Abstract
Mild and minor acute neurological symptoms may lead to diagnostic uncertainty, resulting in a heterogeneous group of patients with true ischemic events and stroke mimics with a potential for poor outcomes. More than half of ischemic stroke patients present as minor strokes (National Institutes of Health Stroke Scale score <6). Whole-brain computed tomography perfusion can be used as a diagnostic test for minor stroke, offering a potential method of reducing diagnostic uncertainty in these patients. We hypothesize that whole-brain computed tomography perfusion imaging features could accurately predict infarction in patients with minor neurological deficits. This retrospective chart review enrolled consecutive patients suspected of acute ischemic stroke with a National Institutes of Health Stroke Scale score <6, who underwent whole-brain computed tomography perfusion and follow-up diffusion-weighted magnetic resonance imaging at our institution. Sensitivity, specificity, positive and negative predictive values, and positive and negative likelihood ratios were calculated for whole-brain computed tomography perfusion, using follow-up diffusion-weighted magnetic resonance imaging as a reference standard. A total of 524 patients (mean age: 67 years; range: 17–96 years; 56% men) met the inclusion criteria. Patients were excluded for non-diagnostic (n = 25) or missing maps (n = 8) scans, non-ischemic findings (n = 7), and lack of follow-up magnetic resonance imaging (n = 336). The final analysis included 148 patients who underwent diffusion-weighted magnetic resonance imaging. Whole-brain computed tomography perfusion has a sensitivity of 0.57 (95% CI: 0.45–0.69) and a specificity of 0.82 (95% CI: 0.71–0.90). The positive and negative predictive values and positive and negative likelihood ratios were 75%, 67%, 3.09, and 0.53, respectively. Our analysis suggests that although whole-brain computed tomography perfusion may offer some value as an adjunctive test for improving confidence in offering stroke treatment, it is not sufficiently sensitive or specific to accurately predict cerebral infarcts in patients with minor neurological symptoms.
Keywords: Stroke, computed tomography perfusion, cerebral infarction, diagnosis
Introduction
More than half of ischemic stroke patients present with a National Institutes of Health Stroke Scale (NIHSS) score of <6, a commonly used clinical criterion for classification of minor stroke.1–4 In current practice, intravenous thrombolysis with tissue plasminogen activator (tPA) is the only recommended pharmacological treatment for acute ischemic stroke.5 Although there is no lower limit on NIHSS for tPA administration, few published trials have evaluated the efficacy of thrombolysis in patients with minor stroke.6 A substantial proportion of otherwise eligible patients are not treated with tPA on the basis of low symptom severity,7,8 despite data suggesting that patients suffering untreated minor ischemic strokes incur substantial rates of disability9,10 and that tPA demonstrates positive outcomes in such patients, with an even lower hemorrhage risk than the overall stroke population.6,11 This may, in part, reflect the diagnostic uncertainty that is faced when evaluating patients with minor symptoms.12 Conversely, some patients initially suspected of experiencing minor stroke symptoms (NIHSS score < 6) are ultimately diagnosed with stroke mimics, such as seizures, migraines and conversion disorder.13–15 Such patients often erroneously receive tPA,16–18 which is associated with substantial hospital costs16 and an underlying risk of hemorrhagic complications,19,20 but provides no therapeutic benefit.
Patients with suspected acute strokes typically undergo evaluation with non-contrast computed tomography (CT) and CT angiography.21 Computed tomography perfusion (CTP) is used in some centers to evaluate patients for penumbra or salvageable tissue,22 and traditionally has limited brain coverage. However, whole-brain computed tomography perfusion (WB-CTP) allows for assessment of any region of ischemia in the brain because of its coverage, and improves diagnostic accuracy for ischemic lesions,23,24 with comparable treatment times to traditional CT scanning protocols.25 Thus, WB-CTP could be a potential diagnostic supplement to the existing clinical pathway for evaluation of acute cerebral events with minor clinical presentations.
Given the clinical and financial consequences of misdiagnosis and therapeutic error, there is a need for an accurate method of distinguishing ischemic strokes from mimics and transient ischemic events in patients presenting with minor neurological symptoms. It is possible that WB-CTP could play a contributory role in guiding this distinction, which would serve to minimize dangerous mistreatment of stroke mimics and facilitate timely identification of patients with minor stroke who may benefit from tPA administration. Thus, we sought to determine the diagnostic accuracy of WB-CTP for identifying acute cerebral ischemic events resulting in infarcts on follow-up diffusion-weighted magnetic resonance imaging (DW-MRI) in individuals with minor clinical presentations.
