Outcomes of high-grade aneurysmal subarachnoid hemorrhage patients treated with coiling and ventricular intracranial pressure monitoring.

BACKGROUND: High-grade aneurysmal subarachnoid hemorrhage is a devastating disease with a low favorable outcome. Elevated intracranial pressure is a substantial feature of high-grade aneurysmal subarachnoid hemorrhage that can result to secondary brain injury. Early control of intracranial pressure including decompressive craniectomy and external ventricular drainage had been reported to be associated with improved outcomes. But in recent years, little is known whether external ventricular drainage and intracranial pressure monitoring after coiling could improve outcomes in high-grade aneurysmal subarachnoid hemorrhage. AIM: To investigate the outcomes of high-grade aneurysmal subarachnoid hemorrhage patients with coiling and ventricular intracranial pressure monitoring. METHODS: A retrospective analysis of a consecutive series of high-grade patients treated between Jan 2016 and Jun 2017 was performed. In our center, followed by continuous intracranial pressure monitoring, the use of ventricular pressure probe for endovascular coiling and invasive intracranial pressure monitoring in the acute phase is considered to be the first choice for the treatment of high-grade patients. We retrospectively analyzed patient characteristics, radiological features, intracranial pressure monitoring parameters, complications, mortality and outcome. RESULTS: A total of 36 patients were included, and 32 (88.89%) survived. The overall mortality rate was 11.11%. No patient suffered from aneurysm re-rupture. The intracranial pressure in 33 patients (91.67%) was maintained within the normal range by ventricular drainage during the treatment. A favorable outcome was achieved in 18 patients (50%) with 6 mo follow-up. Delayed cerebral ischemia and Glasgow coma scale were considered as significant predictors of outcome (2.066 and -0.296, respectively, P < 0.05). CONCLUSION: Ventricular intracranial pressure monitoring may effectively maintain the intracranial pressure within the normal range. Despite the small number of cases in the current work, high-grade patients may benefit from a combination therapy of early coiling and subsequent ventricular intracranial pressure monitoring.

Allicin attenuates early brain injury after experimental subarachnoid hemorrhage in rats.

Early Brain Injury, rather than Cerebral Vasospasm, has been demonstrated to be more important for patients with Subarachnoid hemorrhage. It is considered that allicin can make sense in a wide range of pharmacological areas and can be taken as a therapeutic method in many pathologic situations. We have explored the potential effect of allicin and possible mechanisms in Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats. With therapy (70 mg/kg Allicin, rather than 30 mg/kg) 30 min post SAH, groups showed better neurological scores in 24 h. Significant differences could be found in body weight ratio between the SAH + vehicle groups and SAH + Allicin groups. Treatment with 70 mg/kg, not 30 mg/kg, Allicin significantly reduced brain edema and EB extravasation in 24 h after SAH. Assessments in 24 h after SAH showed that treatment with 70 mg/kg Allicin in 30 min after SAH significantly restrained the expression of cleaved caspase-3, mitigated the severity of neuronal degeneration, decreased the proportion of apoptotic neurons and the elevated MDA levels, and increased the suppressed GSH and SOD levels. We demonstrated for the first time that Allicin extenuated brain edema and blood-brain barrier dysfunction, improved neurological outcomes by the suppression of apoptosis and oxidative stress damage after SAH in experimental models, which may shade new light on the treatments of SAH.

The rise of soluble platelet-derived growth factor receptor ß in CSF early after subarachnoid hemorrhage correlates with cerebral vasospasm.

Platelet-derived growth factor ß (PDGFß) has been proposed to contribute to the development of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH), and soluble PDGFRß (sPDGFRß) is considered to be an inhibitor of PDGF signaling. We aimed at determining the sPDGFRß concentrations in the cerebrospinal fluid (CSF) of patients with aneurysmal SAH (aSAH) and analyzing the relationship between sPDGFRß level and CVS. CSF was sampled from 32 patients who suffered aSAH and five normal controls. Enzyme-linked immunosorbent assay was performed to determine the sPDGFRß concentrations in the CSF. Functional outcome was assessed using modified Rankin scale (mRS) at 6 months after aSAH. CVS was identified using transcranial Doppler or angio-CT or DSA. The cutoff of sPDGFRß for CVS was defined on the ROC curve. The concentrations of sPDGFRß following aSAH were both higher than those of normal controls on days 1-3 and 4-6, and peaked on days 7-9 post-SAH. The cutoff value of sPDGFRß level on days 1-3 for CVS was defined as 975.38 pg/ml according to the ROC curve (AUC = 0.680, p = 0.082). In addition, CSF sPDGFRß concentrations correlated with CVS (r = 0.416, p = 0.018), and multivariate analysis indicated that sPDGFRß level higher than 975.38 pg/ml on days 1-3 was an independent predictor of CVS (p = 0.001, OR = 19.22, 95% CI: 3.27-113.03), but not for unfavorable outcome after aSAH in the current study. CSF sPDGFRß level increases after aSAH and is higher in patients who developed CVS, and sPDGFRß level higher than 975.38 pg/ml on days 1-3 is a potential predictor for CVS after SAH.

Levels of Interleukin-1ß, Interleukin-18, and Tumor Necrosis Factor-α in Cerebrospinal Fluid of Aneurysmal Subarachnoid Hemorrhage Patients May Be Predictors of Early Brain Injury and Clinical Prognosis.

BACKGROUND: Aneurysmal subarachnoid hemorrhage (aSAH) is a severe cerebrovascular accident with high morbidity and mortality. The aim of this study is to investigate the relationship between level of inflammatory cytokines in cerebrospinal fluid (CSF) of aSAH patients, the severity of aSAH, and the outcome of aSAH patients. METHODS: aSAH patients were prospectively included and followed-up for 6 months. CSF samples were collected at 1-3, 4-6, and 7-9 days after aSAH onset. Levels of interleukin (IL)-1ß, IL-18, and tumor necrosis factor-α (TNF-α) in the CSF of aSAH patients were measured by enzyme-linked immunosorbent assay. RESULTS: Eighty-one aSAH patients were enrolled. The levels of IL-1ß, IL-18 and TNF-α in the CSF were especially higher in the group of aSAH patients with cerebral edema, cerebral vasospasm, and a high grade on Hunt-Hess scale, the high World Federation of Neurological Surgeons grades, and Fisher grade (P < 0.01). Higher levels of plasma C-reactive protein in the blood were correlated with poor outcome. The areas under the receiver operating characteristic curves for the levels of inflammatory cytokines in CSF were 0.85, 0.84, and 0.95, respectively. Clinical features (age, Hunt-Hess grade, etc.) were positively correlated with poor outcomes (P < 0.05). CONCLUSIONS: The levels of IL-1ß, IL-18, and TNF-α in CSF were elevated in aSAH patients and were positively associated with cerebral edema and acute hydrocephalus. Our findings suggest that CSF inflammatory cytokines might be biomarkers to assess severity and predict outcomes.