• The Korean Journal of Pain
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• v.12 no.2
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• pp.263-267
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• 1999

We have observed retroperitoneal hematoma after trigger point injections of quadratus lumborum in a patient with chronic low back pain. Severe flank pain and dyspnea was observed three hours after injection of local anesthetic and steroid to the trigger point of quadratus lumborum muscle. There was fuge hematoma in abdominal CT image around the right kidney, which displaced and compressed the kidney anteriorly. Following infusion of contrast media, extravasation through renal vein and IVC was notified. Patient had a past history of having been treated with platelet aggregation inhibitor and lower dose aspirin treatment after cerebral ischemia for a year, but coagulative function was within normal range. Patient was admitted 12 days for bed rest, pain control and transfusion. We need to take greater care with a frequent aspiration and exact direction of needle, during trigger point injection of quadratus lumborum, particu right side, to avoid vascular injury.

• YAKHAK HOEJI
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• v.45 no.4
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• pp.419-425
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• 2001

The neuronal cell death induced by excess glutamate (Glu) has been implicated in many acute and chronic neurodegenerative diseases including cerebral ischemia. Glu-induced elevation of intra-cellular $Ca^{2+}$ plays a critical role in the excitotoxicity, partly through the activation of a variety of $Ca^{2+}$ dependent enzymes. In the present study, we investigated the Glu-induced modulation of $Ca^{2+}$/calmodulin-dependent protein kinase IV (CaMK IV), a multifunctional enzyme abundantly present in the nuclei of neurons. The exposure of cultured rat cortical neurons to $100{\mu}$M Glu for 3 min dramatically increased CaMK IV activity up to 4.5-fold of the control-treated enzyme activity. The activation was very rapid, reaching peak at 3 min and then declined gradually. Under the same experimental conditions, time-dependent acute and delayed neuronal cell death was observed. Immunoblot analyses using specific antibodies showed that the expressions of CaMK IV and $CaMKK_{\alpha}$ were time-dependently modulated by Glu. Taken together, these results imply that the modulation of CaMK IV activity by Glu may be involved in the cascade of events resulting in neuronal cell death in cortical cultures.

• Journal of the Korean neurological association
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• v.36 no.4
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• pp.294-301
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• 2018

Background: Neuroimaging can play a crucial role in discovering potential abnormalities to cause secondary headache. There has been a progress in the fields of headache diagnosis and neuroimaging in the past two decades. We sought to investigate neuroimaging findings according to headache disorders, age, sex, and imaging modalities in first-visit headache patients. Methods: We used data of consecutive first-visit headache patients from 9 university and 2 general referral hospitals. The International Classification of Headache Disorders, third edition, beta version was used in headache diagnosis. We finally enrolled 1,080 patients undertook neuroimaging in this study. Results: Among 1,080 patients (mean age: $47.7{\pm}14.3$, female: 60.8%), proportions of headache diagnosis were as follows: primary headaches, n=926 (85.7%); secondary headaches, n=110 (10.2%); and cranial neuropathies and other headaches, n=43 (4.1%). Of them, 591 patients (54.7%) received magnetic resonance imaging (MRI). Neuroimaging abnormalities were found in 232 patients (21.5%), and their proportions were higher in older age groups and male sex. Chronic cerebral ischemia was the most common finding (n=88, 8.1%), whereas 76 patients (7.0%) were found to have clinically significant abnormalities such as primary brain tumor, cancer metastasis, and headache-relevant cerebrovascular disease. Patients underwent MRI were four times more likely to have neuroimaging abnormalities than those underwent computed tomography (33.3% vs. 7.2%, p<0.001). Conclusions: In this study, the findings of neuroimaging differed according to headache disorders, age, sex, and imaging modalities. MRI can be a preferable neuroimaging modality to identify potential causes of headache.

• Clinical and Experimental Pediatrics
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• v.46 no.10
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• pp.989-995
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• 2003

Purpose : Dexamethasone is frequently administered to prevent or treat chronic lung disease in human neonates who are also prone to hypoxic-ischemic(HI) insults. Recently, meta-analysis of the follow-up studies reveals a significantly increased odd ratio for the occurrence of cerebral palsy or an abnormal neurologic outcome, and there is conflicting evidence regarding the impact of dexamethasone exposure on HI brain injury. This study was conducted to explore the effect of post-HI dexamethasone administration on neuronal injury in neonatal rats. Methods : HI was produced in seven-day-old rats by right carotid artery ligation followed by two hours of 8% oxygen exposure. At the end of HI, the animals were injected intraperitoneally either with dexamethasone(0.5 mg/kg) or saline. Neuronal injury was assessed seven days after the HI by the area of infarction, TUNEL reactivity, Bcl-2 and Bax expression in brain. Results : Post-insult dexamethasone administration resulted in reduction of weight gain and a higher mortality rate during seven days after HI. Dexamethasone treatment revealed no effect on the size of brain infarction induced by HI. Bax protein expression increased in dexamethasone treated brain but Bcl-2 protein expression and TUNEL reactivity revealed no significant differences between dexamethasone treated and non treated brain. Increased Bax protein expression suggest upregulation of the apoptosis by dexamethasone. Conclusion : The result suggests the adverse role of Post-HI administration of dexamethasone in neonatal HI.