Methods
A single center, retrospective analysis was performed in patients with minor deficits on presentation to assess the diagnostic accuracy of WB-CTP in the evaluation of acute cerebral ischemic events. Our hospital research ethics board has approved this study and waived individual patient consent (approval no.: OHSN-REB 2009474-01H). Patients’ demographic data, presenting symptoms, clinical course, and diagnostic imaging results were collected using online patient records: the electronic medical record (vOACIS: Open Architecture Ülinical Information System) and radiological database (PACS: Picture Archiving and Communication System).
Participants
Patients with suspected acute ischemic stroke less than 6 hours from symptom onset, who had CT scans including WB-CTP as per The Ottawa Hospital (tertiary care hospital) stroke protocol and an NIHSS score < 6 were included. Patients were evaluated from August 2008 to June 2015. For any patient whose medical record did not include a formal NIHSS evaluation, an NIHSS score was retrospectively calculated based on the physical exam findings reported during the neurology stroke code consultation.26 Patients were excluded if no CTP was performed or if the CTP was non-diagnostic. Patients were excluded if they did not undergo follow-up DW-MRI sequences within a maximum of 14 days with no intervening clinical events.
Imaging
All CT images were acquired using a Toshiba Aquilion One 320 scanner (Toshiba Medical Systems, Tokyo, Japan). Our acute stroke imaging protocol starts with a non-contrast computed tomography scan (NCCT) followed by combined whole-brain perfusion and cranial computed tomography angiography (CTA) acquisition. In each patient, 40 ml of iodinated intravenous contrast was used for whole-brain CTA/CTP acquisition. This is followed by CTA of the neck, with a separate bolus of contrast injection. A total of 19 dynamic, whole-brain volume acquisitions were obtained over 60 seconds, and CT perfusion was calculated with the scanner workstation. Standard vendor CTP processing was used. The radiation dose from the WB-CTP acquisition is approximately 4.4 mSv (dose-length product of 1930 mGycm); for comparison, the dose-length product of non-contrast CT of the head is 1335 mGycm (∼3 mSv).
Image analysis
All WB-CTP and follow-up DW-MRI scans were interpreted by staff neuroradiologists as part of clinical reporting practice. Outcomes for the purpose of this study were primarily determined based on the original radiology reports. Readers of WB-CTP scans had access to clinical information but were blinded to the result of the follow-up MRI (which had not yet been performed). Readers of the follow-up MRI were not blinded to previous imaging and clinical information. Original WB-CTP images were cross-referenced with radiology reports, and cases of obvious reporting error were reassessed by a staff neuroradiologist (SC) who was blinded to the original radiologist report and the result of the reference test. WB-CTP scans demonstrating focal areas of increased time to peak or mean transit time, or decreased cerebral blood flow, with or without decreased cerebral blood volume, particularly in the context of a mismatched defect or penumbra were considered to be positive for acute ischemic changes, as per standard reporting practice at our institution. Unremarkable scans, and those with WB-CTP findings such as hypoperfusion and matched defects related to area of encephalomalacia (which are characteristic of chronic or remote ischemic changes) were considered to be negative. Follow-up MRI was considered positive for stroke only if it demonstrated restricted diffusion and the reporting radiologist’s impression was ischemic stroke. WB-CTP diagnosis was cross-referenced with DW-MRI diagnosis to establish true positives, false negatives, false positives, and true negatives for the presence of an infarct. In patients with a final diagnosis of stroke on MRI, images were retrieved from hospital archives and diffusion-weighted imaging (DWI) lesion diameters were retrospectively measured.
Statistical methods
We calculated sensitivity, specificity, positive and negative predictive values, and positive and negative likelihood ratios for prediction of infarction by WB-CTP, with associated 95% confidence intervals. DW-MRI is currently the gold standard imaging modality for stroke detection. Confirmatory follow-up imaging is especially important in patients with minor symptoms and clinical diagnostic uncertainty. Thus, the reference standard for this study was MRI performed within 14 days of presentation, without intervening clinical events.
A subanalysis was performed to evaluate for an association between lesion size and location (anterior versus posterior circulation), using a t-test. A second subanalysis was performed to assess for size differences between false negative and true positive CTP results among infarcts in the middle cerebral artery (MCA) territory.
