensation, motion, and consciousness, often linked to humoral imbalances rather than divine causes.^[11] Earlier and medieval views occasionally attributed such events to divine punishment for sins, reflecting a pre-scientific worldview that interpreted sudden paralysis as supernatural retribution, a perspective later supplanted by empirical pathology.^[12] During the 17th and 18th centuries, advances in autopsy-based pathology began to reveal the organic basis of apoplexy. Johann Jakob Wepfer, in his 1658 monograph Historiae Apoplecticorum, conducted postmortem examinations that first identified cerebral hemorrhage as a primary cause, challenging humoral theories and linking apoplexy to vascular rupture.^[13] Building on this, Giovanni Battista Morgagni's seminal 1761 work De Sedibus et Causis Morborum per Anatomen Indagatis analyzed over 600 cases, distinguishing hemorrhagic from non-hemorrhagic forms of apoplexy and describing brain tissue changes like softening, though the term "ramollissement" for infarction emerged later in the 19th century.^[14] The 19th century marked a pivotal shift toward cellular and vascular mechanisms, largely through Rudolf Virchow's contributions. In the 1840s, Virchow introduced the term "infarction" to describe tissue necrosis due to arterial occlusion, emphasizing embolism and thrombosis as key processes in his 1846 studies on cerebral pathology.^[15] By 1856, he formalized Virchow's triad—stasis, endothelial injury, and hypercoagulability—as the foundational factors in thrombosis formation, linking them directly to ischemic brain events and establishing the vascular etiology of cerebral infarction.^[16] The 20th century brought diagnostic revolutions with neuroimaging. The computed tomography (CT) scan, developed by Godfrey Hounsfield and first clinically applied in 1971, enabled rapid differentiation of ischemic infarction from hemorrhage, transforming acute stroke evaluation in the 1970s.^[17] Magnetic resonance imaging (MRI), emerging in the 1980s, further refined detection of early ischemic changes. Therapeutically, the 1995 NINDS trial demonstrated that intravenous tissue plasminogen activator (tPA) administered within 3 hours improved outcomes in acute ischemic stroke, establishing thrombolysis as a standard.^[18] The 2015 MR CLEAN trial then validated endovascular thrombectomy for large-vessel occlusions, showing significant functional recovery benefits.^[19] In 2018, trials such as DAWN and DEFUSE 3 extended thrombectomy windows to 24 hours in select patients using perfusion imaging, reflecting ongoing refinements in time-sensitive interventions.^[20]^[21]

Classification and causes

Types of cerebral infarction

Cerebral infarctions are classified primarily according to the underlying etiology and vascular involvement, enabling targeted diagnostic and therapeutic approaches. The most widely adopted system is the TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification, established in 1993, which categorizes ischemic strokes into five subtypes based on clinical features and diagnostic investigations: (1) large-artery atherosclerosis, involving stenosis or occlusion of major extracranial or intracranial arteries; (2) cardioembolism, resulting from cardiac sources such as atrial fibrillation; (3) small-vessel occlusion, affecting penetrating arteries and leading to lacunar infarcts; (4) stroke of other determined etiology, encompassing rare causes like arterial dissection or hypercoagulable states; and (5) stroke of undetermined etiology, where no clear cause is identified despite evaluation. This framework, validated in clinical trials, guides secondary prevention strategies by subtype, with large-artery atherosclerosis accounting for approximately 20-25% of cases in population-based studies. Classifications also consider vascular territories affected by the infarction, which correlate with specific neurological deficits. Anterior circulation infarcts, primarily in the middle cerebral artery (MCA) territory, often present with contralateral hemiparesis, sensory loss, and aphasia if the dominant hemisphere is involved, while anterior cerebral artery (ACA) infarcts may cause leg weakness and frontal lobe syndromes. Posterior circulation infarcts, such as those in the posterior cerebral artery (PCA), typically result in visual field defects like homonymous hemianopia, and may extend to brainstem involvement with vertigo or cranial nerve palsies. Lacunar infarcts, a subtype of small-vessel occlusion, arise from lipohyalinosis or microatheroma in deep penetrating arteries, producing small (<15 mm) lesions in basal ganglia, thalamus, or pons, and manifesting as pure motor hemiparesis, ataxic hemiparesis, or dysarthria-clumsy hand syndrome in about 25% of ischemic strokes. Special types include watershed infarcts, occurring in border zones between major arterial territories due to hypoperfusion from systemic hypotension or carotid stenosis, leading to cortical laminar necrosis and deficits like proximal arm-leg weakness. Silent cerebral infarcts, detected incidentally on neuroimaging without acute symptoms, represent up to 20-30% of older adults in cohort studies and are linked to future cognitive decline, often involving small subcortical lesions. Refinements in cryptogenic stroke classification, such as embolic stroke of undetermined source (ESUS) defined in 2014, identify a subset of non-lacunar infarcts with embolic features but no identified source, comprising 15-25% of ischemic strokes. However, subsequent randomized controlled trials, including NAVIGATE-ESUS, RE-SPECT ESUS, and ARCADIA, did not demonstrate superiority of direct oral anticoagulants over aspirin in preventing recurrent stroke and showed increased bleeding risk; current guidelines recommend antiplatelet therapy for most ESUS patients.^[22] In 2025, the Ischemic Stroke Phenotyping System (ISPS25) was proposed as an updated framework to enhance subtyping through expanded minimum diagnostic evaluations, potentially reclassifying patients for improved secondary prevention.^[23]

