No abstract available.
Olivopontocerebellar Atrophies*

BACKGROUND: In this study, we assessed the effectiveness of ketamine as an alternative to non-steroidal anti-inflammatory drugs (NSAID), to manage acute postoperative pain after spinal fusion when given intravenously via a patient-controlled analgesia (PCA) pump in which the dose was proportional to that of fentanyl. METHODS: Forty patients undergoing 1-2 level spinal fusion were enrolled in this study. Patients were intraoperatively randomized into two groups to receive intravenous PCA consisting either of fentanyl 0.4 microg/ml/kg (control group) or fentanyl 0.4 microg/ml/kg with ketamine 30 microg/ml/kg (ketamine group) after intravenous injection of a loading dose. The loading dose in the control group was fentanyl 1 microg/kg with normal saline equal to ketamine volume and in the ketamine group it was fentanyl 1 microg/kg with ketamine 0.2 mg/kg. The verbal numerical rating scale (NRS), fentanyl and ketamine infusion rate, and side effects were evaluated at 1, 24, and 48 hours after surgery. RESULTS: There were no significant differences in patient demographics, duration of surgery and anesthesia or intra-operative opioids administration. We did not find any significant differences in the mean infusion rate of intraoperative remifentanil or postoperative fentanyl or in the side effects between the groups, but we did find a significant difference in the NRS between the groups. CONCLUSIONS: Based on our results, we conclude that a small dose of ketamine (0.5-2.5 microg/kg/min) proportional to fentanyl is not only safe, but also lowers postoperative pain intensity in patients undergoing spinal fusion, although the opioid-sparing effects of ketamine were not demonstrated.
Analgesia, Patient-Controlled ; Analgesics, Opioid ; Anesthesia ; Demography ; Fentanyl ; Humans ; Infusion Pumps ; Injections, Intravenous ; Ketamine ; Pain, Postoperative ; Passive Cutaneous Anaphylaxis ; Piperidines ; Prospective Studies ; Spinal Fusion

BACKGROUND AND OBJECTIVES: We investigated the relationship between the degree of enophthalmos and the volume of herniated orbital tissue measured from computed tomography scan in the isolated blowout fractures of orbital wall. SUBJECTS AND METHOD: In this retrospective study, 100 patients with isolated blowout fractures were evaluated. We classified them into 4 groups according to the site of fracture (medial and inferior) and the presence of symptoms like diplopia and limitation of ocular motility, which needs an operation. The volume of orbit and herniated orbital tissue has been measured by computed tomography scans using three-dimensional reconstruction technique, and the degree of enophthalmos was evaluated with Hertel's ophthalmometer. We compared the volume from which we got from the computed tomography scan, the degree of enophthalmos and the presence of symptoms to figure out the mutual relation between the groups. RESULTS: In the case of medial blowout fracture group, the volume of herniated orbital tissues increased significantly with the presence of symptoms and was in proportion to the extent of enophthalmos (p<0.05). The volume expansion of orbit associated with 2 mm of enophthalmos as calculated by the regression curve was 3.1 ml or 12.8 % in the no-symptoms groups. Finally, in the case of inferior blowout fracture group, there was no evidence of mutual relation. CONCLUSION: These results suggest that surgical intervention is required even though there isn't any symptom for medial blowout fractures, especially when the orbit volume is more than 12.8%. In cases of inferior blowout fractures, a close follow-up is needed even though the extent of fracture is small.
Diplopia ; Enophthalmos ; Follow-Up Studies ; Humans ; Orbit ; Retrospective Studies

BACKGROUND: Diffusion-perfusion mismatch (DPM) on MRI has been considered an ischemic penumbra. However, several reports have demonstrated limitation of DPM on MRI as a predictable marker of the ischemic penumbra. In this study, we investigated the relationship between DPM and the clinical progression in acute ischemic stroke patients. METHODS: We consecutively recruited fifty-seven patients showing acute ischemic stroke (within 24 hours) in the middle cerebral artery (MCA) territory. The clinical outcomes were determined by serial measurement of National Institute of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS) during 30 days after their ischemic event. We also evaluated the relationship among the parameters of perfusion MRI and the clinical worsening in patients with DPM on initial MRI. RESULTS: Nineteen (33.3%) patients had DPM on MRI within 24 hours after stroke onset. Even though the frequency of clinical worsening for 30 days after stroke onset was higher in DPM group (26%) than in non-DPM group (11%), it did not reach statistical significance (p=0.143). However, extent of MCA stenosis (p<0.001) and time to peak (TTP) delay on MRI (p<0.001) were significantly greater in patients with DPM than in those without DPM. Among several parameters of the perfusion MRI, only relative cerebral blood volume (rCBV) was significantly related to the clinical worsening (62.9+/-24.7% vs 96.1+/-19.2%, p=0.007) in patients with DPM. CONCLUSIONS: This study shows that DPM on MRI does not always predict the clinical worsening in acute ischemic stroke. To overcome this problem, we should analyze rCBV map based DPM as well as TTP map based DPM.
Blood Volume ; Brain ; Constriction, Pathologic ; Diffusion ; Humans ; Magnetic Resonance Imaging ; Middle Cerebral Artery ; Perfusion ; Stroke ; Thymine Nucleotides

