A Clinical Trial of Topiramate for Weight Loss in Schizophrenia with Overweight or Obesity / 대한정신약물학회지

OBJECTIVE: Antipsychotic-induced weight gain is associated with treatment noncompliance and is also known to be associated with several medical conditions in schizophrenia. Topiramate, a relatively new antiepileptic drug, is currently used for mood and eating disorders, and also offers the advantage of weight loss. This study explored the efficacy and tolerability of topiramate as an adjuvant treatment of schizophrenia with overweight or obesity. METHODS: In this 8-week, prospective open trial, 30 hospitalized, schizophrenic patients took topiramate at a mean maintenance dosage of 159.37+/-61.15 mg/day. The primary measures were weight, body mass index (BMI), waist circumference, hip circumference, and waist-to-hip ratio. The safety measures included adverse events, physical examination, clinical laboratory data, and vital signs. The Clinical Global Impression Severity (CGI-S) Scale was used to quantify changes in schizophrenic symptoms and signs. RESULTS: Body weight, BMI, waist circumference, and hip circumference decreased significantly after treatment but the waist-to-hip ratio did not. The changes of body weight and BMI during 8 weeks treatment with topiramate were significantly correlated with the maintenance dose of topiramate. The high dose group (>100 mg/d) was significantly more changed in body weight and BMI between baseline and 8 weeks than the low dose group (< or =100 mg/d). The scores on the CGI-S scale decreased significantly over the 8 weeks of treatment. CONCLUSION: The results suggest that topiramate is both efficacious and tolerable for the short-term adjuvant treatment of schizophrenia with overweight or obesity. Further placebo controlled studies included larger samples would be needed to confirm these results. And much more clinical researches should be required to establish guideline for the optimal dose and duration of treatment using topiramate as an antiobesity agent in schizophrenia.

Anxiety and Beta Adrenergic Receptor Function / 대한정신약물학회지

OBJECTIVE: There have been many studies to show the close relationship between anxiety and beta-adrenergic receptor function in patients with anxiety disorder. This study examined the relationship between anxiety levels and beta-adrenergic receptor function in a normal population. METHODS: Subjects for this study were 18 men and 28 women from 20 to 40 years of age whose body mass index was between 17.525 and 26.145. All of them were healthy subjects who had no previous history of medical or psychiatric illnesses. We measured the Korean versions of Spielberger State-Trait Anxiety Inventory and Beck Depression Inventory, and a self-report form of physical fitness level. We also measured the Chronotrophic 25 Dose (CD 25) of isoproterenol, previously developed to assess in vivo beta-adrenergic receptor sensitivity. RESULTS: The mean of CD 25 was 2.5 (+/-1.2)microgram, and there was a significant difference in the mean of CD 25 between men and women (t (17)= -3.73, p=0.0009). This gender difference in beta-adrenergic receptor sensitivity might be accounted for by different means of body mass index between men and women. The correlations between CD 25 and state anxiety levels (r=-0.3966, p=0.0064) and between CD 25 and trait anxiety levels (r=-0.3918, p=0.0071) were both statistically significant. The CD 25 was also positively correlated with age (r=0.4827, p=0.0007) and body mass index (r=0.3517, p=0.0166). CONCLUSION: The sensitivity of beta-adrenergic receptors increased as anxiety levels became higher in a normal population. Thus, the relationship between anxiety and beta-adrenergic function in healthy subjects seemed to be different from that in patients with anxiety disorder. This result suggests that we need a new hypothetical model in order to explain how anxiety affects beta-adrenergic receptors in both healthy subjects and patients with anxiety disorder.

Three Cases of Frontotemporal Dementia / 신경정신의학

Frontotemporal dementia is a common cause of dementia and distinguished from Alzheimer's disease. Because its clinical symptoms are characterized by slow progressive social breakdown and change of personality before cognitive impairments become prominent, it may be diagosed as other psychiatric disease. We have presented three cases of frontotemporal dementia. They had typical clinical histories and symptoms which deserve to be considered frontotemporal dementia. They showed appropriate findings of frontotemporal dementia in the neuropsychological tests and brain imaging study with brain magnetic resonance imaging and 18F-FDG positron emission tomography. Their clinical histories and findings are thought to be helpful for clinician to give attention to and diagnose frontotemporal dementia.