Return-to-Work Screening by Linear Discriminant Analysis of Heart Rate Variability Indices in Depressed Subjects.

Using a linear discriminant analysis of heart rate variability (HRV) indices, the present study sought to verify the usefulness of autonomic measurement in major depressive disorder (MDD) patients by assessing the feasibility of their return to work after sick leave. When reinstatement was scheduled, patients' HRV was measured using a wearable electrocardiogram device. The outcome of the reinstatement was evaluated at one month after returning to work. HRV indices including high- and low-frequency components were calculated in three conditions within a session: initial rest, mental task, and rest after task. A linear discriminant function was made using the HRV indices of 30 MDD patients from our previous study to effectively discriminate the successful reinstatement from the unsuccessful reinstatement; this was then tested on 52 patients who participated in the present study. The discriminant function showed that the sensitivity and specificity in discriminating successful from unsuccessful returns were 95.8% and 35.7%, respectively. Sensitivity is high, indicating that normal HRV is required for a successful return, and that the discriminant analysis of HRV indices is useful for return-to-work screening in MDD patients. On the other hand, specificity is low, suggesting that other factors may also affect the outcome of reinstatement.

The regulation of soluble receptor for AGEs contributes to carbonyl stress in schizophrenia.

Our previous study showed that enhanced carbonyl stress is closely related to schizophrenia. The endogenous secretory receptor for advanced glycation end-products (esRAGE) is a splice variant of the AGER gene and is one of the soluble forms of RAGE. esRAGE is considered to be a key molecule for alleviating the burden of carbonyl stress by entrapping advanced glycation end-products (AGEs). In the current study, we conducted genetic association analyses focusing on AGER, in which we compared 212 schizophrenic patients to 214 control subjects. We also compared esRAGE levels among a subgroup of 104 patients and 89 controls and further carried out measurements of total circulating soluble RAGE (sRAGE) in 25 patients and 49 healthy subjects. Although the genetic association study yielded inconclusive results, multiple regression analysis indicated that a specific haplotype composed of rs17846798, rs2071288, and a 63 bp deletion, which were in perfect linkage disequilibrium (r2 = 1), and rs2070600 (Gly82Ser) were significantly associated with a marked decrease in serum esRAGE levels. Furthermore, compared to healthy subjects, schizophrenia showed significantly lower esRAGE (p = 0.007) and sRAGE (p = 0.03) levels, respectively. This is the first study to show that serum esRAGE levels are regulated by a newly identified specific haplotype in AGER and that a subpopulation of schizophrenic patients are more vulnerable to carbonyl stress.

Pathways from life-historical events and borderline personality disorder to symptomatic disorders among suicidal psychiatric patients: A study of structural equation modeling.

AIMS: Suicidal behavior (SB) is a major mental health problem. The research has identified many factors related to SB, such as problems in the developmental period and psychiatric and personality disorders. However, the interrelation of these factors has not been clearly delineated. METHODS: The subjects were 155 patients consecutively admitted with SB to a psychiatric center in Tokyo. Structured interviews, including the Structured Clinical Interview for DSM-IV (SCID)-I and SCID-II, were conducted to determine characteristics of the SB-related factors. To illustrate their interrelation, this study applied the technique of structural equation modeling. The latent constructs of life-historical events, borderline personality disorder (BPD) features and three symptomatic disorders (depression, anxiety disorders and substance dependence) were aligned in the chronological order of their manifestation, and connected one another within the model. Indicator variables of life-historical events were maltreatment in the developmental period and early onset of problematic behaviors. Indicators of BPD features and symptomatic disorders included the scales composed of the items in the SCID-I and II. RESULTS: The constructed model with favorable goodness-of-fit indices confirmed that BPD features had a mediating role in which they were influenced by life-historical events, and exerted an influence on the symptomatic disorders. Outside the BPD-mediating paths, the model suggested three clinically interpretable links between life-historical events and symptomatic disorders. CONCLUSIONS: The model of this study demonstrated the pathways from life-historical events and BPD to symptomatic disorders, and indicated a generating process of psychiatric comorbidity among suicidal patients. The wide-range view this study portrayed has important clinical implications, and deserves further substantiation by future studies.

Physiological paradigm for assessing reward prediction and extinction using cortical direct current potential responses in rats.

