Diagnosis

Stroke

Sudden death of neurons due to inadequate blood flow.

Also known as: Apoplexia cerebri, Apoplexy, Cerebral infarction, Ischemic stroke

Etiology

Cause [mpt][rfd]

Pathophysiology [mpt][rfd]

  1. Embolus pathway: Heart -> Carotid Artery and Vertebral Artery -> Circle of Willis:

    • Anterior Cerebral Artery (medial frontal lobe)

      • Contralateral hemiparesis in the lower extremities

    • Middle Cerebral Artery (lateral frontal lobe, parietal lobe, temporal lobe)

      • Contralateral hemiparesis in the face and upper extremities

      • Facial paralysis

      • Gaze preference toward the side of the lesion

      • Dysarthria

      • Aphasia

      • Neglect

      • Visual field loss (contralateral inferior quadrantanopia)

    • Posterior Cerebral Artery (occipital lobe medial portion of the temporal lobe)

      • Visual cortex: contralateral homonymous hemianopia, cortical blindness

      • Thalamus: hypersomnolence, cognitive impairment, ocular findings, hypoesthesia, and ataxia

      • Larger infarcts --> hemisensory loss and hemiparesis

      • Anmesia

    • Vertebral artery and basilar artery

      Ataxia, vertigo, headache, vomiting, oropharyngeal dysfunction, visual field deficits, abnormal oculomotor findings

    • Cerebellar Infarction

      Ataxia, nausea, vomiting, headache, dysarthria, and vertigo

  2. Insufficient blood supply --> ischemia/cell hypoxia --> irreversible damage (infarction)

  3. Depletion of ATP --> unable to maintain ionic gradients across the cell membrane --> influx of sodium and calcium ions --> passive inflow of water into the cell --> cytotoxic edema

  4. Ischemia --> breakdown of the blood-brain barrier occurring within 4-6 hours after infarction --> proteins and water flood into the extracellular space --> leading to vasogenic edema --> brain swelling and mass effect that peak at 3-5 days and resolve over the next several weeks with resorption of water and proteins

  5. Hemorrhagic transformation occurs in 5% of ischemic strokes

  6. The infarcted tissue eventually undergoes liquefaction necrosis and is removed by macrophages, with the development of parenchymal volume loss.

Risk factors [mpt]

Complications [mpt][rfd]

Epidemiology

Incidence per 100.000 [2nt][fyp][eiz][d5a][bvq][qf8]

Epidemiology chart for Incidence

Approach

Treatment

The goal of therapy is to preserve areas of reversible tissue damage. [mpt]

  1. Vital signs: [mpt]

    • Airway

    • Breathing

    • Circulation --> Blood pressure <180/105

      • Labetalol 10 to 20 mg IV; may repeat once

      • Nicardipine 5 mg/hour IV, increase 2.5 mg/hour (max 15 mg/hour)

      • Clevidipine 1 to 2 mg/hour IV, double dose every 15 minutes (max 21 mg/hour)

      • Hydralazine and enalaprilat may be considered

    • Temperature <38 °C (acetaminophen, exclude infections)

    • Glucose: insuline to achieve normoglycemia

    • Nutrition: Early enteric feeding is encouraged (dysphagia -> nasogastric tube)

    • Thrombosis prophylaxis: heparin or low molecular weight heparin

  2. Ischemic stroke recanalization strategies: Effective if performed quickly

    • Antiplatelet/anticoagulation:

      • Aspirin is recommended within 24 to 48 hours of symptom onset

      • DVT-prophylaxis: low-dose heparin or low molecular weight heparin

      • Atrial fibrillation: oral anticoagulation within 4 to 14 days

    • IV alteplase/tenecteplase (within 4.5 hours of stroke onset)

    • Mechanical thrombectomy (within 6 hours of stroke onset) if large vessel occlusion

  3. Intracerebral Hemorrhage [rfd]

    • Discontinued anticoagulation immediately, rapid reversal

    • Platelet transfusion if treated with antiplatelet or indication for neurosurgery

    • Surgery:

