No abstract

The FOUR score at admission and day 7 post-SAH is associated with mortality, 1-month GOS/mRS, and 6-month GOS/mRS. The FOUR score at day 14 post-SAH is associated with 6-month GOS. The brainstem sub-score was not associated with 1- or 6-month primary outcomes.

Treatment of BBAs is currently challenging and remains difficult despite improvement of microsurgical technique and advancement in endovascular technologies. Therapeutic options are reconstructive and deconstructive open surgeries or endovascular procedures. However, there is a lack of consensus about optimal treatment. We report a case of 38-year old woman with subarachnoid hemorrhage due to a ruptured BBA successfully treated with placement of an endovascular flow-diverting stent.

OBJECTIVECerebral proliferative angiopathy (CPA) is considered a discrete vascular malformation of the brain separate from classical brain arteriovenous malformations (AVMs). It has unique angiographic characteristics and has been hypothesized to result from chronic cortical ischemia and perinidal oligemia. Treatment with cerebral revascularization has been proposed in an attempt to disrupt regional hypoperfusion and interrupt the angiogenesis that defines CPA. A systematic review of the literature pertaining to the role of cerebral revascularization may highlight a treatment paradigm for this rare disease.METHODSA systematic review was performed in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. MEDLINE and Embase were searched from inception for papers relating to CPA. Included articles were categorized according to methodology (case series or imaging study) and treatment modality (conservative, radiation, endovascular, or revascularization). A synthesis was compiled summarizing the current evidence regarding cerebral revascularization in CPA.RESULTSThe initial search revealed 43 articles, of which 28 studies met the inclusion criteria. Nine studies were identified that described imaging findings, which suggested hemodynamic dysregulation and perinidal impairments in the cerebrovascular reserve could be identified compared to unaffected hemispheres and classical brain AVMs. Six studies including 7 patients undergoing indirect forms of cerebral revascularization were identified. Clinical and radiological outcomes following revascularization were favorable in all but one study.CONCLUSIONSA small body of radiological and clinical studies has emerged, suggesting that CPA is a response to perinidal oligemia. While the long-term clinical efficacy of revascularization remains unclear, early results suggest that this may be a novel treatment paradigm for patients with CPA.

Background. During hypertensive therapy for post-subarachnoid hemorrhage (SAH) symptomatic vasospasm, norepinephrine is commonly used to reach target blood pressures. Concerns over aggravation of vasospasm with norepinephrine exist. Objective. To describe norepinephrine temporally related deterioration in neurological examination of two post-SAH patients in vasospasm. Methods. We retrospectively reviewed two charts of patients with delayed cerebral ischemia (DCI) post-SAH who deteriorated with norepinephrine infusions. Results. We identified two patients with DCI post-SAH who deteriorated during hypertensive therapy with norepinephrine. The first, a 43-year-old male presented to hospital with DCI, failed MABP directed therapy with rapid deterioration in exam with high dose norepinephrine and MABP of 140–150 mm Hg. His exam improved on continuous milrinone and discontinuation of norepinephrine. The second, a 39-year-old female who developed DCI on postbleed day 8 responded to milrinone therapy upfront. During further deterioration and after angioplasty, norepinephrine was utilized to drive MABP to 130–140 mm Hg. Progressive deterioration in examination occurred after angioplasty as norepinephrine doses escalated. After discontinuation of norepinephrine and continuation of milrinone, function dramatically returned but not to baseline. Conclusions. The potential exists for worsening of DCI post-SAH with hypertensive therapy directed by norepinephrine. A potential role exists for vasodilation and inotropic directed therapy with milrinone in the setting of DCI post-SAH.

Refractory status epilepticus, in the absence of an identifiable etiology, in elective aneurysm clipping is a rare event. Consideration should be given for the early use of ketamine in refractory status epilepticus.

The risk of intracranial hemorrhage from cerebral cavernous malformations is likely not changed during pregnancy, delivery, or post partum.

Background. Treatment of symptomatic delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is difficult. Recent studies suggest intravenous (IV) high dose milrinone as a potential therapy. The timing to angiographic response with this is unclear. Methods. We reviewed the chart of one patient admitted for SAH who developed symptomatic DCI and was treated with high dose IV milrinone. Results. A 66-year-old female was admitted with a Hunt and Hess clinical grade 4, World Federation of Neurological Surgeons (WFNS) clinical grade 4, and SAH secondary to a left anterior choroidal artery aneurysm which was clipped. After bleed day 6, the patient developed symptomatic DCI. We planned for angioplasty of the proximal segments. We administered high dose IV milrinone bolus followed by continuous infusion which led to clinical improvement prior to angiography. The angiogram performed 1.5 hours after milrinone administration displayed resolution of the CT angiogram and MRI based cerebral vasospasm such that further intra-arterial therapy was aborted. She completed 6 days of continuous IV milrinone therapy, was transferred to the ward, and subsequently rehabilitated. Conclusions. High dose IV milrinone therapy for symptomatic DCI after SAH can lead to rapid neurological improvement with dramatic early angiographic improvement of cerebral vasospasm.