Treatment of Headache in Aneurysmal Subarachnoid Hemorrhage: Multimodal Approach

Sudden severe headache is a cardinal symptom and the most common complaint amongst patients presenting with aneurysmal subarachnoid hemorrhage. The multifactorial etiology of these headaches makes pharmacotherapy problematic. Current aneurysmal subarachnoid hemorrhage guidelines have limited or no recommendations for headache treatment. Our institution utilizes a multimodal pharmacotherapy protocol in the management of aneurysmal subarachnoid hemorrhage headache. The purpose of this study was to evaluate the efficacy of the current aneurysmal subarachnoid hemorrhage headache treatment approach at our institution. This was a retrospective cohort study of patients presenting with aneurysmal subarachnoid hemorrhage. A multimodal aneurysmal subarachnoid hemorrhage headache treatment protocol was implemented in February 2014. After an eight-month washout period, patients treated between September 2014 and November 2017 represented the study cohort. Data collected included severity of aneurysmal subarachnoid hemorrhage and headache, interventions to secure the aneurysm, pain score response related to specific analgesic administered, and discharge status. Multivariate analysis and linear regression were used to identify predictors of treatment efficacy. A total of 249 patients were identified in the study cohort. The majority of patients were female (61.4%) with a median age of 54 years (±12.5), median Hunt and Hess score of 2 (interquartile range 2–3), and mean length of hospitalization of 15.2 days. Magnesium infusion had the largest reduction in mean pain score compared to baseline pain score (−0.75; p = 0.0002). In this retrospective cohort study involving patients presenting with headache secondary to aneurysmal subarachnoid hemorrhage, no agent resulted in a clinically significant improvement on headache pain scores

Role of anesthetics and their adjuvants in neurovascular protection in secondary brain injury after aneurysmal subarachnoid hemorrhage

Aneurysmal rupture accounts for the majority of subarachnoid hemorrhage and is responsible for most cerebrovascular deaths with high mortality and morbidity. Initial hemorrhage severity and secondary brain injury due to early brain injury and delayed cerebral ischemia are the major determinants of outcomes after aneurysmal subarachnoid hemorrhage. Several therapies have been explored to prevent these secondary brain injury processes after aneurysmal subarachnoid hemorrhage with limited clinical success. Experimental and clinical studies have shown a neuroprotective role of certain anesthetics in cerebrovascular disorders including aneurysmal subarachnoid hemorrhage. The vast majority of aneurysmal subarachnoid hemorrhage patients require general anesthesia for surgical or endovascular repair of their aneurysm. Given the potential impact certain anesthetics have on secondary brain injury after SAH, appropriate selection of anesthetics may prove impactful on overall outcome of these patients. This narrative review focuses on the available evidence of anesthetics and their adjuvants in neurovascular protection in aneurysmal subarachnoid hemorrhage and discusses current impact on clinical care and future investigative directions

Commentary [Decompressive craniectomy in patients with cerebral infarction due to malignant vasospasm after aneurysmal subarachnoid hemorrhage]

Commentary: article "Decompressive craniectomy in patients with cerebral infarction due to malignant vasospasm after aneurysmal subarachnoid hemorrhage" on page 251 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505309

Acute management of poor condition subarachnoid hemorrhage patients

Poor condition subarachnoid hemorrhage (SAH) patients present a high mortality and morbidity. In this study, we reviewed the acute interventional (surgical and endovascular) management of 109 SAH-poor condition patients, who were treated as early as logistically possible after confirming stable circulation parameters. Patients over the age of 70 years, without clinical response to painful stimulation were excluded. We recognized at least 3 different postinterventional therapeutic approaches: (1) Norm- or hypovolemic, normotensive hemodilution in 30 patients with space-occupying intracranial hematomas as well as in 31 cases with acute cerebro-spinal-fluid obstruction. (2) Normovolemic, hypertensive hemodilution after unilateral decompressive craniotomy in 23 surgical- and 2 endovascular-treated patients with focalized space occupying lesions and reduced cerebral perfusion. (3) Hypovolemic, normo-, or hypertensive hemodilution after bilateral decompressive craniotomy in 23 cases with massive brain-swelling. We observed a reduced mortality (21%). The overall late outcome was favorable in 56% and unfavorable in 23%. Selective aggressive treatment adapted to increase the cerebral perfusion, seems to be an effective therapy to improve the survival and outcome of several poor condition SAH-patients