Anticipating positive outcomes is a core cognitive function in the process of reward prediction. However, no neurophysiological method objectively assesses reward prediction in basic medical research. In the present study, we established a physiological paradigm using cortical direct current (DC) potential responses in rats to assess reward prediction. This paradigm consisted of five daily 1-h sessions with two tones, wherein the rewarded tone was followed by electrical stimulation of the medial forebrain bundle (MFB) scheduled at 1000 ms later, whereas the unrewarded tone was not. On day 1, both tones induced a negative DC shift immediately after auditory responses, persisting up to MFB stimulation. This negative shift progressively increased and peaked on day 4. Starting from day 3, the negative shift from 600 to 1000 ms was significantly larger following the rewarded tone than that following the unrewarded tone. This negative DC shift was particularly prominent in the frontal cortex, suggesting its crucial role in discriminative reward prediction. During the extinction sessions, the shift diminished significantly on extinction day 1. These findings suggest that cortical DC potential is related to reward prediction and could be a valuable tool for evaluating animal models of depression, providing a testing system for anhedonia.

Increase in the IgG avidity index due to herpes simplex virus type 1 reactivation and its relationship with cognitive function in amnestic mild cognitive impairment and Alzheimer's disease.

After infection with herpes simplex virus type 1 (HSV-1), latent infection persists for life in the trigeminal ganglion and reactivation results in an outbreak of cold sores around the mouth. Many previous studies have reported HSV-1 reactivation to be a risk factor for Alzheimer's disease (AD). This study enrolled subjects with AD (n=85), subjects with amnestic mild cognitive impairment (aMCI; a prodromal stage of AD) (n=34), and healthy controls (n=28). The avidity index of anti-HSV-1 IgG antibodies--a known indicator of HSV-1 reactivation--was measured in order to clarify the relationship between HSV-1 reactivation and symptoms of cognitive function in AD. Cognitive function in AD and aMCI were evaluated using scores from the mini-mental state examination (MMSE) and frontal assessment battery (FAB). The results showed that the subjects with aMCI, for which cerebral function is better preserved than subjects with AD, had a higher anti-HSV-1 IgG antibody avidity index than the AD subjects or healthy controls. Furthermore, the anti-HSV-1 IgG antibody avidity index was even higher in the subjects with high MMSE scores on orientation to time and three-step command subscores. We observed a negative correlation between the anti-HSV-1 IgG antibody avidity index and plasma BDNF concentration, which is an indicator of encephalitis. This suggests that HSV-1 reactivation, as observed through an increase in the anti-HSV-1 IgG avidity index, does not progress to encephalitis. These results suggest that HSV-1 reactivation occurs from the stage of aMCI, which is prodromal to AD, and can affect AD symptoms without an intermediary stage of severe encephalitis. The study demonstrates that the anti-HSV-1 IgG antibody avidity index could be a useful biomarker for the early diagnosis of aMCI as well as AD, and suggests that antiviral medication to treat HSV-1 could play a role in preventing the onset of AD.

Post-hospitalization course and predictive signs of suicidal behavior of suicidal patients admitted to a psychiatric hospital: a 2-year prospective follow-up study.

BACKGROUND: Suicidal patients admitted to a psychiatric hospital are considered to be at risk of suicidal behavior (SB) and suicide. The present study aimed to seek predictors of SB recurrence of the high-risk patients by examining their post-hospitalization course. METHOD: The design was 2-year prospective follow-up study of patients consecutively admitted with SB to a psychiatric center in Tokyo. The DSM-IV diagnoses and SB-related features of subjects were determined in structured interviews. Subsequently, the subjects underwent a series of follow-up assessments at 6-month intervals. The assessment included inquiries into SB recurrence, its accompanying suicidal intent (SI) and SF-8 health survey. Analyses of serial change over time in the follow-up data and Cox proportional hazards regression analyses of SB recurrence were performed. RESULTS: 106 patients participated in this study. The dropout rate during the follow-up was 9%. Within 2 years, incidences of SB as a whole, SB with certain SI (suicide attempt) and suicide were 67% (95% CI 58 - 75%), 38% (95% CI 29 - 47%) and 6% (95% CI 3 - 12%), respectively. Younger age, number of lifetime SBs and maltreatment in the developmental period were predictive of SB as a whole, and younger age and hopelessness prior to index admission were predictive of suicide attempt. Regarding diagnostic variables, anxiety disorders and personality disorders appeared to have predictive value for SB. Additionally, poor physical health assessed during the follow-up was indicated as a possible short-term predictor of SB recurrence. CONCLUSIONS: This study demonstrated a high incidence of SB and suicide and possible predictors of SB recurrence in the post-hospitalization period of psychiatric suicidal patients. Specialized interventions should be developed to reduce the suicide risk of this patient population.

[A flow cytometric postmortem brain study for major depressive disorders: implication for oligodendroglial differentiation and functions].

