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Robotic Brain Universe

Blood supply and stroke

The arteries of the brain and their territories, how flow is regulated, what a stroke destroys minute by minute, and the trials that changed treatment.

Intermediate · about 13 min · updated 2026-10-02 · awaiting clinical review

See it in 3D:

Illustrative simulation excitatory inhibitory

Anterior and posterior circulations, the circle of Willis and the territories of the anterior, middle and posterior cerebral arteries shown in this atlas; autoregulation and flow thresholds; the penumbra; thrombolysis and thrombectomy trials from NINDS to SELECT2; Poiseuille's law, 'time is brain' and the number needed to treat; AI, mobile stroke units and vagus nerve stimulation.

Contents
  1. Every minute counts
  2. What supplies the brain
  3. Why blood flow is regulated so tightly
  4. How a stroke unfolds, and how it is treated
  5. When: the clock and the tissue
  6. What is lost, territory by territory
  7. The mathematics of flow, time and benefit
  8. Technology: imaging, AI and devices
  9. Milestones
  10. Frontiers
  11. Check yourself

Every minute counts

In a typical large-vessel ischaemic stroke left untreated, the brain loses about 1.9 million neurons, 14 billion synapses and 12 km of myelinated fibres every minute. Measured against normal ageing, the ischaemic brain ages 3.6 years for each hour without treatment.[1]

Stroke is one of the world's great killers: in 2021 it caused 7.3 million deaths, 10.7% of all deaths, making it the third most common cause of death after ischaemic heart disease and COVID-19. There were 11.9 million new strokes that year.[2]

This reading follows the blood into the brain: the arteries and the territories they supply (shown in this atlas's Arterial territory colour mode), how blood flow is regulated, what happens when it fails, and the treatments, built on trials and imaging, that now reopen blocked arteries within hours.[3,4]

What supplies the brain

Two sources of arterial blood perfuse the brain: the anterior circulation, from the two internal carotid arteries, and the posterior (vertebrobasilar) circulation, from the two vertebral arteries, which fuse into the single basilar artery. The two meet at the base of the brain in the circle of Willis, an arterial ring around the optic chiasm that joins the carotid and vertebral supplies.[3]

The circle is often incomplete. In MR angiograms of 150 volunteers, 74% had a complete anterior part, 52% a complete posterior part and only 42% an entirely complete circle.[5]

Anterior cerebral artery (ACA). Supplies the medial surface of the hemisphere along the longitudinal fissure: parts of the frontal lobe and the superomedial parietal lobe, but not the medial occipital lobe.[3,6]

Middle cerebral artery (MCA). The largest cerebral artery, supplying most of the lateral surface: all of the insular cortex, the superior and middle temporal gyri, the inferior parietal lobule and much of the postcentral gyrus, the inferior and middle frontal gyri and much of the precentral gyrus. Its lenticulostriate branches supply deep structures including the putamen and parts of the caudate nucleus and internal capsule.[3,6]

Posterior cerebral artery (PCA). Usually arises from the end of the basilar artery and supplies much of the posterior cortex, including the occipital lobe, with a deep territory that covers the thalamus and midbrain. The vertebrobasilar system as a whole supplies the occipital lobe, most of the brainstem and all of the cerebellum.[3]

Key numbers

Share of total cerebral blood flow carried by the anterior circulation (phase-contrast MRI)
72%[3]
Volunteers with an entirely complete circle of Willis
42% of 150[5]
Patients whose stroke lesions defined the arterial atlas shown here
1,298[4]
New strokes worldwide in 2021
11.9 million[2]

Why blood flow is regulated so tightly

Brain function depends on a close match between metabolic demand and the delivery of oxygen and nutrients. That match is kept by four kinds of regulation: autoregulation (the vessels' response to changes in perfusion pressure), reactivity to substances such as carbon dioxide, neurovascular coupling (more flow where neurons are active) and endothelium-dependent responses.[7]

When flow falls, functions fail in order. Protein synthesis stops first, at about 0.55 mL per gram per minute; anaerobic glycolysis begins at 0.35; neurotransmitter release and the disturbance of energy metabolism begin at about 0.20; and below 0.15 cells undergo anoxic depolarisation.[8]

Collaterals. The circle of Willis is the critical junction between the carotid and vertebral supplies and a key collateral pathway. In one study of 976 patients with atherosclerosis, reviewed by Chandra and colleagues, an incomplete anterior circle (present in 23%) carried a hazard ratio of 2.8 for future anterior-circulation ischaemic stroke.[3]

