Direct CBF · INVASIVE FLOW

Direct CBF monitoring

Thermal diffusion (Hemedex / Bowman), laser Doppler, xenon CT, and perfusion CT/MR; the family of methods that report regional cerebral blood flow directly, mostly research-grade in pediatrics.

FlowResearchAdultInvasiveInvestigational
CLast reviewed 2026-05-1720-min read

1. Bedside vignettes: why this matters

Vignette A. SAH day 8 with high TCD velocities but real DCI

A 14-year-old with aneurysmal SAH, day 8, post-coiling. Right MCA TCD MFV has risen to 180 cm/s with Lindegaard ratio 4.2; clinical exam shows subtle right-arm drift. A bedside thermal-diffusion probe was placed at admission in the right frontal white matter. TD-CBF reads 18 mL/100 g/min (down from baseline 42); the patient is at the electrical-failure threshold. DCI is confirmed by direct measurement; haemodynamic augmentation and (if needed) intra-arterial therapy follow. The TCD warned; the TD-CBF confirmed and quantified.

Vignette B. Severe TBI with PbtO₂ low, CPP normal

A 13-year-old severe TBI, day 2. PbtO₂ probe reads 14 mmHg (low), CPP 65 (adequate), ICP 18. The team adds a thermal-diffusion probe at the same trajectory. TD-CBF 22 mL/100 g/min in the pericontusional white matter, consistent with oligemia at the upper end of the Astrup cascade. The CBF deficit is the upstream cause of the low PbtO₂; raising MAP to lift CPP to 70 brings TD-CBF to 38 and PbtO₂ to 22. The combined measurement disambiguates flow vs O₂-delivery problems.

Vignette C. Xe-CT for moyamoya screening

A 9-year-old with confirmed moyamoya, considering bypass surgery. Pre-operative xenon-CT (a research / academic centre offering) shows reduced baseline CBF in both MCA territories (24 mL/100 g/min) with markedly reduced reserve to acetazolamide challenge (no increase). This documents the haemodynamic indication for bypass. The same patient post-bypass returns to a 30+ mL/100 g/min CBF with augmented reserve. Xe-CT here is a tomographic snapshot, not a continuous monitor; it bridges the gap between continuous bedside tools and tomographic imaging.


2. What direct CBF monitoring is, and what it is not

The bedside ICU question "what is the flow?" is answered indirectly by every other modality on this site: TCD measures velocity (proxy for flow if vessel diameter is constant), NIRS measures tissue oxygenation (proxy for the supply-demand ratio), PbtO₂ measures tissue O₂ tension (proxy for the same ratio at the tip), and SjvO₂ measures global O₂ extraction (proxy for whole-brain supply-demand). Direct CBF measures the flow itself, in absolute units, at one or more regions.

2.1 The Astrup cascade

The reason "absolute CBF" matters at all is that the bedside thresholds for neuronal viability are calibrated in absolute flow units:

CBF (mL/100 g/min)Bedside meaning
50–75Normal adult cortex
35–50Oligemia onset; CMRO₂ still met
20–35Oligemia; functional deficit possible
15–20Electrical failure (EEG flattening)
10–15Membrane failure threshold
< 10Imminent infarction
< 6Established infarction

These thresholds come from controlled adult-cortex data (Astrup, Heiss, Hossmann); pediatric thresholds are inferred. Direct CBF measurement is what turns these numbers from a foundational concept into a bedside threshold.

2.2 The four method families

Continuous bedside (research-grade):

  • Thermal diffusion (TD-CBF): Hemedex Bowman QFlow probe. A small parenchymal probe with a heater and two temperature sensors; measures the rate of heat dispersion to compute absolute CBF at the probe tip (~17 mm³ tissue zone).
  • Laser Doppler flowmetry (LDF): a fibreoptic probe; measures the Doppler shift of light reflected from moving red blood cells. Reports relative flux in arbitrary units (perfusion units), not absolute mL/100 g/min.

Intermittent tomographic:

  • Xenon-CT (Xe-CT): inhaled stable xenon (a freely diffusible radioopaque tracer); serial CT scans during washin map absolute regional CBF.
  • CT perfusion (CTP): bolus iodinated contrast; deconvolution analysis gives CBF, CBV, MTT maps. Widely available; the standard for acute stroke imaging.
  • MR perfusion (MRP) and arterial spin labelling (ASL): bolus gadolinium (MRP) or magnetically tagged blood (ASL, no contrast); regional CBF maps. ASL is repeatable, non-contrast; ideal for pediatric serial use.