Etiology and risk factors

Cerebral infarction primarily results from thrombotic or embolic occlusion of cerebral arteries, leading to reduced blood flow and tissue ischemia. Large-artery atherosclerosis, characterized by plaque accumulation and rupture in major vessels such as the carotid arteries, accounts for approximately 20-25% of cases and often involves thrombi formation or distal embolization.^[1] Cardioembolic events, originating from cardiac sources like atrial fibrillation or valvular heart disease, contribute to about 20% of ischemic strokes by dislodging emboli into the cerebral circulation.^[1] Small vessel disease, driven by hypertensive arteriolosclerosis, leads to lacunar infarcts in subcortical regions and represents around 25% of cases, particularly in individuals with chronic hypertension or diabetes.^[1] Less common etiologies include arterial dissection, which may occur spontaneously or post-trauma, and hypercoagulable states such as antiphospholipid syndrome, each comprising under 5% of infarctions but requiring specific diagnostic evaluation.^[1] Modifiable risk factors play a central role in the development of cerebral infarction, with hypertension being the most significant, carrying an odds ratio of approximately 3.0 for ischemic stroke and a population-attributable fraction (PAF) of 39-60% across global populations.^[24] Smoking nearly doubles the risk (relative risk ~1.9) and has a PAF of 4-18% depending on regional prevalence, while diabetes mellitus confers a twofold increased risk (hazard ratio ~2.0) with a PAF contributing to about 10% of stroke burden when combined with other factors.^[25] Dyslipidemia elevates risk through accelerated atherosclerosis, with statin therapy reducing ischemic stroke incidence by 11-40%, and obesity further amplifies susceptibility by promoting endothelial dysfunction and inflammation.^[25] Non-modifiable risk factors include advancing age, where incidence doubles every decade after 55 years, and male sex, which confers higher risk at younger ages despite women's overall greater lifetime incidence due to longevity.^[25] Family history of stroke increases susceptibility through shared genetics, while ethnic disparities show African Americans facing a 50-100% higher risk compared to non-Hispanic whites, and South Asian populations experiencing elevated rates of small vessel disease.^[25]^[26] Emerging factors include obstructive sleep apnea, which independently raises ischemic stroke risk (hazard ratio 2.5), air pollution with long-term PM2.5 exposure linked to a 10-20% increased risk per 10 μg/m³ increment, and prior SARS-CoV-2 infection, associated with 1.8-fold higher odds of ischemic stroke particularly in severe cases.^[27]^[28] Genetic markers like Factor V Leiden mutation modestly elevate risk in young adults (odds ratio 2.0), especially in prothrombotic contexts.^[29]

