Table 1.
(1) Nature of presentation on admission and/or hospitalization history: |
Patient demographics (increasing age, female sex, Caucasian race, etc.)b |
Symptoms (headache, dizziness, blurring or decreased vision in one or both eyes, loss of balance or coordination and/or in combination with other symptoms, weakness, numbness, paralysis of the face, arm, or leg, commonly confinedto one side of the body, etc.)c |
Sudden onset of symptoms, with severity maximal at onset with or without subsequent rapid recovery |
Decreased level of consciousness at onset of event or upon presentation to hospital |
Association of seizure in relation to supratentorial cortical involvement and focal neurological presentation (although infrequent at onset and more common after gliotic scar formation)d |
Symptoms corresponding to the involvement of different/multiple focal cerebral areas |
Clinical evidence or signs established with neurologic testing suggesting focal neurological involvement consistent with lesions in multiple cereberovascular territories |
Symptomatic or clinical findingsof cortical or subcortical lesion that may be localized to specificterritories supplied by branches of the anterior, middle, and posterior cerebral arteries and absence of evidence of proximal vascular stenosis/occlusion |
Specificmiddle cerebral artery neurologic syndromes (opercular, brachial or hand plegia, isolated Broca's or Wernicke's aphasia and left visual neglect syndromes) |
Rapid recovery from major hemispheric deficits(“spectacular shrinking deficit” phenomenon, common with fibrinousthrombi or posttreatment/intervention) |
Absence of lacunar syndrome |
(2) Presence of major risk factors and/or correlates in medical history: |
AF or atrial flutter at time of presentationd |
History of atrial tachyarrhythmias |
Past TIA |
Past stroke |
History of blood dyscrasiasd |
Predisposing coronary vascular risk factors (CAD, HTN, etc.) |
Myocardial infarction (recent or at time of presentation) |
Known LVD or severe congestive heart failure during event |
Iatrogenic (cardiac or great vessel surgery, angiography, endovascular manipulation, intravascular device implantation)d |
Periprocedure risk of embolism (Valsalva‐provoking activity in patients with a patent foramen ovale and other right‐to‐left shunting causes)d |
(3) Presence of new infarct on CT and/or MRI: |
Infarct consistent with embolic lesion and/or able to be differentiated from a nonembolic ischemic lesion with or without known presenting history |
Lesion size and extent of involvement (unlikely involving both gray and white matter; large embolic infarct however may be suggestive of cardiac source) |
Distinguishable cortical or subcortical lesion localization to the territory supplied by the branches of the anterior, middle, and posterior cerebral arteries in the absence of evidence of proximal vascular stenosis/occlusion (beyond main branches) |
Radiographic evidence of embolic infarcts pertaining to multiple vascular territories or to the gray–white matter junction |
In the lenticulostriate or thalamogeniculate territories, lesions >1 cm suggestive of embolism |
Medial subthalamic and thalamic involvement suggestive of basilar artery lesion with corresponding symptoms (sudden sleepiness, impaired upward gaze, and bilateral ptosis) |
Cerebellar hemispheric infarction consistent with presenting symptoms |
Sparing involvement of the deep‐penetrating arteries (although microemboli from valvular sources can occlude small penetrating arteries)d |
aPrior to the identificationof a possible embolic source and in the absence of other etiologies at admission.
bPer outlines of the Lausanne Stroke Registry criteria.
cModifiedOxfordshire Community Stroke Project criteria.
dExcluded from study or were not factors among selected patients in sinus rhythm.