1) Provide a brief review of CNS vasculopathies highlighting the key diagnostic features. 2) Review pertinent differential diagnoses of neuroimaging cases. 3) Provide important imaging pearls for differentiating CNS vasculopathies.

A review of of CNS vasculopathies highlighting the key diagnostic features will be provided. The pertinent differential diagnoses of neuroimaging cases will be reviewed. Important imaging pearls for differentiating CNS vasculopathies will be provided.

To assess the contribution of high-resolution T2-weighted vessel wall MR (VWI) sequences for differential diagnosis of intracranial vasculopathies.

Consecutive patients with intracranial arterial stenosis who had undergone 3T high-resolutioin MR VWI were retrospectively selected. 2D T2-weighted sequences (.4 x .4 mm in-plane resolution, 1 mm thick slices) were scanned and assessed in both axial plane and a plane perpendicular to the artery lumen. Relative vessel wall thickness, eccentricity of disease and signal characteristics were assessed in areas of arterial stenosis or irregularity as seen on luminal imaging by a double blinded rater. Classification of patients was based on the following clinical and imaging criteria: atherosclerosis (>2 atherosclerosis risk factors without evidence of systemic or CSF inflammation or clinical evidence of vasospastic process/reversibility), vasculitis (clinical evidence of CSF infection/inflammation and/or systemic inflammatory disease without atherosclerosis risk factors or clinical evidence of vasospastic process) and reversible cerebral vasoconstriction syndrome (RCVS) (classic clinical presentation, with reversibility of the imaging findings and no evidence of systemic or CNS inflammatory disease).

There were 21 atherosclerosis cases with 45 plaques, 4 vasculitis cases (VZV, PACNS, TB and Behcet vasculitis) with 14 stenoses and 4 RCVS cases with 19 stenoses that could adequately be assessed on T2-weighted VWI. A linear T2 hyperintense band along the intimal surface (presumed to represent fibrous cap) was seen in 36/45 atherosclerotic, 0/14 vasculitic and 0/19 RCVS lesions. All of the atherosclerotic lesions showed appreciable wall thickening, as compared to 11/14 vasculitis and 4/19 RCVS lesions. 42/45 atherosclerotic plaques, 2/14 vasculitis and 2/19 RCVS lesions showed eccentric wall thickening.

High resolution T2-weighted VWI can complement T1 and PD pre and post-contrast VWI for the differentiation of intracranial stenosing vasculopathy, based on disease eccentricity, presence of a T2 hyperintense intimal band and appreciable wall thickening.

High-resolution T2 VWI should be incorporated into intracranial VWI protocols, as this technique can provide complementary information to T1 and PD-weighted techniques.

2D-T1w black-blood sequences are used in atherosclerotic plaque imaging and for the assessment of inflammatory changes of intracranial vessels. However, sequences are limited due to long acquisition times which limits the number of acquired slices and thus the coverage (coverage often 3 cm or less). Aim of the study was to evaluate a commercially not available gadolinium-enhanced isotropic 3D-whole-brain-black-blood T1w-TSE sequence with variable flip angles (T1w-VISTA) for the diagnosis of intra- and extracranial vasculitis.

We prospectively included 26 patients with suspected vasculitis, 3 patients with Sickle-cell disease and 15 tumor patients without any evidence of vascular disease. All patients received a standardized protocol (T1w pre- and post contrast, TOF, DIFF, T2, FLAIR) and a T1w 3D-BB-VISTA sequence pre- and post contrast (resolution=0.8 mm3 isotropic, scan time 4:43 minutes). Left and right arteries of the anterior and posterior circulation (176 segments) and right/left temporal artery (88 segments) were evaluated for the presence of stenosis, wall thickening (eccentric/concentric) and contrast enhancement of the vessel wall (3-point Likert scale).

6 out of 104 arterial segments in patients with suspected intracranial vasculitis (3x right/1x left middle cerebral artery, 1x right and left vertebral artery) and 6 out of 88 temporal arteries showed focal circumferential, concentric wall thickening, luminal narrowing and strong contrast enhancement These findings were found in 8 distinct patients in which vasculitis was clinically confirmed. One patient with sickle-cell disease presented with a stenosis and concentric wall thickening without contrast enhancement. None of the 60 arterial segments of the tumor patients showed vasculitis like lesions but 6 segments (distal vertebral artery) showed an eccentric wall thickening and none to moderate contrast enhancement due to atherosclerotic plaques.

Whole-brain-black-blood MRI is feasible in less than 5 minutes scan time and allows to accurately diagnosing CNS vasculitis and Horton's disease. Future studies will be necessary to evaluate the utility of this sequence for other vascular pathologies, such as arterial dissection and atherosclerosis.