Pathophysiology

Mechanisms of ischemia

Cerebral blood flow is tightly regulated to meet the brain's high metabolic demands, with normal flow rates averaging 50-60 mL/100 g/min under physiological conditions.^[30] Cerebral autoregulation maintains stable perfusion by adjusting vascular resistance in response to changes in mean arterial pressure, typically within a range of 60-150 mmHg, where blood flow remains constant despite fluctuations in systemic pressure.^[30] This mechanism involves myogenic responses in arterioles and metabolic feedback from brain tissue. Collateral circulation, primarily through the circle of Willis—an anastomotic ring connecting the major cerebral arteries—provides alternative pathways to redistribute blood flow when primary vessels are compromised, potentially mitigating ischemia in affected territories.^[31] Ischemia in cerebral infarction arises from disruptions in this regulated blood supply, primarily through three mechanisms: thrombosis, embolism, and hypoperfusion. Thrombosis involves local clot formation within cerebral arteries, often at sites of atherosclerotic plaque, leading to abrupt occlusion and downstream hypoperfusion.^[1] Embolism occurs when thrombi or other particles, such as from cardiac sources or proximal arterial plaques, travel and lodge in distal cerebral vessels, causing sudden territorial ischemia.^[1] Hypoperfusion results from global or regional reductions in blood flow, such as during systemic hypotension from cardiac arrest or severe extracranial stenosis, overwhelming compensatory autoregulation and collaterals.^[32] Underlying vascular pathology contributes to these triggers, particularly endothelial dysfunction and plaque instability in atherosclerosis, a common precipitant of ischemic events. Endothelial dysfunction impairs vasodilation, promotes inflammation, and facilitates thrombus formation by altering the vessel wall's antithrombotic properties.^[33] Plaque instability, characterized by thin fibrous caps and lipid-rich cores, increases the risk of rupture, releasing embolic debris or triggering in situ thrombosis.^[34] Hemodynamic failure becomes critical in cases of significant stenosis, such as greater than 70% narrowing in the carotid artery, where flow limitation exceeds collateral capacity, heightening infarction risk as demonstrated in symptomatic patients.^[35] Quantitative thresholds define the progression from reversible to irreversible ischemia based on cerebral blood flow (CBF) reductions. The infarct core, where irreversible tissue death occurs, develops when CBF falls below approximately 10-12 mL/100 g/min for a sufficient duration.^[36] The ischemic penumbra represents a surrounding zone of viable but compromised tissue with CBF between approximately 12-20 mL/100 g/min, where neuronal function is impaired but cell death is not inevitable, offering a window for therapeutic salvage if perfusion is restored promptly.^[36]

Ischemic cascade

The ischemic cascade refers to the sequential series of biochemical and cellular events triggered by cerebral ischemia in the setting of cerebral infarction, leading to progressive neuronal injury if blood flow is not restored. This process begins rapidly after the onset of reduced cerebral blood flow and unfolds over minutes to days, highlighting the critical time sensitivity for potential interventions to limit damage.^[37] In the hyperacute phase, occurring within 0-30 minutes of ischemia onset, the primary event is energy failure due to oxygen and glucose deprivation, resulting in rapid ATP depletion to approximately 0-25% of normal levels. This ATP shortfall inhibits the Na⁺/K⁺-ATPase pump, which normally maintains ionic gradients by hydrolyzing ATP to exchange intracellular Na⁺ for extracellular K⁺; the basic model of this failure can be represented as pump activity ceasing when ATP falls below a critical threshold, leading to membrane depolarization and cytotoxic edema from Na⁺ and water influx. Anaerobic metabolism predominates, producing lactic acidosis that further acidifies the intracellular environment and exacerbates energy deficits.^[38]^[39] The acute phase, spanning 30 minutes to 6 hours, involves excitotoxicity driven by excessive glutamate release from depolarized neurons, which overactivates NMDA and AMPA receptors, causing massive calcium influx into cells. This calcium overload activates proteases, lipases, and endonucleases, promoting free radical formation—such as reactive oxygen species (ROS)—that damage lipids, proteins, and DNA, while also initiating blood-brain barrier (BBB) breakdown through endothelial dysfunction. In embolic subtypes, this progression may accelerate due to abrupt occlusion, intensifying early excitotoxic damage.^[37]^[38]^[40] During the subacute phase from 6 to 72 hours, inflammation escalates with microglial activation and cytokine release (e.g., TNF-α, IL-1β), recruiting peripheral leukocytes that amplify tissue injury and contribute to vasogenic edema via further BBB permeability. Cell death mechanisms diverge here: necrosis predominates in the severely ischemic core due to uncontrolled swelling and lysis, while apoptosis—a programmed cell death pathway involving caspase activation—occurs more in marginally affected regions, allowing for potential salvage.^[37]^[41]^[39] Central to the cascade is the ischemic penumbra, a rim of viable but hypoperfused tissue surrounding the infarct core, where cells maintain electrophysiological silence but retain metabolic potential for recovery if reperfused promptly. In the core, irreversible neuronal death typically completes within 4-6 hours, but the penumbra offers a therapeutic window, as delayed intervention can still mitigate expansion into this salvageable zone.^[39]^[41]^[40]

