Heterotrophic ossification (HO) is a reactive disease presenting the formation of mature lamellar bone in soft tissues. It is known to occur following surgery, soft tissue injury, or central nervous system anomalies. However, a definite cause has not yet been clearly addressed. During the process of approach, reduction, and fixation while conducting surgeries, partial injury of soft tissue is inevitable. Additionally, secondary injuries may be caused during the active and passive range of motion exercises that should be done for the recovery of joint motion after surgery. The authors experienced cases of HO that may occur during surgery and rehabilitation after surgery. The authors recognized that special care is required for patients complaining of severe pain during the early stage of rehabilitation immediately after surgery. This study aimed to reaffirm the principles of fracture treatment by reviewing the cases and to investigate the occurrence of HO after fracture surgery.
Central Nervous System ; Exercise ; Humans ; Joints ; Range of Motion, Articular ; Rehabilitation ; Soft Tissue Injuries

PURPOSE: This study was designed to provide a basis for building a master plan for a regional trauma system by analyzing the distribution of trauma deaths in the most populous province in Korea.MATERIALS AND METHODS: We investigated the time distribution to death for trauma patients who died between January and December 2017. The time distribution to death was categorized into four groups (within a day, within a week, within a month, and over a month). Additionally, the distribution of deaths within 24 hours was further analyzed. We also reviewed the distribution of deaths according to the cause of death and mechanism of injury.RESULTS: Of the 1546 trauma deaths, 328 cases were included in the final study population. Patients who died within a day were the most prevalent (40.9%). Of those who died within a day, the cases within an hour accounted for 40.3% of the highest proportion. The majority of trauma deaths within 4 hours were caused by traffic-related accidents (60.4%). The deaths caused by bleeding and central nervous system injuries accounted for most (70.1%) of the early deaths, whereas multi-organ dysfunction syndrome/sepsis had the highest ratio (69.7%) in the late deaths. Statistically significant differences were found in time distribution according to the mechanism of injury and cause of death (p<0.001).CONCLUSION: The distribution of overall timing of death was shown to follow a bimodal pattern rather than a trimodal model in Korea. Based on our findings, a suitable and modified trauma system must be developed.
Cause of Death ; Central Nervous System ; Hemorrhage ; Humans ; Korea ; Wounds and Injuries

Recovery from central nervous system (CNS) injury, such as stroke or spinal cord injury (SCI), largely depends on axonal regeneration, and the neuronal and glial cells plasticity in the lesioned tissue. The lesioned tissue following CNS injury forms a scar that is composed of astrocytes and mixed with connective tissues. At the glial scar, the regenerating axon forms dystrophic endbulbs which do not regenerate and grow beyond the glial scar without a suitable environment. Along with the astrocytes, microglia are also suspected of being involved in necrotic and apoptotic neuronal cell death and the early response to axonal damage in CNS injury. The inflammatory response, a major component of secondary injury and controlled by the microglia, plays a pivotal role in nerve injury and control the regenerative response. As a result, it is very important to control the glial cell function in order to assure the recovery of the CNS injury. Studies have suggested that agmatine, a L-arginine derived primary amine, is a potential modulator of glial cell function after CNS injuries. Agmatine was found to possess anti-inflammatory and neuroprotective characteristics that benefited the rehabilitation process following CNS injury. In this review, we will discuss the effect of agmatine on glial cells in the process of recovery after CNS injury.
Agmatine ; Arginine ; Astrocytes ; Axons ; Cell Death ; Central Nervous System ; Cicatrix ; Connective Tissue ; Microglia ; Neuroglia ; Neurons ; Plastics ; Regeneration ; Rehabilitation ; Spinal Cord Injuries ; Stroke

Vertigo, dizziness, and disequilibrium are common symptoms following concussion or traumatic brain injury. Dizziness and vertigo may be the result of trauma to the peripheral vestibular system or the central nervous system, or, in some cases, may be due to anxiety, depression, or posttraumatic stress disorder; these mechanisms are not mutually exclusive. While most peripheral vestibular disorders can be identified by testing and examination, those without inner ear causes that have persisting complaints of dizziness and motion sickness are more difficult to understand and to manage. Some of these patients exhibit features compatible with vestibular migraine and may be treated successfully with migraine preventative medications. This paper reviews the neurological causes of persisting dizziness, the possible mechanisms, and the pathophysiology, as a framework for patient management and for future research.
Anxiety ; Brain Injuries ; Central Nervous System ; Depression ; Diffuse Axonal Injury ; Dizziness ; Ear, Inner ; Humans ; Migraine Disorders ; Motion Sickness ; Stress Disorders, Post-Traumatic ; Vertigo

