OBJECTIVE: The aim of this study was to describe and evaluate the clinical data and short-term treatment response in patients with obsessive-compulsive disorder (OCD) based on an outpatient setting. METHODS: A group of patients with OCD underwent mean 12-weeks treatment with selective serotonin reuptake inhibitors. The patients were divided into two groups according to treatment response, defined as a reduction of the Yale-Brown Obsessive Compulsive Scale total score >35% and CGI of 1 or 2. RESULTS: 1) Among the 249 patients, 24.1% had checking type and 23.7% washing type. Among these two types, 31.9% had mood disorder, 15.0% had anxiety disorder and 24.5% personality disorder as co-morbidity. One hundred fourteen patients (45.8%) responded to the treatment and 135 (54.2%) did not. The responders decreased Y-BOCS scores from 27.9+/-7.2 at baseline to 21.3+/-6.4 and 19.3+/-3.8 at post-treatment 8 and 12 weeks, respectively (repeated measure ANOVA, p=0.039). There were no differences among the treatment responses to serotonin reuptake inhibitors. CONCLUSION: About half of the OCD patients showed a response to pharmacological treatment using SSRI in the outpatient clinic setting for 12 weeks. Long-term and contrast studies of OCD may elucidate further clinical aspects of this disorder in the future.
Ambulatory Care Facilities ; Anxiety Disorders ; Comorbidity ; Humans ; Mood Disorders ; Obsessive-Compulsive Disorder* ; Outpatients ; Personality Disorders ; Serotonin Uptake Inhibitors

OBJECTIVE: The aim of this study was to evaluate which clinical variables might influence the antiobsessional responses to proserotonergic drugs in a sample of patients with obsessive-compulsive disorder (OCD). METHODS: Two hundred forty-nine patients with DSM-IV OCD under-gone mean 13-month treatments with selective serotonin reuptake inhibitors. According to the treatment response, defined as a reductions of the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) total score > or =35%, patients were divided into two groups. RESULTS: One hundred fourteen patients responded to the treatment and the other one hundred thirty five patients did not. Responders had a significant long duration of medication in YUMC OCD clinic, short total duration of past treatment in other institutes, and higher frequency of drug naive cases and lower baseline Y-BOCS scores. CONCLUSION: The pre-treatment factors including total duration of past treatment, drug naive or not, baseline OCD symptoms and the factor of duration of the treatment may influence drug treatment response in OCD patients.
Academies and Institutes ; Diagnostic and Statistical Manual of Mental Disorders ; Humans ; Obsessive-Compulsive Disorder ; Serotonin Uptake Inhibitors

Succinylcholine induces a small increase in serum K+ (0.3~0.5mEq/l) in normal patients, but it may produce fatal increases in sensitive conditions, including severe burn, massive trauma, tetanus and neuromuscular disorders. Recently, interest has been focussed on the role of the adrenergic system in extrarenal potassium hemeostasis. According to this concept, beta-adrenergic stimulation enhances and conversely a blockade imparis celluar uptake of potassium. Meanwhile propranolol, a beta-adrenergic blocker, is an incresingly, common drug among surgical patients. Therefore, the present experiment was carried out on 66 patients in order to determine whether propranolol augments or prolongs the increases in serum K+ following succinylcholine injection(2mg/kg, I.V.). Serum K+ and Na+ levels were measured just prior to induction and at 3,5,10,30,60,90 minutes following succinylcholine administration. The patients were divided into three groups: Group 1: 26 patients without propranolol treatment, Group 2: 20 patients pretreat with divided doses of propranolol (320 mg b.i.d. p.o.). and Group 3: 20 patients on chronic propranolol therapy. The results were as follows. 1) Baseline K+ valuses were significantly higher in propranolol treated patients(Groups 2 and 3) than in non-treated patients(Group 1). 2) The magnitude of maximum increases in serum K+ following succinylcholine was 0.19mEq/l, 0.16mEq/l and 0.21mEq/l in group 1,2 and 3, respectively. 3) The time to peak increases in K+ was 30min, 5min and 3 min following succinylcholine in group 1,2 and 3, respectively. 4) Serum Na+ decreased significantly following succinylcholine administration in all groups, but there was no significant difference among the groups at other times. These results indicate that propranolol neither augments nor prolongs increases in serum K+ following succinylcholin injection. Thus succinylcholine can be used safely in the presence of a beta-adrenergic blockade.
Burns ; Humans ; Potassium ; Propranolol* ; Succinylcholine* ; Tetanus

It is known that the concurrent administration of epinephrine, whether applied subcutaneously or parenterally during halothane anesthesia, can result in the initiation of ventrieular arrhythmias, which may be life threatening. However the mechanism by which halothane sensitizes the heart to catecholamines are not known yet. The purpose of this study was to investigate the mechanism of epinephrine induced cardiac arrhythmias during 1.2 MAC halothane anesthesia in dogs. Thirty-eight dogs were randomly assigned to five groups, halothane anesthesia were measured the arrythmogenic doses of epinephrine(ADE) before and after each treatment with sodium nitroprusside (SNP) (n=9), lidocaine(n=7), propranolol(n=7), prazosin(n=7) and verapamil(n=8), and compared each other. The results were follows. 1) The control ADE to induce ventricular arrhythmias was 2.160.15 ug/kg/min. 2) Treatment with SNP resulted in a decrease(28%) in mean blood pressure, but did not increase the ADE compared to the control. 3) Lidocaine and propranolol significantly increased the control ADE by 1.5 times, respectively, but there was no different between the ADE of lidocaine and that of propranolol. 4) Prazosin and verapamil also significantly increased the control ADE by 3.3 times and 2.6 times respectively, and the increased amplitudes were significant greater than the effect noted after lidocaine or propranolol treatment. There results suggest that the mechanism of epinephrine-induced cardiac arrhythmias during halothane anesthesia is mainly mediated via alpha-1 receptor and calcium channel, and alpha-1 blocker and calcium channel blocker may be useful to prevent the epinephrine-induced cardiac arrhythmias during halothane anesthesia.
Anesthesia* ; Animals ; Arrhythmias, Cardiac* ; Blood Pressure ; Calcium Channels ; Catecholamines ; Dogs* ; Epinephrine* ; Halothane* ; Heart ; Lidocaine ; Nitroprusside ; Prazosin ; Propranolol ; Verapamil