Clinical presentation

Signs and symptoms

Cerebral infarction, a type of ischemic stroke, typically presents with sudden onset of focal neurological deficits corresponding to the affected vascular territory in the brain.^[1] These symptoms arise due to ischemia-induced neuronal dysfunction and can vary based on the location and extent of the infarction.^[1] Focal symptoms often reflect the specific brain region involved. In middle cerebral artery (MCA) infarctions, common manifestations include contralateral hemiparesis affecting the face and upper extremities more than the lower limbs, sensory loss in the same distribution, aphasia or neglect depending on the dominant or nondominant hemisphere, and gaze deviation toward the lesion side.^[1] Anterior cerebral artery (ACA) infarcts typically cause contralateral weakness and sensory deficits predominantly in the lower extremities, with relative sparing of the face and arms, sometimes accompanied by urinary incontinence or abulia.^[42] Posterior cerebral artery (PCA) territory involvement leads to contralateral homonymous hemianopia, often with macular sparing, along with possible thalamic sensory disturbances, memory impairment, or cortical blindness in bilateral cases.^[1] Posterior circulation infarcts, such as those in the vertebrobasilar system or cerebellum, may produce ataxia, vertigo, dysarthria, diplopia, and limb incoordination, with ataxia being prominent in cerebellar lesions.^[43] Non-focal or global symptoms can occur, particularly with larger infarcts or those causing mass effect. Altered mental status, ranging from confusion to coma, may develop due to increased intracranial pressure or widespread ischemia.^[1] Headache is less frequent in cerebral infarction compared to hemorrhagic stroke, occurring in about 25% of cases, and is often mild unless associated with posterior circulation involvement.^[1] Symptom progression patterns vary; most infarcts reach maximal deficit at onset, but stuttering or stepwise worsening can occur over hours to days due to evolving ischemia or edema.^[44] Lacunar infarcts, resulting from occlusion of small penetrating arteries, produce characteristic syndromes without cortical involvement. Pure motor hemiparesis involves contralateral facial, arm, and leg weakness without sensory or visual deficits, often due to internal capsule lesions.^[45] Pure sensory stroke causes numbness or paresthesia on the contralateral side, typically from thalamic involvement.^[45] Ataxic hemiparesis combines hemiparesis with ipsilateral ataxia, commonly from pontine or capsular infarcts.^[45] Variations in presentation include silent infarcts, which occur without noticeable symptoms and are detected incidentally on imaging, accounting for 10% to 30% of cerebral infarctions in older adults.^[46] Transient symptoms lasting less than 24 hours, distinguishing transient ischemic attacks (TIAs) from infarction, may mimic these signs but resolve fully.^[1] Quick recognition aids like the FAST acronym (Face drooping, Arm weakness, Speech difficulty, Time to call emergency services) can help identify potential infarction symptoms.^[47]

Recognition and assessment

The recognition and assessment of cerebral infarction in acute settings rely on rapid, standardized screening tools to identify potential stroke symptoms and facilitate timely intervention. The FAST acronym (Face drooping, Arm weakness, Speech difficulty, Time to call emergency services) serves as a widely adopted prehospital and public education tool derived from the Cincinnati Prehospital Stroke Scale, enabling quick identification of key focal neurological deficits.^[48] An enhanced version, BE-FAST, incorporates additional checks for Balance loss and Eye deviation or vision changes, improving sensitivity for posterior circulation strokes and vertigo-related presentations without compromising specificity.^[49] In clinical and prehospital evaluation, determining the exact time of symptom onset or last known normal is critical to establish eligibility for time-sensitive therapies, often achieved through patient history or witness accounts.^[50] Common stroke mimics, such as seizures or migraines, must be excluded via targeted questioning and basic neurological checks to avoid misdiagnosis, as these conditions can present with unilateral weakness or sensory changes.^[51] Prehospital protocols emphasize emergency medical services (EMS) activation within minutes of symptom recognition, with guidelines targeting on-scene times of 15 minutes or less to expedite transport to stroke-capable facilities.^[52] The urgency of assessment is underscored by the "time is brain" principle, which quantifies irreversible neuronal loss at approximately 1.9 million neurons per minute of untreated ischemia, equating to substantial disability if delays occur.^[53] Hospital protocols aim for door-to-needle times of 60 minutes or less for eligible thrombolytic administration, a benchmark associated with improved functional outcomes.^[54] The National Institutes of Health Stroke Scale (NIHSS) provides a structured quantification of deficits such as those in facial palsy or speech, with scores ranging from 0 (no stroke) to 42 (severe); scores exceeding 4 typically indicate moderate severity warranting escalated care.^[55]^[56] Recent advancements include mobile stroke units (MSUs), specialized ambulances equipped for prehospital neuroimaging and laboratory testing, introduced in trials post-2010. These units have demonstrated reductions in treatment delays by 25-90 minutes compared to standard EMS, enabling earlier thrombolysis decisions and better outcomes in randomized studies like PHANTOM-S and BEST-MSU.^[57]^[58]