We have previously demonstrated that the neurosteroid dehydroepiandrosterone sulfate (DHEAS) induces functional potentiation of N-methyl-D-aspartate (NMDA) receptors via increases in phosphorylation of NMDA receptor GluN1 subunit (pGluN1). However, the modulatory mechanisms responsible for the expression of the DHEA-synthesizing enzyme, cytochrome P450c17 following peripheral nerve injury have yet to be examined. Here we determined whether oxidative stress induced by the spinal activation of nitric oxide synthase type II (NOS-II) modulates the expression of P450c17 and whether this process contributes to the development of neuropathic pain in rats. Chronic constriction injury (CCI) of the sciatic nerve induced a significant increase in the expression of NOS-II in microglial cells and NO levels in the lumbar spinal cord dorsal horn at postoperative day 5. Intrathecal administration of the NOS-II inhibitor, L-NIL during the induction phase of neuropathic pain (postoperative days 0~5) significantly reduced the CCI-induced development of mechanical allodynia and thermal hyperalgesia. Sciatic nerve injury increased the expression of PKC- and PKA-dependent pGluN1 as well as the mRNA and protein levels of P450c17 in the spinal cord at postoperative day 5, and these increases were suppressed by repeated administration of L-NIL. Co-administration of DHEAS together with L-NIL restored the development of neuropathic pain and pGluN1 that were originally inhibited by L-NIL administration alone. Collectively these results provide strong support for the hypothesis that activation of NOS-II increases the mRNA and protein levels of P450c17 in the spinal cord, ultimately leading to the development of central sensitization and neuropathic pain induced by peripheral nerve injury.
Animals ; Central Nervous System Sensitization ; Constriction ; Cytochromes ; Dehydroepiandrosterone ; Dehydroepiandrosterone Sulfate ; Hyperalgesia ; N-Methylaspartate ; Neuralgia ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase ; Nitric Oxide ; Oxidative Stress ; Peripheral Nerve Injuries ; Phosphorylation ; Rats ; RNA, Messenger ; Rodentia ; Sciatic Nerve ; Spinal Cord ; Spinal Cord Dorsal Horn

Central pain, a neuropathic pain caused by an injury or dysfunction of the central nervous system, is a common, annoying sequela of mild traumatic brain injury (mTBI). Clarification of the pathogenetic mechanism of central pain is mandatory for precise diagnosis, proper management, and prognosis prediction. The introduction of diffusion tensor imaging allowed assessment of the association of the central pain and injury of the spinothalamic tract (STT), and traumatic axonal injury (TAI) in mTBI. In this review, 6 diffusion tensor tractography studies on central pain due to TAI of the STT in patients with mTBI are reviewed. The diagnostic approach for TAI of the STT in individual patients with mTBI is discussed, centering around the methods that these studies employed to demonstrate TAI of the STT.
Axons* ; Brain Concussion ; Brain Injuries* ; Central Nervous System ; Diagnosis ; Diffusion ; Diffusion Tensor Imaging ; Humans ; Neuralgia ; Prognosis ; Spinothalamic Tracts*

Carbon monoxide (CO) is a gaseous molecule produced from heme by heme oxygenase (HO). Endogenous CO production occurring at low concentrations is thought to have several useful biological roles. In mammals, especially humans, a proper neurovascular unit comprising endothelial cells, pericytes, astrocytes, microglia, and neurons is essential for the homeostasis and survival of the central nervous system (CNS). In addition, the regeneration of neurovascular systems from neural stem cells and endothelial precursor cells after CNS diseases is responsible for functional repair. This review focused on the possible role of CO/HO in the neurovascular unit in terms of neurogenesis, angiogenesis, and synaptic plasticity, ultimately leading to behavioral changes in CNS diseases. CO/HO may also enhance cellular networks among endothelial cells, pericytes, astrocytes, and neural stem cells. This review highlights the therapeutic effects of CO/HO on CNS diseases involved in neurogenesis, synaptic plasticity, and angiogenesis. Moreover, the cellular mechanisms and interactions by which CO/HO are exploited for disease prevention and their therapeutic applications in traumatic brain injury, Alzheimer’s disease, and stroke are also discussed.
Astrocytes ; Brain Injuries ; Carbon Monoxide* ; Carbon* ; Central Nervous System ; Central Nervous System Diseases ; Endothelial Cells ; Heme ; Heme Oxygenase (Decyclizing) ; Homeostasis ; Humans ; Mammals ; Microglia ; Neural Stem Cells ; Neurogenesis ; Neuronal Plasticity ; Neurons ; Pericytes ; Regeneration ; Stroke ; Therapeutic Uses

