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University students with symptoms of attention-deficit hyperactivity disorder (ADHD) often experience depression. This study examined whether interpersonal counseling (IPC) could be an effective treatment for depression among students with ADHD symptoms.Participants were assigned to either an IPC (N=5) or control (N=7) group. Depression was assessed by using the Self-Rating Depression Scale (SDS) at baseline, postintervention, and at 4-, 8-, and 12-week follow-ups.No significant changes in the SDS total score were observed for either group at each postintervention point. However, the IPC group showed a large effect size at the 4- and 12-week follow-ups. A significant intergroup difference was observed after 4 weeks. No significant intergroup difference was observed after 12 weeks, but there was a large effect size.IPC appeared to have effects at 4 weeks postintervention. Because this was an exploratory study, further research is necessary.

[Purpose] The number of patients with attention deficit hyperactivity disorder has been increasing. These patients show low activity in the prefrontal cortex, which can be improved by pharmacotherapy and neurofeedback training. This exploratory study aimed to examine whether the hemodynamic response in the prefrontal cortex during an inhibition response in patients with attention deficit hyperactivity disorder tendencies increased after interpersonal counseling. [Participants and Methods] Participants (n=5) received three interpersonal counseling sessions. Interpersonal counseling focuses on the patient's current problems and devises specific coping strategies, and it can be performed by healthcare personnel such as physiotherapists. Prefrontal cortex activity during a suppression reaction task was measured by using near-infrared spectroscopy at baseline and post-interpersonal counseling. The outcome was a difference in the oxyhemoglobin level from baseline to post-interpersonal counseling. [Results] The oxyhemoglobin level in the prefrontal cortex significantly increased post-interpersonal counseling. [Conclusion] These results suggested that interpersonal counseling could improve the hemodynamic response in the prefrontal cortex under inhibition in individuals with attention deficit hyperactivity disorder tendencies, suggesting that interpersonal counseling may be effective for treating attention deficit hyperactivity disorder symptoms.

Emi Tsujimoto,1,2 Noa Tsujii,1 Wakako Mikawa,1 Hisae Ono,2 Osamu Shirakawa1 1Department of Neuropsychiatry, Kindai University Faculty of Medicine, Osakasayama, Osaka, Japan; 2Department of Psychological Sciences, Graduate School of Humanities, Kwansei Gakuin University, Nishinomiya, Hyogo, Japan Purpose: The rating discrepancy for patients with major depressive disorder (MDD) is believed to be associated with hopelessness, risk of suicidal behavior, and personality characteristics, such as high neuroticism. However, it remains to be elucidated whether the discrepancy is also mediated by coping styles, which are conceptualized as personality characteristics. Patients and methods: We enrolled 154 participants and divided them into three groups: patients with MDD with a rating discrepancy (MDD-WD; n=46), patients with MDD without a rating discrepancy (MDD-WoD; n=50), and healthy controls (HCs; n=58). A rating discrepancy was defined as a high Beck Depression Inventory score and low Hamilton Depression Rating Scale score. Coping styles and hopelessness were compared among the groups. Results: The MDD-WD group exhibited a higher level of hopelessness than those in the MDD-WoD and HC groups. They also demonstrated a significantly increased number of suicide attempts compared with the MDD-WoD group. Both the MDD-WD and MDD-WoD groups exhibited lesser task-oriented and greater emotion-oriented coping styles than those in the HC group, with the MDD-WD group demonstrating even greater emotion-oribented coping than that in the MDD-WoD group. Overall, high levels of hopelessness, a history of suicide attempts, and frequent use of emotion-oriented coping mechanisms were associated with rating discrepancy. Conclusion: Patients with MDD who showed rating discrepancy tended to use emotion-oriented coping. Planning for minimal use of emotion-oriented coping may be a psychotherapeutic intervention for such patients. Reduced emotion-oriented coping may also reduce the feeling of hopelessness and risk of developing suicidal behavior. Keywords: major depressive disorder, coping styles, emotion-oriented coping, self-rating, observer rating, hopelessness

Background.Subthreshold depression and poor stress coping strategies are major public health problems among undergraduates. Interpersonal counseling (IPC) is a brief structured psychological intervention originally designed for use in primary care to treat depressive patients whose symptoms arose from current life stress.Objectives.This study examined the efficacy of IPC in treating subthreshold depression and coping strategies among undergraduates in school counseling.Materials and Methods.We carried out an exploratory randomized controlled trial comparing the efficacy of IPC with counseling as usual (CAU). Participants were 31 undergraduates exhibiting depression without a psychiatric diagnosis.Results.The Zung Self-Rating Depression Scale total score decreased significantly in the IPC group (n=15;Z=-2.675,p=.007), but not in the CAU group(n=16). The task-oriented coping score of the Coping Inventory for Stressful Situations showed a tendency towards a greater increase in the IPC group than in the CAU group (t=1.919,df=29,p=.065).Conclusions.The IPC might be more useful for student counseling because it can teach realistic coping methods and reduce depressive symptoms in a short period. Further studies using more participants are required.

