JournalGlobal Spine Journal
PublisherSAGE Publications Ltd
MetadataShow full item record
AbstractStudy Design: Literature review. Objective: The aim of this review is to describe the injuries associated with sacral fractures and to analyze their impact on patient outcome. Methods: A comprehensive narrative review of the literature was performed to identify the injuries associated with sacral fractures. Results: Sacral fractures are uncommon injuries that result from high-energy trauma, and that, due to their rarity, are frequently underdiagnosed and mistreated. Only 5% of sacral fractures occur in isolation. Injuries most often associated with sacral fractures include neurologic injuries (present in up to 50% of sacral fractures), pelvic ring disruptions, hip and lumbar spine fractures, active pelvic/ abdominal bleeding and the presence of an open fracture or significant soft tissue injury. Diagnosis of pelvic ring fractures and fractures extending to the lumbar spine are key factors for the appropriate management of sacral fractures. Importantly, associated systemic (cranial, thoracic, and abdominopelvic) or musculoskeletal injuries should be promptly assessed and addressed. These associated injuries often dictate the management and eventual outcome of sacral fractures and, therefore, any treatment algorithm should take them into consideration. Conclusions: Sacral fractures are complex in nature and often associated with other often-missed injuries. This review summarizes the most relevant associated injuries in sacral fractures and discusses on their appropriate management. Copyright 2017, Copyright The Author(s) 2017.
Identifier to cite or link to this itemhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85030243127&doi=10.1177%2f2192568217701097&partnerID=40&md5=d774494d04da959211f40a4ff55dd2c1; http://hdl.handle.net/10713/10037
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Chronic Sensory and Affective Craniofacial Pain After Blast-Induced Traumatic Brain Injury and Peripheral Nerve Injury in RatsStudlack, Paige Elizabeth; Keller, Asaf; Simard, J. Marc; 0000-0002-3626-1865 (2017)Thousands of military members suffer long-term consequences of blast-induced traumatic brain injury (Blast-TBI), including chronic head and face pain. Pain after blast-TBI usually manifests as post-traumatic headaches with a high degree of comorbid mood disorders, suggesting that the affective dimension of pain may burden survivors of blast-TBI. Here, we tested the hypothesis that an innovative model of the unique aspect of blast-TBI over blunt-force TBI, the primary blast injury, directed over the cranium sufficiently modeled long-term conditions of human blast exposure in rats. Rats exposed to cranium-directed primary blast-TBI demonstrated behavioral manifestations of ongoing pain, mechanical hyperalgesia, and cold allodynia three weeks after injury, recapitulating chronic facial pain in patients after blast-TBI. We predicted that maladaptive changes to pain-signaling and -processing nuclei in CNS would induce and maintain pain behavior after blast-TBI. We recorded single units in sensory pain-associated nuclei, the posterior nucleus of the thalamus (PO) and spinal trigeminal nucleus caudalis (SpVc), which have previously been causally associated with pain after spinal cord injury. We observed hyperexcitability at baseline of PO neurons after blast injury in absence of changes to evoked response to cutaneous noxious stimuli. Neuronal hyperexcitability in PO is not associated with persistent gliosis. Affective pain processing through the parabrachial complex (PB) occurs in parallel to information coding the sensory dimension of pain through PO. We assessed central changes to PB neuronal activity in a robust model of post-traumatic pain using the chronic constriction injury of the infraorbital nerve (CCI-ION). PB neurons, weeks to months after injury, are hyper-excitable in chronic pain, as shown by prolonged response after presentation of noxious cutaneous stimulation ("after-discharges"), previously observed to be causally-related to pain due to CCI-ION in SpVc. Further study of PB hyperexcitability in blast-TBI rodent models may elucidate the mechanism underlying blast-TBI-associated affective pain.
