Brain ischemia

Other names| Cerebral ischemia, cerebrovascular ischemia

Brain ischemia is a condition in which there is insufficient bloodflow to the brain to meet metabolic demand.[1] This leads to poor oxygen supply in the brain and may be temporary such as in transient ischemic attack or permanent in which there is death of brain tissue such as in cerebral infarction (ischemic stroke).[2]

The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen deprivation, and may involve impairments in vision, body movement, and speaking.

An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an interruption in flow for more than a few minutes generally results in irreversible brain damage.[3] In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered.[4] Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible.[5]

## Contents

* 1 Symptoms and signs
* 2 Causes and Risk Factors
* 3 Pathophysiology
* 4 Diagnosis
* 4.1 Focal brain ischemia
* 4.2 Global brain ischemia
* 4.3 Management and Treatment
* 4.4 Prognosis and Outcomes
* 5 References

## Symptoms and signs

The clinical presentation of brain ischemia varies depending on the affected vascular territory. Ischemia in the anterior circulation, particularly branches of the internal carotid artery, may present with unilateral weakness, speech disturbances, or visual loss in one eye (amaurosis fugax).Posterior circulation ischemia, involving the vertebrobasilar arteries, often leads to symptoms such as vertigo, diplopia, dysarthria, or bilateral motor deficits.Transient symptoms may indicate a TIA, while prolonged or severe cases may progress to permanent deficits due to cerebral infarction.[6] Sudden loss of consciousness can occur when cerebral blood flow ceases for over 10 seconds, and irreversible brain damage generally follows within minutes.[7]

## Causes and Risk Factors

Brain ischemia results from conditions that reduce or block cerebral blood flow. Common causes of focal ischemia include arterial thrombosis due to atherosclerosis, embolism from cardiac sources such as atrial fibrillation, and small vessel disease associated with hypertension or diabetes. Global ischemia usually arises from systemic hypoperfusion following cardiac arrest or severe hypotension.[8] Additional risk factors include smoking, hyperlipidemia, advanced age, and a history of TIA or stroke. Rare etiologies include sickle cell anemia, which promotes vascular occlusion, and Moyamoya disease, a progressive cerebrovascular disorder affecting the intracranial arteries.[9]

## Pathophysiology

When blood supply to the brain is compromised, neurons are deprived of oxygen and glucose necessary for aerobic metabolism. This leads to rapid depletion of adenosine triphosphate (ATP) within minutes. The failure of ATP-dependent ion pumps disrupts electrochemical gradients, resulting in cellular depolarization and an influx of calcium. Elevated intracellular calcium triggers glutamate release, proteolysis, and ultimately, neuronal injury.[10] Surrounding the infarcted core is the 'ischemic penumbra,' a zone of hypoperfused tissue that retains some metabolic activity and may be salvageable with timely intervention.[7]

## Diagnosis

Diagnosis of brain ischemia begins with prompt clinical assessment of neurological deficits, often using tools such as the NIH Stroke Scale.[11] Immediate brain imaging is essential to confirm ischemia and exclude hemorrhage. Noncontrast computed tomography (CT) is typically the first step due to its availability and speed. Magnetic resonance imaging (MRI) with diffusion-weighted imaging offers higher sensitivity for detecting acute ischemia. Additional studies, including CT or MR angiography and carotid Doppler ultrasound, help identify vascular occlusions or stenosis. Cardiac evaluation, such as echocardiography and ECG monitoring, may be necessary in cases with suspected embolic sources.[12]

### Focal brain ischemia

Focal brain ischemia occurs when a blood clot has occluded a cerebral vessel.[13] Focal brain ischemia reduces blood flow to a specific brain region, increasing the risk of cell death to that particular area.[14] It can be either caused by thrombosis or embolism.

