Evaluation of the Thoracolumbar Injury Classification and Severity (TLICS) Score Over a Two-Year Period at a Level One Trauma Center.

Introduction The use of the Thoracolumbar Injury Classification and Severity Score (TLICS) and other classification systems for guiding the management of traumatic spinal injuries remains controversial. TLICS is one of the few classifications that provides treatment recommendations.We sought to analyze intervention modality selection based on the TLICS scoring system. Methods A retrospective review of patients presenting with traumatic thoracolumbar fractures at a level 1 trauma center over a two-year period was performed. Primary endpoints for comparison analysis included visual analog scale (VAS) scores and Cobb angles during follow-up. Results There were 272 patients with thoracolumbar fractures, of whom 212 had TLICS of ≤3, six with TLICS of 4, and 54 with TLICS of ≥5. Of the 272 total patients, 59 were treated via surgery and 213 via non-surgical conservative methods. The VAS scores significantly decreased from presentation to last follow-up in both surgically treated and conservative groups (p<0.0001). This remained consistent in subgroup analyses of TLICS ≤ 3, TLICS = 4, and TLICS ≥ 5 (p<0.0001). Burst fractures treated conservatively had larger fracture Cobb angles versus those treated via surgery at the last follow-up, although this was not significantly associated (p=0.07). The only significant relationship with Cobb angles was in distraction fractures of the TLICS > 4 conservative group, who had significantly lower Cobb angles at the last follow-up than the TLICS > 4 surgical group (p<0.04). The "surgeon's choice" for TLICS = 4 was surgical intervention (4/6 patients, 66.7%). Conclusion Using the TLICS score, thoracolumbar injuries in a level 1 trauma center are more commonly TLICS ≤ 3. For patients with TLICS = 4, the surgeon's choice was most commonly surgical repair. VAS scores decreased over time from presentation between surgically and conservatively managed patients (as well as within-group analyses). The data concerning Cobb angles were more ambiguous, as larger Cobb angles in burst fractures treated conservatively did not show statistically significant differences with surgery.

Evolution of open surgery for unruptured intracranial aneurysms over a fifteen year period-increased difficulty and morbidity.

OBJECTIVE: The approach to intervention for unruptured intracranial aneurysms (UIAs) remains controversial. Utilization of endovascular techniques for aneurysm repair increased dramatically during the last decade. We sought to analyze recent national trends for electively treated (open and endovascular) UIAs focusing on pre-existing patient disease burden and intervention modality selection. METHODS: The Nationwide Inpatient Sample (NIS) national database was used to identify patients with primary diagnosis codes of unruptured intracranial aneurysm between 1999 and 2014. Patients were dichotomized by intervention into endovascular or open surgical treatment. Analysis of pre-existing disease severity were calculated using the Elixhauser comorbidity index. Complications of combined peri-procedural stroke or death during admission and hospital length of stay were used as primary endpoints for comparison. RESULTS: The percent of total UIAs treated electively with open approach decreased from more than 95 % of cases in 1999 to less than 25 % in 2014. Patients undergoing clipping were 3 years younger than those in the endovascular group (p < 0.001). The rate of primary endpoint complications (stroke and death) and length of stay for open cases saw a decrease throughout the study but remained statistically higher when compared to the endovascular group over the study period (p < 0.001). Additionally, non-neurologic complications increased over the time period for open cases. The average preoperative co-morbid disease severity for all groups treated increased over this interval. Conversely, the relative volume of endovascular cases increased but the rate of complications and average group disease remained statistically lower than the surgical clipping group (p < 0.05). CONCLUSION: The percent of UIAs treated electively with open approach has decreased since 1999 with a concomitant increase in complication rate in particular compared to endovascular cases. However, the health characteristics of patients treated with surgical clipping show an increase in severity of pre-existing co-morbidities. Further research into factors contributing to this finding, including potential socioeconomic differences and changes in surgeon experience are needed.

Anterior Thoracic Diskectomy and Fusion: Surgical Technique and Anatomic Considerations.

