83 yo Fe with previous (one year earlier) subarachnoid hemorrhage related to a left MCA aneurysm: this was treated with endovascular device. Patient now presents with acute headache and change in mental status consistent with suspected recurrent SAH.

CT Head precontrast and CTA; MR T1-w precontrast; MR T1-w postcontrast/MRA; T2-w spin echo; MR flair; MR susceptbility (SWI)

CT head: pre
1. There is evidence of concurrent subarachnoid hemorrhage with subarachnoid clot concentrated in the proximal segment of the sylvian fissure and right lateral suprasellar space plus a large intraparenchymal hematoma in the adjacent mesial right temporal lobe. This complex of SAH & adjacent intraaxial is consistent with a sentinel hemorrhage condition where pial adhesions from prior hemorrhage (which this patient had from the left MCA aneurysm bleed) cause the hemorrhage direction to bleed into brain and subarachnoid space at the same time.
2. There is minimal to moderate external hydrocephalus and papiiledema.
3. There is early downward uncal herniation compressing the right cerebral peduncle.

CT head: CTA
1. There is no residual aneurysm in the left MCA treatment area.
2. There is a right P-com saccular aneurysm with a relatively wide neck for fundal size. There is no vasospasm nor incorporation of the parent artery in the aneurysm neck. It has a small apical daughter aneurysm.
3. There is a small basilar apex pre-aneurysm.

MR T1-w pre contrast
1. The right temporal hematoma is virtually isointense to brain indicating it is in a hyperacute to acute timeframe (2 hrs to 2 days). The existing vasogenic perilesional edema is hypointense on T1 and surrounds the parenchymal hematoma.
2. There is a right posterior saccular aneurysm. It is not as well seen on MRA than on the CTA. There is no residual left MCA aneurysm, and the basilar tip pre-aneurysm is not evident.
3. The large right temporal mass reduces venocapillary filling, But this could be just delay in filling and not necessarily infarction.

MR T1-w post contrast/MRA
1. There is no residual aneurysm in the left MCA treatment area.
2. The active P-com aneurysm is present but is detail concerning the aneurysm is clearer on the CTA.

T2-w spin echo
1. The right temporal hematoma age is in the hyperacute to early acute timeframe

MR flair
1. MR flair demonstrates that the degree of actual transependymal fluid migration is minimal. Most of the periventricular hyper intense signal is likely age-related leukomalacia.
2. The age of the hematoma also matches the hyperacute phase on MR flair.

MR susceptibility
1. SWI reveals evidence of both recent subarachnoid blood and recent parenchymal right temporal hematoma
2. SWI also reveals evidence of wide spread, but mainly right temporal pial surface chronic hemosiderin, which would likely provide the pial adhesions necessary for the right P-com aneurysm to rupture into both the subarachnoid and the mesial right temporal lobe concurrently.

1. This patient had multiple saccular aneurysms, i.e. a prior treated left MCA aneurysm, a currently bleed right P-com aneurysm, and a basilar tip pre aneurysm. Multiple saccular aneurysms occurs in about 10% of patients with any saccular aneurysm. What is unique about this case is the fact that the prior SAH appeared to have left hemosiderin laden pia-arachnoid adhesions including the area of the active right P-com aneurysm. When the current P-com aneurysm bled it did so not into the adjacent subarachnoid space, as expected, but also directly into the mesial right temporal lobe despite the fact that the P-com aneurysm as pointed posteriorly and not laterally. This complex is referred to a "sentinel hemorrhage". The sentinel term refers to a prior bleed leaving pial adhesions that alters the direction of a subsequent aneurysmal hemorrhage. What make this an important observation is that the amount of SAH may be minimal, and the interpretation might misconstrue the parenchymal hematoma as just a spontaneous brain bleed that may possibly be watched. However, rebleed rate in a sentinel hemorrhage context has a very high rate of recurrent bleeding without therapy.

1. Parenchymal hemorrhages that originate along a cisternal surface and them dissect into the parenchyma are unusual. Therefore, when there is a cisternal (basilar) subarachnoid hemorrhage and a parenchymal hemorrhage occurring concurrently, it should be considered that the two events are connected. This situation raises the possibility that there has been a prior aneurysmal bleed that may or may not have been symptomatic, but was enough to cause hemosiderin deposition on the pial surface of the brain, and subsequent saccular burst hemorrhage is driven into both the subarachnoid space and into the adjacent brain which forms the margin of the affected cistern.

2. Most spontaneous dissections that cause brain hemorrhage affect distal, not proximal, arterial segments.

3. Most spontaneous mycotic aneurysms that cause brain hemorrhages also typically effect distal, not proximal arteries plus there are infectious findings as well.