### Global brain ischemia

Due to different susceptibility to ischemia of various brain regions, a global brain ischemia may cause focal brain infarction. The cerebral cortex and striatum are more susceptible than the thalamus, and the thalamus in turn is more sensitive than the brainstem.[15] Partial cerebral cortex infarction from global brain ischemia typically manifests as watershed stroke.[16]

The outcome of brain ischemia is influenced by the quality of subsequent supportive care. Systemic blood pressure (or slightly above) should be maintained so that cerebral blood flow is restored. Also, hypoxaemia and hypercapnia should be avoided. Seizures can induce more damage; accordingly, anticonvulsants should be prescribed and should a seizure occur, aggressive treatment should be undertaken. Hyperglycaemia should also be avoided during brain ischemia.[17]

A closely related disease to brain ischemia is brain hypoxia. Brain hypoxia is the condition in which there is a decrease in the oxygen supply to the brain even in the presence of adequate blood flow. If hypoxia lasts for long periods of time, coma, seizures, and even brain death may occur. Symptoms of brain hypoxia are similar to ischemia and include inattentiveness, poor judgment, memory loss, and a decrease in motor coordination.[18] Potential causes of brain hypoxia are suffocation, carbon monoxide poisoning, severe anemia, and use of drugs such as cocaine and other amphetamines.[19] Other causes associated with brain hypoxia include drowning, strangling, choking, cardiac arrest, head trauma, and complications during general anesthesia. Treatment strategies for brain hypoxia vary depending on the original cause of injury, primary and/or secondary.[18]

### Management and Treatment

Treatment of brain ischemia depends on the type, location, and timing of the event. For acute ischemic stroke, intravenous thrombolysis with tissue plasminogen activator (tPA) is recommended within 4.5 hours of symptom onset.[20] In patients with large vessel occlusions, endovascular mechanical thrombectomy offers substantial benefits when performed within 6 to 24 hours, particularly if imaging shows viable penumbral tissue.[21] Supportive care includes blood pressure optimization, oxygenation, and management of complications such as fever and seizures. In global ischemia due to cardiac arrest, targeted temperature management (32–36 °C) may improve neurologic outcomes.[22] Long-term care focuses on secondary prevention through antithrombotic therapy, control of vascular risk factors, and rehabilitation.[23]

### Prognosis and Outcomes

The clinical outcome of brain ischemia depends on the extent of injury, time to treatment, and patient comorbidities. Rapid reperfusion has been associated with significantly improved functional recovery and reduced mortality.[21] However, delayed treatment or severe ischemia often results in long-term neurological deficits, including motor impairment, aphasia, and cognitive dysfunction. Approximately one-third of ischemic stroke survivors experience significant disability. In cases of global ischemia, outcomes are heavily influenced by the duration of cerebral hypoperfusion and the quality of post-resuscitation care.[24] Vascular depression and vascular dementia may develop after multiple subcortical ischemic insults, particularly in older adults.[25]

