61 research outputs found

    Animal Models in Traumatic Spinal Cord Injury

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    Underlying Causes of Paresthesia

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    Car sunshade-induced craniofacial injury: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>We report the case of a man who sustained a craniofacial injury after spontaneous lateral airbag deployment resulting in his face being struck by a car sunshade. This highlights the potential damage that can be caused by any object placed between a lateral airbag and a car occupant.</p> <p>Case presentation</p> <p>We report the case of a 33-year-old Caucasian man who was the driver in a frontal collision. He had opened the car sunshade and turned it 90° towards the left. As he was driving, he struck a bus, causing the driver's lateral airbag to spontaneously deploy. The airbag pushed the sunshade against his face and injured him.</p> <p>Conclusions</p> <p>Car sunshades can cause significant craniofacial injury. We suggest that sunshade design must be improved to reduce the risk of potential injuries to car occupants. We recommend a new, safer sunshade design.</p

    Functioning Pituitary Adenoma

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    Epidural hematoma in computed tomography scan-based scoring systems of traumatic brain injury

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    Dear Editor Traumatic brain injury (TBI) is a harmful condition that permanently or temporarily damages brain functions and imposes enormous costs on health systems. Computed tomography (CT) scan is the preferred modality to detect injuries and determine TBI patients' prognoses in emergency departments. Thus far, some scoring systems have been introduced for grading TBI based on CT scan findings, including the Marshal,[1] Rotterdam,[2] Helsinki,[3] Stockholm,[4] and NeuroImaging Radiological Interpretation System (NIRIS) [Table 1].[5] This letter aims to briefly raise issues regarding the scoring of epidural hematoma (EDH) in CT scan-based scoring systems of TBI.Epidural hematoma is the gathering of blood between the dura mater and the skull. This intracranial hematoma usually occurs following the bleeding from the middle meningeal artery and, less commonly, from the dural venous sinuses.[6] Some studies have shown that EDH positively affects the outcome, so patients with EDH would have a better overall prognosis.[2] A typical EDH's prognosis is good if diagnosed early and managed before deterioration. Gennarelli et al., showed that the EDH death rate is approximately one-tenth of subdural hematoma.[7] Bricolo et al., reported that mortality should be zero in uncomplicated EDH.[8]On the other hand, EDH can be potentially life-threatening. EDH of venous origin can gradually spread, and its findings may appear late, leading to a delayed diagnosis and treatment. Consequently, EDH expansion can lead to herniation, permanent neurological damage, and death.[9] EDH with a size greater than 30 ml or a midline shift of more than 10 mm does not have a good prognosis.[9] The swirl sign indicating active bleeding also worsens the prognosis.[10]The presence or absence of EDH is evaluated in four CT scan-based scoring systems of TBI [Table 1]. Three scoring systems, including Rotterdam, Helsinki, and Stockholm, consider the presence of EDH as a favorable prognostic factor, i.e., patients with EDH on their brain CT scans get a lower score. However, in the NIRIS, EDH is scored as an adverse prognostic factor based on its volume, leading to a higher score.Hence, EDH cannot always be a favorable prognostic indicator. For instance, the presence of EDH along with diffuse axonal injury (DAI) worsens the outcome.[11] However, according to Rotterdam, Helsinki, and Stockholm systems, the association of EDH with DAI would have a lower score than DAI alone. Besides, high-volume EDH can worsen the situation by causing a midline shift and brain herniation.[9] Nonetheless, the specific size of EDH is not checked in any of these three systems.The scoring systems have been developed from the statistical weighting of variables. However, it is necessary to look at the issue more dynamically and comprehensively for a more accurate outcome prediction. Adjusting CT scoring systems with clinical characteristics and scales such as the Glasgow Coma Scale (GCS) and head injury biomechanics may also be helpful

    Oligodendrogliogenesis and axon remyelination after traumatic spinal cord injuries in animal studies: a systematic review

