Isolated acute nontraumatic cortical subarachnoid hemorrhage

Abstract

Our aim was to review the etiologic background of isolated acute nontraumatic cSAH. While SAH located in the basal cisterns originates from a ruptured aneurysm in approximately 85% of cases, a broad spectrum of vascular and even nonvascular pathologies can cause acute nontraumatic SAH along the convexity. Arteriovenous malformations or fistulas, cortical venous and/or dural sinus thrombosis, and distal and proximal arteriopathies (RCVS, vasculitides, mycotic aneurysms, Moyamoya, or severe atherosclerotic carotid disease) should be sought by noninvasive imaging methods or/and conventional angiography. Additionally, PRES may also be a source of acute cSAH. In elderly patients, cSAH might be attributed to CAA if numerous hemorrhages are demonstrated by GRE T2 images. Finally, cSAH is rarely observed in nonvascular disorders, such as abscess and primitive or secondary brain tumors.

Figures

Fig 1.

Imaging algorithm and main causes of cSAH.

Fig 2.

Cortical venous thrombosis. A, Axial GRE T2 image shows right central sulcus SAH (black arrowhead). B, Axial FLAIR image shows a thrombosed right cortical parietal vein (white arrowhead).

Fig 3.

Dural sinus thrombosis. A, Axial brain CT shows left peri-rolandic SAH. B, Axial FLAIR image confirms the sulcal hemorrhage, which is also visible more anteriorly (arrowhead). C, Sagittal contrast-enhanced T1 shows a filling defect in the superior sagittal sinus.

Fig 4.

RCVS. A, Axial brain CT scan shows bilateral frontoparietal sulcal SAH (white arrowheads). B, Axial FLAIR image confirms the cSAH (white arrowheads). C, Lateral projection of 3D TOF MRA shows multiple arterial stenoses and dilations, mainly on the anterior cerebral artery branches (white arrowheads). D, Lateral projection of a right internal carotid angiogram shows multiple stenoses and dilations on both anterior cerebral and middle cerebral arteries (black arrowheads). Note that DSA, even if it showed more clearly the arterial abnormalities, did not change the previously suspected diagnosis. Follow-up MRA performed at 3 months demonstrated disappearance of the arterial lesions (not shown).

Fig 5.

Endocarditis. A, Axial brain CT scan shows an isolated slight right frontal subarachnoid hyperattenuation. B, Because of clinical aggravation the next day, another brain CT was performed and demonstrated a larger right Sylvian SAH. Subsequent MR imaging showed a right middle cerebral artery infarction due to M1 occlusion (not shown), which precluded the exact identification of this SAH origin.

Fig 6.

Pial vasodilation. A, Axial GRE T2 image shows a left frontal sulcal SAH (black arrowhead), possibly located in the “watershed” territory between the anterior and the middle cerebral arteries. B, Axial maximum-intensity-projection reconstruction of CTA shows an asymmetry of the distal arteries, in favor of left pial vasodilation. C, Frontal projection of 3D angiography of the left carotid artery reveals a severe stenosis at the origin of the M2 branch (white arrowhead).

Fig 7.

Eclampsia-related PRES. A, Axial FLAIR image shows a left frontal SAH and a left parietal subcortical hyperintensity. B, Axial FLAIR image shows bilateral cerebellar hyperintensities, very suggestive of PRES lesions.

Fig 8.

CAA. A, Axial brain CT scan shows a subtle left rolandic hyperattenuation favoring minimal SAH (white arrowhead). B and C, Axial GRE T2 images show left temporal lobar hemorrhage, multiple microbleeds, and cortical hemosiderosis. D, Axial FLAIR image obtained after 7 months shows a new asymptomatic SAH in a left parietal sulcus (white arrowhead), which was previously normal (see B).