Background Endoscopically placed, temporary gastric electrical stimulation (tGES) may relieve symptoms of gastroparesis (Gp) and predict permanent gastric electrical stimulation (GES) outcomes. Objective To measure effects of 72 hours of temporary GES on Gp symptoms. Design, Setting, and Patients From 2005 to 2006, we conducted a hospital-based, randomized, placebo-controlled, crossover trial of two consecutive, 4-day sessions (session 1 and session 2), enrolling 58 patients (11 males, 47 females; mean age 46 years) with GP symptom histories of three etiologies (idiopathic, 38; diabetes mellitus, 13; postsurgical, 7). Intervention 72 continuous hours temporary GES was provided for group A during session 1, and for group B during session 2. Main Outcome Measurements Symptoms measured daily; gastric emptying, electrogastrography, and quality of life measured at baseline and session close. Results In session 1, vomiting decreased in both groups, but was greater with stimulation, resulting in a day 3 difference of −1.02 (95% CI, −1.62 to −0.42; P < .001). Scores did not return to baseline during washout; on day 4, the difference persisted at −1.08 (95% CI, −1.81 to −0.35; P = .005). In session 2, vomiting slightly decreased with stimulation and slightly increased without it; at day 8, the nonactivated group had nonsignificantly greater vomiting, 0.12 (−0.68 to 0.92; P = .762). An overall treatment effect of a slight, nonsignificant daily decrease in average vomiting scores, −0.12 (−0.26 to 0.03; P = .116), was observed by pooling stimulation effects across sessions. Limitations Missing data; potential physiological imbalances between groups. Conclusions Although overall treatment effects were not significant, differences in favor of stimulation were suggested. Barriers to observing treatment effects included a decrease in vomiting for both groups during session 1, insufficient washout, and the absence of baseline vomiting for some patients. Future studies should better define inclusion criteria, use longer washout periods, randomize by etiology and baseline physiological findings, and pursue alternative designs. (Clinical trial registration number: 00432835.)

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Background: Although comprising 7% of all spinal tumors, sacral tumors present with a litany of issues due to their slow growth and difficulty in detection. As a result, sacral tumors can grow unperturbed for years until a patient presents for an incidental workup of an unassociated minor trauma or an offending primary tumor source that has metastasized to the sacrum; in most cases, this includes primary tumors of the breast, prostate, and lung. The goal of this review is to outline the pathophysiology underlying sacral tumors including the various tissues and structures that can be targeted for treatment, along with a discussion of the surgical approach to sacrectomy. Methods: An extensive review of the published literature was conducted through PubMed database with articles simultaneously containing both search terms “sacral tumors” and “sacrectomy.” No date restrictions were used. Results: The search yielded 245 related articles. Cross-checking of articles was conducted to exclude of duplicate articles. The articles were screened for their full text and English language availability. We finalized those articles pertaining to the topic. Conclusion: Once a sacral tumor has reached the point of diagnostic detection, invasive sacrectomy is typically utilized (through an anterior, posterior, or combination approach) to locally isolate and resect the tumor and minimize risk of future tumor growth and additional bone loss. While institutions have varying criteria for surgical approaches, a combination of anterior and posterior approach has traditionally been used in total and high sacrectomies due to the control it provides surgeons toward the rectum and vasculature anterior to the sacrum. A posterior-only approach can be performed for tumors that failed to invade pelvic organs or extend past the lumbosacral junction. Early detection with screenings can help avoid invasive sacrectomy by identifying the onset of tumor formation in the sacrum, particularly for highly metastatic cancers.

Background: Vasogenic edema in the setting of acute ischemic stroke can be attributed to the opening of transient receptor potential 4 channels, which are expressed in the setting of injury and regulated by sulfonylurea receptor 1 (SUR1) proteins. Glibenclamide, also known as glyburide, RP-1127, Cirara, and BIIB093, is a second-generation sulfonylurea that binds SUR1 at potassium channels and may significantly reduce cerebral edema following stroke, as evidenced by recent clinical trials. This review provides a comprehensive analysis of clinical considerations of glibenclamide use and current patient outcomes when administered in the setting of acute ischemic stroke to reduce severe edema. Methods: National databases (MEDLINE, EMBASE, Cochrane, and Google scholar databases) were searched to identify studies that reported on the clinical outcomes of glibenclamide administered immediately following acute ischemic stroke. Results: The pharmacological mechanism of glibenclamide was reviewed in depth as well as the known indications and contraindications to receiving treatment. Eight studies were identified as having meaningful clinical outcome data, finding statistically significant differences in glibenclamide treatment groups ranging from matrix metalloproteinase-9 serum levels, midline shift, modified Rankin Scores, National Institute of Health Stroke Score, and mortality endpoints. Conclusion: Studies analyzing the GAMES-Pilot and GAMES-PR trials suggest that glibenclamide has a moderate, however, measurable effect on intermediate biomarkers and clinical endpoints. Meaningful conclusions are limited by the small sample size of patients studied.

Background: First characterized in the 19th century, spontaneous spinal epidural hematoma (SSEH) is known as the idiopathic accumulation of blood within the spinal canal’s epidural space, causing symptoms varying from general back pain to complete paraplegia. With varying etiologies, a broad spectrum of severity and symptoms, a time-dependent resolution period, and no documented diagnosis or treatment algorithm, SSEH is a commonly misunderstood condition associated with increasing morbidity. While SSEH can occur at any vertebrae level, 16% of all SSEH cases occur in the cervical spine, making it a region of interest to clinicians. Case Description: Herein, the authors present two case examples describing the clinical presentation of SSEH, while also reviewing the literature to provide a comprehensive overview of its presentation, pathology, and treatment. The first case is a patient with nontraumatic sudden onset neck pain with rapidly progressing weakness. The second case is a patient with painless weakness that developed while taking 325 mg of aspirin daily. Conclusion: Clinicians should keep SSEH in their differential diagnosis when seeing patients with nontraumatic sources of weakness in their extremities. The appropriate steps should be followed to diagnose and treat this condition with magnetic resonance imaging and surgical decompression if there are progressive neurological deficits. There is a continued need for more extensive database-driven studies to understand better SSEHs clinical presentation, etiology, and ultimate treatment.