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    © 2019 IBRO Extensive oligodendrocyte death after acute traumatic spinal cord injuries (TSCI) leads to axon demyelination and subsequently may leave axons vulnerable to degeneration. Despite the present evidence showing spontaneous remyelination after TSCI the cellular origin of new myelin and the time course of the axon ensheathment/remyelination remained controversial issue. In this systematic review the trend of oligodendrocyte death after injury as well as the extent and the cellular origin of oligodendrogliogenesis were comprehensively evaluated. The study design was based on Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA)-guided systematic review. PubMed and EMBASE were searched with no temporal or linguistic restrictions. Also, hand-search was performed in the bibliographies of relevant articles. Non-interventional animal studies discussing different types of myelinating cells including oligodendrocytes, Schwann cells and oligodendrocyte progenitor cells (OPCs) were evaluated. The extent of oligodendrocyte death, oligodendrocyte differentiation and remyelination were the pathophysiological outcome measures. We found 12,359 studies, 34 of which met the inclusion criteria. The cumulative evidence shows extensive oligodendrocytes cell death during the first week post-injury (pi). OPCs and peripheral invading Schwann cells are the dominant cells contributing in myelin formation. The maximum OPC proliferation was observed at around 2 weeks pi and oligodendrogliogenesis continues at later stages until the number of oligodendrocytes return to normal tissue by one month pi. Taken together, the evidence in animals reveals the potential role for endogenous myelinating cells in the axon ensheathment/remyelination after TSCI and this can be the target of pharmacotherapy to induce oligodendrocyte differentiation and myelin formation post-injury

    The fate of neurons after traumatic spinal cord injury in rats: a systematic review

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    Objective(s): To reach an evidence-based knowledge in the context of the temporal-spatial pattern of neuronal death and find appropriate time of intervention in order to preserve spared neurons and promote regeneration after traumatic spinal cord injury (TSCI). Materials and Methods: The study design was based on Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA)-guided systematic review. PubMed and EMBASE were searched (24 October, 2015) with no temporal or linguistic restrictions. Hand-search was performed in the bibliographies of relevant articles. Non-interventional animal studies evaluating time-dependent neuronal death following acute mechanical trauma to the spinal cord were included. We separately evaluated the fate of various populations of neurons including propriospinal neurons, ventral motor neurons, Clarke’s column neurons, and supraspinal neurons. Results: We found 11,557 non-duplicated studies. Screening through the titles and abstracts led to 549 articles, 49 of which met the inclusion criteria. Both necrotic and apoptotic neuronal deaths occur after TSCI, though necrosis is the prominent mechanism. There are differences in the responses of intrinsic neurons of the spinal cord to the TSCI. Also, the extent of neuronal death in the supraspinal neurons depends on the anatomical location of their axons. Conclusion: In order to develop new therapies, selection of the injury model and time of intervention has a crucial role in the efficacy of therapy. In addition, examining the safety and efficacy of an intervention by reliable methods not confounded by the injury-related changes would promote translation of therapies to the clinical application

    Sustaining the National Spinal Cord Injury Registry of Iran (NSCIR-IR) in a Regional Center: Challenges and Solutions

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    Background: The National Traumatic Spinal Cord Injury Registry in Iran (NSCIR-IR), was implemented initially in three hospitals as a pilot phase from 11 Oct 2015 to 19 Jun 2016 and has been active in eight centers from 19 Jun 2016. Poursina Hospital, a trauma care referral center in Rasht, Guilan Province of Iran is one of the registry sites, and has been involved in registering eligible patients since 1 Jan 2016. This study aimed to identify the challenges and solutions for sustaining the NSCIR-IR in a regional center. Methods: This was a mixed-methods study. For the quantitative analysis, a retrospective observational design was used to measure case capture or case identification rate, mapping cases in the registry against those eligible for registry inclusion amongst the register of hospital admissions. For the qualitative component, data was collected using focus group discussions and semi-structured interviews, followed by thematic analysis. Results: From 19 Jun 2016 to 24 Jan 2018, the proportion of case capture (case identification rate) was 17%. The median time between case identification and data entry to the system was 30.5 d (range: 2 to 193 d). Thematic analysis identified a lack of trained human resources as the most important cause of low case identification rate and delay in data completion. Conclusion: Recruitment and education to increase trained human resources are needed to improve case capture, the timeliness of data input and registry sustainability in a regional participating site

