• Journal of Korean Neurosurgical Society
• /
• 제29권9호
• /
• pp.1233-1237
• /
• 2000

Objectives : In order to evaluate the metabolic changes associated with pericontusional edematous area in mild head injury, proton magnetic resonance spectroscopy(1H-MRS) was performed in mild head injury patients (initial GCS score 13-15) with focal brain contusion. Methods : Seven head injury patients with initial GCS 13-15(3 males and 4 females : age range 15-65 years, mean age 33 years) have underwent 1H-MRS evaluations. The patients were examined within 7 days after injury(n=7) and 2 months after injury(n=5). The region of interest(ROI) was selected in the edematous area adjacent to traumatic brain contusion upon T2-weighted MR images and a corresponding region of the contralateral hemisphere (ROC, region of contralateral corresponding hemisphere) was examined as well. The metabolic ratios of NAA/Cr and lactate/Cr were compared between ROIs, ROCs and control values. Results : In initial NAA/Cr ratios, the values of ROIs were significantly lower than those of the controls(p=0.009), but there was no difference either between ROIs and ROCs(p=0.410) or between ROCs of patients and the control (p=0.199). In lactate/Cr ratios, the ROIs in all seven patients and the ROCs in two showed increased lactate signals. The lactate/Cr ratios of the ROIs were significantly elevated as compared to those of the ROCs(p=0.02) and the control(p=0.015). In two months follow-up, lactate signals were absent or significantly reduced(p=0.015). In no patients, clinical or radiological deterioration has been observed. Conclusion : Our 1H-MRS results demonstrate that there are significant ischemic changes in pericontusional edematous areas as indicated by elevated lactate signals in the patients with mild head injury. But there were no consistent neural loss or dysfunction in these area. There findings suggest that pericontusional edematous areas can be vulnerable to secondary brain insults even in the patients with mild head injury.

• BMB Reports
• /
• 제35권1호
• /
• pp.94-105
• /
• 2002

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

• 대한의생명과학회지
• /
• 제16권3호
• /
• pp.139-149
• /
• 2010

The present study was carried out to elucidate whether an environmental strain of Cryptococcus neoformans (environmental C. neoformans) isolated from an environmental source in a park of Busan has an acute pathophysiological effect in rats. On the second day after peritoneal inoculation of environmental C. neoformans, adverse effects occurred from the viewpoint of hematology and biochemistry. Eosinophil damages and crystal formations were found in the blood. Disturbances in cytokines production were observed in the cerebral and pulmonary tissues. Fungal budding existed in the brain, lung, liver and kidney. Tissue injury findings such as inflammation, leukocyte infiltration, bleeding, or degeneration were found in the brain, lung, liver and kidney. The present data suggest that the environmental C. neoformans can cause systematically harmful effects even for short periods of infection (two days of cryptococcal infection) and the adverse effects are summarized as immune derangements and biochemical and/or histological dysfunction and injury on major organ such as the brain, lung, liver and kidney in the immunocompetent hosts. Further studies should be focused on comparing the differences between environmental and clinical strains of C. neoformans.

• Investigative Magnetic Resonance Imaging
• /
• 제25권2호
• /
• pp.76-80
• /
• 2021

Post-concussion syndrome (PCS) following mild traumatic brain injury (mTBI) is a major factor that contributes to the increased socioeconomic burden caused by TBI. Myelin loss has been implicated in the development of PCS following mTBI. Diffusion tensor imaging (DTI), a traditional imaging modality for the evaluation of axonal and myelin integrity in mTBI, has intrinsic limitations, including its lack of specificity and its time-consuming and labor-intensive post-processing analysis. More recently, various fast MR techniques based on multicomponent relaxometry (MCR), including QRAPMASTER, mcDESPOT, and MDME sequences, have been developed. These MCR-based sequences can provide myelin water fraction/myelin volume fraction, a quantitative parameter more specific to myelin, which might serve as a surrogate marker of myelin volume, in a clinically feasible time. In this review, we summarize the clinical application of the MCR-based fast MR techniques in mTBI patients.