Diagnosis

Clinical evaluation

The clinical evaluation of cerebral infarction begins with a thorough history to determine the precise timing of symptom onset, which is essential for assessing eligibility for time-sensitive interventions. Elicitation of modifiable and non-modifiable risk factors, including hypertension, diabetes mellitus, hyperlipidemia, atrial fibrillation, smoking, and family history, helps identify underlying etiologies and guide secondary prevention. Inquiry into prior transient ischemic attacks (TIAs) or strokes is critical, as recurrent events may indicate specific vascular pathologies. When the patient cannot provide a reliable account due to aphasia, confusion, or unconsciousness, collateral history from witnesses, family, or prehospital personnel is obtained to clarify the timeline and circumstances. A systematic physical examination follows, encompassing both general and neurological components. The general examination focuses on vital signs, cardiac auscultation to detect irregular rhythms suggestive of atrial fibrillation, and auscultation of the carotid arteries for bruits indicating stenosis or plaque. The neurological examination systematically assesses mental status, cranial nerve function (e.g., pupillary responses, extraocular movements, facial symmetry), motor strength in all limbs, sensory integrity, deep tendon reflexes, plantar responses, coordination, and cerebellar function to localize the infarcted territory and gauge deficit severity. Standardized tools are employed to quantify and characterize impairments. The National Institutes of Health Stroke Scale (NIHSS), a validated 15-item instrument, measures stroke severity with high interrater reliability and supports lesion localization; for instance, high scores on facial palsy and arm drift items often suggest middle cerebral artery territory involvement. In patients with depressed consciousness, the Glasgow Coma Scale (GCS) evaluates eye opening, verbal response, and motor response to stratify coma depth and predict prognosis. Differential diagnosis is integral to avoid misclassification, distinguishing cerebral infarction from mimics such as intracerebral hemorrhage (which may feature more severe headache or vomiting at onset), hypoglycemia (prompting immediate bedside glucose measurement), and Todd's paralysis (a postictal focal weakness resolving within hours). Building on initial recognition tools like the Face Arm Speech Time (FAST) test, this evaluation refines suspicion through detailed history and exam findings. In resource-limited or rural settings, tele-stroke consultations have seen significant expansion during the 2020s, enabling real-time expert review of history and examination via videoconferencing to enhance diagnostic accuracy and expedite care decisions.

