A 60-year-old woman presented with a five-day history of severe headaches and confusion and was found to have aneurysmal subarachnoid hemorrhage (aSAH) secondary to a ruptured basilar artery aneurysm. Her modified Fisher Scale was 2. She underwent external ventricular drainage (EVD) and endovascular coiling. Her Glasgow Coma Scale (GCS) was E4V5M5. On day 10, the patient deteriorated to E1V2M3, requiring intubation and transfer to the Neurosciences Critical Care Unit. Non-contrast CT (NCCT) showed extensive bilateral frontoparietal hypodensities, and CT perfusion (CTP) at a mean arterial pressure (MAP) of 80–90 mmHg demonstrated globally reduced cerebral blood flow (CBF) and cerebral blood volume (CBV), interpreted as infarction (Figure 1).

Figure 1.

CT perfusion and non-contrast CT (NCCT) on day 10 after aneurysmal subarachnoid hemorrhage ictus. Diffusely low cerebral blood flow (CBF) (A) with areas showing corresponding reduction in cerebral blood volume (CBV) (white arrows) (B). Mean transit time prolongation is seen throughout, with areas of mismatch present outside of the areas of reduced CBV (red arrows) (C). Corresponding NCCT, showing diffuse areas of edema (D).

On arrival, MAP was augmented to ≥120 mmHg. She improved to having normal left-sided power, with mild right hemiparesis. Repeat CTP at MAP 120–130 mmHg, with the EVD at 0 cmH₂O, showed delayed time parameters with relative preservation of CBV, more consistent with penumbral tissue (Figure 2A–C), although NCCT at day 20 showed the presence of infarction (Figure 2D). On hospital discharge (day 46), the patient had a modified Rankin Scale of 5. She was still undergoing tracheostomy weaning, could move all four limbs and had increasingly purposeful movements on the left.

Figure 2.

CT perfusion and non-contrast CT (NCCT) on day 18 after aneurysmal subarachnoid hemorrhage ictus, following mean arterial pressure augmentation. Cerebral blood flow (CBF) and cerebral blood volume (CBV) maps (A, B) demonstrate marked improvement compared with the prior study, with near-resolution of previously noted areas of severely reduced CBF/CBV. The mean transit time map (C) shows decreased extent of prolongation. NCCT (D) demonstrates multifocal hypodensities compatible with established ischemic injury.

Delayed cerebral ischemia (DCI) after aSAH reflects a multifactorial cascade involving vasospasm, microcirculatory dysfunction, impaired cerebral autoregulation, cortical spreading depolarization, neuroinflammation and microthromboses culminating in metabolic mismatch and ischemia. ^{Reference Dodd, Laurent and Dumont1} The diagnosis is based on consensus criteria ^{Reference Vergouwen, Vermeulen and van Gijn2} but lacks a gold standard; CT angiography and CTP are used to support it. ^{Reference Hoh, Ko and Amin-Hanjani3} In CTP, irreversibly infarcted tissue is typically characterized by low CBF and CBV with increased mean transit time. ^{Reference Lui, Tang, Allmendinger and Spektor4} In contrast, penumbral tissue is characterized by reduced CBF with preserved or elevated CBV due to compensatory vasodilation mediated by cerebral autoregulation. ^{Reference Leigh, Knutsson, Zhou and van Zijl5}

Our case highlights an important pitfall of CTP interpretation, namely, that low CBF and CBV may not always be synonymous with irreversible infarct. The evolution of CTP with MAP augmentation suggests that low-CBV patterns may reflect loss of autoregulation with pressure-dependent hypoperfusion rather than a completed infarct. Failure of cerebral autoregulation is well described after aSAH, ^{Reference Dodd, Laurent and Dumont1} and cerebral perfusion pressures below calculated optimal levels are associated with DCI and worse outcomes. ^{Reference Kranawetter, Tuzi, Moerer, Mielke, Rohde and Malinova6–Reference Fan, Sun, Huang, Yang, Guo and He8} Serial CTP studies may distinguish reversible ischemia from progression to infarct in DCI cohorts. ^{Reference Cremers, Vos and van der Schaaf9} Another potential explanation relates to the fact that CTP concepts, which are largely derived from the large-vessel occlusion acute ischemic stroke literature, may not translate cleanly to aSAH-related DCI. Whereas the former produces a near-complete flow arrest, the latter causes incomplete and heterogeneous hypoperfusion, such that low CBF and CBV may not necessarily represent completed infarction. Interestingly, ischemic core overestimation, known as the “ghost core phenomenon,” is increasingly reported in acute ischemic stroke patients, especially in those with poor collaterals and those imaged early after symptom-onset. ^{Reference García-Tornel, Campos and Rubiera10} This supports the concept that CTP reflects hemodynamic compromise rather than definitive tissue fate and suggests that a similar interpretive pitfall can be observed in aSAH-related DCI.

The unfavorable clinical functional recovery at discharge highlights the complex nature of DCI, where restoring perfusion with MAP augmentation alone may be insufficient to reverse downstream metabolic and inflammatory injury. Ultimately, this case illustrates reversibility of apparently “irreversible” CTP parameters in a patient with DCI and reinforces that CTP should always be interpreted cautiously and in the context of the wider clinical picture. It further highlights the necessity of neuromonitoring to better characterize cerebral physiology and support tailored treatment decisions.