Mechanisms of single and multiple borderzone infarct: transcranial Doppler ultrasound/magnetic resonance imaging correlates.
OBJECTIVE
Hemodynamic patterns after borderzone (BZ) infarction are variable and dynamic. However, stroke mechanisms in different types of BZ infarctions have not been systematically studied by magnetic resonance angiography (MRA) and transcranial Doppler ultrasonography (TCD).


METHODS
Forty-nine patients who experienced a stroke limited to the territory of either the superficial or internal borderzone proved on MRI included in our registry, corresponding to 4% of 1,200 patients with ischemic stroke, were studied. All these patients underwent MRA, extracranial Doppler ultrasonography, TCD and other investigations from the standard protocol of our registry. Twenty of them (41%) had a posterior BZ infarct, 14 (29%) an anterior BZ infarct, 10 (20%) a subcortical BZ infarct and 5 (10%) bilateral BZ infarcts.


RESULTS
Unilateral internal carotid artery (ICA) tight stenosis or occlusion ipsilateral to the lesion was present in 14 patients (70%) with a posterior BZ infarct, in 72% of those with an anterior BZ infarct, in 80% of those with a subcortical BZ infarct and in 80% of those with bilateral BZ infarcts. TCD showed cross-filling of the middle cerebral artery via the anterior communicating artery in 5 patients (25%) with a posterior BZ infarct and 10% had an increased mean flow velocity (MFV) in the ipsilateral P1 posterior cerebral artery (PCA). In patients with an anterior BZ infarct, 3 (23%) had an MFV increase in the contralateral A1 anterior cerebral artery (ACA), and 2 (15%) had a higher MFV in the ipsilateral PCA. An elevated velocity at midline depths with reversed A1 ACA flow direction was seen in 2 patients (20%) with a subcortical infarct, and 1 patient (10%) had an MFV increase in the ipsilateral P1 PCA. Left ventricular systolic dysfunction (ejection fraction <40%) was present in 50% of patients with a posterior BZ infarct, in 36% of those with an anterior BZ infarct, in 20% of those with a subcortical BZ infarct and bilateral BZ infarcts each.


CONCLUSIONS
The association of severe ICA stenosis or occlusion with cardiopathies and left ventricular dysfunction may play a critical role in those with BZ infarcts having inadequate collateral supply, while a cardioembolism or acute ICA dissection may also cause BZ infarction due to the rapidity of the occlusive process and the inability of the cerebral vasculature to recruit collateral pathways quickly enough.
Kumral
Emre
E
Stroke Unit, Neurology Department, Ege University, Izmir, Turkey. ekumral@med.ege.edu.tr
Bayülkem
Gamze
G
Sağcan
Abdi
A
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016893:Carotid Stenosis / Q000000981:diagnostic imaging / Q000473:pathology; D002544:Cerebral Infarction / Q000000981:diagnostic imaging / Q000209:etiology / Q000473:pathology*; D002560:Cerebrovascular Circulation; D005260:Female; D006321:Heart / Q000503:physiopathology; D006334:Heart Function Tests; D006801:Humans; D020243:Infarction, Anterior Cerebral Artery / Q000000981:diagnostic imaging / Q000473:pathology; D020244:Infarction, Middle Cerebral Artery / Q000000981:diagnostic imaging / Q000473:pathology; D020762:Infarction, Posterior Cerebral Artery / Q000000981:diagnostic imaging / Q000473:pathology; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D012306:Risk; D020521:Stroke / Q000000981:diagnostic imaging / Q000473:pathology; D017585:Ultrasonography, Doppler, Transcranial; D016277:Ventricular Function, Left / Q000502:physiology