The neuropathology of psychiatric disorders has long been of interest in psychiatry. Several abnormalities in the prefrontal cortex have been demonstrated in major depressive disorders; however, only a small number of quantitative studies have been conducted, partly because the stereological techniques often used for such investigations are hampered by intrinsically low throughput, typically requiring long periods of time to complete. Recently, we developed a quantitative cell-counting method for frozen unfixed postmortem brains using a flow cytometer. Anisotropic frozen brain tissue was transformed into an isotropic suspension of nuclei; the numbers and fluorescent intensities of 7-AAD(+), a DNA marker, were quantified; and the nuclei were immunolabeled for the neuronal and oligodendroglial nuclear markers, NeuN and olig2, respectively. Using this method, the frontopolar and inferior temporal cortical gray matter of major depressive disorder patients, as well as that of normal controls, was analyzed. We found that the densities of 7-AAD(+) and olig2(+) nuclei in the gray matter tissue of the frontopolar cortex from major depressive disorder subjects were significantly reduced when compared to those from controls, but not in the inferior temporal cortex. Our findings suggest that the pathogenesis of major depressive disorders may involve some abnormalities in cortical myelination in the adult frontopolar cortex.

Chronic antidepressant treatment rescues abnormally reduced REM sleep theta power in socially defeated rats.

The effects of chronic antidepressant (AD) treatment on sleep disturbances in rodent chronic stress models have not been thoroughly investigated. Here, we show that chronic social defeat stress (SDS) in rats induces prolonged social avoidance, alterations in sleep architecture (increased total rapid eye movement [REM] sleep duration, bout, and shortened REM latency), and contextual but not cued fear memory deficits, even 1 month after the last SDS. These abnormalities were associated with changes in electroencephalography (EEG) spectral powers, including reduced REM sleep theta power during the light phase. Chronic treatment with two different classes of antidepressants (ADs), imipramine and fluoxetine, significantly ameliorated these behavioral, sleep, and EEG abnormalities. Interestingly, REM theta power was normalized by chronic (1 month) but not 1 week AD administration and solely correlated with the ratio (an objective indicator) of social interaction 1 month after the last SDS. These data suggest that reductions in REM sleep theta power, an EEG parameter that has never been directly investigated in humans, is a core sleep symptom in socially defeated rats, and, potentially, also in patients with stress-related psychiatric disorders, including major depressive and posttraumatic stress disorders.

Essential roles of plexin-B3+ oligodendrocyte precursor cells in the pathogenesis of Alzheimer's disease.

The role of oligodendrocyte lineage cells, the largest glial population in the adult central nervous system (CNS), in the pathogenesis of Alzheimer's disease (AD) remains elusive. Here, we developed a culture method for adult oligodendrocyte progenitor cells (aOPCs). Fibroblast growth factor 2 (FGF2) promotes survival and proliferation of NG2+ aOPCs in a serum-free defined medium; a subpopulation (~5%) of plexin-B3+ aOPCs was also found. FGF2 withdrawal decreased NG2+, but increased plexin-B3+ aOPCs and Aß1-42 secretion. Plexin-B3+ aOPCs were distributed throughout the adult rat brain, although less densely than NG2+ aOPCs. Spreading depolarization induced delayed cortical plexin-B3+ aOPC gliosis in the ipsilateral remote cortex. Furthermore, extracellular Aß1-42 accumulation was occasionally found around plexin-B3+ aOPCs near the lesions. In AD brains, virtually all cortical SPs were immunostained for plexin-B3, and plexin-B3 levels increased significantly in the Sarkosyl-soluble fractions. These findings suggest that plexin-B3+ aOPCs may play essential roles in AD pathogenesis, as natural Aß-secreting cells.

Psychiatric disorders and clinical correlates of suicidal patients admitted to a psychiatric hospital in Tokyo.

BACKGROUND: Patients admitted to a psychiatric hospital with suicidal behavior (SB) are considered to be especially at high risk of suicide. However, the number of studies that have addressed this patient population remains insufficient compared to that of studies on suicidal patients in emergency or medical settings. The purpose of this study is to seek features of a sample of newly admitted suicidal psychiatric patients in a metropolitan area of Japan. METHOD: 155 suicidal patients consecutively admitted to a large psychiatric center during a 20-month period, admission styles of whom were mostly involuntary, were assessed using Structured Clinical Interviews for DSM-IV Axis I and II Disorders (SCID-I CV and SCID-II) and SB-related psychiatric measures. Associations of the psychiatric diagnoses and SB-related characteristics with gender and age were examined. RESULTS: The common DSM-IV axis I diagnoses were affective disorders 62%, anxiety disorders 56% and substance-related disorders 38%. 56% of the subjects were diagnosed as having borderline PD, and 87% of them, at least one type of personality disorder (PD). SB methods used prior to admission were self-cutting 41%, overdosing 32%, self-strangulation 15%, jumping from a height 12% and attempting traffic death 10%, the first two of which were frequent among young females. The median (range) of the total number of SBs in the lifetime history was 7 (1-141). Severity of depressive symptomatology, suicidal intent and other symptoms, proportions of the subjects who reported SB-preceding life events and life problems, and childhood and adolescent abuse were comparable to those of the previous studies conducted in medical or emergency service settings. Gender and age-relevant life-problems and life events were identified. CONCLUSIONS: Features of the studied sample were the high prevalence of affective disorders, anxiety disorders and borderline PD, a variety of SB methods used prior to admission and frequent SB repetition in the lifetime history. Gender and age appeared to have an influence on SB method selection and SB-preceding processes. The findings have important implications for assessment and treatment of psychiatric suicidal patients.