Imaging and laboratory tests

Non-contrast computed tomography (CT) of the head is the initial imaging modality of choice for suspected cerebral infarction, primarily to exclude intracranial hemorrhage and identify early signs of ischemia, such as loss of gray-white matter differentiation or hypoattenuation.^[59] Non-contrast computed tomography (CT) of the head should be completed within 20 minutes of patient arrival (door-to-CT time), with interpretation by a physician with stroke expertise occurring within 20 minutes of scan completion, facilitating rapid decision-making for thrombolytic therapy eligibility.^[59] The Alberta Stroke Program Early CT Score (ASPECTS), ranging from 0 to 10, quantifies the extent of early ischemic changes in the middle cerebral artery territory on non-contrast CT, with scores below 6 indicating larger infarcts associated with poorer outcomes.^[60] Magnetic resonance imaging (MRI), particularly diffusion-weighted imaging (DWI), offers superior sensitivity for detecting acute cerebral infarction, identifying cytotoxic edema with over 95% sensitivity within minutes of onset, compared to non-contrast CT's lower early detection rate of approximately 67% within 3 hours.^[1] DWI is especially useful for confirming ischemia in cases where CT is inconclusive or for assessing small infarcts, though MRI is not routinely first-line due to longer acquisition times.^[60] Fluid-attenuated inversion recovery (FLAIR) sequences complement DWI to better delineate infarct age. Vascular imaging, such as CT angiography (CTA) or MR angiography (MRA), is recommended to evaluate for large vessel occlusions, which occur in up to 20-30% of acute ischemic strokes and guide endovascular interventions.^[59] CTA demonstrates high accuracy for intracranial occlusions (sensitivity 92-100%, specificity 82-100%), while MRA serves as a non-contrast alternative.^[60] Carotid Doppler ultrasound noninvasively assesses extracranial stenosis, quantifying plaque burden and flow velocities to identify sources of embolism, with sensitivity exceeding 90% for hemodynamically significant stenoses greater than 70%.^[61] Perfusion imaging via CT or MR techniques identifies the ischemic penumbra—the potentially salvageable tissue surrounding the infarct core—by mapping cerebral blood flow, volume, and mean transit time mismatches.^[59] This modality extends the therapeutic window beyond 4.5 hours in select patients, as validated in trials like DAWN and DEFUSE 3, where penumbra assessment predicted favorable outcomes with thrombectomy up to 24 hours.^[1] Digital subtraction angiography remains the gold standard for detailed intracranial vessel evaluation during endovascular planning, though it is invasive and reserved for procedural guidance.^[60] Recent advancements, including AI-assisted tools for automated ASPECTS calculation and large vessel occlusion detection on CT/CTA, have reduced interpretation times by up to 50%, aligning with 2023 recommendations for integrating such technologies to expedite workflows in high-volume centers.^[62] Laboratory evaluation in suspected cerebral infarction focuses on excluding contraindications to reperfusion therapy, assessing comorbidities, and identifying underlying etiologies. A complete blood count (CBC) is essential to detect thrombocytopenia or polycythemia, which could increase hemorrhagic risk, and should be obtained immediately upon arrival.^[59] Coagulation studies, including prothrombin time (PT), international normalized ratio (INR), and activated partial thromboplastin time (aPTT), are critical for thrombolytic eligibility, with INR greater than 1.7 typically contraindicating intravenous alteplase.^[59] Blood glucose measurement is mandatory to rule out hypo- or hyperglycemia mimicking stroke symptoms, targeting levels between 140-180 mg/dL in acute management.^[1] Additional routine tests include serum electrolytes, renal function (blood urea nitrogen and creatinine), and lipid profile to evaluate metabolic derangements and cardiovascular risk factors.^[59] Cardiac biomarkers such as troponin are recommended to screen for concomitant myocardial injury or embolic sources from atrial fibrillation.^[1] In younger patients (typically under 50 years) without traditional risk factors, a hypercoagulable panel—including antiphospholipid antibodies, protein C/S, antithrombin III, and factor V Leiden—is warranted to identify inherited or acquired thrombophilias contributing to 5-10% of such cases.^[63] All initial labs should be completed with results available no later than 30 minutes after arrival to avoid delaying imaging or therapy, with point-of-care testing considered if standard turnaround times cannot meet this target.^[64]

Treatment

Acute interventions

Intravenous thrombolysis with alteplase (tPA) is a cornerstone of acute intervention for eligible patients with cerebral infarction, administered within 4.5 hours of symptom onset to restore blood flow and minimize ischemic damage.^[59] The recommended dose is 0.9 mg/kg (maximum 90 mg), with 10% given as an initial bolus over 1 minute followed by infusion of the remainder over 60 minutes.^[59] Eligibility requires confirmation of ischemic stroke via non-contrast CT to exclude hemorrhage, with contraindications including active internal bleeding, recent major surgery, or coagulopathy such as an INR greater than 1.7.^[65] For patients with large vessel occlusions (LVOs), such as those in the internal carotid artery (ICA) or middle cerebral artery (MCA), endovascular mechanical thrombectomy using stent retrievers offers a highly effective reperfusion strategy, particularly when thrombolysis is insufficient or contraindicated.^[20] The DAWN trial demonstrated significant functional improvement with thrombectomy performed 6 to 24 hours after last known well in patients selected by perfusion imaging showing a mismatch between infarct core and penumbra.^[20] Similarly, the DEFUSE-3 trial extended the window to 6 to 16 hours for anterior circulation LVOs, showing superior outcomes with endovascular therapy plus medical management compared to medical management alone.^[21] These procedures are guided by multimodal imaging to ensure a favorable mismatch ratio, prioritizing rapid intervention to achieve recanalization rates exceeding 80% in selected cases.^[21] Supportive measures in the hyperacute phase focus on optimizing physiological parameters to facilitate safe reperfusion. Blood pressure should be managed to below 185/110 mmHg prior to and during tPA administration to reduce hemorrhage risk, using agents like labetalol or nicardipine if needed.^[66] In patients not receiving tPA, aspirin at a dose of 325 mg is recommended within 48 hours of onset to prevent early recurrent ischemia, unless contraindicated by thrombolysis.^[67] In 2025, the thrombolysis time window was further extended for selected patients based on imaging; for instance, trials such as HOPE and studies on posterior circulation strokes demonstrated benefits of intravenous thrombolysis (alteplase or tenecteplase) from 4.5 to 24 hours after symptom onset in patients with evidence of salvageable penumbra via perfusion mismatch.^[68]^[69] Tenecteplase, a fibrin-specific thrombolytic administered as a single 0.25 mg/kg bolus, was approved by the U.S. Food and Drug Administration in March 2025 for the treatment of acute ischemic stroke in adults and has shown non-inferiority (and in some cases superiority) to alteplase in achieving excellent functional outcomes at 90 days in multiple phase 3 trials.^[70]^[71] For instance, the AcT trial and pooled analyses confirmed comparable safety profiles, with potential advantages in ease of administration for prehospital settings.^[72] Efforts in neuroprotection, such as the free radical scavenger NXY-059, have largely failed; the SAINT-II trial showed no benefit in reducing disability when added to tPA within 6 hours of onset.^[73]

