0 |
No dissection detected or suspected. Ruling out dissection: negative FAT-saturated MRI of suspected artery or good quality, normal X-ray angiography (too early FAT-saturated MRI performed within 3 days of symptom onset can be falsely negative and then should be repeated). If there is no clinical suspicion of dissection, the patient can be classified D0 provided good-quality extra- or intracranial cerebral artery and cardiac evaluations have been performed |
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No dissection detected or suspected. Ruling out dissection: negative FAT-saturated MRI of suspected artery or good quality, normal X-ray angiography (too early FAT-saturated MRI performed within 3 days of symptom onset can be falsely negative and then should be repeated). If there is no clinical suspicion of dissection, the patient can be classified D0 provided good-quality extra- or intracranial cerebral artery and cardiac evaluations have been performed |
1 |
Potentially causal. (1) arterial dissection by direct demonstration (evidence of mural hematoma: hypersignal on FAT-saturated MRI or at autopsy or on TOF-MRA or CT on axial sections showing both enlargement of the arterial wall by the hematoma with narrowing of the lumen or on echography showing an hypoechoic arterial wall with narrowing of the lumen and sudden enlargement of the carotid or vertebral (V2) artery diameter, (2) arterial dissection by indirect demonstration or by less sensitive or less specific diagnostic test (only long arterial stenosis beyond the carotid bifurcation or in V2, V3 or V4 without demonstration of arterial wall hematoma: on X-ray angiography, and/or echography and/or CTA and/or MRA) or unequivocal US with recanalization during follow-up |
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Potentially causal. (1) arterial dissection by direct demonstration (evidence of mural hematoma: hypersignal on FAT-saturated MRI or at autopsy or on TOF-MRA or CT on axial sections showing both enlargement of the arterial wall by the hematoma with narrowing of the lumen or on echography showing an hypoechoic arterial wall with narrowing of the lumen and sudden enlargement of the carotid or vertebral (V2) artery diameter, (2) arterial dissection by indirect demonstration or by less sensitive or less specific diagnostic test (only long arterial stenosis beyond the carotid bifurcation or in V2, V3 or V4 without demonstration of arterial wall hematoma: on X-ray angiography, and/or echography and/or CTA and/or MRA) or unequivocal US with recanalization during follow-up |
2 |
Causal link is uncertain. (1) arterial dissection by weak evidence (suggestive clinical history, e.g. painful Horner's syndrome or past history of arterial dissection), (2) imaging evidence of fibromuscular dysplasia of a cerebral artery supplying the ischemic field |
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Causal link is uncertain. (1) arterial dissection by weak evidence (suggestive clinical history, e.g. painful Horner's syndrome or past history of arterial dissection), (2) imaging evidence of fibromuscular dysplasia of a cerebral artery supplying the ischemic field |
3 |
Causal link is unlikely but the disease is present. (1) kinking or dolichoectasia without complicated aneurysm or plicature, (2) fibromuscular dysplasia on arteries not supplying the ischemic field |
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Causal link is unlikely but the disease is present. (1) kinking or dolichoectasia without complicated aneurysm or plicature, (2) fibromuscular dysplasia on arteries not supplying the ischemic field |
9 |
Incomplete workup. In patients aged less than 60 years and with no evidence of A1, A2, S1, C1, or O1 category: no FAT-saturated MRI performed on the extra- or intracranial artery supplying the ischemic field or no X-ray angiography performed (all performed within 15 days of symptom onset) |
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Incomplete workup. In patients aged less than 60 years and with no evidence of A1, A2, S1, C1, or O1 category: no FAT-saturated MRI performed on the extra- or intracranial artery supplying the ischemic field or no X-ray angiography performed (all performed within 15 days of symptom onset) |