A novel form of depression, called “modern type depression” (MTD), has been increasing in prevalence in Japan. Patients with MTD present with an overt appeal of depressive mood and a desire to be excused from their work duties; as such, this can cause considerable trouble in the workplace. Psychosocial interventions should be primarily considered for the treatment of MTD. Interpersonal counseling (IPC), which has proven effective for treating subthreshold depression, may be effective for MTD. However, IPC is rarely done in Japan. Herein, we report on a successful case of IPC for a woman in her thirties who was about to quit her job due to MTD (diagnosed by the criteria for research use). After IPC, the patient enjoyed good communication with her boss and continued her job without succumbing to her depression. This case suggests that IPC may be effective for MTD in workers and further highlights the benefits of teaching interpersonal communication methods in the workplace.

Previous neuroimaging studies have revealed frontal and temporal functional abnormalities in patients with major depressive disorder (MDD) and a history of suicidal behavior. However, it is unknown whether multi-channel near-infrared spectroscopy (NIRS) signal changes among individuals with MDD are associated with a history of suicide attempts and a diathesis for suicidal behavior (impulsivity, hopelessness, and aggression). Therefore, we aimed to explore frontotemporal hemodynamic responses in depressed patients with a history of suicide attempts using 52-channel NIRS. We recruited 30 patients with MDD and a history of suicidal behavior (suicide attempters; SAs), 38 patient controls without suicidal behavior (non-attempters; NAs), and 40 healthy controls (HCs) matched by age, gender ratio, and estimated IQ. Regional hemodynamic responses during a verbal fluency task (VFT) were monitored using NIRS. Our results showed that severities of depression, impulsivity, aggression, and hopelessness were similar between SAs and NAs. Both patient groups had significantly reduced activation compared with HCs in the bilateral frontotemporal regions. Post hoc analyses revealed that SAs exhibited a smaller hemodynamic response in the left precentral gyrus than NAs and HCs. Furthermore, the reduced response in the left inferior frontal gyrus was negatively correlated with impulsivity level and hemodynamic responses in the right middle frontal gyrus were negatively associated with hopelessness and aggression in SAs but not in NAs and HCs. Our findings suggest that MDD patients with a history of suicide attempts demonstrate patterns of VFT-induced NIRS signal changes different from those demonstrated by individuals without a history of suicidal behaviors, even in cases where clinical symptoms are similar. NIRS has a relatively high time resolution, which may help visually differentiate SAs from NAs.

An association between serotonergic dysfunction in the brain and suicidal behavior has previously been suggested. The high affinity of some antipsychotic and antidepressant drugs to serotonin 6 (5-HT 6 ) receptors, and the predominant localization of 5-HT 6 receptors in some limbic regions, suggest that 5-HT 6 receptors play a role in the pathogenesis of suicide. The objective of the present study was to examine the association between suicide victims and two polymorphisms of the 5-HT 6 receptor gene: a biallelic polymorphism (267C/T) in exon 1 and a trinucleotide repeat polymorphism ([GCC] 2/3 ) in the 5'-upstream region of the gene. The two polymorphisms were genotyped in 163 suicide victims and 166 controls, and the distribution of genotype and allele frequencies between the two groups were compared. Haplotype frequencies of these two polymorphisms were estimated from genotypic data by the maximum-likelihood method. In both polymorphisms, there were no significant differences in genotype or allele frequencies between the suicide victims and the controls. Moreover, there were no significant differences in the haplotype distributions of these polymorphisms between the two groups. These findings suggest that it is unlikely that the 5-HT 6 receptor gene is involved in the susceptibility to suicide.