Human Herpesvirus 6B Greatly Increases Risk of Depression by Activating Hypothalamic-Pituitary -Adrenal Axis during Latent Phase of Infection.

Little is known about the effect of latent-phase herpesviruses on their host. Human herpesvirus 6B (HHV-6B) is one of the most ubiquitous herpesviruses, and olfactory astrocytes are one of the most important sites of its latency. Here, we identified SITH-1, an HHV-6B latent protein specifically expressed in astrocytes. Mice induced to produce SITH-1 in their olfactory astrocytes exhibited olfactory bulb apoptosis, a hyper-activated hypothalamic-pituitary-adrenal (HPA) axis and depressive symptoms. The binding of SITH-1 to the host protein calcium-modulating ligand (CAML) to form an activated complex promoted the influx of extracellular calcium. The serum antibody titers for depressive patients with respect to this activated complex were significantly higher than for normal controls (p = 1.78 × 10-15), when the antibody positive rates were 79.8% and 24.4%, respectively, and the odds ratio was 12.2. These results suggest that, in the latent phase, HHV-6B may be involved in the onset of depression.

Ergothioneine, a metabolite of the gut bacterium Lactobacillus reuteri, protects against stress-induced sleep disturbances.

The relationships between depression and gut microbiota, particularly those involving the immune system, have become a major focus of recent research. Here, we analyzed changes in gut microbiota and their sulfur metabolites in the feces of a depression rat model using the modified 14-day social defeat stress (SDS) paradigm. Our results showed that SDS increased fecal Lactobacillus reuteri in correlation with ergothioneine levels at around day 11, which continued for at least 1 month following SDS administration. In vitro study further revealed that L. reuteri is capable of producing ergothioneine. Although the known anti-inflammatory and anti-oxidative actions of ergothioneine suggested that the increased fecal ergothioneine levels may be related to intestinal anti-inflammatory defense mechanisms, no change was observed in the plasma ergothioneine levels during the same observation period, indicating that the defense mechanisms may not be sufficiently reflected in the body. As ergothioneine is a natural ingredient that is absorbed mainly from the upper gastrointestinal tract, we hypothesized that oral ergothioneine may exert antidepressant effects. As expected, oral administration of ergothioneine prior to and during the SDS paradigm had a preventative effect on SDS-induced depressive behaviors, such as social avoidance and depression-like sleep abnormalities, particularly those of rapid eye movement sleep. These findings indicate that ergothioneine, a metabolite of L. reuteri, may be a common substance in the microbiota-gut-brain axis that prevents stress-induced sleep disturbances, especially those associated with depression.

Usefulness of heart rate variability indices in assessing the risk of an unsuccessful return to work after sick leave in depressed patients.

AIM: The present study aimed to examine whether heart rate variability (HRV) indices in depressed patients measured at return to work after sick leave are related to the outcome of reinstatement. METHODS: This study included 30 workers who took a leave of absence due to major depressive disorder. HRV was measured twice, once when participants left work and another when they returned to work. One month after returning to work, 19 participants continued their original work (successful return group), while 11 failed to perform their original work (unsuccessful return group). HRV indices including high- and low-frequency components (HF and LF) were calculated in three conditions within a session lasting for about 5 minutes, initial rest (Rest), mental task (Task), and rest after task (After), and were compared between the two participant groups. Psychological states were evaluated using Self-rating Depression Scale and State-Trait Anxiety Inventory. RESULTS: No significant differences were observed in the HRV indices on leaving work between groups. On returning to work, the "unsuccessful return group" exhibited lower HF Rest score, higher HF Task/Rest ratio, and higher LF/HF Rest score than the "successful return group." Psychological scores improved in both groups. CONCLUSION: These results indicate that autonomic dysregulations revealed by HRV measurement at return to work after a leave of absence in MDD patients were related to the outcome of reinstatement and can serve as useful information for the assessment of the risk of unsuccessful return.

