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Cheng-Chung Chen

Bio: Cheng-Chung Chen is an academic researcher from Kaohsiung Medical University. The author has contributed to research in topics: Major depressive disorder & Electroconvulsive therapy. The author has an hindex of 14, co-authored 35 publications receiving 1220 citations. Previous affiliations of Cheng-Chung Chen include Kaohsiung Medical University Chung-Ho Memorial Hospital.

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TL;DR: In this article, the authors have recruited articles mentioning coexisting psychiatric disorders of Internet addiction from the PubMed database as at November 3, 2009, and described the updated results for such disorders of internet addiction, which include substance use disorder, attention-deficit hyperactivity disorder, depression, hostility, and social anxiety disorder.

650 citations

Journal ArticleDOI
TL;DR: Genetic variations in GADL1 are associated with the response to lithium maintenance treatment for bipolar I disorder in patients of Han Chinese descent.
Abstract: Background Lithium has been a first-line choice for maintenance treatment of bipolar disorders to prevent relapse of mania and depression, but many patients do not have a response to lithium treatment. Methods We selected subgroups from a sample of 1761 patients of Han Chinese descent with bipolar I disorder who were recruited by the Taiwan Bipolar Consortium. We assessed their response to lithium treatment using the Alda scale and performed a genomewide association study on samples from one subgroup of 294 patients with bipolar I disorder who were receiving lithium treatment. We then tested the single-nucleotide polymorphisms (SNPs) that showed the strongest association with a response to lithium for association in a replication sample of 100 patients and tested them further in a follow-up sample of 24 patients. We sequenced the exons, exon–intron boundaries, and part of the promoter of the gene encoding glutamate decarboxylase–like protein 1 (GADL1) in 94 patients who had a response to lithium and in 94...

138 citations

Journal ArticleDOI
TL;DR: This study explored whether patients with late‐onset major depressive disorder showed higher carotid artery intima‐medium thickness (IMT) and investigated the relationship between the IMT and white matter hyperintensities on magnetic resonance imaging (MRI) among patients.
Abstract: Background This study explored whether patients with late-onset major depressive disorder showed higher carotid artery intima-medium thickness (IMT) and investigated the relationship between the IMT and white matter hyperintensities on magnetic resonance imaging (MRI) among patients. Methods Fourteen elderly patients with late-onset major depressive disorder from a psychiatric outpatient clinic and 11 non-depressed controls received a comprehensive psychiatric assessment, ultrasound IMT measurements of the carotid arteries, and cerebral MRI. Results The carotid IMT was higher in the patient group vs the control group (1.26 ± 0.30 vs 1.00 ± 0.20 mm; t = 2.40, p < 0.03). The difference was more apparent in the common carotid artery (1.20 ± 0.32 vs 0.97 ± 0.13 mm; t = 2.31, p < 0.04). There was a high correlation (r = 0.55, p < 0.05) between the carotid IMT and white matter hyperintensities among patients with late-onset major depressive disorder. Conclusion Results of this study suggest that atherosclerosis represented by the carotid IMT contributes to the development of late-onset major depressive disorder. The findings support the vascular depression hypothesis. Copyright © 2005 John Wiley & Sons, Ltd.

51 citations

Journal ArticleDOI
TL;DR: In this article, the authors investigated the risk of acute myocardial infarction associated with antipsychotic treatment in 56 910 patients with schizophrenia, mood disorders, or dementia first hospitalized or visiting an emergency room for AMI in 1999 to 2009.
Abstract: Background—Antipsychotic medications have been increasingly and more widely prescribed despite continued uncertainty about their association with the incidence of acute myocardial infarction (AMI). Methods and Results—We investigated the risk of AMI associated with antipsychotic treatment in 56 910 patients with schizophrenia, mood disorders, or dementia first hospitalized or visiting an emergency room for AMI in 1999 to 2009. A case-crossover design was used to compare the distributions of antipsychotic exposure for the same patient across 1 to 30 and 91 to 120 days just before the AMI event. Adjustments were made for comedications and outpatient visits. The adjusted odds ratio of AMI risk was 2.52 (95% confidence interval, 2.37–2.68) for any antipsychotics, 2.32 (95% confidence interval, 2.17–2.47) for first-generation antipsychotics, and 2.74 (95% confidence interval, 2.49–3.02) for second-generation antipsychotics. The risk significantly increased (P<0.001) with elevations in dosage and in short-term ...

43 citations

Journal ArticleDOI
TL;DR: The central cognitive impairments among the elderly with major depressive disorder in remission were memory and information-processing speed, and over half of the subjects met the MCI diagnostic criteria.
Abstract: Background Cognitive impairment in remitted late-life depression varies and might be associated with greater risk of dementia in some individuals. This study aimed to classify the subtypes of mild cognitive impairment (MCI) in late-life major depressive disorder in remission and to examine their clinical correlates and structural magnetic resonance imaging (MRI) features. Methods Elderly patients with major depressive disorder in remission and elderly comparisons were examined by a comprehensive battery of cognitive tasks. Proposed diagnostic criteria were used for MCI classification, and the degree of brain atrophy and white matter hyperintensity on MRI were evaluated. Results We found information-processing speed and memory were independent cognitive domains associated with late-life remitted major depressive disorder. Of the study cohort, 52.3% met the definition of MCI, including 28.5% with amnestic MCI (aMCI) and 23.8% with nonamnestic MCI (naMCI). A clinical correlate of aMCI was the late-onset of disorder (OR = 4.76; 95% CI=1.57, 14.40) and of naMCI was a higher score on the Framingham stroke risk scale (OR = 1.39; 95% CI=1.12, 1.72). The odds ratio of highest quartile of ventricular atrophy for aMCI compared to the comparisons was 3.65 (95% CI=1.22, 10.96). Conclusions The central cognitive impairments among the elderly with major depressive disorder in remission were memory and information-processing speed, and over half of the subjects met the MCI diagnostic criteria. Different risk factors existed for the subtypes of aMCI and naMCI. Later-age onset of first episode and ventricular atrophy were associated with aMCI, whereas vascular risk factor were associated with naMCI. We suggest there were different pathogeneses between aMCI and naMCI in late-life major depressive disorder.