Suicide has been suggested to involve catecholaminergic dysfunction and to be related to genetics. Catechol-O-methyltransferase (COMT) 158Val/Met polymorphism (GenBank Accession No. Z26491) is a polymorphism of the gene encoding COMT, a major enzyme in catecholamine inactivation. The COMT 158Val/Met polymorphism affects COMT activity, that is, the alleles encoding Val and Met are associated with relatively high and relatively low COMT activity, respectively. In this study, we hypothesized that the COMT 158Val/Met polymorphism is associated with suicide. The study population consisted of 163 suicide completers (112 males and 51 females). We found that the genotype distribution of the COMT 158Val/Met polymorphism was significantly different between male suicide completers and male controls (p=0.036), while the frequency of the Val/Val genotype, a high-activity COMT genotype, was significantly less in male suicide completers than in male controls (OR: 0.52; 95% CL: 0.31-0.89; p=0.016). However, this was not the case in females. Our results suggest that the Val/Val genotype is a protective factor against suicide in males.

Several lines of evidence suggest that a partly genetically controlled serotonergic dysfunction is involved in the biological pathogenesis of suicide. In this study, we measured tryptophan hydroxylase (TPH) immunoreactivity as a pre-synaptic marker, and serotonin receptor 2A (5HT2A receptor) density as a post-synaptic marker in the serotonergic system in 10 postmortem brains of suicide victims. We also examined whether TPH gene polymorphisms (A218C and A-6526G polymorphisms) could affect TPH immunoreactivity and 5HT2A receptor gene polymorphism (A-1438G polymorphism) could affect 5HT2A receptor density in 28 postmortem brain samples. No significant differences were found in TPH immunoreactivity or 5HT2A receptor density between suicide victims and controls. The AA genotype of the A218C polymorphism of the TPH gene showed higher TPH immunoreactivity along with lower 5HT2A receptor density than did any other genotypes in the postmortem brains of both suicide victims and controls. Our findings suggest that the A218C polymorphism of the TPH gene can be expected to provide new insights not only for neurobiological studies of suicide, but also for research into the behavioral characteristics that may be associated with serotonergic dysfunction.

Several lines of evidence indicate that a serotonergic dysfunction is involved in the biological susceptibility to suicide. Recently, the A-1438G polymorphism of the serotonin 2A (5-HT2A) receptor gene has been suggested to be associated with suicide, but the results are inconsistent. We examined whether the A-1438G polymorphism of the 5-HT2A receptor gene was associated with suicide itself using 151 Japanese completed suicides. No significant difference in genotype distribution or allele frequencies of the polymorphism was found between the completed suicides and the comparison group. We conclude that the A-1438G polymorphism of the 5-HT2A receptor gene is not likely to have a major effect on the biological susceptibility of suicide.

Dysfunction of neuronal signal transduction via G-protein has previously been speculated to be involved in the pathophysiology of schizophrenia. Regulator of G-protein signaling (RGS) is a protein that acts as a GTPase-activator for Galpha protein. A total of 33 Japanese patients with schizophrenia were screened for mutations in the coding region of the RGS10 gene, and a novel missense polymorphism (Val38Met) in the RGS domain was detected. A case-control study did not reveal a significant association between this polymorphism and schizophrenia. The results do not provide evidence that the RGS10 gene is involved in biological vulnerability to schizophrenia.

A serotonergic dysfunction in the brain has been reported to be involved in suicidal behavior independently of the presence of a specific psychiatric disorder. Serotonin 1A (5-HT1A) receptors are known to be located on serotonergic nerve terminals and to be involved in the presynaptic regulation of serotonin release. Genetic factors partly explain the risks for suicide, and a suicide completion group is thought to be more uniform than a suicide attempt group. To explore the hypothesis that the 5-HT1A receptor-induced serotonergic dysfunction is implicated genetically in suicide, we focused on the structural polymorphisms, Pro16Leu and Gly272Asp, of the 5-HT1A receptor gene, and examined the association between suicide victims who completed suicide and these two polymorphisms. In both polymorphisms, we found no significant difference in genotype distribution or allele frequencies between suicide victims and controls. These findings suggest that neither of these two polymorphisms is associated with suicide victims and it is unlikely that the 5-HT1A receptor gene is implicated in the susceptibility to suicide. © 2002 Wiley-Liss, Inc.

An association between serotonergic dysfunction in the brain and suicidal behavior has previously been suggested. The high affinity of some antipsychotic and antidepressant drugs to serotonin 6 (5-HT6) receptors, and the predominant localization of 5-HT6 receptors in some limbic regions, suggest that 5-HT6 receptors play a role in the pathogenesis of suicide. The objective of the present study was to examine the association between suicide victims and two polymorphisms of the 5-HT6 receptor gene: a biallelic polymorphism (267C/T) in exon 1 and a trinucleotide repeat polymorphism ([GCC](2/3)) in the 5'-upstream region of the gene. The two polymorphisms were genotyped in 163 suicide victims and 166 controls, and the distribution of genotype and allele frequencies between the two groups were compared. Haplotype frequencies of these two polymorphisms were estimated from genotypic data by the maximum-likelihood method. In both polymorphisms, there were no significant differences in genotype or allele frequencies between the suicide victims and the controls. Moreover, there were no significant differences in the haplotype distributions of these polymorphisms between the two groups. These findings suggest that it is unlikely that the 5-HT6 receptor gene is involved in the susceptibility to suicide.