Ossification of the posterior longitudinal ligament (OPLL) is a rare condition that can lead to progressive spinal cord compression.1 Currently, surgical decompression remains the optimal treatment in symptomatic patients.2,3 In cases with significant thoracic stenosis and concern for ventral erosion of the dura, an anterior approach may be necessary for direct decompression.4 In Video 1, we demonstrate the successful application of a multidisciplinary approach for surgical resection of a large OPLL lesion located at the T2-3 disk space. A 37-year-old female with medical history significant for rickets presented a year after a fall with bilateral lower extremity paraparesis and saddle anesthesia. Exposure consisted of a manubrial window, followed by thoracic diskectomy and fusion with drilling of the calcified posterior longitudinal ligament. Major steps within this video include 1) a summary of the patient presentation and preoperative imaging, 2) exposure of thoracic vertebrae via a manubrial window approach, 3) thoracic diskectomy and fusion with take-down of calcified posterior longitudinal ligament, and 4) a review of the postoperative imaging. The patient tolerated the procedure well with immediate relief of symptoms and was subsequently discharged on postoperative day 1 with no complications. This operative video illustrates the technical steps and capabilities of an anterior approach, achieving near-complete gross total resection of an OPLL lesion using a multidisciplinary approach. The patient consented to this procedure.

Combined Transcranial and Endoscopic Endonasal Approach for Resection of a Complex Sinonasal Squamous Cell Carcinoma: Two-Dimensional Operative Video.

Sinonasal squamous cell carcinoma (SCC) is a rare head-and-neck neoplasm that has a propensity to locally invade vital structures. Currently, the combination of surgical resection and radiation remains the optimal treatment. 1 However, the extent of disease burden and involvement of surrounding anatomy may make these inoperable. Here, we demonstrate the successful application of multidisciplinary approach for surgical resection of a large, complex SCC lesion centered at the superior nasal cavity with extension into the eye orbits and brain. A two-step approach was performed; transcribiform, endoscopic piecemeal resection with reconstruction of the skull base, followed by a bifrontal craniotomy. Reconstruction was achieved using an inlay of DuraMatrix allograft (Stryker Inc., Kalamzoo, Michigan, United States) followed by an inlay of AlloDerm (Allergan Inc., Irvine, California, United States), anchored anteriorly and posteriorly with wide wings placed over the respective orbital roofs. Major steps include (1) a summary of the patient presentation and preoperative imaging, (2) resection of the tumor endonasally, (3) resection of the tumor intracranially from a bifrontal craniotomy, and (4) a review of the postoperative imaging. The patient tolerated the procedure ( Fig. 1 ) well, returned to his baseline with no new neurologic deficits, and was placed on 6-week antibiotics regimen for osteomyelitis discovered during the operation. Approximately, 2 months after discharge, the patient unfortunately returned with altered mental status, was found to have sepsis, and expired shortly thereafter. This operative video illustrates the technical steps and capabilities of surgical treatment, achieving near-complete gross total resection of a complex SCC lesion using a multidisciplinary approach. The link to the video can be found at: https://youtu.be/8ffckKIuBzM .

The prevalence of 11 ribs and its potential implications in spine surgery.

INTRODUCTION: Wrong level surgery is a preventable event in spine surgery. The thoracic spine given its length and anatomical landmarks remains the most challenging spine section for accurate localization during surgery. Traditionally, counting the ribs with intraoperative fluoroscopy is the preferred method. The incidence of 11 ribs instead of the conventional 12 ribs is not examined in current scientific literature, even though the incidence of 11 ribs may have a substantial impact on spinal procedures and the outcomes. This is especially relevant if patients have a potential surgical pathology of their thoracic spine. In this case series we sought to investigate the prevalence of 11 ribs in a trauma population. METHODS: A retrospective review was conducted of patients presenting with thoracolumbar fractures at our Level I Trauma Center between 2017 and 2018. CT scans were obtained and analyzed by counting the number of ribs. RESULTS: Out of 234 patients who were consulted for thoraco-lumbar fractures by spine specialists, 8 patients had 11 ribs which results in a prevalence of 3.4 % in this population. Within these 8 patients, 5 were male (62.5 %). CONCLUSIONS: Spine surgeons should consider the possibility of numeric variation of ribs when evaluating thoracolumbar spine imaging. In a trauma population with spine fractures, the prevalence of 11 ribs is 3.4 %. Given the not insignificant prevalence of this variant in potentially surgical spine patients, the spine surgeon should remain vigilant of this anatomical variant.