How a stroke unfolds, and how it is treated

Most strokes are ischaemic, caused by a blocked artery: in 2021, 65.3% of new strokes were ischaemic, 28.8% intracerebral haemorrhages and 5.8% subarachnoid haemorrhages.[2]

Core and penumbra. Around the core, where energy is exhausted, lies the ischaemic penumbra: a region of constrained blood supply in which energy metabolism is still preserved. Without reperfusion the core gradually expands into the penumbra until, after a few hours, the penumbra has disappeared; waves of peri-infarct depolarisation are thought to drive that expansion.[8,9]

Dissolving the clot. In the NINDS trial, intravenous tissue plasminogen activator (t-PA) given within three hours of onset made patients at least 30% more likely to have minimal or no disability at three months, despite more symptomatic brain haemorrhage (6.4% vs 0.6%). ECASS III extended benefit to 3–4.5 hours, after a CT scan had excluded haemorrhage.[10,11]

Removing the clot. For occlusion of the internal carotid or proximal middle cerebral artery, endovascular thrombectomy removes the clot from inside the artery. Pooling five trials (1,287 patients), the HERMES collaboration found that thrombectomy reduced disability at 90 days, with a number needed to treat of 2.6 to reduce disability by at least one level on the modified Rankin Scale.[12]

From symptom onset to reperfusionSymptom onsetthe clock starts: about 1.9million neurons lost per minutein a typical large-vessel strokeBrain imaging (CT or MRI)haemorrhage must be excludedbefore thrombolysisThrombolysis if eligiblewithin 4.5 hours in ECASS IIILarge-vessel occlusion?internal carotid or proximalmiddle cerebral artery; AIsoftware can flag itThrombectomywithin 6 hours, or up to 16–24hours in patients selected byimagingRecovery and rehabilitationincluding newer device-pairedtherapies
From symptom onset to reperfusion. A simplified path through acute ischaemic stroke care as tested in the trials cited here; real pathways depend on local guidelines and on each patient.[1,11,12,13,14,15,16]
Text version of the diagram
  1. Symptom onset: the clock starts: about 1.9 million neurons lost per minute in a typical large-vessel stroke. Leads to Brain imaging (CT or MRI).
  2. Brain imaging (CT or MRI): haemorrhage must be excluded before thrombolysis. Leads to Thrombolysis if eligible; Large-vessel occlusion?.
  3. Thrombolysis if eligible: within 4.5 hours in ECASS III. Leads to Large-vessel occlusion?; Recovery and rehabilitation.
  4. Large-vessel occlusion?: internal carotid or proximal middle cerebral artery; AI software can flag it. Leads to Thrombectomy.
  5. Thrombectomy: within 6 hours, or up to 16–24 hours in patients selected by imaging. Leads to Recovery and rehabilitation.
  6. Recovery and rehabilitation: including newer device-paired therapies.

When: the clock and the tissue

Time is brain. Saver estimated that a typical large-vessel stroke reaches a final volume of 54 mL over about 10 hours, losing 120 million neurons an hour.[1]

From the clock to the tissue. Later trials selected patients by imaging rather than by time alone. DAWN treated patients 6 to 24 hours after they were last known to be well whose deficit was disproportionately severe for their infarct volume: 49% were functionally independent at 90 days with thrombectomy, against 13% without. DEFUSE 3 used perfusion imaging to find ischaemic but not yet infarcted tissue 6 to 16 hours after onset and also found better outcomes with thrombectomy.[13,14]

Getting there faster. Mobile stroke units are ambulances that carry a CT scanner. In the BEST-MSU trial, the median time from onset to t-PA was 72 minutes with a mobile unit against 108 minutes with standard emergency services, and outcomes at 90 days were better.[17]

Across a lifetime. Between 1990 and 2019, age-standardised stroke incidence fell by 17% worldwide, but among people younger than 70, incidence rates rose by 15% and prevalence rates by 22%.[18]

What is lost, territory by territory

Because each artery supplies particular regions, the deficits after a stroke follow the territory. The MCA, with its vast lateral territory, is the most common site of stroke.[3,6]

Posterior cerebral artery. PCA infarcts most commonly (84–100%) cause visual field loss; alexia and agnosias such as prosopagnosia can also occur, and deep structures are involved in almost 30% of pure PCA infarcts. One report cited in the same review gives a mortality of 85% for basilar artery occlusion.[3]

