Angiographic Treatment of Asymptomatic Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage for the Prevention of Delayed Cerebral Ischemia.

OBJECTIVE: Angiographic treatment of asymptomatic cerebral vasospasm (CVS) in aneurysmal subarachnoid hemorrhage remains controversial. We sought to investigate its relationship with the development of delayed cerebral ischemia. METHODS: Consecutive patients admitted between July 2017 and June 2019, with a diagnosis of aneurysmal subarachnoid hemorrhage, were retrospectively analyzed. The rate of development of delayed cerebral ischemia was compared between a group of patients who underwent cerebral angiography for asymptomatic CVS and those who did not. The Mann-Whitney U test or χ2 test was used to compare the 2 groups. RESULTS: Thirty-seven of the 94 patients with aneurysmal subarachnoid hemorrhage were screened for CVS, of whom 16 (43%) had moderate-severe vasospasm. When patients who underwent therapeutic cerebral angiography were compared with those who did not and after adjusting for sex, age, and grade of subarachnoid hemorrhage, treatment was not found to be significantly associated with delayed cerebral ischemia (hazard ratio = 0.82, 95% confidence interval: 0.19-3.52, P = 0.79). We found that the median length of stay in the intensive care unit and hospital increased significantly with the severity of CVS (P < 0.001). CONCLUSIONS: Cerebral angiography has a low rate of detecting moderate-severe CVS in asymptomatic patients. Moreover, there was no statistically significant difference in the rate of delayed cerebral ischemia between asymptomatic patients treated versus those not treated for CVS. There was significant association between the severity of CVS and the intensive care unit and hospital length of stay. More studies are needed to evaluate the utility of treating asymptomatic CVS in high-grade aneurysmal subarachnoid hemorrhage.

Predictors of Opiate Utilization in the Treatment of Headache and Impact on Three-Month Outcomes Following Subarachnoid Hemorrhage.

Despite multiple investigational drugs, headache due to subarachnoid hemorrhage (SAH) remains inadequately controlled and requires high opiate utilization. This study investigates the factors associated with increased opiate usage for the management of headache in SAH in the first 14 days of admission, the association between opiate usage and hospital length of stay, and the incidence of opiate consumption during the outpatient follow up. This is a single-center cross-sectional study. A total of 138 patients admitted between January 1, 2017, and May 31, 2019, with a diagnosis of SAH, were identified through a neurocritical care dashboard. Outpatient electronic medical records were evaluated at three months. Statistical analysis included descriptive statistics, Mann-Whitney U test, stepwise regression, and multiple regression analysis. We found that of 138 patients, the majority (90%) were prescribed opiates during their hospitalization, and the mean daily morphine equivalent dosage was 18.74 mg. Steroid usage was associated with an increase in 14-day opiate usage (r = 0.4, p = 0.0001); however, the cerebral spinal fluid profile did not show a statistically significant correlation. Over 14 days, smokers significantly used more opiates compared to nonsmokers (353 mg vs. 184 mg, p = 0.01). In addition, peri-mesencephalic SAH required less morphine compared to aneurysmal SAH (195 mg vs. 283 mg, p = 0.004). Aneurysm clipping was associated with less opiate usage compared to aneurysm coiling (186 vs. 320, p = 0.08). Only the high Hunt and Hess scale score predicted opiate usage, and the high modified Fisher scale score, aneurysmal SAH, and more opiate usage predicted hospital length of stay. A total of 48 patients (42%) suffered from headaches during their outpatient follow-up within three months of discharge; however, only six (5%) were still on opiates. There was a significant association between the amount of opiate used in the first 14 days of admission and the rate of post-discharge headache. In summary, even though patients admitted with SAH require a large amount of opiate for headache management, this did not lead to more opiate consumption in the outpatient setting. However, patients continued to suffer from headaches at three months follow-up. This high opiate consumption is associated with increased hospital length of stay. Studies are needed to identify opiate sparing analgesics that target the pathogenesis of headaches in this patient population.

Ketamine for empiric treatment of cortical spreading depolarization after subdural hematoma evacuation.