• Journal of Korean Neurosurgical Society
• /
• 제65권3호
• /
• pp.334-341
• /
• 2022

Traumatic brain injury (TBI) is one of the leading causes of death in the pediatric population in Korea. In addition, it can cause disability in children and adolescents, with physical and mental consequences. This causes a substantial burden on the health care system and occurs globally and not just in Korea. We searched and reviewed current data on the epidemiologic characteristics of pediatric TBI in Korea. Our review provides the recent epidemiological trend mainly focusing on incidence and mortality along with worldwide reported data. This review will be helpful to understand the global epidemiology of pediatric TBI and its differences between countries.

• Neonatal Medicine
• /
• 제15권1호
• /
• pp.94-99
• /
• 2008

저자들은 저혈당증에 의해 발생한 뇌후두엽의 신생아 저혈당 뇌증과 이로 인한 시각유발전위검사 이상을 보인 2례를 경험하였기에 보고하는 바이다.

• 생물정신의학
• /
• 제9권2호
• /
• pp.152-158
• /
• 2002

Background & Purpose:Neuropsychological disorders after traumatic brain injury(TBI) are poorly correlated with structural lesions detected by structural neuroimaging techniques such as computed tomography(CT) scan or magnetic resonance imaging(MRI). It is well known that patients with TBI have cognitive and behavioral disorders even in the absence of structural lesions of the brain. This study investigated whether there are abnormalities of regional cerebral blood flow(rCBF) in TBI patients without structural abnormality on MRI, using technetium 99m ethyl cysteinate dimer(Tc-99m-ECD) single photon emission computed tomography(SPECT) scans. Materials and Methods:Twenty-eight TBI patients without structural abnormality on MRI(mild, n=13/moderate, n=9/severe, n=6) and fifteen normal controls were scanned by SPECT. A voxel-based analysis using statistical parametric mapping(SPM) was performed to compare the patients with the normal controls. Results:rCBF was reduced in the right uncus and the right lateral orbitofrontal gyrus in the TBI patients. However, no increase of rCBF was noted in the patients in comparison to the normal controls. Conclusions:These results suggest that the TBI patients, even in the absence of structural lesion of the brain, may have dysfunction of the brain, particularly of the orbitofrontal and anterior pole of the temporal cortex. They also suggest that SPECT can be a useful method to identify brain dysfunctions in combination with structural brain imaging and neuropsychological tests.

• Molecules and Cells
• /
• 제37권4호
• /
• pp.345-355
• /
• 2014

Mitigating secondary delayed neuronal injury has been a therapeutic strategy for minimizing neurological symptoms after several types of brain injury. Interestingly, secondary neuronal loss appeared to be closely related to functional loss and/or death of astrocytes. In the brain damage induced by agonists of two glutamate receptors, N-ethyl-D-aspartic acid (NMDA) and kainic acid (KA), NMDA induced neuronal death within 3 h, but did not increase further thereafter. However, in the KA-injected brain, neuronal death was not obviously detectable even at injection sites at 3 h, but extensively increased to encompass the entire hemisphere at 7 days. Brain inflammation, a possible cause of secondary neuronal damage, showed little differences between the two models. Importantly, however, astrocyte behavior was completely different. In the NMDA-injected cortex, the loss of glial fibrillary acidic protein-expressing ($GFAP^+$) astrocytes was confined to the injection site until 7 days after the injection, and astrocytes around the damage sites showed extensive gliosis and appeared to isolate the damage sites. In contrast, in the KA-injected brain, $GFAP^+$ astrocytes, like neurons, slowly, but progressively, disappeared across the entire hemisphere. Other markers of astrocytes, including $S100{\beta}$, glutamate transporter EAAT2, the potassium channel Kir4.1 and glutamine synthase, showed patterns similar to that of GFAP in both NMDA- and KA-injected cortexes. More importantly, astrocyte disappearance and/or functional loss preceded neuronal death in the KA-injected brain. Taken together, these results suggest that loss of astrocyte support to neurons may be a critical cause of delayed neuronal death in the injured brain.