## References

1. ↑ Sullivan, Jonathon. "What is Brain Ischemia?". WSU Emergency Medicine Cerebral Resuscitation Laboratory. http://sullydog.com/sullysites/qm/brainischemia101syllabus/syllabus/presentation1_9_1.html.
2. ↑ "Brain Ischemia (Cerebral Ischemia)". Cure Hunter Incorporated. 2003. pp. Relationship Network. http://www.curehunter.com/public/keywordSummaryD002545.do.
3. ↑ Raichle, Marcus (1983). "The Pathophysiology of Brain Ischemia". Neurological Progress. http://www.nil.wustl.edu/labs/raichle/MER_chapters/C55_The Pathophysiology of Brain Ischemia.pdf.
4. ↑ Hossmann, Konstantin-Alexander; Zimmermann, Volker (1974). "Resuscitation of the monkey brain after 1 H complete ischemia. I. Physiological and morphological observations" (in en). Brain Research 81 (1): 59–74. doi:10.1016/0006-8993(74)90478-8. PMID 4434196.
5. ↑ Raichle, Marcus; Ann Neurol (1983). "The pathophysiology of brain ischemia". Neurological Process. http://www.nil.wustl.edu/labs/raichle/MER_chapters/C55_The Pathophysiology of Brain Ischemia.pdf.
6. ↑ The Merck manual of medical information (2nd home, [all new & completely rev.] ed.). Whitehouse Station, NJ: Merck Research Laboratories. 2003. ISBN 9780911910353.
7. ↑ 7.0 7.1 Hakim, Antoine M. (September 1998). "Ischemic penumbra". Neurology 51 (3_suppl_3): S44–S46. doi:10.1212/WNL.51.3_Suppl_3.S44. PMID 9744833. https://doi.org/10.1212/WNL.51.3_SUPPL_3.S44.
8. ↑ Murphy, Robert; Damasceno, Albertino; Reddin, Catriona; Hankey, Graeme J; Iversen, Helle K; Oveisgharan, Shahram; Lanas, Fernando; Czlonkowska, Anna et al. (1 June 2024). "Variations in the prevalence of atrial fibrillation, and in the strength of its association with ischemic stroke, in countries with different income levels: INTERSTROKE case–control study" (in EN). International Journal of Stroke 19 (5): 559–568. doi:10.1177/17474930241227783. PMID 38204182. https://doi.org/10.1177/17474930241227783.
9. ↑ Rupareliya, Chintan; Lui, Forshing (2025). Moyamoya Disease. StatPearls Publishing. PMID 30571076. https://www.ncbi.nlm.nih.gov/books/NBK535455/.
10. ↑ Lipton, Peter (10 January 1999). "Ischemic Cell Death in Brain Neurons". Physiological Reviews 79 (4): 1431–1568. doi:10.1152/physrev.1999.79.4.1431. PMID 10508238. https://doi.org/10.1152/physrev.1999.79.4.1431.
11. ↑ Caplan, Louis R; Kasner, Scott E; Dashe, John F. "Differential diagnosis of transient ischemic attack and acute stroke". https://www.uptodate.com/contents/differential-diagnosis-of-transient-ischemic-attack-and-acute-stroke?search=Differential diagnosis of brain ischemia. UpToDate.&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2.
12. ↑ "Pathophysiology Of Disease An Introduction To Clinical Medicine, 7th Ed [ PDF[tahir 99] VRG"]. https://archive.org/details/PathophysiologyOfDiseaseAnIntroductionToClinicalMedicine7thEdPDFtahir99VRG.
13. ↑ Sullivan, Jonathon. "Two Flavors of Ischemia". Brain Ischemia 101 (Emergency Medicine Cerebral Resuscitation Lab). http://sullydog.com/sullysites/qm/brainischemia101syllabus/syllabus/presentation1_9_2.html.
14. ↑ Miettinen, S.; Fusco, F. R.; Yrjanheikki, J.; Keinanen, R.; Hirvonen, T.; Roivainen, R.; Narhi, M.; Hokfelt, T. et al. (1997). "Spreading depression and focal brain ischemia induce cyclooxygenase-2 in cortical neurons through N-methyl-D-aspartic acid-receptors and phospholipase A2". Proceedings of the National Academy of Sciences 94 (12): 6500–5. doi:10.1073/pnas.94.12.6500. PMID 9177247. Bibcode: 1997PNAS...94.6500M.
15. ↑ Dimitri P. Agamanolis, M.D.. "Neuropathology - Chapter 2: Cerebral ischemia and stroke". https://neuropathology-web.org/chapter2/chapter2aHIE.html. Updated: October, 2017
16. ↑ Porth, C.M. (2009). Pathophysiology: Concepts of Altered Health States (Eighth ed.). Philadelphia: Wolters Kluwer Health | Lippincott Williams & Wilkins. pp. 1301. ISBN 978-16054-7390-1.
17. ↑ "Prevention and treatment of brain ischaemia". British Medical Journal 291 (6498): 758–60. 1985. doi:10.1136/bmj.291.6498.758. PMID 3929929.
18. ↑ 18.0 18.1 "Cerebral Hypoxia Information Page". National Institute of Neurological Disorders and Stroke (National Institutes of Health). 2008-05-07. http://www.ninds.nih.gov/disorders/anoxia/anoxia.htm.
19. ↑ Tsatsakis, Aristides; Docea, Anca Oana; Calina, Daniela; Tsarouhas, Konstantinos; Zamfira, Laura-Maria; Mitrut, Radu; Sharifi-Rad, Javad; Kovatsi, Leda et al. (23 August 2019). "A Mechanistic and Pathophysiological Approach for Stroke Associated with Drugs of Abuse". Journal of Clinical Medicine 8 (9): 1295. doi:10.3390/jcm8091295. PMID 31450861.
20. ↑ Powers, William J.; Rabinstein, Alejandro A.; Ackerson, Teri; Adeoye, Opeolu M.; Bambakidis, Nicholas C.; Becker, Kyra; Biller, José; Brown, Michael et al. (December 2019). "Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke 50 (12): e344–e418. doi:10.1161/STR.0000000000000211. PMID 31662037. https://doi.org/10.1161/STR.0000000000000211.
21. ↑ 21.0 21.1 Nogueira, Raul G.; Jadhav, Ashutosh P.; Haussen, Diogo C.; Bonafe, Alain; Budzik, Ronald F.; Bhuva, Parita; Yavagal, Dileep R.; Ribo, Marc et al. (4 January 2018). "Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct". New England Journal of Medicine 378 (1): 11–21. doi:10.1056/NEJMoa1706442. PMID 29129157. https://doi.org/10.1056/NEJMoa1706442.
22. ↑ Bernard, Stephen A.; Gray, Timothy W.; Buist, Michael D.; Jones, Bruce M.; Silvester, William; Gutteridge, Geoff; Smith, Karen (21 February 2002). "Treatment of Comatose Survivors of Out-of-Hospital Cardiac Arrest with Induced Hypothermia". New England Journal of Medicine 346 (8): 557–563. doi:10.1056/NEJMoa003289. PMID 11856794. https://doi.org/10.1056/NEJMoa003289.
23. ↑ Powers, William J.; Rabinstein, Alejandro A.; Ackerson, Teri; Adeoye, Opeolu M.; Bambakidis, Nicholas C.; Becker, Kyra; Biller, José; Brown, Michael et al. (December 2019). "Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association". Stroke 50 (12): e344–e418. doi:10.1161/STR.0000000000000211. PMID 31662037. https://doi.org/10.1161/STR.0000000000000211.
24. ↑ Hinds, C J (21 September 1985). "Prevention and treatment of brain ischaemia." (in en). BMJ 291 (6498): 758–760. doi:10.1136/bmj.291.6498.758. PMID 3929929. PMC 1417168. https://doi.org/10.1136/bmj.291.6498.758.
25. ↑ Baldwin, Robert C. (2005). "Is vascular depression a distinct sub-type of depressive disorder? A review of causal evidence" (in en). International Journal of Geriatric Psychiatry 20 (1): 1–11. doi:10.1002/gps.1255. PMID 15578670. https://doi.org/10.1002/gps.1255.