Results
Patient selection
A summary of patient selection is provided in Figure 1. A total of 1440 patients received CT by our institutional stroke imaging protocol. Of these, 361 patients were excluded based on the presence of intracranial hemorrhage. An additional 446 patients presented with an NIHSS score > 5, and were excluded. One hundred and sixty-seven patient charts did not report an NIHSS value and required retrospective calculation. Of these, 82 were excluded because of absent documentation, illegible notes, or incomplete physical examination, and 27 exceeded the maximum inclusion value of 5. A total of 524 patients met the inclusion criteria of NIHSS score < 6. Twenty-one patients were found to have non-diagnostic WB-CTP scans due to motion artifacts, eight patients’ charts contained no CT perfusion scan record and missing maps, and four patients demonstrated suboptimal CT acquisition, resulting in exclusion of 33 patients. Seven patients were excluded because of the presence of distinct CTP abnormalities consistent with non-ischemic pathologies (five with mass lesions, one with non-specific inflammatory changes, and one with dural arteriovenous fistula). Three hundred and thirty-six patients were excluded for not undergoing follow-up DW-MRI. After applying inclusion and exclusion criteria, 148 patients presenting with an NIHSS score < 6, adequate WB-CTP imaging on presentation, and appropriate follow-up DW-MRI were included in our analysis.
Figure 1.
Patient selection details. CT: computed tomography; CTP, computed tomography perfusion; DW-MRI, diffusion-weighted magnetic resonance imaging; H&N, head and neck; NIHSS, National Institutes of Health Stroke Scale.
The median age of included patients was 67 years (range: 17–96 years), including 83 males and 96 females. Disease prevalence was 54% in our study population. Clinical characteristics of the study population are presented in Table 1.
Table 1.
Summary of clinical data in study population.
| All patients (n = 148) | CTP-positive (n = 55) | CTP-negative (n = 93) | |
|---|---|---|---|
| Event severity by NIHSS | |||
| Zero | 19 | 4 | 15 |
| One | 20 | 9 | 11 |
| Two | 43 | 9 | 34 |
| Three | 29 | 16 | 13 |
| Four | 18 | 8 | 10 |
| Five | 19 | 9 | 10 |
| Laterality of symptoms | |||
| Left | 54 | 21 | 33 |
| Right | 64 | 26 | 38 |
| Bilateral | 4 | 2 | 2 |
| Not applicable | 26 | 6 | 20 |
| Final clinical diagnosis | |||
| Stroke (infarct on MRI) | 80 | 48 | 32 |
| Transient ischemic attack | 38 | 4 | 34 |
| Seizure | 6 | 0 | 6 |
| Migraine | 5 | 1 | 4 |
| Syncope | 3 | 1 | 2 |
| Psychogenic | 3 | 0 | 3 |
| Other | 13 | 1 | 12 |
CTP: computed tomography perfusion; MRI: magnetic resonance imaging; NIHSS, National Institutes of Health Stroke Scale.
Imaging analysis
Fifty-five patients had positive CTP findings and the remaining 93 patients had negative CTP findings. Four CTP scan reports were falsely reported as negative on the initial report and treated as positive in the analysis.
Eighty patients had confirmed infarcts on DW-MRI follow-up. The most commonly affected territory was MCA (n = 35), followed by posterior cerebral artery (n = 14), basilar artery (n = 8), superior cerebellar artery (n = 5), posterior inferior cerebellar artery (n = 4), anterior cerebral artery (n = 2), and anterior choroidal artery (n = 1). The remaining 11 cases involved multiple vascular territories.
The mean lesion size in patients with infarcts on DWI (measured by the longest axis) was 1.85 cm (range: 0.20–7.48). The mean lesion size was significantly greater for anterior circulation infarcts (2.26 cm) compared with posterior circulation infarcts (1.39 cm), with a mean diameter difference of 0.86 cm (95% CI: 0.25–1.58; P = 0.0189).
Among confirmed infarcts in the MCA territory, the mean lesion size on DWI was 1.24 cm in those that were not detected by CTP (i.e. false negatives) and 2.54 cm in those that were detected by CTP (i.e. true positives), although the difference between groups was not statistically significant (P = 0.0973).