    Volume Changes After Traumatic Spinal Cord Injury in Animal Studies - A Systematic Review

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    There are limited data on the lesion volume changes following spinal cord injury (SCI). In this study, a meta-analysis was performed to evaluate the volume size changes of the injured spinal cord over time among animal studies in traumatic SCI. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we conducted a comprehensive electronic search of English literature of PubMed and EMBASE databases from 1946 to 2015 concerning the time-dependent changes in the volume of the spinal cord following mechanical traumatic SCI. A hand-search was also performed for non-interventional, non-molecular, and non-review studies. Quality appraisal, data extraction, qualitative and quantitative analyses were performed afterward. Of 11,561 articles yielded from electronic search, 49 articles were assessed for eligibility after reviewing of titles, abstracts, and references. Ultimately, 11 articles were eligible for quantitative synthesis. The ratio of lesion volume to spinal cord total volume increased over time. Avascularity appeared in spinal cord 4 hours after injury. During the first week, the spinal subarachnoid space decreased. The hemorrhagic lesion size peaked in 1 week and decreased thereafter. Significant loss of gray and white matter occurred from day 3 with a slower progression of white matter damage. Changes of lesion extent over time is critical in pathophysiologic processes after SCI. Early avascularity, rapid loss of gray matter, slow progression of white matter damage, and late cavitation are the pathophysiologic key points of SCI, which could be helpful in choosing the proper intervention on a timely basis

    Population based estimates of non-fatal injuries in the capital of Iran

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    <p>Abstract</p> <p>Background</p> <p>Fatal injuries are at the top of the injury pyramid; however, non-fatal injuries are quite common and impose huge medical expenses on the population. Relying on hospital data will underestimate the incidence of non-fatal injuries. The aim of this study was to estimate the annual incidence and out of pocket medical expenses of all injuries in urban population of Tehran (the capital city of Iran).</p> <p>Methods</p> <p>Using the cluster random sampling approach, a household survey of residents of greater Tehran was performed on April 2008. At randomly selected residential locations, interviewers asked one adult person to report all injuries which have occurred during the past year for all household members, as well as the type of injury, place of occurrence, the activity, cause of accidents resulting in injuries, the amount of out of pocket medical expenses for injury, and whether they referred to hospital.</p> <p>Results</p> <p>This study included 2,450 households residing in Tehran during 2007-8. The annual incidence of all injuries was 188.7 (180.7-196.9), significant injuries needing any medical care was 68.8 (63.7-74.2), fractures was 19.3 (16.6 - 22.4), and injuries resulted in hospitalization was 16.7 (14.2 - 19.6) per 1000 population. The annual incidence of fatal injuries was 33 (7-96) per 100,000 Population. In children aged 15 or less, the annual incidence of all injuries was 137.2 (120.0 - 155.9), significant injuries needing any medical care was 64.2 (52.2 - 78.0), fractures was 21.8 (15.0 - 30.7), and injuries resulted in hospitalization was 6.8 (3.3 - 12.5) per 1000 population. The mean out of pocket medical expense for injuries was 19.9 USD.</p> <p>Conclusion</p> <p>This population based study showed that the real incidence of non-fatal injuries in the capital of Iran is more than the formal hospital-based estimates. These injuries impose non trivial medical and indirect cost on the community. The out of pocket medical expense of non-fatal injuries to Tehran population is estimated as 27 million USD per year. Effective strategies should be considered to minimize these injuries and decrease the great financial burden to public and the health system.</p
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