Background: Cerebral palsy is due to static encephalopathy during perinatal period. Selective dorsal rhizotomy (SDR) involves selective division of posterior nerve roots to reduce spasticity and improve function in children with spastic cerebral palsy. Anesthesia during SDR must preserve muscle contraction in response to direct electrical stimulation of the dorsal nerve roots. We did this study to get the better management of anesthesia for SDR. Methods: Anesthetic records were reviewed for 16 patients who underwent SDR during January 1996 to August 1997. Demographic data; anesthetic drugs and doses; changes of vital signs and end tidal CO2; dorsal root stimulation; postoperative pain control were analysed. Results: The mean age of patients was 4.9+/-1.7 years old. The mean weight was 16.3+/-4.0 kg. The under 1 MAC concentration of isoflurane and 2~3 mcg/kg/hr fentanyl did not interfere with electrophysiologic monitoring. Esophageal temperature was increased significantly during electrical stimulation of dorsal roots. End tidal CO2 concentration had a tendency to increase after electrical stimulation too. Direct installation of 10~15 mcg/kg intrathecal morphine prior to dural closure, and postoperative 0.5 mcg/kg/hr fentanyl had a good postoperative analgesia without complication. Conclusions: Isoflurane and fentanyl during anesthesia, and intrathecal morphine with continuous infusion of fentany postoperatively are suggested a good anesthetic method for SDR.
Analgesia ; Anesthesia ; Anesthetics ; Cerebral Palsy ; Child ; Electric Stimulation ; Fentanyl ; Humans ; Isoflurane ; Morphine ; Muscle Contraction ; Muscle Spasticity ; Pain, Postoperative ; Rhizotomy* ; Spinal Nerve Roots ; Vital Signs

A case of acute febrile neutrophilic dermatosis (Sweet's syndrome) characterized by tender erythematous plaques on the face, neck, and limbs was reported. This 43-year-old male patient has been suffering from fever and sore throat prior to development of skin lesions. Positive laboratory findings were polymorphonuclear leukocytosis and elevated erythrocyte sedimentation rate. The symptoms well responded to corticosteroid therapy.
Adult ; Blood Sedimentation ; Extremities ; Fever ; Humans ; Leukocytosis ; Male ; Neck ; Pharyngitis ; Skin ; Sweet Syndrome*

No abstract available.
Ultrasonography, Prenatal*

Microcystic meningioma is a rare variant of meningiomas. This unusual variant was originally described by Masson, who labeled it "humid". The computed tomographic scan or magnetic resonance images of these tumors resemble those of a glial or metastatic tumor with cystic or necrotic changes. There is no definitive method for differentiating cystic meningiomas from these more common tumors. But immunohistochemically, they share a similar pattern of positive staining for epithelial membrane antigen and vimentin with other meningiomas. Our case was a 34-year-old woman with a tumor mass on the right frontal area. She was admitted to hospital because of generalized tonic seizure. Grossly all of the tumor could be removed, and histopathologically this tumor was revealed to be a microcystic meningioma.
Adult ; Female ; Humans ; Meningioma* ; Mucin-1 ; Seizures ; Vimentin

BACKGROUND: Trimetazidine(Vastinan(R)) is a new antianginal agent of different action mechanism specifically targeted at the metabolic cellular consequences of myocardial ischemia. The clinical efficacy of the Trimetazidine in angina pectoris is still to be defined. METHOD: To determine the antianginal effect of trimetazidine in the treatment of ischemic heart disease, 15 patients with stable angina(12 male, 3 female, mean age : 59.3 years) were studied. In 6 cases as a single agent and in 9 cases as an additive regimen to conventional antianginal medications. Trimetazidine(20mg 3 times daily) was given for 30 days or more to evaluate the clinical effect. Graded exercise tests were carried out before the trial of Trimetazidine and on the 30th day of the treatment period. RESULTS: 1) The number of episodes of anginal attacks decreased from 4.2+/-2.7 to 2.0+/-0.5 a week(p<0.05) after treatment with Trimetazidine. 2) Trimetazidine also significantly increased the duration of total exercise from 12.1+/-4.7 min to 14.5+/-3.3 min(p<0.05), and the time to 1mm ST segment depression from 7.7+/-5.9 min to 11.7+/-5.2 min(p<0.05) on treadmill exercise by modified Bruce protocol. 3) Total workload (METs) and rate pressure double product(heart rate x systolic blood pressure) slightly increased, but the differences were not significant statistically. 4) No serious clinical side effects were observed during the treatment. CONCLUSION: These results suggest that the Trimetazidine is an effective and safe as an antianginal drug in the treatment of stable angina patients as a single agent and as an additive regimen when the patients are refractory to conventional drugs.
Angina Pectoris ; Angina, Stable* ; Depression ; Exercise Test ; Female ; Humans ; Male ; Myocardial Ischemia ; Trimetazidine