Thalamus. Strokes in the thalamus's vascular territories produce distinct syndromes. Tuberothalamic strokes impair arousal, orientation, learning, memory, personality and executive function; paramedian strokes reduce arousal, especially when bilateral; inferolateral strokes cause sensory loss, weakness and ataxia on the opposite side and pain syndromes. Language deficits follow left paramedian or left tuberothalamic lesions, and right-sided lesions can cause hemispatial neglect.[19]

Risk factors. In the INTERSTROKE study of 26,919 people in 32 countries, ten potentially modifiable risk factors together accounted for 90.7% of the population attributable risk of stroke. Hypertension was the largest, with a population attributable risk of 47.9%.[20]

The mathematics of flow, time and benefit

Blood flow follows the physics of fluids, and the benefit of a treatment can be summarised in a single number.[21,22]

Poiseuille's law[7,21]
Q=ΔPR,R=8μLπr4Q = \frac{\Delta P}{R}, \qquad R = \frac{8 \mu L}{\pi r^{4}}

Flow through a tube equals the pressure difference divided by the resistance, and resistance rises with the inverse fourth power of the radius: halving a vessel's radius raises its resistance 16-fold. Autoregulation is the response of the brain's vessels to changes in perfusion pressure; because resistance depends so steeply on radius, small changes in vessel calibre can offset large changes in pressure.

Symbols in Poiseuille's law
SymbolMeaningUnit
QQvolume flow ratem³/s
ΔP\Delta Ppressure difference along the vesselPa
RRresistance to flowPa·s/m³
μ\muviscosity of the fluidPa·s
L,rL, rlength and radius of the vesselm
Flow thresholds of ischaemia[8]
CBF  (mL g−1 min−1):0.55→protein synthesis stops,0.35→anaerobic glycolysis,0.20→energy metabolism disturbed,<0.15→anoxic depolarisation\mathrm{CBF}\;(\mathrm{mL\,g^{-1}\,min^{-1}}):\quad 0.55 \to \text{protein synthesis stops},\quad 0.35 \to \text{anaerobic glycolysis},\quad 0.20 \to \text{energy metabolism disturbed},\quad <0.15 \to \text{anoxic depolarisation}

A ladder of cerebral blood flow thresholds from studies of focal ischaemia. Multiply by 100 for the more familiar unit of millilitres per 100 g per minute (for example, 0.20 is 20 mL/100 g/min).

Symbols in Flow thresholds of ischaemia
SymbolMeaningUnit
CBFCBFcerebral blood flow per gram of tissuemL/(g·min)
Time is brain[1,17]
Nlost(t)≈r t,r≈1.9×106 neurons/minN_{\text{lost}}(t) \approx r\,t, \qquad r \approx 1.9 \times 10^{6}\ \text{neurons/min}

Saver's average rate for a typical untreated large-vessel stroke. Saving 30 minutes corresponds to about 1.9×106×30≈571.9 \times 10^6 \times 30 \approx 57 million neurons. As an illustration only, the 36-minute difference in median time to t-PA between mobile stroke units and standard care corresponds to about 68 million neurons at this rate.

Symbols in Time is brain
SymbolMeaningUnit
NlostN_{\text{lost}}neurons lost—
rraverage rate of neuron lossneurons/min
tttime without reperfusionmin
Number needed to treat[11,13,22]
NNT=1ARR=1ptreated−pcontrol\mathrm{NNT} = \frac{1}{\mathrm{ARR}} = \frac{1}{p_{\text{treated}} - p_{\text{control}}}

How many patients must be treated for one extra good outcome. In ECASS III, 52.4% had a favourable outcome with alteplase and 45.2% with placebo: an absolute difference of 7.2 percentage points, so NNT ≈ 1/0.072 ≈ 14. In DAWN, 49% against 13% were functionally independent, a crude difference of 36 points and NNT ≈ 3. These are simple unadjusted calculations from the published percentages.