Objective: Due to the special anatomical structure and pathophysiological mechanism of the central nervous system (CNS), there is a big difference between the repair of brain injury and other systems of the body. More and more evidence shows that targetedly reducing the autoimmune response of brain tissue without affecting the immune function in other parts of the body will be the best optimized treatment for brain injury. Data Sources: This review was based on data in articles published in PubMed up to June 5, 2017, with the following keywords: "immune tolerance", "traumatic brain injury", and "central nervous system". Study Selection: Original articles and critical reviews on immune tolerance and brain damage were selected for this review. References of the retrieved articles were also screened to search for potentially relevant papers. Results: The CNS is isolated from the immune system through the blood-brain barrier. After brain injury, brain antigens are released into the systemic circulation to induce damaging immune responses. Immune tolerance can effectively reduce the brain edema and neurological inflammatory response after brain injury, which is beneficial to the recovery of neurological function. The clinical application prospect and theoretical research value of the treatment of immune tolerance on traumatic brain injury (TBI) is worth attention. Conclusions The establishment of immune tolerance mechanism has a high clinical value in the treatment of TBI. It opens up new opportunities for the treatment of brain damage.
Brain ; immunology ; Brain Injuries, Traumatic ; immunology ; therapy ; Central Nervous System ; Humans ; Immune Tolerance ; Immunotherapy

BACKGROUND: Organic solvent-induced chronic toxic encephalopathy (CTE) is known as a non-progressive disorder that does not progress after diagnosis. The authors present a case those symptoms worsened after continued exposure to organic solvent after returning to work. Because such a case has not been reported in South Korea to the best of our knowledge, we intend to report this case along with literature review. CASE PRESENTATION: A 59-year-old man, who performed painting job at a large shipyard for 20 years, was receiving hospital treatment mainly for depression. During the inpatient treatment, severe cognitive impairment was identified, and he visited the occupational and environmental medicine outpatient clinic for assessing work relatedness. In 1984, at the age of 27, he began performing touch-up and spray painting as a shipyard painter. Before that he had not been exposure to any neurotoxic substances. In 2001, at the age of 44, after 15 years of exposure to mixed solvents including toluene, xylene and others, he was diagnosed with CTE International Solvent Workshop (ISW) type 2A. After 7 years of sick leave, he returned to work in 2006. And he repeated return-to-work and sick leave in the same job due to worsening of depressive symptoms. He had worked four times (2006–2010, 2011–2011, 2011–2011, 2016–2017) for a total of 5 years as a shipyard painter after first compensation. During the return-to-work period, the mean values of the mixed solvent index ranged from 0.57 to 2.15, and except for a one semiannual period, all mean values were above the standard value of 1. We excluded other diseases that can cause cognitive impairment like central nervous system diseases, brain injury, psychological diseases and metabolic diseases with physical examinations, laboratory tests, and brain image analysis. And finally, throughout neuropsychological tests, an overall deterioration in cognitive function was identified compared to 2002, and the deterioration types was similar to that often shown in the case of CTE; thus a diagnosis of CTE (ISW) type 3 was made. CONCLUSION: This case is showing that CTE can go on with continued exposure to mixed solvents. Appropriate “fitness to work” should be taken to prevent disease deterioration especially for the sick leave workers.
Ambulatory Care Facilities ; Brain ; Brain Injuries ; Central Nervous System Diseases ; Cognition ; Cognition Disorders ; Compensation and Redress ; Depression ; Diagnosis ; Education ; Environmental Medicine ; Humans ; Inpatients ; Korea ; Metabolic Diseases ; Middle Aged ; Neuropsychological Tests ; Neurotoxicity Syndromes ; Occupational Diseases ; Paint ; Paintings ; Physical Examination ; Return to Work ; Sick Leave ; Solvents ; Toluene ; Xylenes

Traumatic pseudoaneurysms of middle meningeal artery (MMA) and medial sphenoid wing dural arteriovenous fistula (dAVF) are rare. These lesions usually result from traumatic brain injury, and associated with skull fracture. In this paper, the authors report a case of a patient with a ruptured traumatic pseudoaneurysm of MMA and medial sphenoid wing dAVF presented with an intracerebral hemorrhage in the left temporal region and subarachnoid hemorrhage. These lesions were completely obliterated by endovascular treatment, and the patient was recovered without any neurologic deficit. However, 18-day after the procedure, delayed neurologic deficits were developed due to cerebral vasospasm.
Aneurysm, False* ; Arteriovenous Fistula ; Brain Injuries ; Central Nervous System Vascular Malformations* ; Cerebral Hemorrhage ; Humans ; Meningeal Arteries* ; Neurologic Manifestations ; Skull Fractures ; Subarachnoid Hemorrhage* ; Subarachnoid Hemorrhage, Traumatic ; Temporal Lobe ; Vasospasm, Intracranial