Abstract
Early ischemic changes seen on non‐contrast computed tomography secondary to cerebral edema is believed to indicate irreversible cellular injury. Computed tomography perfusion may overpredict the infarct core in patients with large vessel occlusion presenting in acute phase as these changes are potentially reversible if successful endovascular reperfusion is performed in a timely manner. This has led to the concept of “ghost infarct core” which is the mismatch in the infarct core as seen on follow‐up imaging. We present a case which potentially supports the concept of “ghost infarct core” evaluated not only by computed tomography perfusion but also non‐contrast computed tomography in a patient with large vessel occlusion following successful thrombectomy.
In patients with acute ischemic stroke from large vessel occlusion presenting within the first 6 hours of stroke symptom onset, non‐contrast computed tomography (NCCT) is the primary imaging modality used to evaluate the extent of ischemia and determine patient's eligibility for mechanical thrombectomy (MT). Early ischemic hypodensity on NCCT is considered the hallmark of cerebral infarction. These changes are attributed to the cerebral edema secondary to irreversible tissue damage. 1 The Alberta Stroke Program Early CT Score (ASPECTS) is a 10‐point quantitative scale used to measure total stroke burden. 2 The score of 6 to 10 is generally considered to represent favorable imaging profile when determining patient's eligibility for MT.
The use of computed tomography perfusion in the first 6‐hour window is not recommended given evidence of computed tomography perfusion in overestimating final infarct core (the term known as “ghost infarct core”), which may exclude patients who would potentially benefit from MT. 3 Broocks et al. showed that lesion hypodensity on NCCT representative of early infarct in acute stroke may also be reversible following complete recanalization with MT in some case. 4
Here, we present a case of a patient in their 50s who presented with a classic left hemispheric syndrome within the first 1.5 hours of symptom onset. The National Institutes of Health Stroke Scale was 25. The initial NCCT was reviewed and ASPECTS was estimated as “poor” (0–5 range; Figure 1A). Automated NCCT processing with RapidAI (iSchemaView) calculated ASPECTS of 5, including 2 cortical regions (Figure 1B). Computed tomography angiography demonstrated a tandem left internal carotid artery and middle cerebral artery occlusion (Figure 1C). Given early presentation and stroke symptom severity, the patient was taken for emergent thrombectomy with excellent recanalization (TICI 3) achieved at approximately 2.5 hours from stroke symptom onset. Repeat NCCT within 12 hours after MT revealed a smaller area of hypodensity, consistent with ASPECTS>6 on visual inspection (Figure 2A). Furthermore, ASPECTS of 6 was calculated with automated RapidAI, with no infarct assigned to the 2 left cortical regions originally detected on the admission NCCT (Figure 2B). Follow‐up magnetic resonance imaging on day 1 revealed the infarct burden mainly in the basal ganglia region with additional more subtle regions of cortical injury in the frontal and temporal lobes (Figure 2C,D).
FIGURE 1.

Baseline imaging. (A) Admission NCCT slices. Early ischemic changes within the left temporal lobe, insula, and basal ganglia can be appreciated on visual inspection of the images. Total ASPECTS is less than 6. (B) Admission NCCT processed with RapidAI (iSchemaView) showing ASPECTS of 5. Two points are added for early ischemic changes in cortical regions M2 and M3, and 3 points are added for subcortical regions (caudate, internal capsule, lentiform). (C) Computed tomography angiography showing left middle cerebral artery M1 occlusion (arrow). ASPECTS indicates Alberta Stroke Program Early CT Score; and NCCT, non‐contrast computed tomography.
FIGURE 2.

Follow‐up imaging. (A) Repeat NCCT study. Residual hypodensity is present mainly within the left basal ganglia region. The previously affected left temporal region (M2, M3) where early ischemic changes were present on the initial NCCT study demonstrates marked reduction in tissue hypodensity. (B) Repeat NCCT with automated ASPECTS, total score of 6. Only subcortical regions are “scored” for ischemia (caudate, internal capsule, lentiform, insula). (C) Diffusion‐weighted magnetic resonance imaging (DWI) and FLAIR showing mainly subcortical strokes. However, less pronounced cortical injury can also be noted on both DWI and FLAIR, indicating that the apparent reversal of ischemic hypodensity on follow‐up NCCT represents pseudo‐normalization phenomenon. (D) NCCT at day 5. More defined residual hypodensity in left basal ganglia and M2, M3 region. ASPECTS indicates Alberta Stroke Program Early CT Score; DWI, diffusion‐weighted imaging; FLAIR, fluid‐attenuated inversion recovery; and NCCT, non‐contrast computed tomography.
This case demonstrates the reversal of edema progression of acute ischemic infarct after a successful endovascular recanalization at early time window. It suggests that the concept of “ghost infarct core” in early stroke may apply to large vessel occlusion cases evaluated not only with computed tomography perfusion but also with NCCT. Whether this phenomenon is due to reversibility of vasogenic brain edema, an early fogging effect (observation of initially hypodense infarct becoming transiently isodense on NCCT after successful reperfusion with its later reappearance), or a new mechanism remains to be determined. 4 , 5
In our case, at 60‐day follow‐up, the patient had significant improvement in motor ability but continued to have significant aphasia with a National Institutes of Health Stroke Scale of 6.
Disclosures
Maxim Mokin – Grants: principal investigator NIH R21NS109575 consultant: Medtronic, Cerenovus Stock options: Brain Q, Endostream, Serenity medical, Synchron.
Shail Thanki and Karl A. Kasischke – none.
Acknowledgments
None
References
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