Diagnostic accuracy
With follow-up DW-MRI as a reference standard, WB-CTP has sensitivity of 0.61 (95% CI: 0.50–0.72) and specificity of 0.91 (95% CI: 0.82–0.96) for detection of acute cerebral infarction. The positive and negative predictive values and positive and negative likelihood ratios were 89% (95% CI: 79–95%), 67% (95% CI: 60–73%), 6.94 (95% CI: 3.17–15.20), and 0.42 (95% CI: 0.32–0.57), respectively.
There were 49 true positives, 62 true negatives, six false positives, and 31 false negatives (Figure 2). Of the correctly identified cases of cerebral infarction, 16 cases (32.7%) involved the posterior circulation, 31 cases (63.3%) involved the anterior circulation, and two cases (4.1%) involved scattered, tiny foci of ischemia. The vascular territory of the abnormality on WB-CTP was congruent with the infarcted region on follow-up MRI in 41 cases (83.7%). Of the false negatives, 15 cases (48.4%) involved the posterior circulation, nine cases (29.0%) involved the anterior circulation, and seven cases (22.7%) involved scattered, tiny foci of ischemia. A comparison of the vascular territories of abnormalities on CTP versus follow-up DW-MRI in all patients with confirmed infarcts is summarized in Appendix 1.
Figure 2.
Case 1 (top row, a–d) is a 51-year-old male who presented with acute onset of bilateral hand ataxia and dysphagia. Admission computed tomography (CT) perfusion time to peak (TTP) map (a) shows increased TTP abnormality in bilateral superior cerebellar hemispheres (white arrows). Coronal reformats of CT angiogram (b) shows non-opacification of bilateral superior cerebellar arteries (black arrow). Diffusion-weighted imaging (c) and apparent diffusion coefficient (ADC) mapping (d) shows corresponding bilateral superior cerebellar small acute infarcts (white arrow; true positive example).
Case 2 (bottom row, e–h) is an 81-year-old male with prior history of right-sided stroke and right internal carotid artery (ICA) stenosis who presented with possible new dysarthria. Admission non-contrast CT (e) shows atrophy changes and old infarcts. CT perfusion TTP (f) and cerebral blood volume (CBV) (g) maps show matched perfusion defect in the right hemisphere thought to be representing changes due to patient’s known ICA stenosis. Diffusion-weighted imaging (h) shows small peripheral acute infarcts in the right posterior frontal lobe (white arrows; false negative example).
When considering the diagnostic accuracy of WB-CTP for localizing a specific region of cerebral infarction, there were 41 true positives (positive WB-CTP finding with DW-MRI abnormality in the corresponding region), 62 true negatives, 14 false positives (positive WB-CTP finding with no corresponding DW-MRI lesion or DW-MRI lesion in different vascular territory), and 31 false negatives. These values correspond to a sensitivity of 0.57 (95% CI: 0.45–0.69) and specificity of 0.82 (95% CI: 0.71–0.90). The positive and negative predictive values and positive and negative likelihood ratios were 0.75 (95% CI: 0.64–0.83), 0.67 (95% CI: 0.60–0.73), 3.09 (95% CI: 1.85–5.17), and 0.53 (95% CI: 0.40–0.70), respectively.
Discussion
The main advantage of WB-CTP in acute stroke diagnosis is its complete brain coverage, allowing for detection of peripheral perfusion defects. This makes WB-CTP a plausible diagnostic tool rather than only a penumbral assessment tool. As part of standard acute stroke protocol, WB-CTP has the theoretical potential to improve the diagnostic performance for differentiating minor stroke from stroke mimics. The moderate specificity observed in this study suggests that, in patients with minor neurological symptoms, positive CTP findings may be an acceptable adjunct for stroke diagnosis as it can help to identify patients at high risk of eventual cerebral infarct. However, the poor sensitivity indicates that negative CTP findings do not reliably rule out ischemic stroke, and therefore preventative and reperfusion therapies cannot be confidently and safely withheld from patients on the sole basis of negative CTP imaging.