Symbols in Number needed to treat
SymbolMeaningUnit
ARRARRabsolute difference in the proportion with a good outcome—
ppproportion with a good outcome in each group—

Technology: imaging, AI and devices

Imaging selects patients. CT excludes haemorrhage before thrombolysis, and perfusion imaging can show tissue that is ischaemic but not yet infarcted; DEFUSE 3 required an initial infarct smaller than 70 mL and a ratio of ischaemic tissue to infarct of at least 1.8.[11,14]

AI on the scan. A 2020 systematic review found 20 machine-learning studies in acute stroke. Convolutional neural networks were typically used to detect large-vessel occlusions and were more sensitive for image features than random-forest methods (85% vs 68%). Commercial platforms named in the review include Brainomix, General Electric, iSchemaView and Viz.ai, which uses convolutional networks to detect occlusions and then automatically activates emergency stroke treatment systems. The authors note that differing performance standards prevent fair comparison.[15]

CT angiogram voxelsConvolution filtersPooled featuresDense layerOcclusion: yes / no
A convolutional network flags an occlusion (schematic). A schematic of the kind of network the review describes: learned filters pick out vessel features, and a final unit outputs the probability of a large-vessel occlusion. Real systems differ in architecture and are validated separately.[15]

Mapping territories. The arterial colour mode in this atlas uses the first publicly available digital 3D atlas of arterial territories, built from stroke lesions in 1,298 patients traced on diffusion-weighted MRI. It defines ACA, MCA, PCA and vertebrobasilar territories and sub-territories such as the lenticulostriate and thalamoperforating territories. It builds on earlier maps of the dominant arterial territories on 12 axial sections of the hemispheres, and of the brainstem and cerebellum.[4,6,23]

Stimulation in rehabilitation. In the VNS-REHAB trial, all 108 participants, who had moderate-to-severe arm weakness at least nine months after ischaemic stroke, had a vagus nerve stimulator implanted, and rehabilitation was paired with active or sham stimulation. Arm impairment scores improved by 5.0 points with active stimulation against 2.4 with sham, and 47% against 24% had a clinically meaningful response 90 days after therapy.[16]

Landmark acute-stroke trials[10,11,12,13,14,24,25]
TrialTreatment and windowMain result
NINDS (1995)t-PA within 3 hAt least 30% more likely to have minimal or no disability
ECASS III (2008)Alteplase at 3–4.5 hFavourable outcome 52.4% vs 45.2%
HERMES (2016)Thrombectomy within 12 h, five trialsNNT 2.6 for one-level improvement
DAWN (2018)Thrombectomy at 6–24 h, mismatchIndependence 49% vs 13%
DEFUSE 3 (2018)Thrombectomy at 6–16 h, perfusion imagingBetter functional outcome
AcT (2022)Tenecteplase vs alteplase within 4.5 hNon-inferior: mRS 0–1 in 36.9% vs 34.8%
SELECT2 (2023)Thrombectomy for large infarcts within 24 hBetter outcome; vascular complications

Milestones

From physiology to thrombectomy

  1. 1959Lassen reviews cerebral blood flow and oxygen consumption in man.[26]
  2. 1981Astrup, Siesjö and Symon describe flow thresholds and the ischaemic penumbra.[9]
  3. 1988The number needed to treat is proposed as a measure of treatment effect.[22]
  4. 1995The NINDS trial shows benefit from t-PA within three hours.[10]
  5. 1998Arterial territory maps of the hemispheres; the circle of Willis is complete in only 42% of volunteers.[5,6]
  6. 2006'Time is brain' is quantified: 1.9 million neurons a minute.[1]
  7. 2008ECASS III extends thrombolysis to 4.5 hours.[11]
  8. 2016HERMES pools five thrombectomy trials; INTERSTROKE quantifies modifiable risk.[12,20]
  9. 2018DAWN and DEFUSE 3 extend thrombectomy to selected patients up to 24 hours.[13,14]
  10. 2021Mobile stroke units and vagus nerve stimulation for rehabilitation are tested in trials.[16,17]
  11. 2022Tenecteplase is shown non-inferior to alteplase.[24]
  12. 2023A digital 3D arterial territory atlas; thrombectomy for large infarcts.[4,25]

Frontiers

A simpler clot-buster. In the AcT trial of 1,600 patients, a single bolus of tenecteplase was non-inferior to the alteplase bolus and hour-long infusion: 36.9% against 34.8% had a score of 0 or 1 on the modified Rankin Scale at 90–120 days, with similar rates of symptomatic haemorrhage (3.4% against 3.2%).[24]

Larger strokes. Earlier thrombectomy trials included patients with large infarcts only in limited numbers. In SELECT2, patients with a large ischaemic core still had better functional outcomes with thrombectomy than with medical care alone, although thrombectomy brought vascular complications.[25]

The global picture. The Global Burden of Disease 2021 analysis found stroke burden rising from 1990 to 2021, the fall in incidence stalling from 2015 onwards, and growing contributions from high body-mass index, high ambient temperature and high fasting plasma glucose.[2]

Check yourself

Check yourself

  1. Which arteries form the anterior and posterior circulations?
    Show answer

    The internal carotid arteries form the anterior circulation; the vertebral arteries, joining as the basilar artery, form the posterior (vertebrobasilar) circulation.

