No abstract available.

No abstract available.
Antipsychotic Agents

Attention is a phenomenon hard to define, but can be conceptualized as a mental function ranging from sustaining readiness to perceive stimuli to understanding the nature and value and selecting stimuli that are most relevant to the given situation. Manifestations of attention include vigilance, and focused, directed, selective, divided, and sustained attentions. While basic attentional tone is controlled by the interaction among reticular activating system, thalamus, and prefrontal cortex, direction and selection of attention is controlled by neural circuits of prefrontal, posterior parietal, and limbic cortex. It is expected that understanding of attention and its neural could provide answers to the relationship between pathophysiology and clinical symptoms of some major psychiatric disorders. More effort are required to develop tools to assess more detailed and various aspects of attention in Korea.
Attention ; Korea ; Prefrontal Cortex ; Rabeprazole ; Thalamus

Recently atypical antipsychotics have been used as first line agent in the treatment of schizophrenia, and also played a significant role in the treatment of many kinds of psychiatric disorders. The pharmacokinetic and pharmacodynamic properties of these newer antipsychotics are well know through preclinical and early clinical trials. However, it is important to note the limitations of the results due to its relatively short experience. Clozapine is eliminated principally by the hepatic P450 1A2 and 3A4 cytochrome enzymes. 1A2 inducers such as carbamazepine and smoking can reduce its half-life, while 1A2 inhibitors such as SSRIs especially fluvoxamine can increase its duration of action. Carbamazepine should be avoided in a patient on clozapine because of carbamazepine's potential effects on bone marrow. Benzodiazepines tend to increase the chances of sedation delirium and respiratory depression. Risperidone is metabolized to 9-hydroxyriperidone by the hepatic P450 2D6 cytochrome enzymes. Fluoxetine and paroxetine, 2D6 inhibitors interfere with metabolism, but 9-hydroxyrisperidone has similar biological activity as parental drug, so it has little affect on the outcome. Olanzapine shows minimal capacity to inhibit cytochrome P450 isoenzymes and shows minimal chance of drug interaction. It is eliminated principally by the hepatic P450 1A2 and 2D6 cytochrome enzymes.
Antipsychotic Agents* ; Benzodiazepines ; Bone Marrow ; Carbamazepine ; Clozapine ; Cytochrome P-450 Enzyme System ; Cytochromes ; Delirium ; Drug Interactions* ; Fluoxetine ; Fluvoxamine ; Half-Life ; Humans ; Isoenzymes ; Metabolism ; Parents ; Paroxetine ; Respiratory Insufficiency ; Risperidone ; Schizophrenia ; Smoke ; Smoking

We described a case of a 30-year-old female patient with bipolar disorder who experienced the anticonvulsant hypersensitivity syndrome (AHS) during treatment with lamotrigine and aripiprazole. She developed fever (38.4 degrees C), leukopenia, skin rash, and elevated serum transaminase levels on the 11th day of lamotrigine treatment (20th day of aripiprazole). Hypersensitivity to lamotrigine was suspected; lamotrigine was discontinued and prednisolone (30 mg/day) was administered to the patient. The clinical manifestations and laboratory findings showed improvement. However, on the 11th day of lamotrigine discontinuation (7th day of prednisolone treatment), she developed maculopapular skin rash over the entire body except the mucosa. There were no other symptoms and the laboratory findings were within normal limits. Skin biopsy showed erythema multiforme. After prescribing 55 mg/day of predisolone for additional 8 days, the recovery was uneventful, and it took 4 weeks from the onset of the second skin rash. Lamotrigine induced AHS showed broad spectrum of presentation and some manifestations can be flared up several days after discontinuation as did in this case. If unexplained systemic symptoms or a skin rash of unknown cause develop during the use of lamotrigine, clinicians should discontinue lamotrigine promptly and monitor the patient carefully at least for several weeks.
Adult ; Biopsy ; Bipolar Disorder ; Erythema Multiforme ; Exanthema ; Female ; Fever ; Humans ; Hypersensitivity* ; Leukopenia ; Mucous Membrane ; Prednisolone ; Skin ; Aripiprazole