What direct CBF does well

  • Absolute units: anchors the Astrup cascade at the bedside.
  • Regional specificity: probe-tip resolution for continuous methods; whole-brain regional for tomographic methods.
  • DCI surveillance: continuous TD-CBF in the at-risk SAH territory provides quantitative warning before clinical signs.
  • Bridge to therapy: a measured CBF deficit can guide haemodynamic augmentation, transfusion, or intra-arterial intervention.

What direct CBF cannot do

  • TD-CBF requires steady-state thermal conditions: shivering, fever spikes, body-temperature changes invalidate the measurement for the duration of the perturbation.
  • LDF reports relative, not absolute: useful for trend, not for thresholding against Astrup.
  • Xe-CT requires patient transport and is no longer routinely available in most centres.
  • CT perfusion requires iodinated contrast and radiation: limits repeatability.
  • MRP / ASL require MRI scanner time and patient stability for transport.
  • Pediatric data are sparse: most evidence is adult; pediatric thresholds inferred.
  • All methods are operator- and centre-dependent: routine clinical use is uncommon.
Clinical pearl

Direct CBF tells you the flow. Every other modality in the ICU tells you a proxy. The clinical question "is the brain ischaemic?" maps cleanly onto direct CBF values; the proxies require interpretation chains. Where the budget and expertise allow, direct CBF is the missing piece.

In children
  • Pediatric experience with direct CBF monitoring is limited: most published series are adult.
  • TD-CBF probes in pediatric severe TBI have been used in academic centres; pediatric Astrup thresholds are inferred from adult data.
  • ASL is the pediatric-friendly tomographic method: no contrast, repeatable, increasingly available on modern MRI scanners.
  • Routine bedside direct CBF in pediatric SAH or TBI is uncommon; the modality is most relevant in research-active centres.

3. Anatomy and probe placement (TD-CBF)

Fig. 1
THERMAL-DIFFUSION CBF PROBEHemedex / Bowman QFlow · heat-clearance gives absolute CBFPLACEMENT (parenchymal, via bolt)scalp / skullwhite matter, away from large vessels + CSFbolt~17 mm3 zoneheater(proximal)temp sensor(distal)~2-3 cmPRINCIPLE: HEAT-PULSE DECAYTtimebaselineheat pulsehigh CBF (fast)low CBF (slow)faster flow removes heat faster;the decay rate gives absolute local CBFMNM-Edu schematic
Thermal-diffusion CBF probe (Hemedex Bowman QFlow). The parenchymal probe is placed via a bolt at the same trajectory as ICP / PbtO2 monitoring. The probe tip carries a heater (the proximal element) and a temperature sensor (the distal element). A controlled heat pulse is delivered; the rate at which the temperature equilibrates back to baseline depends on the local CBF (faster flow = faster heat removal). The interrogated tissue zone is approximately 17 mm³ at the probe tip. The probe is typically placed in white matter at 2–3 cm depth, away from large vessels and CSF spaces.
MNM-Edu, original schematic.

3.1 TD-CBF probe placement

The thermal-diffusion probe is a 1.0 mm diameter parenchymal probe inserted via a cranial bolt:

StepAction
1Pre-procedure imaging review; identify the at-risk territory
2Cranial bolt placement under sterile technique; same trajectory as ICP / PbtO₂
3Advance the TD-CBF probe 2–3 cm into white matter; secure at the bolt
4Confirm position with post-procedure CT
5Allow 60–120 min equilibration for thermal stability
6Begin recording; pair with core temperature and ICP / PbtO₂

The probe interrogates a small tissue zone (~17 mm³) at the tip. It does not survey the whole brain; placement must target the at-risk territory.

3.2 LDF probe placement

The laser Doppler probe is similar in size; placement is via the same bolt trajectory. The interrogation depth is shallower (~1 mm³ at the tip).

3.3 Tomographic methods

Xe-CT, CTP, MRP, and ASL require transport to the imaging scanner. Patient stability and scheduling drive the feasibility; the result is a single tomographic snapshot rather than a continuous trend.

