Citations

Case Report. Spine surgery in patients with Parkinson’s disease (PD) involves increased risk. We describe a case of cervical myelopathy in a patient with PD, multiple fractures involving the atlas and axis vertebrae, and spasmodic torticollis. The patient was successfully treated with an upper cervical decompression and occipital-cervical (OC) fusion surgery. Strategies for torticollis reduction and successful surgical outcome are discussed. Risks and benefits must be carefully weighed when considering occipital cervical fusion in PD patients. Conclusion. Intraoperative manual reduction of laterocollis is possible after general endotracheal anesthesia, and continuous neuromonitoring is established. Use of optimizing strategies such as perioperative botulinum injections and intraoperative O-arm navigation should be considered.

Case Report. Escherichia coli is a rare cause of vertebral osteomyelitis. It is more common in adults and males. We present a case of an immunocompetent adult male presenting with a several month history of progressive systemic symptoms and subsequent neurologic compromise. We discuss the neurosurgical evaluation of a patient with a progressive vertebral osteomyelitis and treatment options. Surgical debridement and spinal stabilization were performed and confirmed the diagnosis. The patient successfully completed a prolonged antimicrobial therapy course. The patient made a complete neurologic recovery. We discuss the presentation of a patient with Escherichia coli vertebral osteomyelitis and the successful surgical management.

Lumbar spondylolysis is a unilateral or bilateral defect of the pars interarticularis, an isthmus of bone connecting the superior and inferior facet surfaces in the lumbar spine at a given level. Spondylolysis is common in young athletes participating in sports, particularly those requiring repetitive hyperextension movements. The majority of young athletes are able to return to full sport participation following accurate diagnosis and conservative management, including a structured treatment program. Surgical intervention for isolated pars injuries is seldom necessary. A progressive physical therapy (PT) program is an important component of recovery after sustaining an acute pars fracture. However, there is a paucity of literature detailing PT programs specific to spondylolysis. Here, we provide an overview of the epidemiology, natural history, radiographic evaluation, and management of pars fractures in young athletes. In addition, a detailed description of a physiotherapy program for this population that was developed at a spine center within an academic medical center is provided.

Abstract Increased pro‐inflammatory cytokine levels and proliferation of activated microglia have been found in Parkinson's disease (PD) patients and animal models of PD, suggesting that targeting of the microglial inflammatory response may result in neuroprotection in PD. Microglial proliferation is regulated by many factors, but colony stimulating factor‐1 receptor (CSF1R) has emerged as a primary factor. Using data mining techniques on existing microarray data, we found that mRNA expression of the CSF1R ligand, CSF‐1, is increased in the brain of PD patients compared to controls. In two different neurotoxic mouse models of PD, acute MPTP and sub‐chronic LPS treatment, mRNA and protein levels of CSF1R and CSF‐1 were significantly increased. Treatment with the CSF1R inhibitor GW2580 significantly attenuated MPTP‐induced CSF1R activation and Iba1‐positive cell proliferation, without a reduction of the basal Iba1‐positive population in the substantia nigra. GW2580 treatment also significantly decreased mRNA levels of pro‐inflammatory factors, without alteration of anti‐inflammatory mediators, and significantly attenuated the MPTP‐induced loss of dopamine neurons and motor behavioral deficits. Importantly, these effects were observed in the absence of overt microglial depletion, suggesting that targeting CSF1R signaling may be a viable neuroprotective strategy in PD that disrupts pro‐inflammatory signaling, but maintains the beneficial effects of microglia.

Case Report.Aspergillusosteomyelitis is a destructive and progressive infection that has been described both in immunosuppressed and in immunocompetent hosts. We describe a case of lumbar vertebral osteomyelitis in a 61-year-old immunocompetent patient due toAspergillus nidulansthat was successfully treated with a combination of extensive surgical debridement, spinal stabilization, and a prolonged course of antifungal therapy. Imaging demonstrated findings consistent with L3 discitis. The biopsy grewAspergillusfungus and was treated with vorconizole. Imaging showed progressive destructive osteomyelitis at L3-L4. Patient underwent anterior L3 and L4 partial corpectomies, anterior interbody fusion L3-L5, and posterior T11-S2 pedicle screw and rod fixation. Antifungal treatment resulted in resolution of infection.Aspergillusmarkers remain negative. One year following definitive treatment, the patient’s back pain remains resolved.Conclusion. Definitive surgical resection of the infection, spinal stabilization, and aggressive antifungal therapy were required to eradicate the infection.

Abstract BACKGROUND AND IMPORTANCE Deep brain stimulation (DBS) is a well-established treatment for medically refractory Parkinson's disease (PD), essential tremor (ET), and dystonia. The field of DBS is expanding and techniques are under investigation for the treatment of several neurological disorders. A critical component of the success of these procedures depends significantly on the reliability and durability of devices implanted. Immediate feedback during surgery often gives the surgeon and patient a sense of confidence of long term success. When impedances are found to be elevated during the implantation of the DBS leads, appropriate trouble shooting measures are critical. CLINICAL PRESENTATION We present a 73-yr-old male undergoing awake subthalamic DBS with microelectrode recordings for severe PD. Once the optimal trajectory and depth were ascertained, the permanent DBS electrode was placed. High impedances were recorded. Troubleshooting procedures were performed and were all negative as to the cause of the values. Correct impedance levels of the DBS electrode was confirmed with extracranial testing, but continued high values were found again with intracranial positioning of the electrode. A postoperative computerized tomography (CT) scan confirmed intracranial air surrounding all of the contacts. The patient went on to outpatient programming with excellent clinical results. CONCLUSION The presence of pneumocephalus surrounding the DBS lead contacts at the target nucleus may have accounted for the intraoperative impedance findings. When all troubleshooting checks have not identified an explanation for the high impedances, intraoperative imaging may demonstrate pneumocephalus around the lead contacts, which should resolve and impedances return to normal values.

SummaryPolymorphonuclear (PMN) leucocytes participate in acute inflammatory pathologies such as acute respiratory distress syndrome (ARDS) following traumatic injury and shock, which also activates the coagulation system systemically. Trauma can prime the PMN nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex for an enhanced respiratory burst, but the relative role of various priming agents in this process remains incompletely understood. We therefore set out to identify mediators of PMN priming during coagulation and trauma-shock and determine whether PMN reactive oxygen species (ROS) generated in this manner could influence organ injury and coagulation. Initial experiments demonstrated that PMN are primed for predominantly extracellular ROS production by products of coagulation, which was abrogated by CD88/C5a receptor(C5aR) inhibition. The importance of this was highlighted further by demonstrating that known PMN priming agents result in fractionally different amounts of extracellular versus intracellular ROS release depending on the agent used. Plasma from trauma patients in haemodynamic shock (n = 10) also primed PMN for extracellular ROS in a C5a-dependent manner, which correlated with both complement alternative pathway activation and thrombin generation. Furthermore, PMN primed by preincubation with products of blood coagulation directly caused loss of endothelial barrier function in vitro that was abrogated by C5aR blockade or NADPH oxidase inhibition. Finally, we show in a murine model of trauma-shock that p47phox knock-out (KO) mice with PMN incapable of generating ROS were protected from inflammatory end-organ injury and activated protein C-mediated coagulopathy. In summary, we demonstrate that trauma-shock and coagulation primes PMN for predominantly extracellular ROS production in a C5a-dependent manner that contributes to endothelial barrier loss and organ injury, and potentially enhances traumatic coagulopathy.