Can Convexity Subarachnoid Hemorrhage be Caused by Rupture of a Saccular Aneurysm?

Abstract

A 51-year-old female came to emergency service with
the complaint of a sudden-onset, one-hour-duration
long, witnessed episode of aphasia. No headache was
declared. When she arrived to the hospital three hours
later, she had no symptoms. Her neurological examination was normal. Medical history elicited alcoholism,
heavy cigarette smoking, and depression. She used irregularly quetiapine, diazepam, paroxetine, and mirtazapine
for a long time. An emergent head CT, obtained four
hours after symptom onset, showed a subarachnoid convexity hemorrhage (cSAH) located in the precentral sulcus of the frontal lobe. There was no subarachnoid
hyperdensity within the Sylvian and basal cisterns (Figure 1).
Given the presence of strokelike episode and a plenty of
vasoactive drugs were used, a CT angiography was
ordered with the provisional diagnosis of cerebrovascular arteriopathy. Of very much surprise to us, a sevenmillimeter left middle cerebral artery (MCA) bifurcation
saccular aneurysm was seen (Figure 2). Of note, no vasospasm or venous thrombosis was present.
At this point, the aneurysm was presumed to be coincidental given absence of spatial relationship between the
locations of the aneurysm and subarachnoid blood.
However, MR imaging obtained 12 hours after symptom
onset, clearly documented that SAH was indeed present
in the stem of the Sylvian fissure, next to the aneurysmal
dome, pushing arachnoidal blood upward to the cortical
sulci (Figure 3).
A complete obliteration of the aneurysm was achieved
uneventfully with a technique utilizing Y-stenting plus
coiling on the first morning after the event (Figure 4).
Convexity SAH, also known as cortical or convexal
SAH, is not a rare entity. Based on our own analysis of
nine published series [1–10] enrolling minimum 10
cases (n = 272), two most prevalent causes are cerebral
amyloid angiopathy (CAA, in 24%) and reversible cerebral vasoconstriction syndrome (RCVS, in 20%). Etiology remained undetermined in 21%. Other prevalent
causes are carotid artery steno-occlusive lesions in 7.4%,
posterior reversible encephalopathy syndrome (PRES) in
7%, cerebral venous thrombosis in 6.6%, endocarditis in
3.7% and vasculitis in 2.4%. Cerebrovascular malformations such as cavernoma, thrombosed developmental
venous anomaly, and dural fistula, were detected in 3%.
Hemostatic abnormalities such as overanticoagulation
and thrombocytopenia were found in 2.2%. The remaining causes, extracted from a diversity of case reports,
include Moya Moya disease [11], hyperperfusion syndrome [10], cerebral hypotension [3], malignant hypertension [2], cerebral abscess [1], and cortical infarct [4].
No cSAH caused by ruptured saccular aneurysm was
reported in the germane literature. Aneurysmal rupture
can cause pure acute subdural hemorrhage [12] or intracerebral hemorrhage but never cause an isolated cSAH.
Saccular aneurysms found in RCVS patients with cSAH

are considered as coincidental, if not being a predisposing factor of RCVS [13].
If we rely on head CT scan alone, the case presented
herein could be diagnosed as aneurysm-related cSAH.
However, this is a misdiagnosis because brain MRI
demonstrates certainly the presence of acute blood in the
cisterns immediately adjacent to the culprit aneurysm.
This case clearly reminds us the necessity to always perform brain MRI in every case of cSAH. This is critical
not only for elucidation of frequent etiologies, such as
CAA and PRES, but also to achieve accurate diagnosis
and classification of SAH as nicely documented in this
case vignette.