Caveat

Probe placement determines what you measure. A probe in normal-appearing brain remote from the at-risk territory may read normal flow while the lesion territory is ischaemic. Match probe placement to the question, just as with PbtO₂.


4. The signal: thermal diffusion physics

The TD-CBF method exploits the fact that flowing blood removes heat from tissue. A small heater on the probe tip delivers a controlled heat pulse; the probe's distal temperature sensor records the temperature rise and the subsequent decay back to baseline. The decay rate is converted, via a calibrated heat-transfer model, to local CBF in absolute units.

4.1 The measurement cycle

Each measurement cycle:

  1. Establish thermal equilibrium with surrounding tissue (~60 s).
  2. Deliver a controlled heat pulse (raise tip temperature ~ 2 °C).
  3. Record the temperature decay over ~ 90 s.
  4. Compute CBF from the decay constant.

A full measurement cycle takes approximately 2–3 minutes; continuous monitoring delivers a CBF value every 2–3 minutes.

4.2 Limitations

  • Thermal stability required: the calculation assumes steady-state tissue temperature; shivering, fever spikes, body-temperature changes invalidate the measurement.
  • Probe-tip CBF only: small interrogation zone (~17 mm³).
  • Calibration drift: every probe requires periodic recalibration; long-term continuous use needs maintenance.
  • Cost: the disposable probe and the dedicated cart limit availability.

4.3 LDF physics

Laser Doppler delivers near-infrared light into tissue; light backscattered from moving red blood cells is Doppler-shifted. The frequency distribution of the backscattered light yields a flux value (perfusion units). The relationship to absolute CBF is approximate; calibration to absolute units requires assumptions about haematocrit and tissue scattering properties.


5. The numbers to record: the direct-CBF six-pack

VariableSymbolWhat to record
Regional CBFTD-CBF (mL/100 g/min)Primary; with probe location
Baseline CBFTD-CBF baselineEstablished in first 12 h
CBF trendΔCBF/hA sustained 25% fall is a clinical event
Probe locationDocumented on CTAt-risk territory vs normal control
Concurrent ICP / CPP / MAPmmHgThe perfusion-pressure context
Patient temperatureT_coreThermal stability is required for valid measurement

Always pair direct-CBF readings with the time since insult, the most recent imaging, the multimodal context (PbtO₂, microdialysis, TCD, qEEG), and the clinical exam.


6. What is normal? Age-banded reference

Pediatric CBF is higher per gram than adult, peaks in the preschool window, and falls into adolescence and adulthood. The Astrup cascade thresholds are referenced to adult cortex; pediatric thresholds are inferred and may be different.

Age bandHealthy CBF (mL/100 g/min)Notes
Preterm < 32 wk10–30Low baseline; passive flow common
Term newborn20–40Lower than older child
6 months50–80Rising rapidly
1–3 years80–120Peak years
4–6 years80–110Peak window
7–12 years70–100Declining
Adolescent55–75Approaching adult
Adult50–75Reference

Sources: . The Astrup cascade thresholds (electrical failure ~ 15, membrane failure ~ 10, infarction ~ 6) are adult-cortex values; pediatric thresholds are inferred and may be lower in absolute terms but proportionally similar.

In children

Healthy pediatric MFV by TCD parallels pediatric CBF. The reference values above are derived from PET, Xe-CT, and ASL studies in healthy children. Use within-patient trend over absolute values where possible; the pediatric Astrup cascade should be informed by the patient's own baseline plus the proportional thresholds.


7. What is abnormal? Pattern library

PatternBedside meaningWhat to do
TD-CBF < 20 mL/100 g/minOligemia at electrical-failure thresholdTreat: raise CPP, transfuse, escalate; pair with qEEG and PbtO₂
TD-CBF < 15Electrical failure thresholdUrgent intervention; impending injury
TD-CBF < 10Membrane failure / impending infarctionAggressive intervention; consider intra-arterial therapy in SAH
TD-CBF falling > 25% over hoursEvolving ischaemiaTreat the trend; do not wait for absolute threshold
TD-CBF normal with low PbtO₂Diffusion limitation, oedema, mitochondrial dysfunctionMicrodialysis; targeted treatment of oedema
TD-CBF high with normal CMRO₂Luxury perfusion; hyperaemic phase of injuryIdentify cause; consider seizure, fever
TD-CBF high with collapsed CMRO₂Luxury without demand; severe injuryPair with cEEG, SSEP; poor prognostic signature
LDF flux change > 50%Real perfusion event (LDF is relative)Correlate with absolute CBF or other modalities
Xe-CT or ASL deficit in territory at riskConfirmed regional ischaemiaAnatomical correlate; targeted intervention
Acetazolamide challenge non-responder (moyamoya)Exhausted vasodilatory reserveSurgical bypass indication