The overall results of this study suggest that WB-CTP is a moderately accurate tool for ruling in acute cerebral ischemia, but is unsuitable for ruling out these events. The observed values for sensitivity, specificity, negative predictive value and positive predictive value are fairly consistent with the overall body of literature surrounding CTP diagnostic value in the general stroke population.27 However, sensitivity and specificity were toward the lower ends of the ranges reported in the literature, likely because of smaller infarct sizes in the minor stroke subgroup assessed. A recent study similarly noted that a subgroup of patients in their study with minor clinical presentations demonstrated a drastically lower CTP sensitivity compared with the full stroke population.28 In our study, seven out of nine cases (78%) of scattered, tiny ischemic foci went undetected on WB-CTP, redemonstrating the previously established low sensitivity of CTP for small scatter lesions.29 In previous studies this difference could have been attributed to both inadequate spatial resolution and limited perfusion coverage,28,30 however, the use of WB-CTP in our study eliminates the latter issue. Even with whole-brain perfusion coverage, it appears that some anatomical areas remain problematic, where approximately half of posterior circulation strokes were missed on CTP compared with a 29% miss rate for anterior circulation strokes. The cause of this regional discrepancy is not entirely clear, although it is likely related to the limited spatial resolution of WB-CTP as well as differences in image quality between regions. Posterior circulation infarcts may tend to be smaller in size compared with anterior circulation infarcts. For example, >90% of cerebellar infarcts (nearly one-third of the posterior circulation infarcts in our study) are smaller than 1 cm,31 whereas <50% of lacunar MCA infarcts are in this size range, with the majority being larger.32 Given the limited ability of WB-CTP to detect smaller lesions, a relative abundance of small lesions in the posterior circulation could predispose to false negative results. Accordingly, in our study, the mean posterior circulation infarct size was significantly lower than that in the anterior circulation, which may have hindered detection of these lesions. In addition, a beam-hardening artifact in the form of the adjacent petrous bone is known to limit CTP evaluation of the posterior fossa,33,34 which could decrease certainty when identifying lesions.
The reason for the infarct localization discrepancies between WB-CTP and DW-MRI in eight patients is unclear. One potential mechanism that could produce this phenomenon is if these patients experienced reversible ischemic lesions followed by subclinical intervening events in the interim before DW-MRI follow-up. Alternatively, as we used radiology reports rather than blinded reanalysis of images, it is possible that these could represent simple errors in radiologist interpretation. It is also possible that poorly understood CTP post-processing errors resulted in mislocalization of these lesions on the displayed image. Finally, a strong possibility exists that the positive findings on WB-CTP in these discrepant situations are mere artifacts, and that these cases in fact represented false negative findings. Given this possibility, clinicians would be well advised to err on the side of caution regarding the presented diagnostic accuracy estimates, by focusing on the analysis of accurate localization of ischemia.
Given the established effectiveness of CTP in detecting MCA infarcts, the six false negative cases observed in this study were unexpected. These cases are most likely attributable to limited spatial resolution: the mean lesion size was >1 cm smaller in this false negative group compared with the group of detected lesions. Although this difference was not statistically significant, the small sample size in the false negative group likely may have limited the power of this analysis to detect a significant difference. Also, as CTP images were not comprehensively reassessed for the purpose of this study, these false negative cases might also be attributable to radiologist error or post-processing issues.
There are several limitations to this study. The main limitation of this study is its retrospective nature, depending on previously documented radiology reports rather than blinded reanalysis of all scans, and not accounting for the volume of CTP abnormalities or the numeric values of perfusion parameters. Also, as this study used a single center design, it does not take into account the variability in CTP post-processing techniques that may exist between centers. It should also be noted that 56 patients in the study population were eligible for inclusion partially on the basis of a retrospectively calculated NIHSS score, which might introduce a degree of bias. Another important limitation to note is that DW-MRI can be subject to false negatives, especially when performed soon after stroke onset, in patients with lacunar or posterior circulation strokes, and in early infarcts due to stroke warning syndromes.35,36 With a 14 day maximum follow-up interval, we also cannot rule out the occurrence of subclinical ischemic events occurring between WB-CTP and follow-up MRI, which would be incorrectly interpreted as false negatives in this study.
For this study, we did not exclude patients on the basis of having received tPA. The potential for bias with tPA administration lies in the possibility that a completely reversible abnormality on WB-CTP could resolve with treatment before follow-up DW-MRI, thereby mimicking a false positive finding. Fourteen patients received tPA during the intervening period between initial WB-CTP and follow-up DW-MRI, where nine of these patients had positive ischemic findings on WB-CTP. However, none of the patients who received tPA had completely reversible deficits on WB-CTP, and all of them were found to have infarcts on follow-up MRI. None of the false positive patients in our study had received tPA. Therefore, the bias introduced by tPA administration in this study was negligible.
