Convexal subarachnoid hemorrhage and acute ischemic stroke: a border zone matter?

Abstract

Background Convexal subarachnoid hemorrhage (c-SAH) is an infrequent condition with variable causes. c-SAH concomitant to acute ischemic stroke (AIS) is even less frequent, and the relationship between the two conditions remains unclear. Methods Between January 2016 and January 2018, we treated four patients who were referred to our stroke unit with ischemic stroke and concomitant nontraumatic c-SAH. The patients underwent an extensive diagnostic workup, including digital subtraction angiography (DSA). Results All four patients developed acute focal neurological symptoms with restricted MRI diffusion in congruent areas. In three of the patients, infarcts were in a border zone between the main cerebral arteries and c-SAH was nearby. The fourth patient showed a small cortical infarct, and c-SAH was in a border zone territory of the contralateral hemisphere. An embolic source was discovered or strongly suspected in all cases. One patient was treated with intravenous thrombolysis, but this treatment was not related to c-SAH. None of the four patients showed microbleeds or further cortical siderosis, thus excluding cerebral amyloid angiopathy. In addition, DSA did not show signs of vasculitis, reversible cerebral vasoconstriction syndrome, or intracranial arterial dissection. Conclusions We proposed the embolism or hemodynamic changes of the border zone arterioles as a unifying pathogenetic hypothesis of coexisting c-SAH and AIS.

Acute ischemic stroke and convexity subarachnoid hemorrhage in large vessel atherosclerotic stenosis: Case series and review of the literature

“…Contralateral cSAH is much rarer than ipsilateral and may have slightly different underlying pathophysiology. It is well documented that chronic ICA stenosis causes several compensatory mechanisms to maintain blood flow to the brain 5 . One compensatory mechanism is the contralateral dilatation of vasculature in order to preserve blood flow as explained previously.…”

“…It is well documented that chronic ICA stenosis causes several compensatory mechanisms to maintain blood flow to the brain. 5 One compensatory mechanism is the contralateral dilatation of vasculature in order to preserve blood flow as explained previously. However, this compensatory mechanism can be harmful if the vessels expand beyond physiological limits leading to increased vessel fragility and rupture.…”

“…However, this compensatory mechanism can be harmful if the vessels expand beyond physiological limits leading to increased vessel fragility and rupture. 4 , 5 …”

“…In addition, another studied compensatory mechanism is the establishment of contralateral collateral circulation to maintain blood and perfuse the areas of the brain supplied by the occluded vessels. 5 Nonetheless, similar to dilated vessels, collateral vessels are usually fragile in structure, making them highly susceptible to rupture, causing hemorrhage in the form of cSAH. 4 , 5 …”

The clinical and neuroradiological features of patients of coexisting atraumatic convexity subarachnoid hemorrhage and large artery atherosclerosis stroke

“…The mainstream theory is that long-standing severe stenosis or occlusion of ICA results in rupture of dilated fragile collateral pal vessels, accompanied by emboli entering into marginally perfused vessels leading to necrosis and rupture. [ 8 , 11 , 12 ] Another possible explanation is that systemic disturbances, such as a sudden rise in blood pressure or a coagulation disorder in the predamaged vessels, may promote the occurrence of c-SAH. [ 3 ] The site of the severe stenosis or occlusion of large artery may occur both intracranially and extracranially, especially for extracranial segment of ICA.…”