41 citations


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TL;DR: A rating scale for drug-induced akathisia has been derived that incorporates diagnostic criteria for pseudoakathisio, and mild, moderate, and severe akath isia, and there is an item for rating global severity.
Abstract: A rating scale for drug-induced akathisia has been derived that incorporates diagnostic criteria for pseudoakathisia, and mild, moderate, and severe akathisia. It comprises items for rating the observable, restless movements which characterise the condition, the subjective awareness of restlessness, and any distress associated with the akathisia. In addition, there is an item for rating global severity. A standard examination procedure is recommended. The inter-rater reliability for the scale items (Cohen's kappa) ranged from 0.738 to 0.955. Akathisia was found in eight of 42 schizophrenic in-patients, and nine had pseudoakathisia, where the typical sense of inner restlessness was not reported.

1,942 citations

01 Jan 1998
TL;DR: The self-medication hypothesis of addictive disorders derives primarily from clinical observations of patients with substance use disorders as mentioned in this paper, who discover that the specific actions or effects of each class of drugs relieve or change a range of painful affect states.
Abstract: The self-medication hypothesis of addictive disorders derives primarily from clinical observations of patients with substance use disorders. Individuals discover that the specific actions or effects of each class of drugs relieve or change a range of painful affect states. Self-medication factors occur in a context of self-regulation vulnerabilities--primarily difficulties in regulating affects, self-esteem, relationships, and self-care. Persons with substance use disorders suffer in the extreme with their feelings, either being overwhelmed with painful affects or seeming not to feel their emotions at all. Substances of abuse help such individuals to relieve painful affects or to experience or control emotions when they are absent or confusing. Diagnostic studies provide evidence that variously supports and fails to support a self-medication hypothesis of addictive disorders. The cause-consequence controversy involving psychopathology and substance use/abuse is reviewed and critiqued. In contrast, clinical observations and empirical studies that focus on painful affects and subjective states of distress more consistently suggest that such states of suffering are important psychological determinants in using, becoming dependent upon, and relapsing to addictive substances. Subjective states of distress and suffering involved in motives to self-medicate with substances of abuse are considered with respect to nicotine dependence and to schizophrenia and posttraumatic stress disorder comorbid with a substance use disorder.

1,907 citations

Journal ArticleDOI
TL;DR: A disconnection hypothesis, wherein focal vascular damage and white matter lesion location is a crucial factor, influencing neural connectivity that contributes to clinical symptomatology is proposed, and inflammatory and hypoperfusion hypotheses, concepts that link underlying vascular processes with adverse effects on brain function that influence the development of depression are proposed.
Abstract: The 'Vascular Depression' hypothesis posits that cerebrovascular disease may predispose, precipitate or perpetuate some geriatric depressive syndromes. This hypothesis stimulated much research that has improved our understanding of the complex relationships between late-life depression (LLD), vascular risk factors, and cognition. Succinctly, there are well-established relationships between LLD, vascular risk factors and cerebral hyperintensities, the radiological hallmark of vascular depression. Cognitive dysfunction is common in LLD, particularly executive dysfunction, a finding predictive of poor antidepressant response. Over time, progression of hyperintensities and cognitive deficits predicts a poor course of depression and may reflect underlying worsening of vascular disease. This work laid the foundation for examining the mechanisms by which vascular disease influences brain circuits and influences the development and course of depression. We review data testing the vascular depression hypothesis with a focus on identifying potential underlying vascular mechanisms. We propose a disconnection hypothesis, wherein focal vascular damage and white matter lesion location is a crucial factor, influencing neural connectivity that contributes to clinical symptomatology. We also propose inflammatory and hypoperfusion hypotheses, concepts that link underlying vascular processes with adverse effects on brain function that influence the development of depression. Testing such hypotheses will not only inform the relationship between vascular disease and depression, but also provide guidance on the potential repurposing of pharmacological agents that may improve LLD outcomes.

659 citations

Journal ArticleDOI
TL;DR: To what degree medication‐specific and patient‐specific risk factors interact, and how adverse outcomes can be minimized, allowing patients to derive maximum benefits from these medications, requires adequate clinical attention and further research.

566 citations

Journal ArticleDOI
TL;DR: There is growing evidence that genetic, personality and individual differences in automatic and controlled aspects of self-regulation may promote the development of PIU, and Pharmacological and psychotherapeutic treatments specific to PIU have received limited testing in large, rigorous studies.

479 citations