OBJECTIVE: Leiomyomas of the bladder and urethra in women is very rare. We present five cases of histologically proven the female urethral and bladder leiomyomas identified over a 15-years period at our institution, together with review of the literature focused on the symptom and proper management. METHODS: Five women pathologically confirmed bladder or urethral leiomyoma were reviewed by the medical record, retrospectively. RESULTS: One patient with bladder leiomyoma was asymptomatic, but four patients with urethral leiomyoma had a palpable mass on physical examination. The leiomyomas posited laterally were less symptomatic than other leiomyomas posited medially, and the symptoms were especially obstructive ones. All of them were removed by excision, and any complication or recurrence was not occurred. CONCLUSION: Leiomyomas of the bladder and urethra are rare and associated with variable symptoms depending on their locations and sizes. It is not necessary immediate operation except to excessive bleeding or acute complete obstruction. Complete excision followed by histological examination is the most reliable means of distinguishing leiomyoma from other more common and usually malignant tumors of the genitourinary tract.
Female* ; Hemorrhage ; Humans ; Leiomyoma* ; Medical Records ; Physical Examination ; Recurrence ; Retrospective Studies ; Urethra* ; Urinary Bladder*

Reexpansion pulmonary edema (RPE) is a rare but sometimes fatal complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion, or atelectasis. We experienced a case of RPE that developed following decortication. A 46 year-old female had a decortication for pyothorax under one-lung anesthesia. There was no event during the operation and results of arterial blood gas analysis were within normal limits. After the operation, tracheal extubation was performed and 100% oxygen saturation on a pulse oximeter (SpO2) was maintained with 100% O2, (8 L/min) via mask ventilation with self-respiration. The patient, with 50% Venturi mask, was transported to the intensive care unit (ICU). On arrival at the ICU, a SpO2 of 80% was detected and arterial blood gas analysis revealed hypoxemia with acute hypercapnic respiratory acidosis. Fortunately, reexpansion pulmonary edema was detected early and intensive treatment was performed using mechanical ventilation with positive end-expiratory pressure. Tracheal extubation was performed after 1 day of mechanical ventilation. The reexpansion pulmonary edema was successfully treated and the patient recovered without any complications.
Acidosis, Respiratory ; Airway Extubation ; Anesthesia ; Anoxia ; Blood Gas Analysis ; Empyema, Pleural ; Female ; Humans ; Intensive Care Units ; Masks ; Oxygen ; Pleural Effusion ; Pneumothorax ; Positive-Pressure Respiration ; Pulmonary Atelectasis ; Pulmonary Edema ; Respiration, Artificial ; Ventilation

BACKGROUND: Use of corticosteroid appears to increase the risk of upper gastrosintestinal side effects associated with NSAIDs. But, there is no study for the effects of these drugs to NSAID induced small intestinal damage. Therefore, we examed the effects of corticosteroid to NSAID induced enteropathy and bacterial translocation. METHODS: Rat received no drug, NSAID alone (diclofenac 80 mg/kg per os), corticosteroid alone (dexamethasone 5 mg/kg intraperitoneal, 2 times) or NSAID with corticosteroid. Amounts of food intakes, body weight, intestinal permeability, enteric aerobic bacterial counts in small and large intestine, serum biochemical profiles, and pathologic findings of ileum were measured. Cultures of the mesenteric lymph nodes, as well as liver, spleen and systemic blood were taken. RESULTS: Diclofenac or dexamethasone alone administration caused gut barrier damage, enteric bacterial overgrowth and increased bacterial translocation. The supplements with dexamethasone increased NSAID induced gut barrier damage, villous atrophy, enteric bacterial overgrowth and bacterial translocation to mesenteric lymph nodes, liver, spleen and systemic blood. Also, these increased diclofenac induced body weight loss, but not hypoproteinemia. CONCLUSION: Corticosteroid increase NSAID induced body weight loss, gut barrier dysfunction, villous atrophy, enteric bacterial overgrowth and bacterial translocation in experimental animals.
Animals ; Anti-Inflammatory Agents, Non-Steroidal ; Atrophy ; Bacterial Load ; Bacterial Translocation* ; Body Weight ; Dexamethasone ; Diclofenac ; Hypoproteinemia ; Ileum ; Intestine, Large ; Intestine, Small ; Liver ; Lymph Nodes ; Permeability ; Rats* ; Spleen