Decision tree: TD-CBF in DCI surveillance


8. Try it: interactive widget

ThermalCBFDemo
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9. Management: CBF-anchored decision-making

9.1 DCI surveillance in SAH

The most evidence-supported application. In high-risk SAH patients (Hunt-Hess 4–5, modified Fisher 3–4), continuous TD-CBF in the at-risk territory provides quantitative early warning:

  1. Establish baseline TD-CBF in the at-risk territory within the first 12–24 h after admission.
  2. Continuous monitoring for the 14-day vasospasm window.
  3. A 25% fall from baseline over hours, or absolute TD-CBF < 20, triggers:
    • Re-examine: clinical exam, TCD, qEEG.
    • Haemodynamic augmentation: raise MAP within autoregulatory range.
    • Transfusion if Hb low.
    • Angiography / intra-arterial therapy if clinical or quantitative deterioration confirmed.
  4. Documentation: every event, every intervention, every quantitative response.

9.2 CPP titration in severe TBI

In centres with TD-CBF available, the probe complements PbtO₂ for CPP titration:

  1. Establish TD-CBF and PbtO₂ baseline at current CPP.
  2. Trial small CPP changes (5 mmHg).
  3. Observe TD-CBF and PbtO₂ response.
  4. Identify the CPP range that maintains TD-CBF in the normal-to-oligemia upper range (35–50 mL/100 g/min) without driving hyperaemia.
  5. Document the operational CPP window.

9.3 Moyamoya pre-operative assessment

Xe-CT or ASL with acetazolamide challenge documents baseline CBF and vasodilatory reserve:

  1. Baseline resting CBF map.
  2. Repeat after acetazolamide IV (1 g adult equivalent, weight-adjusted in pediatrics).
  3. Calculate the increase in CBF; the failure to increase (cerebrovascular reserve exhausted) is a surgical indication for bypass.
  4. Post-operative re-assessment confirms restored reserve.
Caveat

Decision support, not a clinical protocol. Every threshold and workflow above is centre-, patient-, and protocol-dependent. Pair with the full multimodal stack and defer to your unit's protocols.

Educational algorithm, not a clinical protocol. This walkthrough is a teaching aid. Defer to your unit's pediatric protocols, current PBTF / Kochanek / local guidelines, and your senior clinical team. Doses, thresholds, and decision points are starting points, not prescriptions.

10. Clinical contexts

10.1 Aneurysmal SAH and DCI

The leading clinical use case. Continuous TD-CBF in the at-risk territory provides quantitative DCI early warning; absolute thresholds (TD-CBF < 20 mL/100 g/min) trigger intervention. The combined surveillance bundle (TCD + qEEG + TD-CBF) is the modern academic-centre approach. Pediatric SAH data are limited.

10.2 Severe TBI

TD-CBF in severe TBI complements PbtO₂ for CPP titration and identifies regional flow deficits that contribute to low PbtO₂. The 2019 BTF pediatric guidelines do not specifically recommend direct CBF monitoring but acknowledge it as a research modality.

10.3 Pediatric arterial ischaemic stroke

CT perfusion is the standard acute-stroke imaging modality. ASL is the pediatric-friendly serial alternative. Direct continuous CBF is rare in pediatric AIS.

10.4 HIE and post-cardiac-arrest

CBF in HIE evolves through hypoperfusion, reperfusion, and (in severe injury) luxury perfusion. Direct measurement is research-grade in this context; the bedside surrogates (TCD, NIRS) carry the routine clinical signal.

10.5 Moyamoya disease

Xe-CT and ASL with acetazolamide challenge are part of the pre-operative work-up for moyamoya bypass surgery. The CBF reserve is the haemodynamic indication.

10.6 Pediatric ECMO

Direct CBF in pediatric ECMO is research-grade; NIRS is the bedside non-invasive standard.