Whole-brain-black-blood MRI is a relevant additional tool for diagnosing and monitoring cranial vasculitis.

We aimed to assess the ability of arterial spin labeling (ASL) to identify an impaired cerebrovascular reactivity (CVR) relative to single photon emission computed tomography (SPECT) in patients with moyamoya disease (MMD).

The institutional review board of our hospital approved this prospective study and written informed consent was obtained from all patients. We conducted a prospective study to determine the ability of ASL to identify CVR relative to SPECT in 78 subjects with MMD. Among these patients, 31 patients performed unilateral direct arterial anastomosis, and in these patients, follow up ASL perfusion MR and SPECT were performed additionally (for ASL, 1 weeks, 3 months, and 6 months after operation; for SPECT, 6 months after operation). Volumes of interests based on internal carotid artery territories were applied to the cerebral blood flow maps from the basal stress ASL and SPECT. And, the concordance between the CVR indexes (CVRIs) from ASL and SPECT was assessed using Bland-Altman analysis, and the area under the receiver-operating characteristic curve (AUC) was used to evaluate diagnostic accuracy of ASL relative to that of SPECT using various CVRI cutoff points.

The CVRI from ASL had a negative bias as compared to the CVRI from SPECT (systemic bias, -3.5%). In addition, the differences between the CVRI from ASL and SPECT tended to be larger when the CVRI is more impaired. The analysis of the diagnostic accuracy of ASL for detecting the impaired CVR revealed an AUC of 0.81 with a sensitivity of 81%, a specificity of 100%, a positive predictive value of 100%, and a negative predictive value of 12%. ASL performed in 6 months after anastomosis showed significant increase in CVRI than that performed preoperatively as well as SPECT (for ASL, -2.7 ± 7.3 and -11.2 ± 9.3, P < 0.001; for SPECT, -3.7 ± 2.9 and -6.2 ± 5.2, P = 0.013, respectively).

ASL can identify impaired CVR with excellent performance in patients with MMD and has the potential to serve as a non-invasive imaging tool for determining CVR in patients with cerebrovascular disease.

1. ASL can identify impaired CVR with excellent performance in patients with MMD

2. ASL has the potential to serve as a non-invasive imaging tool for determining CVR in patients with cerebrovascular disease.

The most devastating complication of sickle cell disease (SCD) is overt stroke, which occurs in more than 10% of children. Patients with cerebral blood flow velocities (CBFv) >200cm/s on Transcranial Doppler (TCD) are at highest risk of stroke. There are two models that explain how increased CBFv in SCD increases risk of stroke: the vasculopathy-stenosis and the hemodynamic insufficiency (HI) models. The stenosis model was originally used to attribute stroke onset to high CBFv. However, in the STOP trial, 79% of children with SCD had minor/no stenosis. This favours the HI model, which postulates that cerebral vessels have only a finite capacity to dilate, which is compromised in SCD due to chronic anemia. As a result it poises the cerebral vasculature for ischemia and subsequent stroke. The aim of the study was to investigate the HI model in children with SCD by quantifying the capacity of vasodilation using an MR- based cerebrovascular reactivity (CVR) defined as a change in cerebral blood flow (CBF) in response to a vasoactive stimulus. We hypothesize that CVR is reduced and correlates with the degree of anemia.

30 SCD patients (10-18 years) were imaged on a clinical MRI system. A hypercapnic challenge (CO2) was administered in synchrony with a blood-oxygen-level dependent (BOLD) MRI to measure relative CBF changes. Anatomical images were also acquired and reviewed by a radiologist to exclude with significant stenosis, large white matter lesions or vascular abnormalities. CVR maps were generated by correlating the BOLD MRI signal change with the corresponding CO2 values. Mean CVR values were then calculated based on gray and white matter segmentation. Hct values were obtained from hematology records. Pearson correlation coefficients were calculated for CVR and hct as well as CVR and CBF.

CVR demonstrated a moderately strong correlation with hct, r=0.68 (p=0.01). The correlation between CVR and gray matter CBF was moderately strong, r=-0.63 (p=0.021).

Our results show that CVR is associated with the degree of anemia in children with SCD who do not have a stenosis. This seems to support the HI model of stroke risk in this population.

The degree of anemia needs to be considered when assessing stroke risk in SCD. CVR seems to be superior to TCD measures of high CBFv, as CVR can fully describe the status of the cerebral vasculature.

1) Understand how to protocol imaging studies for a child with new onset of localized neurologic impairment and, in particular, when ultrasound or CT may be useful as opposed to performing MRI as the initial procedure. 2) Recognize which studies and, in particular, what sequences should be performed on MRI and in what order. 3) Understand the causes of pediatric stroke, which are different from those in adult stroke. 4) The stroke is easy to identify; to find the cause of the stroke is not easy in children, but will be easier after attending this session.