Randomized, open-label, phase 1/2a study to determine the maximum tolerated dose of intraventricular sustained release nimodipine for subarachnoid hemorrhage (NEWTON [Nimodipine Microparticles to Enhance Recovery While Reducing Toxicity After Subarachnoid Hemorrhage])

BACKGROUND AND PURPOSE—: We conducted a randomized, open-label, phase 1/2a, dose-escalation study of intraventricular sustained-release nimodipine (EG-1962) to determine safety, tolerability, pharmacokinetics, and clinical effects in aneurysmal subarachnoid hemorrhage. METHODS—: Subjects with aneurysmal subarachnoid hemorrhage repaired by clipping or coiling were randomized to EG-1962 or enteral nimodipine. Subjects were World Federation of Neurological Surgeons grade 2 to 4 and had an external ventricular drain. Cohorts of 12 subjects received 100 to 1200 mg EG-1962 (9 per cohort) or enteral nimodipine (3 per cohort). The primary objective was to determine the maximum tolerated dose. RESULTS—: Fifty-four subjects in North America were randomized to EG-1962, and 18 subjects were randomized to enteral nimodipine. The maximum tolerated dose was 800 mg. One serious adverse event related to EG-1962 (400 mg) and 2 EG-1962 dose-limiting toxicities were without clinical sequelae. There was no EG-1962-related hypotension compared with 17% (3/18) with enteral nimodipine. Favorable outcome at 90 days on the extended Glasgow outcome scale occurred in 27/45 (60%, 95% confidence interval 46%–74%) EG-1962 subjects (5/9 with 100, 6/9 with 200, 7/9 with 400, 4/9 with 600, and 5/9 with 800 mg) and 5/18 (28%, 95% confidence interval 7%–48%, relative risk reduction of unfavorable outcome; 1.45, 95% confidence interval 1.04–2.03; P=0.027) enteral nimodipine subjects. EG-1962 reduced delayed cerebral ischemia (14/45 [31%] EG-1962 versus 11/18 [61%] enteral nimodipine) and rescue therapy (11/45 [24%] versus 10/18 [56%]). CONCLUSIONS—: EG-1962 was safe and tolerable to 800 mg, and in this, aneurysmal subarachnoid hemorrhage population was associated with reduced delayed cerebral ischemia and rescue therapy. Overall, the rate of favorable clinical outcome was greater in the EG-1962-treated group. CLINICAL TRIAL REGISTRATION—: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01893190

Poor-Grade Aneurysmal Subarachnoid Hemorrhage: Diagnosis, Therapeutical Management, and Prognosis

Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating neurological condition and these patients often have unfavorable outcomes at the long-term follow-up. Poor-grade aSAH is a severe subtype of aSAH and is defined as World Federation of Neurosurgical Surgeon (WFNS) grade IV or V. All patients should be treated by a multidisciplinary team that consists of vascular neurosurgeons, interventional neuroradiologists, neurologists, and anesthetists. Aneurysm rebleeding occurs in the poor-grade aSAH within the first 72 h after ictus. Timing of treatment for aSAH has shifted from delayed to early treatment of ruptured aneurysms, and there will be a trend toward early or ultra-early treatment for poor-grade aSAH. However, there is no consensus regarding the optimal timing of treatment for poor-grade aSAH. Endovascular coiling has provided a viable alternative to surgical clipping. An increasing number of patients have received endovascular treatment. There are limited data on high-level clinical trials focused on the treatment of poor-grade aSAH. An accurate prediction model remains challenging. Predicting long-term outcome is essential to support treatment decision-making. We reviewed the current therapeutical management and prognosis of poor-grade aSAH