  2. In the MR angiography study of 150 volunteers, how often was the circle of Willis entirely complete?
    Show answer

    In 42% of them (63 of 150).

  3. Which artery supplies the insula and most of the lateral surface of the hemisphere?
    Show answer

    The middle cerebral artery.

  4. What is the ischaemic penumbra?
    Show answer

    A region of constrained blood supply around the infarct core in which energy metabolism is still preserved; without reperfusion it is absorbed into the core within hours.

  5. About how many neurons does a typical untreated large-vessel stroke destroy each minute?
    Show answer

    About 1.9 million.

  6. In ECASS III, 52.4% had a favourable outcome with alteplase against 45.2% with placebo. What is the crude number needed to treat?
    Show answer

    1 / 0.072 ≈ 14.

  7. What did DAWN and DEFUSE 3 change?
    Show answer

    They showed benefit from thrombectomy 6 to 24 (DAWN) or 6 to 16 (DEFUSE 3) hours after onset in patients selected by imaging.

  8. Which modifiable risk factor had the largest population attributable risk in INTERSTROKE?
    Show answer

    Hypertension (47.9%).

Glossary[2,3,7,8,11,12,22]

Ischaemic stroke
Brain injury caused by a blocked artery.
Intracerebral haemorrhage
Bleeding into the brain tissue.
Circle of Willis
The arterial ring at the base of the brain that joins the carotid and vertebral supplies.
Arterial territory
The region of brain supplied by a particular artery.
Penumbra
Under-perfused tissue around the infarct core that can still be saved.
Autoregulation
The response of brain vessels that keeps flow steady as perfusion pressure changes.
Thrombolysis
Dissolving a clot with a drug such as alteplase or tenecteplase.
Thrombectomy
Removing a clot from inside a blocked artery, working from within the blood vessels.
Large-vessel occlusion
Blockage of a major artery such as the internal carotid or proximal middle cerebral artery.
Modified Rankin Scale
A 0–6 scale of disability after stroke, from no symptoms to death.
Number needed to treat
How many patients must be treated for one extra good outcome.