Localized stroke is an important cause of morbidity and mortality in childhood and one of the top ten causes of childhood death. Approximately 25% of all pediatric strokes occur in neonates and approximately 50% occur in children less than 1 year of age. Despite these numbers, the misconception remains that stroke is a rare and relatively unimportant illness in childhood. Fortunately, the medical community has recently become more aware of this entity and its importance in pediatric health. Presenting signs and symptoms depend upon the region of brain affected and the age of the patient at the time of the infarct. Perinatal/prenatal stroke is much more common than generally recognized, with a prevalence of 1 in 2300-5000 live births. Patients may present with neonatal encephalopathy or seizures or may remain undetected until early hand preference is manifested. In older children, presentation is one of abrupt onset of seizure or neurological deficit. Once a stroke is suspected, clinically or by imaging, it is imperative to determine whether hemorrhage is present in order to determine whether anticoagulation is in order. Vascular imaging is essential and in either case should be obtained with high resolution, as dissections and post-infectious vasculopathy can be extremely subtle and both require anticoagulation. If the stroke is hemorrhagic and if there are regions of increased diffusivity, venography should be obtained. If vasculopathy is suspected because of location of the infarct or history of recent illness, we obtain vascular wall imaging with 1mm partition size after administration of contrast to look for irregularity or enhancement of the arterial wall; the latter seems to be associated with inflammation. If dissection is identified in the vertebral artery at the upper cervical level, careful attention should be paid to anomalies of the upper cervical vertebrae that may stretch or damage the vessel with abrupt head motion, usually secondary to trauma.

1) Understand the concept of the diffusion-perfusion (DWI-PWI) mismatch concept in acute stroke. 2) Review the recent results of stroke trials using the DWI-PWI concept. 3) Appreciate the potential role of other markers, such as collateral flow, oxygenation, pH, and resting-state fMRI for assessing the ischemic brain.

In IMS-III trial patients, we evaluate if clot characteristics on baseline non-contrast CT (NCCT) or CT-angio (CTA) determine recanalization with IV-tPA using classification and regression tree analysis (CART).

IMS-III protocol is published. Two readers assessed clot characteristics on NCCT [hyperdense(HD) sign location, length, ratio of maximal Hounsfield Unit (HU) HDS/contralateral MCA (rHU)] and CTA [Clot burden score, length, residual flow through clot, ratio of contrast HU at proximal/distal clot interface (cirHU)] by consensus. Very early arterial weighted CTAs were excluded; appropriate imputation techniques used whenever distal clot interface was not measured. Early recanalization with IV-tPA was assessed on first angio (only in the endovascular arm) while 24-hour recanalization with IV-tPA was assessed on follow-up CTA (only in the IV-tPA alone arm).

Of 263 patients with anterior circulation clots on baseline CTA, after excluding patients with missing data, 64 in the IV-tPA and 175 in the endovascular arm were analyzed. CART models for early and 24-hr recanalization with IV-tPA are shown in Figures 1 and 2 respectively.

Clot characteristics on NCCT and CTA can help physicians estimate a range of early and late recanalization rates with IV-tPA.

Clot characteristics on both NCCT and CTA can help determine the effecay of tPA and should be considered when deciding to treat patients with tPA over endovascular.

Acute ischemic stroke studies emphasize a difference between reperfusion and recanalization but predictors of reperfusion have not been elucidated. This study aims to identify predictors of reperfusion and to investigate the relation between recanalization and reperfusion.

From the XXX trial 178 patients were selected with a middle cerebral artery territory perfusion deficit on admission CT perfusion (CTP) and complete day 3 follow-up CTP and CT-angiography (CTA). Reperfusion and recanalization were evaluated on the follow-up imaging. The association between reperfusion and recanalization was calculated using absolute and relative risks. Patient admission and treatment characteristics as well as admission CT imaging parameters regarding occlusion site and stroke severity were collected. Their association with complete reperfusion was analyzed using logistic regression.

Absolute risk for complete reperfusion was 0.60 in the complete recanalization group and 0.23 in the incomplete recanalization group, with a relative risk of 2.60 (CI 1.63-4.13), but around 40% showed a discrepancy between recanalization and reperfusion status. Lower clot burden (OR 1.35, CI 1.14-1.58), more distal thrombus location (OR 2.28, CI 1.18-4.39) and good collateral score (OR 2.84, CI 1.34-6.02) increased the odds of complete reperfusion whilst higher NIHSS score (OR 0.95, CI 0.90-1.00), larger infarct core size (OR 0.32, CI 0.15-0.69) and larger total ischemic area (OR 0.31, CI 0.15-0.67 for 2001-5000 mm2 and OR 0.16, CI 0.07-0.37 for >5000 mm2) decreased the odds of complete reperfusion. None of the patients with ipsilateral intracranial ICA occlusion showed complete reperfusion.