Stem cell-paved biobridges facilitate stem transplant and host brain cell interactions for stroke therapy.

Distinguished by an infarct core encased within a penumbra, stroke remains a primary source of mortality within the United States. While our scientific knowledge regarding the pathology of stroke continues to improve, clinical treatment options for patients suffering from stroke are extremely limited. Tissue plasminogen activator (tPA) remains the sole FDA-approved drug proven to be helpful following stroke. However, due to the need to administer the drug within 4.5h of stroke onset its usefulness is constrained to less than 5% of all patients suffering from ischemic stroke. One experimental therapy for the treatment of stroke involves the utilization of stem cells. Stem cell transplantation has been linked to therapeutic benefit by means of cell replacement and release of growth factors; however the precise means by which this is accomplished has not yet been clearly delineated. Using a traumatic brain injury model, we recently demonstrated the ability of transplanted mesenchymal stromal cells (MSCs) to form a biobridge connecting the area of injury to the neurogenic niche within the brain. We hypothesize that MSCs may also have the capacity to create a similar biobridge following stroke; thereby forming a conduit between the neurogenic niche and the stroke core and peri-infarct area. We propose that this biobridge could assist and promote interaction of host brain cells with transplanted stem cells and offer more opportunities to enhance the effectiveness of stem cell therapy in stroke. This article is part of a Special Issue entitled SI: Cell Interactions In Stroke.

Neuroinflammatory responses to traumatic brain injury: etiology, clinical consequences, and therapeutic opportunities.

Traumatic brain injury (TBI) is a serious public health problem accounting for 1.4 million emergency room visits by US citizens each year. Although TBI has been traditionally considered an acute injury, chronic symptoms reminiscent of neurodegenerative disorders have now been recognized. These progressive neurodegenerative-like symptoms manifest as impaired motor and cognitive skills, as well as stress, anxiety, and mood affective behavioral alterations. TBI, characterized by external bumps or blows to the head exceeding the brain's protective capacity, causes physical damage to the central nervous system with accompanying neurological dysfunctions. The primary impact results in direct neural cell loss predominantly exhibiting necrotic death, which is then followed by a wave of secondary injury cascades including excitotoxicity, oxidative stress, mitochondrial dysfunction, blood-brain barrier disruption, and inflammation. All these processes exacerbate the damage, worsen the clinical outcomes, and persist as an evolving pathological hallmark of what we now describe as chronic TBI. Neuroinflammation in the acute stage of TBI mobilizes immune cells, astrocytes, cytokines, and chemokines toward the site of injury to mount an antiinflammatory response against brain damage; however, in the chronic stage, excess activation of these inflammatory elements contributes to an "inflamed" brain microenvironment that principally contributes to secondary cell death in TBI. Modulating these inflammatory cells by changing their phenotype from proinflammatory to antiinflammatory would likely promote therapeutic effects on TBI. Because neuroinflammation occurs at acute and chronic stages after the primary insult in TBI, a treatment targeting neuroinflammation may have a wider therapeutic window for TBI. To this end, a better understanding of TBI etiology and clinical manifestations, especially the pathological presentation of chronic TBI with neuroinflammation as a major component, will advance our knowledge on inflammation-based disease mechanisms and treatments.

Stem cell therapy for neonatal hypoxic-ischemic encephalopathy.