Glutamate dysfunction has been hypothesized to be involved in the pathophysiology of schizophrenia. The human homolog of Drosophila discs large protein (hDLG) and post-synaptic density-95-associated protein-1 (DAP-1) is one of the major proteins that are involved in intracellular signal transduction via N-methyl-d-aspartate receptors. In the present study 33 Japanese patients with schizophrenia were screened for mutations in the DAP-1 gene. A single nucleotide polymorphism was identified in the DAP-1 gene (1618A/G). A case–control study using a larger sample of unrelated patients and controls did not reveal a significant association between this polymorphism and schizophrenia. The results do not provide evidence that the DAP-1 gene is involved in vulnerability to schizophrenia.

Monoamine oxidase A (MAOA) has been implicated in the control of aggression and/or impulsivity in humans and been involved in suicide. This gene has a functional polymorphism in which there is a variable number tandem repeat (VNTR) in the upstream region (MAOA-uVNTR). We hypothesized that MAOA dysfunction due to this polymorphism was associated with suicide genetically through the disinhibition of aggression and/or impulsivity. We performed an association study between completed suicides and the MAOA-uVNTR polymorphism. No significant difference in genotype distribution or allele frequencies was found between completed suicides and comparison groups either in males or females. These results show no evidence of an association between the MAOA-uVNTR polymorphism and completed suicides and suggest that MAOA is not involved in the susceptibility to suicide.

Serotonergic systems have been reported to mediate the control of aggression and/or impulsivity in humans and to be involved in suicidal behavior. Neurochemical studies showing serotonergic dysfunction in suicide appear to support the functional alteration of serotonergic systems due to gene polymorphisms. Knock-out mice of the 5HT1B receptor gene have been reported to result in increased aggression. We hypothesized that the 5HT1B receptor-mediated serotonergic dysfunction was implicated in suicide through disinhibition of aggression and/or impulsivity. To explore this hypothesis, we examined the association between suicide victims who completed suicide and the 5HT1B receptor gene G861C polymorphism. No significant differences in genotype distribution and allele frequencies were found between suicide victims and controls. Though there is the possibility of failing to detect small effects, these results show no evidence of an association between the 5HT1B receptor gene G861C polymorphism and suicide victims in a Japanese population and indicate that it is unlikely that the 5HT1B receptor is implicated in the susceptibility to suicide.

Several lines of evidence suggest a serotonergic dysfunction involved in the biological susceptibility of suicide. Abnormalities of serotonergic markers such as 5-hydroxyindoleacetic acid and prolactin response to fenfluramine have been demonstrated in suicide subjects. Tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin biosynthesis, is one of the most important regulating factors in the serotonergic system. Recently, polymorphisms of the TPH gene have been identified and some of these polymorphisms have been suggested to be associated with suicide, but the results are still inconsistent. We examined whether the −6526A/G polymorphism in the promoter region and the 218A/C polymorphism in intron 7 of the TPH gene were associated with suicide using 132 Japanese suicide victims. No significant difference in genotype distribution and allele frequencies of these polymorphisms was found between the suicide victims and the controls. We concluded neither the −6526A/G polymorphism nor the 218A/C polymorphism of the TPH gene is likely to have a major effect on the susceptibility of suicide. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:861–863, 2000. © 2000 Wiley-Liss, Inc.

N-methyl-D-aspartate (NMDA) receptor antagonists are known to produce a syndrome resembling schizophrenia, probably due to their blockade of NMDA receptors. The NMDA receptor 2B (NR2B) subunit has been identified as one of the major proteins in the postsynaptic density at glutamatergic synapses, suggesting that the carboxyl-terminal domain of the NR2B subunit may play a significant role in intracellular signal transduction.The authors screened for genetic variations in the region of the NR2B subunit gene encoding the carboxyl-terminal intracellular domain in patients with schizophrenia and studied the association between schizophrenia and a novel polymorphism of the NR2B subunit gene.One silent mutation (2664C/T) was identified. No significant differences in the frequencies of 2664C/T genotypes and alleles were found between patients with schizophrenia and healthy comparison subjects.The findings provided no evidence of an association between schizophrenia and the 2664C/T polymorphism of the NR2B subunit gene.