In the present study, neuroprotective property of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, and its underlying mechanism were examined in the animal model of kainic acid (KA)-induced excitotoxicity. KA, administered intracerebroventricularly (i.c.v.), induced marked neuronal cell death with concurrent microglial activation and subsequent induction of inducible nitric oxide synthase (iNOS) in the hippocampus. Histopathological analysis demonstrated that celecoxib (100 mg/kg), pre-treated 1 hr before or post-treated 2 hr after KA i.c.v. injection, significantly attenuated KA-induced death of pyramidal neurons in CA3 region. Celecoxib obviously suppressed KA-induced microglial activation and subsequent iNOS expression. KA- induced phosphorylation of c-Jun N-terminal kinases (JNK) was attenuated with celecoxib treatments. The results of the present study demonstrate that suppression of JNK phosphorylation by celecoxib contributes to its neuroprotective action against KA-induced excitotoxicity suggesting that celecoxib may be a potentially valuable in the treatment of acute brain pathologies associated with excitotoxic neuronal damage such as epilepsy, stroke, and traumatic brain injury.
Brain ; Brain Injuries ; Cell Death ; Cyclooxygenase 2 ; Epilepsy ; Hippocampus ; JNK Mitogen-Activated Protein Kinases ; Kainic Acid ; Microglia ; Models, Animal ; Neurons ; Nitric Oxide Synthase Type II ; Phosphorylation ; Phosphotransferases ; Pyrazoles ; Stroke ; Sulfonamides ; Celecoxib

Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice (iNOS-/-) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.
Animals ; Guanidines ; Hippocampus ; Kainic Acid ; Mice ; Mice, Knockout ; Microglia ; Models, Theoretical ; Neurons ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Nitric Oxide Synthase ; Protein Isoforms ; Seizures

Experimental animals were inhalated 50 ppm formaldehyde gas for 3 times with one hour exposure and one hour rest. The olfactory mucosa were taken from the animals on 4, 7, 9, 11 days and 2-6 weeks after the inhalation. The characteristics of the various glycoproteins and the mitotic activity of the olfactory epithelial cells were investigated using lectins and 5'-bromodeoxyuridine (BrdU, 50 mg/kg) which injected one hour before sacrifice of the animals. The results were as follows; 1. In experimental animals, the degenerative changes of the olfactory epithelium such as atrophy and squamous metaplasia were observed until 2 weeks after formaldehyde gas inhalation. 2. In control animals, positive reactions appeared in the supporting cell to PNA, SBA, WGA, ECL, PHA-L and in the olfactory cells to PNA, SBA, WGA, UEA and in the proper basal cell to GS-I, SBA, WGA, PHA-L. In experimental groups, the positive reaction was increased in the supporting cells to SBA, ECL, PHA-L and in Bowman's gland to used lectins except ECL, GS-I. 3. The number of BrdU labelled cells in the olfactory epithelium was 14.8+/-1.2/mm in the control animals. The mitotic activities were decreased to 4.8+/-0.8 mm in 2 weeks and recovered in 3 weeks after the gas inhalation. 4. To find the stem cells of olfactory receptor cells, double labelling method was performed with lectins which were specific for proper basal cells (GS-I or PHA-L) and BrdU immunohistochemistry. The ratio of globose/proper basal cells in BrdU labelled cells with GS-I lectin positive reaction was 82%/18% in control group, 39.3%/60.7% in lesion group and 55.5%/44.5% in recovery group.
Animals ; Atrophy ; Bromodeoxyuridine ; Epithelial Cells ; Formaldehyde* ; Glycoproteins ; Immunohistochemistry ; Inhalation ; Lectins ; Metaplasia ; Olfactory Mucosa* ; Rats* ; Stem Cells