Treatments for neonatal hypoxic-ischemic encephalopathy (HIE) have been limited. The aim of this paper is to offer translational research guidance on stem cell therapy for neonatal HIE by examining clinically relevant animal models, practical stem cell sources, safety and efficacy of endpoint assays, as well as a general understanding of modes of action of this cellular therapy. In order to do so, we discuss the clinical manifestations of HIE, highlighting its overlapping pathologies with stroke and providing insights on the potential of cell therapy currently investigated in stroke, for HIE. To this end, we draw guidance from recommendations outlined in stem cell therapeutics as an emerging paradigm for stroke or STEPS, which have been recently modified to Baby STEPS to cater for the "neonatal" symptoms of HIE. These guidelines recognized that neonatal HIE exhibit distinct disease symptoms from adult stroke in need of an innovative translational approach that facilitates the entry of cell therapy in the clinic. Finally, new information about recent clinical trials and insights into combination therapy are provided with the vision that stem cell therapy may benefit from available treatments, such as hypothermia, already being tested in children diagnosed with HIE.

Mannitol-enhanced delivery of stem cells and their growth factors across the blood-brain barrier.

Ischemic brain injury in adults and neonates is a significant clinical problem with limited therapeutic interventions. Currently, clinicians have only tPA available for stroke treatment and hypothermia for cerebral palsy. Owing to the lack of treatment options, there is a need for novel treatments such as stem cell therapy. Various stem cells including cells from embryo, fetus, perinatal, and adult tissues have proved effective in preclinical and small clinical trials. However, a limiting factor in the success of these treatments is the delivery of the cells and their by-products (neurotrophic factors) into the injured brain. We have demonstrated that mannitol, a drug with the potential to transiently open the blood-brain barrier and facilitate the entry of stem cells and trophic factors, as a solution to the delivery problem. The combination of stem cell therapy and mannitol may improve therapeutic outcomes in adult stroke and neonatal cerebral palsy.

Vascular damage: a persisting pathology common to Alzheimer's disease and traumatic brain injury.

Alzheimer's disease (AD) and traumatic brain injury (TBI) are both significant clinical problems characterized by debilitating symptoms with limited available treatments. Interestingly, both neurological diseases are characterized by neurovascular damage. This impaired brain vasculature correlates with the onset of dementia, a symptom associated with hippocampal degeneration seen in both diseases. We posit that vascular damage is a major pathological link between TBI and AD, in that TBI victims are predisposed to AD symptoms due to altered brain vasculature; vice versa, the progression of AD pathology may be accelerated by TBI especially when the brain insult worsens hippocampal degeneration. Our hypothesis is supported by recent data reporting expedited AD pathology in presymptomatic transgenic AD mice subjected to TBI. If our hypothesis is correct, treatments targeted at repairing the vasculature may prove effective at treating both diseases and preventing the evolution of AD symptoms in TBI victims.

Diabetes insipidus contributes to traumatic brain injury pathology via CD36 neuroinflammation.

Each year, over one million people in the United States are affected by traumatic brain injury (TBI). Symptoms of both acute and chronic neuroinflammation follow TBI, coinciding with a robust immune response and activation of the brain's endogenous repair mechanisms. TBI can lead to endocrine failure as a result of damage to the thalamic region of the brain, evidenced by excessive thirst and polyuria often accompanying TBI. These symptoms indicate the presence of diabetes insipidus (DI), a disruption of water homeostasis due to antidiuretic hormone deficiency. This deficiency accompanies a mechanical or neuroinflammatory damage to the thalamic region during TBI, evidenced by increased expression of inflammatory microglial marker MHCII in this brain region. Excessive thirst and urinations, which are typical DI symptoms, in our chronic TBI rats also suggest a close connection between TBI and DI. We seek to bridge this gap between TBI and DI through investigation of the Cluster of Differentiation 36 (CD36) receptor. This receptor is associated with Low-Density Lipoprotein (LDL) deregulation, pro-inflammatory events, and innate immunity regulation. We posit that CD36 exacerbates TBI through immune activation and subsequent neuroinflammation. Indeed, scientific evidence already supports pathological interaction of CD36 in other neurological disorders including stroke and Alzheimer's disease. We propose that DI contributes to TBI pathology via CD36 neuroinflammation. Use of CD36 as a biomarker may provide insights into treatment and disease pathology of TBI and DI. This unexplored avenue of research holds potential for a better understanding and treatment of TBI and DI.