Efficacy of Ultra-Early (< 12 h), Early (12-24 h), and Late (>24-138.5 h) Surgery with Magnetic Resonance Imaging-Confirmed Decompression in American Spinal Injury Association Impairment Scale Grades A, B, and C Cervical Spinal Cord InjuryAarabi, B.; Chryssikos, T.; Shanmuganathan, K.; Schwartzbauer, G.T.; Simard, J.M.; Olexa, J.; Sansur, C.A.; Crandall, K.M.; Mushlin, H.; Kole, M.J.; et al. (Mary Ann Liebert Inc., 2020)In cervical traumatic spinal cord injury (TSCI), the therapeutic effect of timing of surgery on neurological recovery remains uncertain. Additionally, the relationship between extent of decompression, imaging biomarker evidence of injury severity, and outcome is incompletely understood. We investigated the effect of timing of decompression on long-term neurological outcome in patients with complete spinal cord decompression confirmed on postoperative magnetic resonance imaging (MRI). American Spinal Injury Association (ASIA) Impairment Scale (AIS) grade conversion was determined in 72 AIS grades A, B, and C patients 6 months after confirmed decompression. Thirty-two patients underwent decompressive surgery ultra-early (< 12 h), 25 underwent decompressive surgery early (12-24 h), and 15 underwent decompressive surgery late (> 24-138.5 h) after injury. Age, gender, injury mechanism, intramedullary lesion length (IMLL) on MRI, admission ASIA motor score, and surgical technique were not statistically different among groups. Motor complete patients (p = 0.009) and those with fracture dislocations (p = 0.01) tended to be operated on earlier. Improvement of one grade or more was present in 55.6% of AIS grade A, 60.9% of AIS grade B, and 86.4% of AIS grade C patients. Admission AIS motor score (p = 0.0004) and pre-operative IMLL (p = 0.00001) were the strongest predictors of neurological outcome. AIS grade improvement occurred in 65.6%, 60%, and 80% of patients who underwent decompression ultra-early, early, and late, respectively (p = 0.424). Multiple regression analysis revealed that IMLL was the only significant variable predictive of AIS grade conversion to a better grade (odds ratio, 0.908; confidence interval [CI], 0.862-0.957; p < 0.001). We conclude that in patients with post-operative MRI confirmation of complete decompression following cervical TSCI, pre-operative IMLL, not the timing of surgery, determines long-term neurological outcome. Copyright Bizhan Aarabi et al., 2020
The voltage-gated proton channel Hv1 contributes to neuronal injury and motor deficits in a mouse model of spinal cord injuryMurugan, Madhuvika; Zheng, Jiaying; Wu, Gongxiong; Mogilevsky, Rochelle; Zheng, Xin; Hu, Peiwen; Wu, Junfang; Wu, Long-Jun (Springer Nature, 2020-10-20)Traumatic injury to the spinal cord initiates a series of pathological cellular processes that exacerbate tissue damage at and beyond the original site of injury. This secondary damage includes oxidative stress and inflammatory cascades that can lead to further neuronal loss and motor deficits. Microglial activation is an essential component of these secondary signaling cascades. The voltage-gated proton channel, Hv1, functionally expressed in microglia has been implicated in microglia polarization and oxidative stress in ischemic stroke. Here, we investigate whether Hv1 mediates microglial/macrophage activation and aggravates secondary damage following spinal cord injury (SCI). Following contusion SCI, wild-type (WT) mice showed significant tissue damage, white matter damage and impaired motor recovery. However, mice lacking Hv1 (Hv1-/-) showed significant white matter sparing and improved motor recovery. The improved motor recovery in Hv1-/- mice was associated with decreased interleukin-1β, reactive oxygen/ nitrogen species production and reduced neuronal loss. Further, deficiency of Hv1 directly influenced microglia activation as noted by decrease in microglia numbers, soma size and reduced outward rectifier K+ current density in Hv1-/- mice compared to WT mice at 7 d following SCI. Our results therefore implicate that Hv1 may be a promising potential therapeutic target to alleviate secondary damage following SCI caused by microglia/macrophage activation.