Despite the stated limitations, a strength of this study is the use of a large sample size from a standard tertiary care acute stroke practice. Overall, the results of this study suggest that that WB-CTP may be an accurate add-on test for identification of patients with true ischemic events in a suspected minor stroke population, but it is not sufficiently sensitive to rule out ischemic events.
Further prospective studies are needed to assess the influence of lesion size and specific perfusion parameters on the diagnostic performance of WB-CTP for ischemic stroke, as well as how this information might influence clinical decision-making and whether it modifies clinical outcomes for these patients.
Conclusion
In our study, positive WB-CTP findings performed moderately well for predicting eventual cerebral infarction in patients with vague clinical presentation requiring imaging follow-up, suggesting the presence of acute ischemia at the time of presentation. In the right clinical context, the ability to detect true ischemic events may help establish a diagnosis, thereby supporting the initiation of an appropriate treatment plan. A negative WB-CTP result, however, does not reliably exclude the possibility of a minor stroke and cannot independently justify withholding thrombolytic therapy. Although it may offer some value as an adjunctive test for improving confidence in offering stroke treatment, the modest sensitivity and specificity of WB-CTP for stroke detection in patients with minor neurological symptoms limit its utility as an independent diagnostic tool.
Appendix 1. Vascular territories of abnormality
Table 2.
Vascular territory of abnormality on CTP versus follow-up DW-MRI in patients with confirmed cerebral infarction at follow-up (n = 80).
| Sex | Age | NIHSS | Vascular territory of CTP abnormality | Vascular territory of DW-MRI abnormality | Congruity of imaging modalities |
|---|---|---|---|---|---|
| Male | 72 | 4 | Left global hemisphere | Left hemisphere scattered Infarcts | Congruent |
| Male | 55 | 1 | Left ACA | Left MCA | Region discrepancy |
| Male | 73 | 5 | Right MCA and PCA | Right MCA | Congruent |
| Male | 37 | 5 | Left MCA | Left MCA | Congruent |
| Female | 46 | 3 | Left MCA | Left MCA | Congruent |
| Male | 46 | 5 | Right MCA | Right MCA | Congruent |
| Male | 51 | 4 | Left MCA | Left MCA | Congruent |
| Female | 51 | 3 | Left MCA | Left MCA | Congruent |
| Female | 64 | 2 | Left MCA | Left MCA | Congruent |
| Male | 65 | 3 | Left MCA | Left MCA | Congruent |
| Female | 69 | 2 | Left MCA | Left hemisphere scattered infarcts | Region discrepancy |
| Male | 71 | 5 | Left MCA | Left MCA | Congruent |
| Male | 72 | 5 | Left MCA | Left MCA | Congruent |
| Male | 79 | 2 | Left MCA | Left MCA | Congruent |
| Female | 81 | 3 | Left MCA | Left MCA | Congruent |
| Female | 82 | 3 | Left MCA | Left MCA | Congruent |
| Female | 87 | 2 | Left MCA | Left MCA | Congruent |
| Female | 96 | 1 | Left MCA | Left MCA | Congruent |
| Female | 49 | 3 | Right MCA | Right MCA | Congruent |
| Male | 52 | 5 | Left MCA | Left MCA | Congruent |
| Female | 64 | 3 | Right MCA | Left MCA | Side discrepancy |
| Female | 83 | 5 | Right MCA | Right MCA | Congruent |
| Female | 77 | 1 | Left MCA | Left MCA | Congruent |
| Male | 51 | 4 | Bilateral SCA | Bilateral SCA | Congruent |
| Male | 86 | 0 | Bilateral PCA | Bilateral PCA | Congruent |
| Male | 50 | 1 | Left PCA | Left PCA | Congruent |
| Female | 62 | 3 | Right PCA | Basilar | Region discrepancy |
| Female | 73 | 4 | Right PCA | Right PCA | Congruent |
| Male | 88 | 3 | Right PCA | Right PCA | Congruent |
| Male | 77 | 3 | Bilateral PCA | Bilateral PCA | Congruent |
| Female | 86 | 3 | Basilar | Basilar | Congruent |
| Female | 64 | 4 | Right MCA | Right MCA | Congruent |
| Male | 69 | 2 | Basilar | Basilar | Congruent |
| Male | 74 | 4 | Right PICA | Right PICA | Congruent |