Fundamental difficulties in psychiatric nosology lie in the most basic fact that it deals with subjective states of the human mind. Modern instrumental diagnostic classification systems, which amount to lists of symptom inventories, could not provide accurate concepts of psychiatric disorders. This is also true for schizophrenia, a representative mental disorder. Kraepelin's dementia praecox was a collection of controversially proposed diseases, which had some critical similarities in their clinical features, i.e., the course and outcome. Despite initial debates on the adequacy of this concept, dementia praecox was recognized as a disease entity quite early, so that the concept of dementia praecox or schizophrenia proliferated, became diversified, and was then altered. We can now find large discrepancies between Kraepelin's dementia praecox and today's schizophrenia. However, the myth of disease entity was seldom challenged and psychiatrists today implicitly believe that they are dealing with what Kraepelin had proposed. In order to navigate this impasse, we thought that historical studies on the concept of dementia praecox and underlying taxonomic principles established by 19th century alienists including Kraepelin would shed some light. The aim of this article is to comprehensively review the history of concepts of dementia praecox or schizophrenia, and to question critically how much today's schizophrenia has received the conceptual inheritance from original concepts. Through this process, we expect to attain a renewed understanding of schizophrenia.
Classification ; Equipment and Supplies ; Humans ; Mental Disorders ; Psychiatry ; Schizophrenia* ; Wills

The adverse cardiovascular effects of some psychotropic drugs are well known. The brain and the heart share same neurotransmitter receptors and ion channels. This means that the medications affecting the central nervous system also have effects on the cardiovascular system and vice versa. In the patients with psychiatric disorders such as depression, the prevalence of cardiovascular disorder is increased. Conversely, depression is common in the patients with cardiovascular diseases and the presence of depression affects the prognosis of cardiovascular diseases. Moreover, recent increase in the geriatric population accompanies the increase in the patients with comorbid chronic cardiovascular and mental disorders. These suggest that an adequate consideration about the cardiovascular problems is mandatory in the treatment of psychiatric disorders. In this article, the author reviews the adverse cardiovascular effects of psychotropic medications in the theoretical and clinical aspects. The author also briefly summarizes the interactions between cardiovascular and psychotropic medications. Finally, the author presents two cases of potentially serious cardiovascular adverse effects of psychotropics, and then proposes a brief strategy for the prevention of these problems.
Arrhythmias, Cardiac ; Brain ; Cardiovascular Diseases ; Cardiovascular System ; Central Nervous System ; Depression ; Drug Interactions ; Heart ; Humans ; Ion Channels ; Mental Disorders ; Prevalence ; Prognosis ; Psychotropic Drugs ; Receptors, Neurotransmitter

OBJECTIVES: This study aimed to demonstrate the activities and phosphorylation changes induced by acute ethanol treatment and withdrawal conditions in the intracellular signal transduction molecules [such as extracellular signal-regulated kinase (ERK), glycogen synthase kinase 3beta (GSK3beta), and Akt] of the SH-SY5Y neuroblastoma cell line. METHODS: The acute treatment exposed SH-SY5Y cells to 100 mM ethanol, and we took samples 30 minutes, 60 minutes, and 24 hours after initiating this treatment. After 24 hours' continuous ethanol treatment, we initiated ethanol withdrawal, taking samples at 30 minutes and 60 minutes. We assayed the kinase phosphorylations via an immunoblot analysis using phosphorspecific antibodies, quantified by optical densitometry. RESULTS: Ethanol treatment induced a transient increase in phosphorylation of GSK3beta and Akt at 30 minutes but failed to change the phosphorylation level of ERK. Ethanol withdrawal induced a transient ERK phosphorylation increase at 30 minutes, but it had no effect on the phosphorylation of GSK3beta or Akt. CONCLUSION: The results indicate that the ethanol-induced cellular response includes the ERK, GSK3beta, and Akt systems. In particular, the ERK pathway may play a role in the acute withdrawal response. This also suggests that a relatively short exposure to ethanol, such as the 24-hour exposure in this study, can induce functional adaptation within a cell.
Antibodies ; Cell Line ; Densitometry ; Ethanol ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; MAP Kinase Signaling System ; Neuroblastoma ; Phosphorylation ; Phosphotransferases ; Signal Transduction