* v
* t
* e

Cerebrovascular diseases

Brain ischemia/
cerebral infarction
(ischemic stroke/TIA)|

| TACI, PACI|

* precerebral: Carotid artery stenosis

* cerebral: MCA
* ACA
* Amaurosis fugax

* Moyamoya disease

|

POCI|

* precerebral: Anterior spinal artery syndrome
* Vertebrobasilar insufficiency
* Subclavian steal syndrome

* brainstem: medulla
* Medial medullary syndrome
* Lateral medullary syndrome
* pons
* Medial pontine syndrome/Foville's
* Lateral pontine syndrome/Millard-Gubler
* midbrain
* Weber's
* Benedikt
* Claude's

* cerebral: PCA
* Lacunar stroke
* Dejerine–Roussy syndrome

* cerebellar

General|

* cerebral: Cerebral venous sinus thrombosis
* CADASIL
* Binswanger's disease
* Transient global amnesia

Intracranial hemorrhage
(hemorrhagic stroke)|

| Extra-axial|

* Epidural
* Subdural
* Subarachnoid

|

Cerebral/Intra-axial|

* Intraventricular

Brainstem|

* Duret haemorrhages

Aneurysm|

* Cerebral aneurysm
* Intracranial berry aneurysm
* Charcot–Bouchard aneurysm

Other/general|

* Cerebral vasculitis

* v
* t
* e

Disorders of blood flow

Decreases|

| Clots|

* Thrombus
* Thrombosis
* Renal vein thrombosis

|

Ischemia|

* Brain ischemia
* Ischaemic heart disease
* large intestine: Ischemic colitis
* small intestine: Mesenteric ischemia

Infarction|

* Types
* Anemic
* Hemorrhagic
* Location
* Heart
* Brain
* Spleen
* Limb

Increases|

| Hemorrhage|

* Bruise]]/Hematoma
* Petechia
* Purpura
* Ecchymosis

* head
* Epistaxis
* Hemoptysis
* Intracranial hemorrhage
* Hyphema
* Subconjunctival hemorrhage
* torso
* Hemothorax
* Hemopericardium
* Pulmonary hematoma
* abdomen
* Gastrointestinal bleeding
* Haemobilia
* Hemoperitoneum
* Hematocele
* Hematosalpinx
* joint
* Hemarthrosis

Edema|

* Anasarca
* Angioedema/Lymphedema
* Exudate/Transudate

* Cerebral edema
* Pulmonary edema
* Hydrothorax
* Ascites/hydroperitoneum
* Hydrosalpinx

Other|

* Hyperemia

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