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Sleep electroencephalograms (EEGs) typically showed correlated fluctuations that became random-like oscillations beyond a characteristic time scale. To investigate this behavior quantitatively, the detrended fluctuation analysis (DFA) was applied to EEGs of 10 narcoleptic patients (22.0 ± 4.0 yrs; 6 males) and 8 healthy controls (24.0 ± 2.0 yrs; 5 males). The characteristic time scales of the narcoleptics and controls were estimated as 1.8 ± 0.7 and 4.4 ± 1.2s, respectively (significance level, p0.01). We further performed DFA of the EEGs segmented into 30s epochs and found that the DFA scaling exponents increased in deep sleep stages. These results were verified with power spectrum and auto-correlation analysis, and reproduced by a mathematical model. We thus concluded that characteristics of EEGs of narcoleptic patients could be differentiated from those of healthy subjects, suggesting a potential application of DFA in diagnosing narcolepsy.

Aims: The Short Post-traumatic Stress Disorder (PTSD) Rating Interview (SPRINT) is a validated, eight-item, brief global assessment scale for PTSD. This report investigated the psychometric properties of the Korean version of the SPRINT (K-SPRINT). Methods: Eighty-seven PTSD patients, 47 other psychiatric patients, and 63 healthy control subjects were enrolled in the study. All subjects completed a psychometric assessment package that included the K-SPRINT and the Korean versions of the Clinician-Administered PTSD Scale (CAPS), the Beck Depression Inventory (BDI), and the State Trait Anxiety Inventory (STAI). Results: The K-SPRINT showed good internal consistency (Cronbach's α = 0.86) and test–retest reliability (r = 0.82). K-SPRINT showed moderatecorrelations with CAPS (r = 0.71). An exploratory factor analysis produced one K-SPRINT factor. The optimal diagnostic efficiency (91.9%) of the K-SPRINT was found at a total score of 15, at which point the sensitivity and specificity were 90.8% and 92.7%, respectively. Conclusions: The present findings demonstrate that the K-SPRINT had good psychometric properties and can be used as a reliable and valid instrument for the assessment of PTSD.

For diagnosis and management of post-traumatic stress disorder (PTSD), the easily administered assessment tool is essential. Structured Interview for PTSD (SIP) is a validated, 17-item, simple measurement being used widely. We aimed to develop the Korean version of SIP (K-SIP) and investigated its psychometric properties. Ninety-three subjects with PTSD, 73 subjects with mood disorder or anxiety disorder as a psychiatric control group, and 88 subjects as a healthy control group were enrolled in this study. All subjects completed psychometric assessments that included the K-SIP, the Korean versions of the Clinician-Administered PTSD Scale (CAPS) and other assessment tools. The K-SIP presented good internal consistency (Cronbach's alpha=0.92) and test-retest reliability (r=0.87). K-SIP showed strong correlations with CAPS (r=0.72). Among three groups including PTSD patients, psychiatric controls, and normal controls, there were significant differences in the K-SIP total score. The potential cut-off total score of K-SIP was 20 with highest diagnostic efficiency (91.9%). At this point, the sensitivity and specificity were 95.5% and 88.4%, respectively. Our result showed that K-SIP had good reliability and validity. We expect that K-SIP will be used as a simple but structured instrument for assessment of PTSD.