BACKGROUND: It is widely known that some patients surgically treated for subdural hematoma (SDH) experience neurologic deficits not clearly explained by the acute brain injury or known sequelae like seizures. There is increasing evidence that cortical spreading depolarization (CSD) may be the cause. A recent article demonstrated that CSD occurred at a rate of 15 % and was associated with neurological deterioration in a subset of patients following chronic subdural hematoma evacuation. Furthermore, CSD can lead to ischemia leading to worsening neurologic deficits. CSD is usually detected on electrocorticography (ECoG) and needs cortical strip electrode placement with equipment and expertise that may not be readily available. CASE DESCRIPTION: We report three cases of patients with subdural hematoma (SDH) not undergoing ECoG in whom CSD was suspected to be the cause of their neurologic deficits post evacuation. Extensive workup including neuroimaging and electroencephalography (EEG) were inconclusive. Patients were subsequently treated with ketamine infusion and had resultant neurological recovery. CONCLUSIONS: Ketamine infusion can help reverse neurologic deficits in patients with SDH in whom the deficits are not explained by neuroimaging or electrographic seizure. CSD is a known phenomenon that can result in neurological injury and must remain in the differential diagnosis of such patients. Though only limited cases are discussed (n = 3), this small case series provides the basis for conducting clinical trials evaluating the efficacy of ketamine in improving functional outcome in brain-injured patients demonstrating evidence of CSD.

Portable Magnetic Resonance Imaging for ICU Patients.

OBJECTIVES: Patients in ICUs often require neuroimaging to rule out a wide variety of intracranial problems. CT may be available in the ICU itself, but MRI has greater sensitivity for many conditions that affect the brain. However, transporting patients who are on ventilators and other life-sustaining devices is a labor-intensive process and involves placing the patient at risk for adverse events. This is a report of portable MRI in a clinical setting. DESIGN: This is a prospective, nonrandomized, observational study at one institution, utilizing a 0.064-T, self-shielding, portable MRI in ventilated patients in an ICU setting. SETTING: Academic medical center. PATIENTS: Nineteen patients with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 infection. Patients selected for imaging had any of the following: 1) unexplained encephalopathy or coma, 2) seizures, 3) focal neurologic deficit, or 4) abnormal head CT. Imaging was performed in each patient's ICU room with a portable, self-shielding, 0.064-T MRI. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Among 19 patients, 20 MRI scans in seven ICUs were acquired between April 13, 2020, and April 23, 2020. No adverse events to patients or staff from MRI acquisition were reported. In 12 patients, abnormal findings were seen, which included increased fluid attenuated inversion recovery signal (n = 12), hemorrhage (n = 3), and diffusion-weighted imaging positivity (n =3). Imaging led to changes in clinical management in five patients. CONCLUSIONS: In this case series of patients, use of portable MRI has been found to be safe, feasible, and led to changes in clinical management based on imaging results. However, future studies comparing results with other imaging modalities are required to understand fully the extent of its clinical utility.

Inhibition of IL-6 signaling: A novel therapeutic approach to treating spinal cord injury pain.

To characterize the contribution of interleukin-6 (IL-6) to spinal cord injury pain (SCIP), we employed a clinically relevant rat contusion model of SCIP. Using Western blots, we measured IL-6 levels in lumbar segments (L1-L5), at the lesion site (T10), and in the corresponding lumbar and thoracic dorsal root ganglia (DRG) in 2 groups of similarly injured rats: (a) SCI rats that developed hind-limb mechanical allodynia (SCIP), and (b) SCI rats that did not develop SCIP. Only in SCIP rats did we find significantly increased IL-6 levels. Immunocytochemistry showed elevated IL-6 predominantly in reactive astrocytes. Our data also showed that increased production of IL-6 in hyperreactive astrocytes in SCIP rats may explain still-poorly understood astrocytic contribution to SCIP. To test the hypothesis that IL-6 contributes to mechanical allodynia, we treated SCIP rats with neutralizing IL-6 receptor antibody (IL-6-R Ab), and found that one systemic injection abolished allodynia and associated weight loss; in contrast to gabapentin, the analgesic effect lasted for at least 2weeks after the injection, despite the shorter presence of the Ab in the circulation. We also showed that IL-6-R Ab partially reversed SCI-induced decreases in the protein levels of the glutamate transporter GLT-1 12hours and 8days after Ab injection, which may explain the lasting analgesic effect of the Ab in SCIP rats. A link between reactive astrocytes IL-6-GLT-1 has not been previously shown. Given that the humanized IL-6-R Ab tocilizumab is Food and Drug Administration-approved for rheumatoid arthritis, we are proposing tocilizumab as a novel and potentially effective treatment for SCIP.