10.7 Bacterial meningitis / encephalitis

CT perfusion and ASL may document hypoperfusion in vasculitis or large infarct territories complicating severe meningitis. Continuous direct CBF monitoring is uncommon.

10.8 Brain-death determination (supportive)

In brain death, CBF is zero or near-zero by direct measurement; CTA and TCD are the preferred ancillary tests in the World Brain Death Project framework.

10.9 Refractory status epilepticus

Continuous seizure activity drives hyperaemic CBF. Direct CBF monitoring is uncommon; TCD MFV trends provide the bedside surrogate.


11. Multimodal integration: direct CBF in the MMM/MNM stack

Fig. 2
DIRECT CBF IN THE MMM/MNM STACKThe missing absolute-flow channel, flow itself in absolute unitsDISCORDANCE LOCALISES THE DOMINANT PROBLEMThe four neighboursTCD = velocity · NIRS = oxygenation · PbtO2 = tissue O2· SjvO2 = global extractionlow CBF + low PbtO2ischaemicnormal CBF + low PbtO2diffusion or metabolichigh CBF + high SjvO2luxury perfusion in a dying brainMNM-Edu schematic · Figaji 2025, Helbok 2024, Tasker 2023
Direct CBF is the missing absolute-flow channel in the multimodal stack. TCD measures velocity (flow proxy); NIRS measures tissue oxygenation; PbtO2 measures tissue O2 tension; SjvO2 measures global O2 extraction. Direct CBF measures the flow itself, in absolute units, at the probe tip or as a tomographic map. Discordance among these channels often localises the dominant pathophysiology: low CBF + low PbtO2 = ischaemic; normal CBF + low PbtO2 = diffusion or metabolic; high CBF + low CMRO2 (high SjvO2) = luxury perfusion in a dying brain.
MNM-Edu, original schematic.
Pair with…What you gainWorked scenario
PbtO₂Flow + O₂ tension; localises supply vs delivery problemPbtO₂-CPP titration
TCDVelocity + absolute flow; calibrates the TCD trend in absolute unitsTCD vs ICP vasospasm
NIRSTissue oxygenation + flow; cortical vs probe-tip cross-checkPRx vs COx discordance
MicrodialysisFlow + metabolism; the L/P ratio contextMultimodal discordance
qEEGElectrophysiologic function at the CBF threshold; the Astrup correlateSAH DCI surveillance
ICP / CPP / PRxCBF response to CPP titration; autoregulation curve in absolute flowCPPopt targeting

12. Setup and technique

12.1 Equipment

  • TD-CBF system: Hemedex Bowman QFlow 500; the cart-based monitor and the disposable probe.
  • LDF system: research-grade fibreoptic probes; less commonly deployed clinically.
  • Bolt and adapter: same cranial bolt as ICP / PbtO₂; multi-channel adapter.
  • Tomographic modalities: Xe-CT (rare), CTP (widely available), MRP (MRI-dependent), ASL (modern MRI).
  • Trained operator: probe placement and signal interpretation require dedicated training.

12.2 TD-CBF placement: 6-step protocol

  1. Pre-procedure imaging review to identify the at-risk territory (pericontusional in TBI; at-risk vascular territory in SAH).
  2. Cranial bolt placement under sterile technique; multi-channel adapter accommodates ICP, PbtO₂, and TD-CBF probes through a single bolt.
  3. Advance the TD-CBF probe 2–3 cm into white matter; secure at the bolt.
  4. Confirm probe position with post-procedure CT; document the territory.
  5. Allow 60–120 minutes equilibration: thermal stabilisation is required for valid measurement; CBF values during the first hour are unreliable.
  6. Begin continuous recording: 2–3 minute measurement cycles; pair with ICP, PbtO₂, MAP, core temperature.

12.3 Validity checks

  • Thermal stability: shivering, fever spikes, body-temperature changes invalidate the measurement. Annotate every such event.
  • Probe-tip position: a probe that has migrated into CSF or against bone gives unreliable values; daily check.
  • Calibration drift: weekly recalibration is typical for long-term use.
  • Concurrent ICP: a probe-tip CBF in the presence of unstable ICP needs cautious interpretation.

12.4 Reading routine

  • Establish baseline in the first 12 h: the patient's own reference.
  • Track trend: 25% fall over hours is more informative than a single absolute value.
  • Annotate clinical events: suction, intubation, fever, sedation changes, transfusion.
  • Correlate with the other channels: PbtO₂, microdialysis, TCD, qEEG.