According to the recommended guidelines by Novartis, neutropenia in the range of a white blood cell count less than 3000 per mm 3 , or an absolute neutrophil count (ANC) less than 1500 per mm 3 , is classified as being in the 'red-alert zone' during clozapine treatment If a patient's blood test result falls into this zone, immediate discontinuation of clozapine is recommended, and reinstitution is prohibited. However, in some patients, it is not entirely feasible to implement this standard guideline because of the lack of effective alternatives to clozapine treatment Through retrospective chart reviews, five patients who had been maintained on clozapine treatment despite red-alert zone neutropenia were selected. The haematological and clinical courses of these patients were followed for more than 600 days and were compared with those of two control patients who discontinued clozapine due to neutropenia. In all five patients, no additional episodes of neutropenia occurred during the observation period despite continued clozapine treatment However, three of them maintained a lower neutrophil count for the remaining observation period. Four patients responded favourably to clozapine treatment as judged by Clinical Global Impression score. Given the limitations of a retrospective chart review and the small number of patients, we cannot draw any definite conclusions. However, while the guidelines for the prevention of agranulocytosis should be generally followed, it may be that judicious continuation of clozapine treatment is less risk-prone than previously considered in selected cases where only a few feasible alternatives to clozapine are available. Moreover, there is an apparent necessity to develop new measures or methods that can differentiate between benign neutropenia and that leading to fatal agranulocytosis.

This study investigated the incidence and nature of clozapine-associated electroencephalographic (EEG) abnormalities and the relationship between EEG abnormality and clozapine dosage in Korean schizophrenic patients. Fifty schizophrenic patients with normal baseline EEG and with additional EEG record examined during clozapine treatment more than once were included. Thirty-one patients (62%) showed abnormal EEGs after clozapine treatment, and two of them had seizures. The majority of EEG abnormalities presented as nonspecific slow waves (SW). Spikes (or spike and wave complexes; SP) and frontal intermittent rhythmic delta activity (FIRDA) were relatively rarely observed. The probability of EEG abnormality was linearly dependent on the daily dose of clozapine and patient's age. Our results can be summarized as follows: (1) a substantial proportion of Korean patients treated with clozapine develops EEG abnormalities, and its incidence is comparable to the published results in Caucasian patients; (2) EEG abnormalities occurred in a dose-dependent manner; and (3) the occurrence of EEG abnormalities did not necessarily lead to future seizure development, except in a small number of cases.

1. In order to find the electroencephalographic (EEG) parameters that reflect the effect of clozapine in schizophrenic patients, the authors applied various non-linear analyses on multi-channel EEG data drawn from patients before and after a therapeutic trial of clozapine. 2. The correlation dimension was difficult to extract from our limited time series EEG data and the authors did not find a meaningful assocation with clozapine use. The primary Lyapunov exponent could be reliably calculated but also did not reflect the effect of clozapine. 3. However, the mutual cross-prediction (MCP) algorithm showed potentially meaningful results. The driving system was shifted to the frontal channels after a 4-week trial with clozapine. Moreover, MCP might have a value as a predictor of treatment response. 4. Although preliminary in nature, the MCP might have greater power for interpreting complex changes from channel to channel in EEG induced by clozapine.

Background Cardiovascular side effects of clozapine are not uncommon, but few systematic studies of these effects have been performed. In this study, we reviewed data on the electrocardiographic (ECG) abnormalities in patients treated with clozapine. Method Sixty-one patients treated with clozapine were selected from the Seoul National University Hospital Treatment-Resistant Schizophrenia Clinic. A retrospective chart review was conducted to identify ECG abnormalities and cardiovascular side effects. Results The prevalence of ECG abnormalities in patients who had been using antipsychotics other than clozapine was 13.6% at baseline, which increased significantly to 31.1% after commencement of clozapine treatment. Among the 53 patients without baseline ECG abnormalities, 13 showed new-onset ECG abnormalities after using clozapine. Normal ECG under previous antipsychotic medication reduced the risk of new-onset ECG abnormalities, whereas increased age was found to increase the risk. The occurrence of orthostatic hypotension or tachycardia was not related to the development of ECG abnormalities. Most of the newly developed abnormalities had little clinical significance, and they tended to occur during the initial phase of treatment. In 10 patients, ECGs normalized despite the continued use of clozapine. Clozapine increased corrected QT interval (QTc) in a dose-dependent fashion; however, the clinical significance of this observation is uncertain. Pathologic prolongation of QTc was found to be rare. Conclusion Although a substantial portion of patients treated with clozapine developed ECG abnormalities, most of the abnormalities were benign and did not hinder further treatment.