      • Minimally invasive hematoma evacuation with endoscopic/stereotactic aspiration

      • External ventricular drain insertion

      • Craniotomy

  4. Subarachnoid Hemorrhage [rfd]

    • Early (<72 hours) endovascular coiling (or clipping) of aneurysm to decrease the risk of rebleeding

    • Seizure --> antiepileptic drugs

  5. Cerebellar/Cerebral edema:

    • Peaks in 3 to 5 days after an ischemic stroke

    • Correlate with the size of the stroke

    • May increase ICP/herniation/hydrocephalus --> apnea, pupillary dilatation, death

    • Treatment: ventriculostomy, decompressive craniectomy, surgical evacuation

  6. Post-stroke seizure: Antiepileptic drugs for 1 month (or longer if late seizures)

  7. Cardiac evaluation: Treatment of atrial fibrillation

Differential diagnoses

Amphetamine toxicity, Bell's Palsy, Benign paroxysmal positional vertigo, Brain abscess, Brain tumor, Cerebral venous sinus thrombosis, Cocaine toxicity, Drug side effects, Epilepsy, Hepatic encephalopathy, Hyperglycemic hyperosmolar nonketotic state, Hypoglycemia, Hyponatremia, Intracranial hemorrhage, Migraine, Multiple sclerosis, Myocardial infarction, Postseizure encephalopathy, Psychotropic drugs, Sepsis, Subarachnoid hemorrhage, Syncope, Transient global amnesia, Transient ischemic attack, Wernicke encephalopathy


References

[1] Lui F, Hui C, Khan Suheb MZ, et al. Ischemic Stroke. Updated 2025 Feb 21: https://www.ncbi.nlm.nih.gov/books/NBK499997/

[2] Tadi P, Lui F. Acute Stroke. [Updated 2023 Aug 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK535369/

[3] Nawaz B, Eide GE, Fromm A, Øygarden H, Sand KM, Thomassen L, Næss H, Waje-Andreassen U. Young ischaemic stroke incidence and demographic characteristics - The Norwegian stroke in the young study - A three-generation research program. Eur Stroke J. 2019 Dec;4(4):347-354.

[4] Kissela BM, Khoury JC, Alwell K, Moomaw CJ, Woo D, Adeoye O, Flaherty ML, Khatri P, Ferioli S, De Los Rios La Rosa F, Broderick JP, Kleindorfer DO. Age at stroke: temporal trends in stroke incidence in a large, biracial population. Neurology. 2012 Oct 23;79(17):1781-7.

[5] Ramirez L, Kim-Tenser MA, Sanossian N, Cen S, Wen G, He S, Mack WJ, Towfighi A. Trends in Acute Ischemic Stroke Hospitalizations in the United States. J Am Heart Assoc. 2016 May 11;5(5):e003233.

[6] Hong KS, Bang OY, Kang DW, Yu KH, Bae HJ, Lee JS, Heo JH, Kwon SU, Oh CW, Lee BC, Kim JS, Yoon BW. Stroke statistics in Korea: part I. Epidemiology and risk factors: a report from the korean stroke society and clinical research center for stroke. J Stroke. 2013 Jan;15(1):2-20.

[7] Feigin VL, Krishnamurthi R, Nair B, Rautalin I, Parag V, Anderson CS, Arroll B, Barber PA, Barker-Collo S, Bennett D, Brown P, Cadilhac DA, Douwes J, Exeter D, Ranta A, Ratnasabapathy Y, Swain A, Tautolo ES, Te Ao B, Thrift A, Tunnage B. Trends in stroke incidence, death, and disability outcomes in a multi-ethnic population: Auckland regional community stroke studies (1981-2022). Lancet Reg Health West Pac. 2025 Mar 10;56:101508.

[8] Chau PH, Woo J, Goggins WB, Tse YK, Chan KC, Lo SV, Ho SC. Trends in stroke incidence in Hong Kong differ by stroke subtype. Cerebrovasc Dis. 2011;31(2):138-46.

[9] http://emedicine.medscape.com/article/1916852 (2014-02-05); [Medscape]

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