ASCOD Algorithm for Ischemic Stroke

Grades of predefined ASCOD phenotypes: Finding ASCOD Grade Workup is insufficient to grade the disease 9 Disease is present and potentially a cause 1 Disease is present but causal link is uncertain 2 Disease is present but causal link is unlikely 3 Disease is absent 0 Specific definitions: A: Causality grades for atherothrombosis A9: Incomplete workup Ultrasound (Duplex or TCD), angiogram (CTA, MRA, or conventional), or autopsy not performed (a minimum workup is extra- and intracranial assessment of cerebral arteries - maximum workup also includes transesophageal assessment of the aortic arch (or a default CTA of the aortic arch)) A1: Potentially causal (atherothrombotic stroke) 50-99% ipsilateral atherosclerotic stenosis in intra/extracranial artery supplying the ischemic field Ipsilateral atherosclerotic stenosis <50% in intra/extracranial artery with endoluminal thrombus supplying ischemic field Mobile thrombus in aortic arch Ipsilateral arterial occlusion in intra/extracranial artery with evidence of underlying atherosclerotic plaque supplying ischemic field A2: Causal link uncertain 30-50% ipsilateral atherosclerotic stenosis in intra/extracranial artery supplying the ischemic field Aortic plaque ≥4 mm without mobile lesion A3: Causal link unlikely but disease is present <30% stenosis in intra/extracranial artery ipsilateral to infarct area Aortic plaque <4 mm without mobile thrombus Stenosis (any degree) or occlusion in a cerebral artery not supplying infarct area (e.g. contralateral side, opposite circulation) History of MI, coronary revascularization, or peripheral arterial disease 50-99% ipsi/bilateral atherosclerotic stenosis with bihemispheric MR-DWI lesion A0: Atherosclerosis not detected and ruled out Any of the following done and negative for extracranial arterial stenosis: duplex US, CTA, MRA, conventional angiogram, or autopsy Any of the following done and negative for intracranial arterial stenosis: transcranial Doppler US, MRA, CTA, conventional angiogram, or autopsy TEE with specific assessment of the aortic arch (when the probe is pulled back at end of cardiac examination, turn probe counterclockwise and watch aortic arch), or specific aortic arch assessment with CTA to rule out aortic arch atheroma S: Causality grades for small-vessel disease S9: Incomplete workup MRI or CT not done S1: Potentially causal Lacunar infarction, defined as small deep infarct <15 mm in perforator branch territory on MRI-DWI or default CT in area corresponding to symptoms, plus ≥1 of the following: ≥1 small deep older infarct(s) of lacunar type in other territories Severe (confluent/Fazekas III) leukoaraiosis, or microbleeds, or severe dilatation of perivascular spaces (‘état criblé’) Repeated, recent (<1 month), TIAs attributable to the same territory as the index infarct S2: Causal link uncertain Only one recent lacunar infarction and no other abnormality on MRI/CT Clinical syndrome suggestive of deep branch artery stroke, without ischemic lesion in appropriate area on MRI/CT (main clinical syndrome suggesting a deep branch artery/lacunar stroke: pure hemiparesis, pure hemisensory loss, ataxic hemiparesis, dysarthria-clumsy hand syndrome, unilateral sensorimotor deficit, others: hemichorea, hemiballism, pure dysarthria, etc) S3: Causal link unlikely, but disease is present Severe (confluent/Fazekas III) leukoaraiosis visible on MRI and/or CT scan, and/or microbleeds visible on T2-weighted MRI, and/or severe dilatation of perivascular spaces (visible on T2-weighted MRI), and/or one or several old, small deep infarcts of lacunar type S0: Small-vessel disease not detected Negative MRI (T2, FLAIR, GRE, DWI) and no clinical syndrome suggestive of deep branch artery stroke C: Causality grades for cardiac pathology C9: Incomplete workup Minimum is EKG and examination by trained cardiologist in absence of cardiac imaging C1: Potentially causal Acute cardiogenic stroke, or recent stroke and older bihemispheric, supra/infratentorial territorial, or cortical ischemic lesions and signs of systemic embolism with ≥1 of the following: Mitral stenosis (surface area <1.5 cm²) Mechanical valve MI within 4 weeks before stroke Mural thrombus in the left cavities Left ventricular aneurysm History or presence of documented afib (paroxysmal (>60 seconds), persistent, or permanent) or flutter, with or without left atrial thrombus or spontaneous echo Atrial disease (tachy-brady syndrome) Dilated or hypertrophic cardiomyopathies Left ventricle ejection fraction <35% Endocarditis Intracardiac mass PFO and thrombus in situ PFO and concomitant