OBJECTIVES: Sensory gating dysfunctions in patients with schizophrenia and bipolar disorder have been investigated through two similar methods ; P50 suppression and prepulse inhibition paradigms. However, recent studies have demonstrated that the two measures are not correlated but rather constitute as distinct neural processes. Recent studies adopting spectral frequency analysis suggest that P50 suppression reflects the interaction between gamma and other frequency bands. The aim of the present study is to investigate which frequency component shows more significant interaction with gamma band. METHODS: A total of 108 mood disorder patients and 36 normal subjects were included in the study. The P50 responses to conditioning and test stimuli with an intra-pair interval of 500 msec were measured in the study population. According to P50 ratio (amplitude to the test stimulus/amplitude to the conditioning stimulus), the subjects with P50 ratio less than 0.2 were defined as suppressed group (SG) ; non-suppressed group (NSG) consisted of P50 ratio more than 0.8. Thirty-five and 25 subjects were included in SG and NSG, respectively. Point-to-point correlation coefficients (PPCCs) of both groups were calculated between two time-windows : the first window (S1) was defined as the time-window of one hundred millisecond after the conditioning auditory stimulus and the second window (S2) was defined as the time-window of 100 msec after the test auditory stimulus. Spectral frequency analysis was performed to investigate which frequency band results in the difference of PPCC between SG and NSG. RESULTS: Significant reduction of PPCC between S1 and S2 was observed in the SG (Pearson's r = 0.24), compared to PPCC of the NSG (r = 0.58, p < 0.05). In spectral frequency analysis, gamma band showed "phase-reset" and similar responses after the two auditory stimuli in suppressed and non-suppressed group. However in the case of alpha band, comparison showed significantly low PPCC in SG (r = -0.14) compared to NSG (r = 0.36, p < 0.05). This may be reflecting "phase-out" of alpha band against gamma band at approximately 50 msecs after the test stimulus in the SG. CONCLUSIONS: Our study suggests that normal P50 suppression is caused by phase-out of alpha band against gamma band after the second auditory stimulus. Thus it is demonstrated that normal sensory gating process is constituted with attenuated alpha power, superimposed on consistent gamma response. Implications of preserved gamma and decreased alpha band in sensory gating function are discussed.
Bipolar Disorder ; Humans ; Mood Disorders ; Schizophrenia ; Sensory Gating

BACKGROUND: The aim of the study was to examine the characteristics of alpha wave peak frequency, power, and coherence in patients with schizophrenia. METHODS: Thirty-one patients with schizophrenia and age- and sex-matched subjects with no psychopathology were enrolled. All study participants underwent quantitative electroencephalography (QEEG). Alpha-related values, including peak frequency, power, and coherence, were evaluated. RESULTS: Alpha peak frequency on the Oz area was slower in the schizophrenia group than that in the control group. However, no differences in absolute or relative power were observed between the two groups. Significant reductions in absolute and relative coherence were observed at the C3–C4 and T3–T4 nodes in the patients with schizophrenia. Relative coherence was reduced at the P3–P4 nodes. CONCLUSION: This study focused on alpha variables detected in QEEG as intrinsic values to distinguish schizophrenia from a healthy control. The results suggest decreased alpha peak frequency of the occipital lobe and decreased coherence between the two hemispheres in patients with schizophrenia. A further study could elucidate the causal relationship and biological meaning of the variations in alpha waves in patients with schizophrenia.
Electroencephalography* ; Humans ; Occipital Lobe ; Psychopathology ; Schizophrenia*