Benign perimesencephalic hemorrhage occurring after previous aneurysmal subarachnoid hemorrhage: a case report

<p>Abstract</p> <p>Introduction</p> <p>Both aneurysmal subarachnoid hemorrhage and benign perimesencephalic hemorrhage are well-described causes of spontaneous subarachnoid hemorrhage that arise as a result of different pathologic processes. To the best of the authors' knowledge, there have been no reports of both vascular pathologies occurring in the same individual.</p> <p>Case presentation</p> <p>A 51-year-old Caucasian woman with a history of aneurysmal subarachnoid hemorrhage presented five years after her initial treatment with ictal headache, meningismus, nausea and emesis similar to her previous bleeding event. Computed tomographic imaging revealed perimesencephalic bleeding remote from her previously coiled anterior communicating artery aneurysm. Both immediate and delayed diagnostic angiography revealed no residual filling of the previously coiled aneurysm and no other vascular anomalies, consistent with benign perimesencephalic hemorrhage. The patient had an uneventful hospital course and was discharged to home in good condition.</p> <p>Conclusions</p> <p>This report for the first time identifies benign perimesencephalic hemorrhage occurring in the setting of previous aneurysmal subarachnoid hemorrhage. The presence of a previously treated aneurysm can complicate the process of diagnosing benign perimesencephalic hemorrhage. Fortunately, in this case, the previously treated anterior communicating artery aneurysm was remote from the perimesencephalic hemorrhage and could be ruled out as a source. The patient's prior aneurysmal subarachnoid hemorrhage did not worsen the anticipated good outcome associated with benign perimesencephalic hemorrhage.</p

Эндоваскулярные методики профилактики и лечения сосудистого спазма вследствие разрыва церебральных аневризм: за и против

This review highlights current approaches to endovascular therapy of cerebral angiospasm in non-traumatic subarachnoid hemorrhage due to a ruptured cerebral aneurysm (CA). The main clinical guidelines for the management of patients with CA rupture are highlighted, clinical studies on the use of balloon angioplasty, intra-arterial administration of various vasodilators are presented, the advantages and complications of using various techniques are described. В данном обзоре освещены современные подходы к эндоваскулярной терапии церебрального ангиоспазма при нетравматическом субарахноидальном кровоизлиянии вследствие разрыва церебральной аневризмы (ЦА). Освещены основные клинические рекомендательные протоколы по ведению пациентов с разрывом ЦА, представлены клинические исследования, посвященные применению баллонной ангиопластики, интраартериальному введению различных вазодилататоров, описаны преимущества и осложнения использования различных методик.

Intravenous magnesium in subarachnoid hemorrhage

Contains fulltext : 97062.pdf (publisher's version ) (Open Access

Pharmacological treatment of delayed cerebral ischemia and vasospasm in subarachnoid hemorrhage

Subarachnoid hemorrhage after the rupture of a cerebral aneurysm is the cause of 6% to 8% of all cerebrovascular accidents involving 10 of 100,000 people each year. Despite effective treatment of the aneurysm, delayed cerebral ischemia (DCI) is observed in 30% of patients, with a peak on the tenth day, resulting in significant infirmity and mortality. Cerebral vasospasm occurs in more than half of all patients and is recognized as the main cause of delayed cerebral ischemia after subarachnoid hemorrhage. Its treatment comprises hemodynamic management and endovascular procedures. To date, the only drug shown to be efficacious on both the incidence of vasospasm and poor outcome is nimodipine. Given its modest effects, new pharmacological treatments are being developed to prevent and treat DCI. We review the different drugs currently being tested