OBJECTIVE Deep brain stimulation is an effective surgical treatment for managing some neurological and psychiatric disorders. Infection related to the deep brain stimulator (DBS) hardware causes significant morbidity: hardware explantation may be required; initial disease symptoms such as tremor, rigidity, and bradykinesia may recur; and the medication requirements for adequate disease management may increase. These morbidities are of particular concern given that published DBS-related infection rates have been as high as 23%. To date, however, the key risk factors for and the potential preventive measures against these infections remain largely uncharacterized. In this study, the authors endeavored to identify possible risk factors for DBS-related infection and analyze the efficacy of prophylactic intrawound vancomycin powder (VP). METHODS The authors performed a retrospective cohort study of patients who had undergone primary DBS implantation at a single institution in the period from December 2005 through September 2015 to identify possible risk factors for surgical site infection (SSI) and to assess the impact of perioperative (before, during, and after surgery) prophylactic antibiotics on the SSI rate. They also evaluated the effect of a change in the National Healthcare Safety Network's definition of SSI on the number of infections detected. Statistical analyses were performed using the 2-sample t-test, the Wilcoxon rank-sum test, the chi-square test, Fisher's exact test, or logistic regression, as appropriate for the variables examined. RESULTS Four hundred sixty-four electrodes were placed in 242 adults during 245 primary procedures over approximately 10.5 years; most patients underwent bilateral electrode implantation. Among the 245 procedures, 9 SSIs (3.7%) occurred within 90 days and 16 (6.5%) occurred within 1 year of DBS placement. Gram-positive bacteria were the most common etiological agents. Most patient- and procedure-related characteristics did not differ between those who had acquired an SSI and those who had not. The rate of SSIs among patients who had received intrawound VP was only 3.3% compared with 9.7% among those who had not received topical VP (OR 0.32, 95% CI 0.10-1.02, p = 0.04). After controlling for patient sex, the association between VP and decreased SSI risk did not reach the predetermined level of significance (adjusted OR 0.32, 95% CI 0.10-1.03, p = 0.06). The SSI rates were similar after staged and unstaged implantations. CONCLUSIONS While most patient-related and procedure-related factors assessed in this study were not associated with the risk for an SSI, the data did suggest that intrawound VP may help to reduce the SSI risk after DBS implantation. Furthermore, given the implications of SSI after DBS surgery and the frequency of infections occurring more than 90 days after implantation, continued follow-up for at least 1 year after such a procedure is prudent to establish the true burden of these infections and to properly treat them when they do occur.

Object The primary goal of this study was to review the immediate postoperative neurological function in patients surgically treated for symptomatic cervical spine disease without intraoperative neurophysiological monitoring. The secondary goal was to assess the economic impact of intraoperative monitoring (IOM) in this patient population. Methods This study is a retrospective review of 720 consecutively treated patients who underwent cervical spine procedures. The patients were identified and the data were collected by individuals who were not involved in their care. Results A total of 1534 cervical spine levels were treated in 720 patients using anterior, posterior, and combined (360°) approaches. Myelopathy was present preoperatively in 308 patients. There were 185 patients with increased signal intensity within the spinal cord on preoperative T2-weighted MR images, of whom 43 patients had no clinical evidence of myelopathy. Three patients (0.4%) exhibited a new neurological deficit postoperatively. Of these patients, 1 had a preoperative diagnosis of radiculopathy, while the other 2 were treated for myelopathy. The new postoperative deficits completely resolved in all 3 patients and did not require additional treatment. The Current Procedural Terminology (CPT) codes for IOM during cervical decompression include 95925 and 95926 for somatosensory evoked potential monitoring of the upper and lower extremities, respectively, as well as 95928 and 95929 for motor evoked potential monitoring of the upper and lower extremities. In addition to the charge for the baseline [monitoring] study, patients are charged hourly for ongoing electrophysiology testing and monitoring using the CPT code 95920. Based on these codes and assuming an average of 4 hours of monitoring time per surgical case, the savings realized in this group of patients was estimated to be $1,024,754. Conclusions With the continuing increase in health care costs, it is our responsibility as providers to minimize expenses when possible. This should be accomplished without compromising the quality of care to patients. This study demonstrates that decompression and reconstruction for symptomatic cervical spine disease without IOM may reduce the cost of treatment without adversely impacting patient safety.

Owing to pain limiting mobilization, a quarter of neurologically intact patients with thoracolumbar burst fractures and a TLICS score of 2 failed nonsurgical management. The greater the kyphosis, stenosis, and fragmentation of the fracture, the more likely patients required surgery. In addition to the TLICS classification, other radiographic and clinical parameters should be included in selecting appropriate treatment strategy. The cost savings with nonoperative treatment of intact burst fractures, when appropriate, are significant.

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Neural tube defects (NTDs) are a set of disorders that occur from perturbation of normal neural development. They occur in open or closed forms anywhere along the craniospinal axis and often result from a complex interaction between environmental and genetic factors. One burgeoning area of genetics research is the effect of cilia signaling on the developing neural tube and how the disruption of primary cilia leads to the development of NTDs. Recent progress has implicated the hedgehog (Hh), wingless-type integration site family (Wnt), and planar cell polarity (PCP) pathways in primary cilia as involved in normal neural tube patterning. A set of disorders involving cilia function, known as ciliopathies, offers insight into abnormal neural development. In this article, the authors discuss the common ciliopathies, such as Meckel-Gruber and Joubert syndromes, that are associated with NTDs, and review cilia-related signaling cascades responsible for mammalian neural tube development. Understanding the contribution of cilia in the formation of NTDs may provide greater insight into this common set of pediatric neurological disorders.