PE or proximal DVT preceding the index stroke Aforementioned cardiac pathologies (C1) with single or without obvious cerebral ischemic lesion C2: Causal link is uncertain (one of the following, regardless of stroke pattern) PFO and atrial septal aneurysm PFO and PE or proximal DTV concomitant but NOT preceding the index stroke Intracardiac spontaneous echo-contrast Apical akinesia of the left ventricle and decreased ejection fraction (but >35%) History of MI or palpitation and multiple brain infarction, repeated either bilateral or in two different arterial territories (e.g. both anterior and posterior circulation) No direct cardiac source identified, but multiple brain infarction, repeated either bilateral or in two different arterial territories (e.g. both anterior and posterior circulation) and/or evidence of systemic emboli: renal or splenic or mesenteric infarction (on CT, MRI, or autopsy) or embolism in peripheral artery supplying arm or leg C3: Causal link unlikely but disease is present (one of the following abnormalities present in isolation) PFO, ASA , strands, mitral annulus calcification, aortic valve calcification, nonapical akinesia of left ventricle, transient afib <60 sec, or atrial hyperexcitability C0: Cardiac pathology not detected or not suspected Ruling out a cardiac source of embolism: minimum is negative EKG and examination by a cardiologist; maximum is negative EKG/telemetry/24-hour Holter EKG/long-term EKG recording (implantable device, transtelephonic EKG, loop recorder), negative TEE for atrium, valves, and septal abnormalities, negative TTE for PFO and assessment of left ventricle, negative cardiac CT/MRI, and negative abdominal CT/MRI (search for old or simultaneous subdiaphragmatic visceral infarction) O: Causality for other causes O9: Incomplete workup Unable to reasonably exclude other causes based on best available diagnostic tests and stroke-specific history O1: Potentially causal Dolichoectasia with complicated aneurysm Polycythemia vera or thrombocythemia >800,000/mm³ Systemic lupus Disseminated intravascular coagulation Antiphospholipid antibody syndrome (including >100 GPL units or lupus anticoagulant) Fabry’s disease Coexisting meningitis Sickle cell disease Ruptured intracranial aneurysm with or without vasospasm of the artery supplying the infarcted area Severe hyperhomocysteinemia Horton’s disease Other cerebral inflammatory or infectious angiitis Moyamoya disease, etc. O2: Causal link is uncertain Saccular aneurysm (with suspicion of embolism) Coincidental migraine attack with neurological deficit lasting >60 min in patients with history of migraine aura O3: Causal link is unlikely but disease is present Arteriovenous malformation Thrombocytosis <800,000/mm³ Antiphospholipid antibody <100 GPL units Homocysteinemia <40 μmol/L Malignoma with associated hypercoagulation (high D-dimer levels), DVT/PE and/or recent chemotherapy O0: Cardiac pathology not detected or not suspected Ruling out other causes: negative: CSF , complete hemostasis, cerebral arterial imaging, family history of inherited disease, inflammatory markers ( ESR and CRP ), hematologic tests (platelet, leukocytes, and eosinophilic counts; hematocrit), specific tests according to suspected disease (e.g. genetic test, retinal angiography for Susac syndrome) D: Causality grades for dissection D9: Incomplete workup In patients <60 years old and no evidence of A1, A2, S1, C1, or O1 category: no fat-saturated MRI performed on the extra/intracranial artery supplying the ischemic field or no x-ray angiography performed (all performed within 15 days of symptom onset) D1: Potentially causal 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 Arterial dissection by indirect demonstration or by less sensitive/less specific diagnostic test (only long arterial stenosis beyond 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 D2: Causal link uncertain Arterial dissection by weak evidence (suggestive clinical history, e.g. painful Horner’s syndrome or past history of arterial dissection) Imaging evidence of fibromuscular dysplasia of a cerebral artery supplying ischemic field D3: Causal link unlikely but disease is present Kinking or dolichoectasia without complicated aneurysm or plicature Fibromuscular dysplasia on arteries not supplying ischemic field D0: 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 three days of symptom onset can be falsely negative and then should be repeated). If no clinical suspicion of dissection, patient can be classified D0 provided good-quality extra/intracranial cerebral artery and cardiac evaluations have been done