Recanalization and reperfusion are strongly related but not always equivalent in acute ischemic stroke. Lower clot burden, distal thrombus location, collateral score, NIHSS score, infarct core size and total ischemic area are predictors of reperfusion.

Lower clot burden, distal thrombus location, collateral score, NIHSS score, infarct core size and total ischemic area are predictors of reperfusion and can be used to aid treatment decisions in acute ischemic stroke patients.

Stroke poses a major health challenge in today's world. "Time is Brain" in stroke and every minute counts in stroke management. To what extent are we able to provide timely imaging to these patients globally and if not what can be done? Our aim was to survey radiologists across developing countries in Asia, Europe and South America to assess the stroke care and find out what in their opinion are the most effective ways to improvise imaging and management.

A standardized questionnaire containing 18 questions was sent to radiologists in 20 developing countries across the world. Radiologists from 18 countries responded (response rate=90%). These include Kenya, Algeria, Rwanda, Sri Lanka, Malaysia, Costa Rica, Macedonia, Bulgaria, Mexico, China, India, Uruguay, Burma and Venezuela among others.

Survey results indicated that most of the countries (72%), lack access to CT scanners. Intravenous tissue plasminogen activator (t PA) is the standard of care of ischemic stroke and cannot be given unless hemorrhage is excluded on CT. Also, this can only be administered for a specific time window after symptom onset. To maximize patients who can benefit from thrombolysis, the key is to have a short Emergency Room Door to CT scan time. Unfortunately, Door to CT scanner time is more than 30 minutes in 83% (95% CI being 80.5-85.4%). Moreover, 77% of the countries had shortage of the drug tPA. Overall, radiologists rated their knowledge as "average" in reading stroke imaging and 77% (95% CI being 74.5-79%) believed that further training would be helpful. Minority had access to Neurointerventionalist (33%) and Telestroke services (27%). When questioned about the three most powerful ways to improvise stroke imaging in their respective countries, the highest rated choices were: training prrograms on stroke imaging to improvise knowledge among radiologists, campaigns to increase awareness in the community and improvising access to CT.

This survey helps radiologists around the world communicate the imaging needs in stroke in their respective countries and how can they be met. This can help radiologists who want to reach out in their humanitarian efforts to improve imaging around the world.

Global outreach programs can use this survey to determine more effective ways of improving stroke imaging and care in developing countries.

The recent shift of endovascular treatment (ET) methods for acute ischemic stroke towards better outcome. We hypothesized that bigger core volume may be tolerable to further ET. This study was retrospectively designed to predict the prognosis using ADC volume in endovascular revascularization therapy for acute ischemic stroke.

Patients with acute ischemic stroke in anterior circulation territory and intra-arterial (IA) revascularization therapy were retrieved. ADC volume taken before the IA therapy was calculated quantitatively with the margin thresholds of ADC value as 700x10^-5 mm²/s. Futile prognosis was defined as modified Rankin Scale 5-6 at 3 months. We divided patients into 3 groups. Group 1 represented with ADC volume less than 50 cm³, group 2 with 50 to 100 cm³ and group 3 with more than 100 cm³. Baseline characteristics (age, initial NIHSS score), imaging data (successful revascularization, TICI 2a-3) and clinical outcomes (good outcome, mRS 0-2 at 3months; poor outcome, mRS 5-6) were compared among groups. Logistic regression and Receiver Operating Characteristic (ROC) curve analyses were done.

Finally, 76 patients were enrolled in this study. There is no difference of age and successful revascularization among the groups. Larger volume group show significantly high initial NIHSS score (p=0.027) and poor outcome (p < 0.001). ADC volume more than 100 cm3 was significantly associated with futile prognosis (p=0.001, Odds ratio, 25.4 [95%CI, 3.874-166.673]). The area under the ROC curve for ADC volumes was 0.675 (p=0.009). For predicting futile prognosis, sensitivity and specificity were 57.6% and 69.8% at ADC volume 50 cm3, 48.5% and 95.3% at 100 cm3 and 33.3% and 97.7% at 150 cm3, respectively.

A huge DWI volume was associated with the futile prognosis. This imaging marker, however, could not be a single sign for stopping further aggressive IA treatment for acute ischemic stroke because the area under the ROC curve was relatively small. When IA therapy is considered, well known harmful factors including old age, high NIHSS score and huge ADC volume should be combined altogether for 'no more to go'.

Recent progress of ET methods might be attributed to a tolerance of bigger ADC volume than previously recommended.

1) Assess the impact of recent stroke clinical trials. 2) Compare the outcomes with various thrombectomy devices. 3) Develop a simple systematic approach to thrombectomy.