Rehabilitation and long-term care

Rehabilitation following cerebral infarction typically begins early in the acute phase to optimize recovery and minimize secondary complications. Early mobilization in the intensive care unit, initiated within 24 to 48 hours for medically stable patients, involves gentle physical therapy to reduce the risk of deep vein thrombosis, pneumonia, and muscle atrophy.^[74] This phase transitions to inpatient rehabilitation, where multidisciplinary interventions such as physical therapy for mobility, occupational therapy for daily activities, and speech-language therapy for communication and swallowing impairments are provided intensively, often in specialized stroke units.^[75] Outpatient rehabilitation extends these efforts for 3 to 6 months post-discharge, focusing on community reintegration and sustained functional gains through tailored exercise programs.^[76] Specific therapeutic approaches target common deficits like hemiparesis and dysphagia. Constraint-induced movement therapy (CIMT) restricts the unaffected limb to encourage intensive use of the paretic arm, demonstrating significant improvements in upper extremity function for chronic stroke patients with moderate impairment.^[77] Dysphagia screening, using validated bedside tools like the Toronto Bedside Swallow Screen, is performed immediately upon stabilization to identify aspiration risk and prevent pneumonia, with early screening reducing the risk of pneumonia by approximately 40% (OR 0.60) in acute stroke patients.^[78] Psychological support is integral, addressing post-stroke depression, which affects approximately 30% of survivors in the first year, through cognitive behavioral therapy and antidepressants to enhance adherence to rehabilitation.^[79] Long-term care emphasizes multidisciplinary teams comprising physicians, therapists, nurses, and social workers to coordinate ongoing management and prevent recurrent events or complications such as spasticity.^[80] Assistive devices, including orthotics, wheelchairs, and adaptive utensils, are prescribed based on individual needs to promote independence in activities of daily living. Resumption of driving requires a minimum 1-month abstinence post-stroke, with clearance typically after 3 to 6 months contingent on comprehensive cognitive, visual, and motor evaluations to ensure safety.^[81] Recent advancements include the expansion of telerehabilitation, accelerated by the COVID-19 pandemic in the 2020s, which delivers remote physical and occupational therapy via video platforms, achieving comparable outcomes to in-person sessions while improving access for rural patients.^[82] Experimental stem cell therapies, such as allogeneic mesenchymal stem cells administered intravenously, are in phase II/III trials as of 2025, showing preliminary safety and potential for neuroregeneration in subacute ischemic stroke without established efficacy.^[83]