BACKGROUND: Reciprocal ST-segment depression in precordial leads is a common finding in acute inferior myocardial infarction. The responsible mechanism and the significance of this finding, however, are still controversial. METHODS: Clinical characteristics, serial eletrocardiograms, angiographic findings of coronary artery and left ventricle were reviewed in 33 patients with acute inferior myocardial infarction. Reciprocal ST-segment depression was defined as ST-segment depression > or =1.0mm in two or more adjacent chest leads, I and aVL in patients with acute inferior myocardial infarction showing ST-segment elevation in II, III, aVF. Coronary angiography and left ventriculography were performed 15,2+/-16.9 hours after arrival. RESULTS: Eleven patients did not have reciprocal ST-segment depression(group A) and 22 patients had reciprocal ST-segment depression(group B). There was no significant difference in the demographic data of the patients except age and peak CK-MB, which were significantly higher in group B than group A. Left anterior descending coronary artery(LAD) stenosis was significantly more frequent in group B than group A(54.5% vs 18.2%, p<0.05). However the distribution of left ventricular regional wall motion abnormality and global ejection fraction showed no difference between two groups. In addition, there was no difference in in-hospital complications. CONCLUSIONS: These results suggest that reciprocal ST-segment depression in acute inferior myocardial infarction can be explained by anterior ischemia due to concomitant LAD stenosis in some cases, but its clinical significance is limited at least in terms of in-hospital complications.
Constriction, Pathologic ; Coronary Angiography ; Coronary Stenosis* ; Coronary Vessels* ; Depression* ; Heart Ventricles ; Humans ; Inferior Wall Myocardial Infarction* ; Ischemia ; Thorax

Congenital atresia of left main coronary ostium is a rare congenital coronary anomaly. This anomaly was detected during elective coronary angiogram in a 40 year-old female patient with chest pain and exertional dyspnea. Treadmill exercise test demonstrated 2 mm upslope depression of ST segment at stage I and the test was terminated due to chest pain. Myocardial stress SPECT using 201 Tl-dipyridamole showed reversible perfusion defects at anterior, apex and lateral wall. It was impossible to select left coronary artery ostium and right coronary angiogram revealed 30% eccentric stenosis at proximal right coronary artery with grade 3 collateral flow to left anterior descending and circumflex arteries. Operative finding revealed totally occluded left coronary ostium with membrane-like, non-atheromatous tissue similar to aortic wall. The patient was successfully treated with coronary artery bypass grafts (CABG) using left internal mammary artery and great saphenous vein. She underwent follow-up coronary angiogram, which revealed patent grafts, at one year after CABG and no cardiovascular event was observed on 5-year clinical follow-up.
Adult ; Arteries ; Chest Pain ; Constriction, Pathologic ; Coronary Artery Bypass ; Coronary Vessels ; Depression ; Dyspnea ; Exercise Test ; Female ; Follow-Up Studies ; Humans ; Mammary Arteries ; Perfusion ; Saphenous Vein ; Tomography, Emission-Computed, Single-Photon ; Transplants

