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ence of an intracranial occlusion (RR 9.6, 95% CI 4–22). Sites of occlusion were as follows: intracranial internal carotid artery (ICA) 12/52 (23%), middle cerebral artery (MCA) 31/52 (60%; MCA-M1 7/52; MCA-M2 15/52; MCA-M3 9/52), posterior cere-bral artery (PCA) 5/52 (10%; PCA-P1 3/52, PCA-P2 2/52), and basilar artery (BA) 2/52 (4%). Detailed sites of occlusion and pro-gression rates are shown in table 1 . Our analysis was limited due to the small number of patients in each group, but neurological worsening was seen in patients with both proximal and distal ves-sel occlusions.In this retrospective sub-study of the CATCH study [2], we did not find any clear pattern in the site of vessel occlusion and risk of stroke progression. This finding leads us to suggest that studies us-ing intracranial occlusion as an entry criterion in a TIA and minor stroke population should not exclude patients based simply on oc-clusion location. Finally, this study did not allow us to determine the mechanism explaining neurological deterioration, although we suspect that hemodynamic fluctuations [7] or support by the col-lateral circulation play a determinant role. Future studies could further analyze the relationship between site of occlusion, collat-eral circulation, and symptom progression. Patients affected by TIA and minor stroke are at a high risk of recurrent events, symptom progression, and disability, especially if an intracranial occlusion is documented on a CT-angiogram (CTA) [1, 2] . Despite a risk of poor outcome, these patients are often excluded from thrombolysis treatment because of mild or improving symptoms [3] . Recurrent events are phenomenologi-cally either distinct recurrent strokes or symptomatic progression of the presenting event [4]. Unlike in major stroke, where proximal occlusion is an independent predictor [5] , it remains unclear whether the exact site of vessel occlusion influences outcome in TIA and minor stroke patients [6]. Our aim was to explore the re- lationship between the location of intracranial occlusion and stroke progression in this population. The CATCH study [2] prospectively enrolled consecutive pa-tients with minor stroke (NIHSS 1 or were treated with thrombolysis for this event. All patients had a brain CT and CTA of neck and circle of Willis within 24 h of symptom onset. A neuroradiologist identified the site of vessel occlusion. Stroke progression was defined as clin-ical worsening referable to the same arterial territory as the base-line symptoms without any imaging evidence of a new infarct sep-arate from the baseline imaging [4] . Experienced stroke neurolo-gists assessed the outcomes within 24 h of the index event. The relationship between vessel occlusion site and stroke progression was explored. If a patient had more than one intracranial occlu-sion, the most proximal site was used for analysis. Fisher’s exact test was used to compare proportions, and interpreted with a Bon-ferroni correction for multiple comparisons. For each individual comparison, patients with other sites of intracranial occlusion were removed from the analysis. 510 patients were enrolled. Intracranial occlusion was ob-served in 10% (52/510) of patients. Overall, stroke progression occurred in 4% (19/510) and was more likely to occur in the pres

Background: The assortment of patients based on the underlying pathophysiology is central to preventing recurrent stroke after a transient ischemic attack and minor stroke (TIA-MS). The causative classification of stroke (CCS) and the A-S-C-O (A for atherosclerosis, S for small vessel disease, C for Cardiac source, O for other cause) classification schemes have recently been developed. These systems have not been specifically applied to the TIA-MS population. We hypothesized that both CCS and A-S-C-O would increase the proportion of patients with a definitive etiologic mechanism for TIA-MS as compared with TOAST. Methods: Patients were analyzed from the CATCH study. A single-stroke physician assigned all patients to an etiologic subtype using published algorithms for TOAST, CCS and ASCO. We compared the proportions in the various categories for each classification scheme and then the association with stroke progression or recurrence was assessed. Results: TOAST, CCS and A-S-C-O classification schemes were applied in 469 TIA-MS patients. When compared to TOAST both CCS (58.0 vs. 65.3%; p < 0.0001) and ASCO grade 1 or 2 (37.5 vs. 65.3%; p < 0.0001) assigned fewer patients as cause undetermined. CCS had increased assignment of cardioembolism (+3.8%, p = 0.0001) as compared with TOAST. ASCO grade 1 or 2 had increased assignment of cardioembolism (+8.5%, p < 0.0001), large artery atherosclerosis (+14.9%, p < 0.0001) and small artery occlusion (+4.3%, p < 0.0001) as compared with TOAST. Compared with CCS, using ASCO resulted in a 20.5% absolute reduction in patients assigned to the ‘cause undetermined' category (p < 0.0001). Patients who had multiple high-risk etiologies either by CCS or ASCO classification or an ASCO undetermined classification had a higher chance of having a recurrent event. Conclusion: Both CCS and ASCO schemes reduce the proportion of TIA and minor stroke patients classified as ‘cause undetermined.' ASCO resulted in the fewest patients classified as cause undetermined. Stroke recurrence after TIA-MS is highest in patients with multiple high-risk etiologies or cryptogenic stroke classified by ASCO.