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Acute Ischemic Stroke: Pathophysiology, Cerebrovascular Anatomy, and Stroke Syndromes
Last updated: 04/20/2023
Key Points
- Acute ischemic stroke (AIS) occurs when arterial occlusion leads to lack of brain tissue oxygenation resulting in irreversible neuronal injury and neurological signs and symptoms.
- AIS remains one of the leading causes of death and disability globally.
- Fundamental knowledge of cerebral vasculature anatomy and associated stroke syndromes is essential in the recognition and treatment of AIS.
Introduction
- Stroke is a debilitating disease and represents the second most common cause of death worldwide and the leading cause of serious long-term disability in adults.
- Globally, 60% of all strokes are due to ischemia.1
- In the United States, the etiology of strokes include2
- 87% are due to ischemia;
- 10% are due to intracerebral hemorrhage (ICH); and
- 3% are due to subarachnoid hemorrhage (SAH).
- AIS subtypes according to the mechanism of injury:3
- 30% are due to cerebral small vessel disease;
- 18% are due to large-artery atherosclerosis;
- 20% are due to a cardiac source of emboli;
- 30% are without an identified cause (cryptogenic infarcts); and
- 2% are due to other determined causes, such as arterial dissection or hypercoagulable states.3
- Among the common causes of AIS, large-artery atherosclerosis carries the highest risk of early stroke recurrence, while cardioembolism portrays the highest mortality rate.
- Traditional vascular risk factors associated with common causes of AIS include4
- hypertension
- smoking
- diabetes
- hyperlipidemia
- cardiovascular disease
- obesity
- physical inactivity
- family history of stroke prior to age 65
Pathophysiology
- Cerebral tissue is highly dependent on consistent cerebral blood flow (CBF) for the delivery of oxygen and glucose.
- Acute occlusion of an artery supplying the brain leads to cell injury (ischemia) and death (infarct) when CBF falls below 20mL/100g/minute.
- CBF is directly affected by arterial pCO2 levels. Increases in pCO2 will increase CBF, whereas decreases in pCO2 will decrease CBF.4
- Cerebral vasculature adapts to provide a relatively constant CBF despite changes in systemic mean arterial pressure (MAP), referred to as autoregulation.5 This adaptive mechanism may be overwhelmed when extreme variances in MAPs occur (Figure 1).
- Loss of cerebrovascular autoregulation following ischemic injury further impairs the delivery of oxygen to at-risk tissue, leading to cell death.
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Figure 1. CBF autoregulation curves depicting the relationship between MAP and CBF. The solid curve is the classical representation, with a relatively broad plateau phase. The solid vertical arrow indicates an average lower limit of autoregulation for normotensive adult humans of approximately 70mmHg. The 2 dotted line curves represent the variations that occur within a normal population, with some subjects having effectively shorter plateaus and some having very little autoregulatory capacity. Used with permission from Drummond, JC. Blood pressure and the brain: How low can you go? Anesth Analg. 2019;128(4):759-71.5
Cerebrovascular Anatomy
- Focal and abrupt reduction in CBF rapidly leads to cell injury; however, rapid treatment can prevent progression to cell death.
- A fundamental knowledge of cerebral vasculature is essential in the recognition and management of AIS.
- Cerebrovascular anatomy originates at the aortic arch from which the brachiocephalic, left common carotid and left subclavian artery are derived (Figure 2).
- The brachiocephalic artery forms the right common carotid and subclavian artery shortly after takeoff.
- The vertebral arteries originate from the subclavian arteries.
- The extracranial segments enter the transverse foramen at C6 level and ultimately pierce the dura in the vertebral canal, becoming the intracranial segments.
- Common carotid arteries divide into external and internal carotid arteries at the level of C3-C4 vertebrae (Figure 3).
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Figure 2. Branches of the aortic arch. Source: Wkimedia Commons. Henry Vaandyke Carter. Public Domain. Link.
- The circle of Willis connects the anterior (carotid) and posterior (vertebrobasilar) circulation as the major intracranial arterial system (Figure 4).
- The intracranial carotid artery bifurcates into the middle cerebral artery (MCA) and anterior cerebral artery (ACA).
- Prior to bifurcation, the ICA provides smaller branches including the
- ophthalmic artery;
- posterior communicating artery (PCom); and
- anterior choroidal artery.
- Prior to bifurcation, the ICA provides smaller branches including the
- The vertebral arteries form the basilar artery at the pontomedullary junction, which later bifurcates to form the right and left posterior cerebral arteries (PCA).
- The posterior inferior cerebellar artery (PICA) is derived from the vertebral artery prior to the vertebrobasilar junction, while the anterior inferior cerebellar artery (AICA) is a branch of the basilar artery.
- The superior cerebellar artery (SCA) originates immediately prior to the termination of the basilar artery.
- The communicating arteries provide anastomosis between arterial branches:
- Anterior communicating artery connects the bilateral ACAs.
- Posterior communicating artery connects each MCA to the respective posterior cerebral artery (PCA).4
- The intracranial carotid artery bifurcates into the middle cerebral artery (MCA) and anterior cerebral artery (ACA).
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Table 1. Anatomical arterial supply
Stroke Syndromes
- The rapid identification of stroke syndromes can assist in timely treatment and improved outcomes.
- Cortical signs can assist in the identification of large vessel occlusion (LVO):
- aphasia
- gaze preference
- visual field cut
- neglect
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Table 2. Anterior circulation stroke syndromes.6
- Posterior circulation stroke syndromes may be overlooked as they frequently present with nonspecific, nonlocalizing signs and symptoms, including nausea, vomiting, and dizziness.
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Table 3. Posterior circulation syndromes6
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Table 4. Lacunar syndromes6
References
- GBD 2019 Stroke Collaborators. Global, regional, and national burden of stroke and its risk factors, 1990-2019; a systematic analysis for the Global Burden of Disease Study 2019. The Lancet Neurology. 2021; 20(10):P795-820. PubMed
- Ovbiagele B, Nguyen-Huynh MN. Stroke epidemiology: Advancing our understanding of disease mechanism and therapy. Neurotherapeutics. 2011; 8:319-29. PubMed
- Sacco, RL. Risk factors, outcomes, and stroke subtypes for ischemic stroke. Neurology. 1997, 49 (5 Suppl 4): S39-S44. PubMed
- Grotta, JC., et al. Stroke: Pathophysiology, diagnosis, and management. Elsevier Health Sciences. 7th Ed. 2021.
- Drummond, JC. Blood pressure and the brain: How low can you go? Anesth Analg. 2019;128(4):759-71. PubMed
- Brazis PW, Masdeu, JC, Biller, J. Localization in Clinical Neurology. Lippincott Williams & Wilkins. 3rd Edition. 1996.
Other References
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