| Male | 76 | 0 | Right PCA | Right MCA | Region discrepancy |
| Male | 47 | 1 | Left MCA | Left MCA | Congruent |
| Female | 50 | 4 | Right SCA | Right SCA | Congruent |
| Female | 51 | 4 | Bilateral ACA/MCA | Bilateral ACA/MCA | Congruent |
| Male | 60 | 3 | Right MCA | Right MCA | Congruent |
| Male | 66 | 1 | Left MCA | Basilar | Region discrepancy |
| Male | 67 | 0 | Right MCA | Right MCA | Congruent |
| Female | 73 | 3 | Basilar | Basilar | Congruent |
| Male | 73 | 1 | Left MCA | Left MCA | Congruent |
| Female | 75 | 1 | Right SCA | Right SCA | Congruent |
| Male | 83 | 1 | Left MCA | Left SCA | Region discrepancy |
| Male | 86 | 3 | Left ACA | Left ACA | Congruent |
| Female | 88 | 2 | Left MCA | Left PCA | Region discrepancy |
| Male | 73 | 2 | Right MCA | Right MCA | Congruent |
| Male | 68 | 2 | No perfusion defects | Scattered, tiny, bilateral hemispheres | False negative |
| Female | 64 | 2 | Left MCA | Left MCA | Congruent |
| Male | 68 | 2 | No perfusion defects | Right MCA | False negative |
| Female | 78 | 1 | No perfusion defects | Basilar | False negative |
| Male | 61 | 5 | No perfusion defects | Right PICA | False negative |
| Male | 66 | 0 | No perfusion defects | Scattered, tiny, bilateral hemispheres | False negative |
| Male | 68 | 0 | No perfusion defects | Scattered, tiny, bilateral hemispheres | False negative |
| Male | 41 | 1 | No perfusion defects | Left AChA | False negative |
| Male | 43 | 5 | No perfusion defects | Left PCA | False negative |
| Male | 54 | 4 | No perfusion defects | Left PCA | False negative |
| Male | 55 | 2 | No perfusion defects | Left PCA | False negative |
| Female | 58 | 5 | No perfusion defects | Scattered, tiny, bilateral hemispheres | False negative |
| Female | 58 | 0 | No perfusion defects | Left ACA | False negative |
| Female | 59 | 2 | No perfusion defects | Left PCA | False negative |
| Male | 60 | 2 | No perfusion defects | Right PCA | False negative |
| Male | 66 | 2 | No perfusion defects | Basilar | False negative |
| Male | 66 | 4 | No perfusion defects | Left PCA | False negative |
| Female | 68 | 4 | No perfusion defects | Right SCA | False negative |
| Male | 69 | 2 | No perfusion defects | Basilar | False negative |
| Male | 70 | 0 | No perfusion defects | Left PICA | False negative |
| Female | 73 | 2 | No perfusion defects | Left MCA | False negative |
| Male | 79 | 5 | No perfusion defects | Right PICA | False negative |
| Male | 80 | 3 | No perfusion defects | Left MCA | False negative |
| Female | 80 | 2 | No perfusion defects | Scattered, tiny, bilateral hemispheres | False negative |
| Male | 81 | 3 | No perfusion defects | Scattered, tiny, bilateral hemispheres | False negative |
| Male | 84 | 5 | No perfusion defects | Bilateral MCA | False negative |
| Male | 90 | 3 | No perfusion defects | Bilateral MCA | False negative |
| Female | 92 | 4 | No perfusion defects | Left PCA | False negative |
| Male | 76 | 3 | No perfusion defects | Left MCA/PCA | False negative |
| Male | 40 | 4 | No perfusion defects | Right MCA | False negative |
| Male | 69 | 2 | No perfusion defects | Left PCA | False negative |
| Female | 58 | 2 | No perfusion defects | Scattered, tiny, bilateral hemispheres | False negative |
ACA: anterior cerebral artery; AChA: anterior choroidal artery; CTP: computed tomography perfusion; DW-MRI: diffusion-weighted magnetic resonance imaging; MCA: middle cerebral artery; NIHSS: National Institutes of Health Stroke Scale; PCA: posterior cerebral artery; PICA: posterior inferior cerebellar artery; SCA: superior cerebellar artery.
Funding
Financial support for this research was received in the form of a stipend from the University of Ottawa Summer Studentship Program.
Conflict of interest
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
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