Prognosis and prevention

Outcomes and complications

The prognosis following cerebral infarction depends on factors such as infarct size, location, initial stroke severity, and patient comorbidities, with outcomes ranging from full recovery to significant disability or death. Short-term mortality is substantial, with 10-20% of patients succumbing within 30 days, and rates exceeding 30% in cases of large-vessel occlusion or extensive infarcts.^[84]^[85] Long-term survival improves but remains guarded; for instance, overall survival probability is approximately 82% at 3 months and 77% at 1 year for first-ever ischemic strokes.^[86] Globally, ischemic stroke accounts for 7.8 million incident cases annually, with 3.6 million deaths and 70.4 million disability-adjusted life years lost.^[7] Functional recovery is commonly evaluated using the modified Rankin Scale (mRS), a 7-point ordinal scale from 0 (no symptoms) to 6 (death), focusing on disability in daily activities. At 3 months, roughly 50% of survivors achieve independence (mRS 0-2), though this drops in severe cases, with only 20-30% reaching good outcomes in large infarcts.^[87] The risk of recurrent stroke is notable, affecting about 8-10% of patients in the first year, often linked to inadequate secondary prevention.^[88] Intravenous tissue plasminogen activator (tPA) administration can enhance the odds of a favorable mRS score by around 30% relative to placebo in eligible patients. Complications of cerebral infarction can arise acutely or persist long-term, significantly impacting survival and quality of life. Early adverse events include hemorrhagic transformation, a breakdown of the blood-brain barrier leading to bleeding into the infarcted area; after tPA thrombolysis, symptomatic cases occur in approximately 6% of patients, often worsening neurological deficits.^[89] Vascular complications such as deep vein thrombosis (DVT) develop in 10-20% of immobilized patients without prophylactic anticoagulation, increasing the risk of pulmonary embolism. Late complications frequently involve neurocognitive and neuropsychiatric sequelae. Post-stroke dementia affects 20-30% of survivors within the first year, doubling the risk compared to age-matched controls without stroke.^[90] Epilepsy emerges in 5-10% of cases, typically within the first 1-2 years, with higher incidence in cortical infarcts.^[91] Depression complicates recovery in 30-50% of patients, correlating with poorer functional outcomes and reduced adherence to rehabilitation.^[90] Key predictors of poor prognosis include high initial stroke severity, as indicated by a National Institutes of Health Stroke Scale (NIHSS) score greater than 16, which is associated with over 50% risk of death or severe disability at 3 months.^[92] Advanced age over 80 years halves the odds of achieving functional independence compared to younger adults, due to reduced neuroplasticity and comorbidities.^[92] Socioeconomic and equity factors exacerbate outcomes, with racial and ethnic minorities—particularly Black Americans—experiencing worse neurologic, functional, and cognitive recovery at 90 days, often due to disparities in access to timely care.^[93]^[94] During the COVID-19 era, stroke outcomes worsened, with infected patients showing increased severity (higher NIHSS scores at admission) and mortality rates up to 2-3 times higher than non-infected counterparts, attributed to hypercoagulability and delayed treatments.^[95]^[96] Quality of life post-infarction is notably diminished, as reflected in SF-36 health survey scores, where survivors typically score 20-30 points lower on physical and mental component summaries than population norms, with persistent deficits in mobility and emotional well-being.^[97]

Preventive strategies

Primary prevention of cerebral infarction focuses on modifiable risk factors through lifestyle interventions and targeted screening. Smoking cessation is a cornerstone, as quitting tobacco use can reduce the risk of stroke by up to 50% within five years, approaching levels seen in never-smokers.^[98] Adopting a healthy diet and regular physical activity to maintain a body mass index below 25 kg/m² further lowers risk by addressing obesity-related hypertension and dyslipidemia.^[99] Blood pressure control to below 130/80 mmHg is critical, with evidence showing that achieving this target through lifestyle changes and pharmacotherapy prevents a significant portion of first-time strokes.^[100] For individuals at elevated risk, such as those with cardiovascular disease history, screening via carotid ultrasound is recommended if stenosis exceeds 50%, enabling interventions like endarterectomy to mitigate embolic events.^[101] Secondary prevention targets those with prior cerebral infarction or transient ischemic attack to avert recurrence. Antiplatelet therapy is standard, with low-dose aspirin (81 mg daily) or clopidogrel (75 mg daily) recommended to inhibit platelet aggregation and reduce ischemic events by 20-25%.^[102] For patients with atrial fibrillation, direct oral anticoagulants (DOACs) such as apixaban are preferred over warfarin; the ARISTOTLE trial demonstrated apixaban's superiority in preventing stroke or systemic embolism (hazard ratio 0.79) with lower bleeding risk.^[103] High-intensity statin therapy, aiming for low-density lipoprotein cholesterol below 70 mg/dL, is advised to stabilize atherosclerotic plaques and decrease recurrent stroke risk by 16-22%, as shown in the Treat Stroke to Target trial.^[104] Public health measures complement individual efforts. Annual influenza vaccination reduces stroke risk by approximately 20-30%, particularly in high-risk groups, by mitigating infection-triggered inflammation and thrombosis.^[105] Population-level policies, such as salt reduction campaigns, promote lower sodium intake (target <2 g/day), which can prevent up to 83,000 stroke deaths over a decade by curbing hypertension prevalence.^[106] Current guidelines from the American Heart Association/American Stroke Association (AHA/ASA 2024) emphasize integrated approaches, including screening for sedentary behavior and social determinants of health, with sodium-glucose cotransporter-2 (SGLT2) inhibitors for diabetic patients to reduce cardiovascular events, including stroke, by 14% compared to other glucose-lowering agents.^[99] For refractory hyperlipidemia, emerging therapies like PCSK9 inhibitors (e.g., evolocumab) further lower LDL cholesterol by 50-60% and stroke risk by 25%, offering benefits when statins alone are insufficient.^[107]

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