Physiological provocation compared to acetazolamide in the assessment of cerebral hemodynamics – A case report

Author:

Henriksen Alexander Cuculiza1,Thomsen Gerda Krog2,Knudsen Gitte M2,Stavngaard Trine1,Rosenbaum Sverre1,Marner Lisbeth1ORCID

Affiliation:

1. Copenhagen University Hospital Bispebjerg

2. Copenhagen University Hospital: Rigshospitalet

Abstract

Abstract

Background: Severe large vessel disease may lead to cerebral hemodynamic failure that critically impairs cerebral blood flow (CBF) regulation elevating the risk of ischemic events. Assessment of the condition is often based on changes in CBF during vasodilatation; however, pharmacologically induced vasodilation does not reflect the physiological condition during an ischemic event caused by hemodynamic failure. We compared a [15O]H2O PET brain scan during vasodilation to a [99mTc]HMPAO SPECT brain scan during an ongoing transient ischemic attack (TIA). Case presentation: A single patient presenting with limb-shaking TIA underwent CT, Digital Subtraction Angiography, and two cerebral perfusion scans: [15O]H2O PET and [99mTc]HMPAO SPECT. Acetazolamide was used in the PET scan to induce vasodilatation, and during the SPECT scan physiological stress, standing up rapidly, was used to induce limb-shaking TIA. CT-angiography and Digital Subtraction Angiography demonstrated an occluded anterior cerebral artery distal to the circle of Willis on the left side, with a corresponding infarction in the watershed area. Collaterals supplied the main vascular territory of the anterior cerebral artery. During rest, neither perfusion scans demonstrated reduced perfusion outside of the ischemic core. However, we found a pronounced difference between the PET utilizing acetazolamide and the SPECT during the TIA. The PET scan demonstrated a reduced CBF in vascular territory supplied by collaterals, while the area around the ischemic core was not affected. Contrary, the SPECT had only a minor decrease in the collateral-supplied area, whereas the watershed area proximal to the infarct core had a pronounced decrease. Conclusions: The observed discrepancy in compromised areas during physiological provocation compared to pharmacological induced vasodilation questions the use of an unphysiological stressor for assessment of cerebrovascular hemodynamics. A physiological provocation test may achieve more clinically relevant evaluation.

Publisher

Springer Science and Business Media LLC

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