Little is known as to why elevated red cell distribution width (RDW) is associated with adverse clinical outcomes in patients with atrial fibrillation (AF). We hypothesized that RDW value might predict the intensity of anticoagulation, resulting in higher adverse events in patients with AF taking warfarin. We analyzed 657 patients with non-valuvular AF who took warfarin. The intensity of anticoagulation was assessed as mean time in the therapeutic range (TTR) and defined TTR ≥60% as an optimal intensity. The primary end-point was the composite of stroke/systemic embolism and major bleeding. The secondary end-point was the composite of stroke/systemic embolism, major bleeding and death. The relationship between the baseline RDW with TTR and clinical outcomes was assessed using categorical variables as quartiles or dichotomous variables. The mean value of TTR decreased as an increment of the RDW (45.2% vs. 44.7% vs. 40.8% vs. 35.2%, p < 0.001). Primary and secondary end-points were significantly increased when TTR was less than 60% and RDW was more than 13.6%. Ratio of patients achieving optimal anticoagulation were significantly decreased as an increment of RDW. A RDW of ≥13.6% was a significant predictor for poor anticoagulation control (adjusted Odds ratio [OR] 0.43, 95% confidence interval [CI] 0.23–0.82), stroke (adjusted hazard ratio [HR] 3.86, 95% CI 1.11–13.40), primary (adjusted HR 1.88, 95% CI 1.12–3.16) and secondary end-point (adjusted HR 2.46, 95% CI 1.26–4.81). RDW was negatively associated with TTR in patients with AF. Therefore, RDW might be a useful marker for the prediction of anticoagulation response and clinical outcomes in patients with AF.
Anticoagulants ; Atrial Fibrillation* ; Embolism ; Erythrocyte Indices* ; Hemorrhage ; Humans ; Odds Ratio ; Prognosis ; Stroke ; Warfarin

Background: The mechanism of Brugada syndrome (BrS) is still unclear, with different researchers favoring either the repolarization or depolarization hypothesis. Prolonged longitudinal activation time has been verified in only a small number of human right ventricles (RVs). The purpose of the present study was to demonstrate RV conduction delays in BrS. Methods: The RV outflow tract (RVOT)-to-RV apex (RVA) and RVA-to-RVOT conduction times were measured by endocardial stimulation and mapping in 7 patients with BrS and 14 controls. Results: Patients with BrS had a longer PR interval (180 ± 12.6 vs. 142 ± 6.7 ms, P = 0.016). The RVA-to-RVOT conduction time was longer in the patients with BrS than in controls (stimulation at 600 ms, 107 ± 9.9 vs. 73 ± 3.4 ms, P= 0.001; stimulation at 500 ms, 104 ± 12.3 vs. 74 ± 4.2 ms, P = 0.037; stimulation at 400 ms, 107 ±12.2 vs. 73 ± 5.1 ms, P= 0.014). The RVOT-to-RVA conduction time was longer in the patients with BrS than in controls (stimulation at 500 ms, 95 ± 10.3 vs. 62 ± 4.1 ms, P= 0.007; stimulation at 400 ms, 94 ±11.2 vs. 64 ± 4.6 ms, P= 0.027). The difference in longitudinal conduction time was not significant when isoproterenol was administered. Conclusion The patients with BrS showed an RV longitudinal conduction delay obviously. These findings suggest that RV conduction delay might contribute to generate the BrS phenotype.

Background: The mechanism of Brugada syndrome (BrS) is still unclear, with different researchers favoring either the repolarization or depolarization hypothesis. Prolonged longitudinal activation time has been verified in only a small number of human right ventricles (RVs). The purpose of the present study was to demonstrate RV conduction delays in BrS. Methods: The RV outflow tract (RVOT)-to-RV apex (RVA) and RVA-to-RVOT conduction times were measured by endocardial stimulation and mapping in 7 patients with BrS and 14 controls. Results: Patients with BrS had a longer PR interval (180 ± 12.6 vs. 142 ± 6.7 ms, P = 0.016). The RVA-to-RVOT conduction time was longer in the patients with BrS than in controls (stimulation at 600 ms, 107 ± 9.9 vs. 73 ± 3.4 ms, P= 0.001; stimulation at 500 ms, 104 ± 12.3 vs. 74 ± 4.2 ms, P = 0.037; stimulation at 400 ms, 107 ±12.2 vs. 73 ± 5.1 ms, P= 0.014). The RVOT-to-RVA conduction time was longer in the patients with BrS than in controls (stimulation at 500 ms, 95 ± 10.3 vs. 62 ± 4.1 ms, P= 0.007; stimulation at 400 ms, 94 ±11.2 vs. 64 ± 4.6 ms, P= 0.027). The difference in longitudinal conduction time was not significant when isoproterenol was administered. Conclusion The patients with BrS showed an RV longitudinal conduction delay obviously. These findings suggest that RV conduction delay might contribute to generate the BrS phenotype.