References

  1. Saver JL. Time is brain—quantified. Stroke 2006;37(1):263-266. doi:10.1161/01.STR.0000196957.55928.ab
  2. Feigin VL, Abate MD, Abate YH, Abd ElHafeez S, Abd-Allah F, Abdelalim A, et al. (GBD 2021 Stroke Risk Factor Collaborators). Global, regional, and national burden of stroke and its risk factors, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021. The Lancet Neurology 2024;23(10):973-1003. doi:10.1016/S1474-4422(24)00369-7
  3. Chandra A, Li WA, Stone CR, Geng X, Ding Y. The cerebral circulation and cerebrovascular disease I: Anatomy. Brain Circulation 2017;3(2):45-56. doi:10.4103/bc.bc_10_17
  4. Liu CF, Hsu J, Xu X, Kim G, Sheppard SM, Meier EL, Miller MI, Hillis AE, Faria AV. Digital 3D Brain MRI Arterial Territories Atlas. Scientific Data 2023;10(1):74. doi:10.1038/s41597-022-01923-0
  5. Krabbe-Hartkamp MJ, van der Grond J, de Leeuw FE, de Groot JC, Algra A, Hillen B, Breteler MM, Mali WP. Circle of Willis: morphologic variation on three-dimensional time-of-flight MR angiograms. Radiology 1998;207(1):103-111. doi:10.1148/radiology.207.1.9530305
  6. Tatu L, Moulin T, Bogousslavsky J, Duvernoy H. Arterial territories of the human brain. Neurology 1998;50(6):1699-1708. doi:10.1212/WNL.50.6.1699
  7. Claassen JAHR, Thijssen DHJ, Panerai RB, Faraci FM. Regulation of cerebral blood flow in humans: physiology and clinical implications of autoregulation. Physiological Reviews 2021;101(4):1487-1559. doi:10.1152/physrev.00022.2020
  8. Hossmann KA. Viability thresholds and the penumbra of focal ischemia. Annals of Neurology 1994;36(4):557-565. doi:10.1002/ana.410360404
  9. Astrup J, Siesjö BK, Symon L. Thresholds in cerebral ischemia - the ischemic penumbra. Stroke 1981;12(6):723-725. doi:10.1161/01.STR.12.6.723
  10. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. New England Journal of Medicine 1995;333(24):1581-1588. doi:10.1056/NEJM199512143332401
  11. Hacke W, Kaste M, Bluhmki E, Brozman M, Dávalos A, Guidetti D, et al.. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. New England Journal of Medicine 2008;359(13):1317-1329. doi:10.1056/NEJMoa0804656
  12. Goyal M, Menon BK, van Zwam WH, Dippel DWJ, Mitchell PJ, Demchuk AM, et al.. Endovascular thrombectomy after large-vessel ischaemic stroke: a meta-analysis of individual patient data from five randomised trials. The Lancet 2016;387(10029):1723-1731. doi:10.1016/S0140-6736(16)00163-X
  13. Nogueira RG, Jadhav AP, Haussen DC, Bonafe A, Budzik RF, Bhuva P, et al.. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. New England Journal of Medicine 2018;378(1):11-21. doi:10.1056/NEJMoa1706442
  14. Albers GW, Marks MP, Kemp S, Christensen S, Tsai JP, Ortega-Gutierrez S, et al.. Thrombectomy for stroke at 6 to 16 hours with selection by perfusion imaging. New England Journal of Medicine 2018;378(8):708-718. doi:10.1056/NEJMoa1713973
  15. Murray NM, Unberath M, Hager GD, Hui FK. Artificial intelligence to diagnose ischemic stroke and identify large vessel occlusions: a systematic review. Journal of NeuroInterventional Surgery 2020;12(2):156-164. doi:10.1136/neurintsurg-2019-015135
  16. Dawson J, Liu CY, Francisco GE, Cramer SC, Wolf SL, Dixit A, et al.. Vagus nerve stimulation paired with rehabilitation for upper limb motor function after ischaemic stroke (VNS-REHAB): a randomised, blinded, pivotal, device trial. The Lancet 2021;397(10284):1545-1553. doi:10.1016/S0140-6736(21)00475-X
  17. Grotta JC, Yamal JM, Parker SA, Rajan SS, Gonzales NR, Jones WJ, et al.. Prospective, multicenter, controlled trial of mobile stroke units. New England Journal of Medicine 2021;385(11):971-981. doi:10.1056/NEJMoa2103879
  18. Feigin VL, Stark BA, Johnson CO, Roth GA, Bisignano C, Abady GG, et al. (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):795-820. doi:10.1016/S1474-4422(21)00252-0
  19. Schmahmann JD. Vascular Syndromes of the Thalamus. Stroke 2003;34(9):2264-2278. doi:10.1161/01.STR.0000087786.38997.9E
  20. O'Donnell MJ, Chin SL, Rangarajan S, Xavier D, Liu L, Zhang H, et al.. Global and regional effects of potentially modifiable risk factors associated with acute stroke in 32 countries (INTERSTROKE): a case-control study. The Lancet 2016;388(10046):761-775. doi:10.1016/S0140-6736(16)30506-2
  21. Sutera SP, Skalak R. The history of Poiseuille's law. Annual Review of Fluid Mechanics 1993;25:1-20. doi:10.1146/annurev.fl.25.010193.000245
  22. Laupacis A, Sackett DL, Roberts RS. An assessment of clinically useful measures of the consequences of treatment. New England Journal of Medicine 1988;318(26):1728-1733. doi:10.1056/NEJM198806303182605
  23. Tatu L, Moulin T, Bogousslavsky J, Duvernoy H. Arterial territories of human brain. Neurology 1996;47(5):1125-1135. doi:10.1212/WNL.47.5.1125
  24. Menon BK, Buck BH, Singh N, Deschaintre Y, Almekhlafi MA, Coutts SB, et al.. Intravenous tenecteplase compared with alteplase for acute ischaemic stroke in Canada (AcT): a pragmatic, multicentre, open-label, registry-linked, randomised, controlled, non-inferiority trial. The Lancet 2022;400(10347):161-169. doi:10.1016/S0140-6736(22)01054-6
  25. Sarraj A, Hassan AE, Abraham MG, Ortega-Gutierrez S, Kasner SE, Hussain MS, et al.. Trial of endovascular thrombectomy for large ischemic strokes. New England Journal of Medicine 2023;388(14):1259-1271. doi:10.1056/NEJMoa2214403
  26. Lassen NA. Cerebral blood flow and oxygen consumption in man. Physiological Reviews 1959;39(2):183-238. doi:10.1152/physrev.1959.39.2.183

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Template anatomy for education. Not patient-specific. Not for clinical decision-making.