Non-aneurysmal subarachnoid hemorrhage in 173 patients: a prospective study of long-term outcome.

BACKGROUND AND PURPOSE: In some patients with subarachnoid hemorrhage (SAH) a bleeding source cannot be identified. Perimesencephalic (PM) SAH is assumed to have an excellent outcome. Our objective was to analyze the long-term physical and psychological outcome of patients after non-aneurysmal SAH. METHODS: One hundred and seventy-three patients met the inclusion criteria. Short-term follow-up 6 months after SAH was assessed according to the modified Rankin Scale (0-2 favorable). A short-form health survey with 36 questions (SF-36) and eight scales was used as questionnaire for long-term follow-up. RESULTS: Thirty-seven answers were received from the two groups, PM and non-perimesencephalic (NPM) SAH, on average 76 months after ictus (range 1.5-14 years). PM- and NPM-SAH without Fisher grade 3 blood pattern have excellent short-term outcomes. The quality of life (QoL) is significantly reduced after non-aneurysmal SAH, especially in NPM-SAH. In particular, patients with a Fisher 3 blood pattern had significantly higher risks for cerebral vasospasm, delayed cerebral ischaemia, unfavorable outcome, reduced QoL and mortality in short- and long-term follow-up. CONCLUSIONS: Excluding rolph, only patients with a PM-SAH have a similar QoL at long-term follow-up compared to the standard population. Patients with NPM-SAH have a significantly decreased QoL in long-term follow-up. Furthermore, the Fisher 3 blood pattern group in particular had a significantly worse outcome - at short-term and long-term follow-up. Therefore the NPM-SAH group was stratified into patients with Fisher 3 blood pattern and patients without Fisher 3 in further investigations.

Hematoma expansion in experimental intracerebral hemorrhage is not altered by peracute treatment with recombinant tissue plasminogen activator.

Recombinant tissue-type plasminogen activator (rt-PA) is the mainstay of acute stroke treatment and the only approved medical therapy so far. Because of its fibrinolytic action, it is presumed to aggravate intracerebral hemorrhage (ICH). Since clinical features do not discriminate between ischemic stroke and ICH, brain imaging is strictly required before the initiation of thrombolysis. A recent study has shown that rt-PA does not worsen (primary) ICH in two different experimental mouse models. Here, we further explored this surprising finding and examined hematoma expansion and long-term outcome after rt-PA treatment in a murine model of ICH. We induced ICH by collagenase injection into the right basal ganglia of C57BL/6 mice. At 30 min, 90 min or 4h after ICH induction, respectively, mice were treated with vehicle or 10mg/kg rt-PA. In parallel, we administered the vascular tracer Evans Blue (EB) and sacrificed the mice 2h after injection to assess EB extravasation as a marker of ongoing bleeding and rt-PA induced rebleeding. Additionally, we observed mice which were treated with vehicle or rt-PA 30 min after ICH induction for 72 h and quantified functional outcome and hematoma volume. EB extravasation was highest in the groups that were treated after 30 min and decreased thereafter according to a cessation of active bleeding. At all three time points covering the early phase of ICH, treatment with rt-PA did not increase EB extravasation. In the 72 h observation, there was also no difference in functional outcome and hematoma volume. In our experimental study, we were not able to demonstrate that peracute rt-PA treatment in (primary) ICH has detrimental effects on hematoma expansion, hematoma volume or functional outcome. This finding needs careful consideration in future translational studies.