• Journal of Trauma and Injury
• /
• 제20권2호
• /
• pp.138-143
• /
• 2007

Purpose: $S100{\beta}$, a marker of traumatic brain injury (TBI), has been increasingly focused upon during recent years. $S100{\beta}$, is easily measured not only in cerebrospinal fluid (CSF) but also in serum. After TBI, serum S 10019, has been found to be increased at an early stage. The purpose of this study was to evaluate the clinical correlations between serum $S100{\beta}$, and neurologic outcome, and severity in traumatic brain injury. Methods: From August 2006 to October 2006, we made a protocol and studied prospectively 42 patients who visited the emergency room with TBI. Venous blood samples for $S100{\beta}$, protein were taken within six hours after TBI and vital signs, as well as the Glasgow Coma Scale (GCS), were recorded. The final diagnosis and the severity were evaluated using the Abbreviated Injury Score (AIS), and the prognosis of the patients was evaluated using the Glasgow Outcome Score (GOS). Results: Thirty-eight patients showed a favorable prognosis (discharge, recovery, transfer), and four showed an unfavorable prognosis. Serum $S100{\beta}$, was higher in patients with an unfavorable prognosis than in patients with a favorable prognosis, and a significant difference existed between the two groups ($0.74{\pm}1.50\;{\mu}g/L$ vs $7.62{\pm}6.53\;{\mu}g/L$ P=0.002). A negative correlation existed between serum $S100{\beta}$, and the Revised Traumatic Score (R2=-0.34, P=0.03), and a positive correlation existed between serum $S100{\beta}$, and the Injury Severity Score (R2=0.33, P=0.03). Furthermore, the correlation between serum $S100{\beta}$, and the initial GCS and the GCS 24 hours after admission to the ER were negative (R2=-0.62, P<0.001; R2=-0.47, P=0.005). Regarding the GOS, the mean serum concentration of $S100{\beta}$, was $7.62\;{\ss}{\partial}/L$ (SD=${\pm}6.53$) in the expired patients, $1.15\;{\mu}g/L$ in the mildly disable patient, and $0.727\;{\mu}g/L$ (SD=${\pm}0.73$) in the recovered patients. These differences are statistically significant (p<0.001). Conclusion: In traumatic brain injury, a higher level of serum concentration of $S100{\beta}$, has a poor prognosis for neurologic outcome.

• Journal of Korean Neurosurgical Society
• /
• 제29권4호
• /
• pp.461-470
• /
• 2000

Objective : Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury(TBI) in both animals and humans. It has long been recognized that mild to moderate hypothermia improves neurologic outcomes as well as reduces histologic and biochemical sequelae after TBI. In this study, two immunohistochemical staining using terminal deoxynucleotidyl-transferase-mediated biotin dUTP nick end labeling(TUNEL), staining of apoptosis, and ${\beta}$-amyloid precursor protein(${\beta}$-APP), a marker of axonal injury, were done and the authors evaluated the protective effects of hypothermia on axonal and neuronal injury after TBI in rats. Material and Method : The animals were prepared for the delivery of impact-acceleration brain injury as described by Marmarou and colleagues. TBI is achieved by allowing of a weight drop of 450gm, 1 m height to fall onto a metallic disc fixed on the intact skull of the rats. Fourty Sprague-Dawley rats weighing 400 to 450g were subjected to experimental TBI induced by an impact-acceleration device. Twenty rats were subjected to hypothermia after injury, with their rectal temperatures maintained at $32^{\circ}C$ for 1 hour. After this 1-hour period of hypothermia, rewarming to normothermic levels was accomplished over 30-minute period. Following 12 hours, 24 hours, 1 week and 2 weeks later the animals were killed and semiserial sagittal sections of the brain were reacted for visualization of the apoptosis and ${\beta}$-APP. Results : The density of ${\beta}$-APP marked damaged axons within the corticospinal tract at the pontomedullary junction and apoptotic cells at the contused cerebral cortex were calculated for each animal. In comparison with the untreated controls, a significant reduction in ${\beta}$-APP marked damaged axonal density and apoptotic cells were found in all hypothermic animals(p<0.05). Conclusion : This study shows that the posttraumatic hypothermia result in substantial protection in TBI, at least in terms of the injured axons and neurons.