12.5 Xenon-CT and tomographic methods

Xe-CT requires patient transport, inhalation of stable xenon, and serial CT scans; the resulting absolute CBF map is a single time-point. CTP and MRP / ASL are similar in workflow: scanner time, contrast (CTP, MRP) or no contrast (ASL), reconstruction, and interpretation. The result is a tomographic snapshot, not a continuous trend.

12.6 Removal

The TD-CBF probe is removed when monitoring is no longer required, typically at the same time as ICP and PbtO₂. Complications are similar (small haemorrhage, infection, malposition); the probe is small and removal is straightforward.


13. Pitfalls

  • Thermal instability invalidates TD-CBF measurements; fever spikes, shivering, body-temperature changes pause the measurement for the duration.
  • Single-region measurement: probe tip samples ~17 mm³; misses remote ischaemia.
  • LDF is relative: useful for trend, not for thresholding against Astrup.
  • Xe-CT availability is limited: most centres no longer offer the modality.
  • CT perfusion radiation and contrast limit repeatability; not a continuous monitor.
  • ASL motion sensitivity: pediatric patients may need sedation for high-quality ASL acquisitions.
  • Pediatric Astrup thresholds are inferred: the cascade values are adult-cortex calibrated; pediatric application is approximate.
  • Probe drift / dislodgement: same risks as ICP / PbtO₂ probes.
  • Calibration drift: TD-CBF systems require periodic calibration; uncalibrated values drift.
  • Interpretation requires training: not a plug-and-play modality; clinical use is centre- and operator-dependent.

14. Combine with…


15. Evidence summary

TopicSourceGrade
Kety-Schmidt CBF measurementfoundational
Lassen autoregulationfoundational
Thermal diffusion CBF (Vajkoczy)B
Laser Doppler flowmetry B
AHA SAH guidelinesexpert
Modern DCI reviewreview
Pediatric severe TBI (BTF 4th ed.)expert
BOOST-II (PbtO₂ feasibility)A
BOOST-III (PbtO₂ outcome)A
HIE NICHD cooling trialA
AHA pediatric post-arrestexpert
Pediatric brain injury post-arrestreview
Pediatric AIS / thrombectomy expert
Bacterial meningitis expert
ECMO neuro outcomes C
Brain-death determination expert
Pediatric MMM consensus expert
Pediatric neurocritical care reviewreview
Autoregulation reviewreview
TCD post-HIE prognosis (pediatric)C

16. Recent literature (2022–2025)

  • BOOST-III (Bernard 2025): PbtO₂-guided care reduces brain hypoxia episodes; direct CBF complements PbtO₂ where available.
  • Modern DCI surveillance in SAH continues to evolve toward multimodal bundles (TCD + qEEG + TD-CBF where available); pediatric data remain sparse.
  • Tasker 2023 (pediatric neurocritical care review): direct CBF monitoring listed as tier-3 research modality in pediatric centres.
  • Pediatric MMM consensus (Figaji 2025): direct CBF monitoring acknowledged as research-grade with potential bedside utility in academic centres.
  • ASL adoption in pediatric MRI continues to expand; the non-contrast, repeatable nature makes it the pediatric-friendly tomographic CBF modality of choice.
  • TD-CBF in adult TBI / SAH continues to be used in academic centres; the cost and complexity limit broader adoption.

17. Self-check

Retrieval check
A 14-year-old aneurysmal SAH, day 8, post-coiling. Baseline TD-CBF in the right MCA territory was 42 mL/100 g/min on day 1. Today TD-CBF reads 18 mL/100 g/min; right MCA TCD MFV 180 with Lindegaard ratio 4.2; subtle right-arm drift on exam. Best next step?
A 13-year-old severe TBI, day 2. PbtO₂ 14 mmHg (low), TD-CBF 22 mL/100 g/min in the same pericontusional territory, CPP 65, MAP 88, ICP 23. The low PbtO₂ is most likely due to:
A 9-year-old with moyamoya disease is being evaluated for surgical bypass. Pre-operative ASL CBF maps show baseline CBF 24 mL/100 g/min in both MCA territories; after IV acetazolamide, repeat ASL shows no significant CBF increase. Interpretation?

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