[Psychiatric and personality disorders and clinical characteristics of admitted suicidal patients: data from Matsuzawa Suicidal Behavior Study].

Psychiatric patients who have shown suicidal behavior (SB) are belived to be at a particularly high risk of suicide. However, the number of studies that have sought ways to prevent suicide in this patient population is limited. The present study investigated the diagnosis and SB-related characteristics of psychiatric inpatients showing suicidal behavior prior to admission. One-hundred and fifty-seven eligible subjects were recruited from patients consecutively admitted to a large psychiatric facility during a 20-month period in 2006 and 2007, and underwent extensive research interviews. Percentages of diagnoses based on the Structured Clinical Interview for DSM-IV, Clinician Version (SCID-I, CV) in this series were: affective disorders, 62%; anxiety disorders, 55%; substance use disorders, 38%; psychotic disorders, 27%; and eating disorders, 10%. Eighty-seven percent of the subjects were diagnosed as having some type of personality disorder (PD) in the SCID-II interview. Borderline PD was diagnosed in 56% of the subjects, making it the most frequent type of PD in this series. Frequent SB in these subjects involved: self-cutting, 40%; overdosing, 32%; self-strangulation, 14%; and jumping, 11%. Step-wise logistic regression analyses were conducted to examine the association of dichotomized SB-related clinical characteristics with diagnostic categories (affective disorders, psychotic disorders, substance use disorders, anxiety disorders, and cluster A, B and C PDs). The analysis demonstrated that three diagnostic categories were dominant in the association with clinical characteristics. Cluster B PD was associated with a history of overdosing, greater aggressiveness, interpersonal and life-situational life events, and childhood maltreatment (physical abuse and neglect). Anxiety disorders were related to histories of overdosing, dissociative symptoms in SB, excessive worry concerning life problems, and childhood neglect. Affective disorders were mainly associated with the characteristics of SB or SB-related symptoms: severe depressive symptoms and hopelessness, potentially fatal SB before admission such as self-strangulation, and dissociative symptoms in SB, though they did not show a significant relationship with pre-SB characteristics such as life events or childhood maltreatment. These findings will be helpful to develop treatment guidelines, SB-prevention strategies, and future research regarding suicidal psychiatric patients.

Therapy-refractory schizophrenia in a patient who previously suffered from Meige's syndrome.

The main symptoms of Meige's syndrome are involuntary eye blinking with muddled speech and uncontrollable contraction of the platysma muscle characterized by segmental, primarily oromandibular, dystonia (hyperkinesia). It can also develop after long-term medication of first- and second-generation antipsychotics. Here, we report the case of a Japanese female schizophrenic patient comorbid with Meige's syndrome and hyperthyroidism. We discuss the relationship between the three diseases, that is, schizophrenia, Meige's syndrome, and hyperthyroidism. Our intention is to consider the important role of the cerebral basal ganglia, where little attention has been given in regard to schizophrenia and Meige's syndrome. A part of this article was presented in a poster section at the joint congress of the 28th Annual Meeting of the Japanese Society of Clinical Neuropsychopharmacology and the 48th Annual Meeting of the Japanese Society of Neuropsychopharmacology held in 2018.

Insulin dysfunction induces in vivo tau hyperphosphorylation through distinct mechanisms.

Hyperphosphorylated tau is the major component of paired helical filaments in neurofibrillary tangles found in Alzheimer's disease (AD) brains, and tau hyperphosphorylation is thought to be a critical event in the pathogenesis of the disease. The large majority of AD cases is late onset and sporadic in origin, with aging as the most important risk factor. Insulin resistance, impaired glucose tolerance, and diabetes mellitus (DM) are other common syndromes in the elderly also strongly age dependent, and there is evidence supporting a link between insulin dysfunction and AD. To investigate the possibility that insulin dysfunction might promote tau pathology, we induced insulin deficiency and caused DM in mice with streptozotocin (STZ). A mild hyperphosphorylation of tau could be detected 10, 20, and 30 d after STZ injection, and a massive hyperphosphorylation of tau was observed after 40 d. The robust hyperphosphorylation of tau was localized in the axons and neuropil, and prevented tau binding to microtubules. Neither mild nor massive tau phosphorylation induced tau aggregation. Body temperature of the STZ-treated mice did not differ from control animals during 30 d, but dropped significantly thereafter. No change in beta-amyloid (Abeta) precursor protein (APP), APP C-terminal fragments, or Abeta levels were observed in STZ-treated mice; however, cellular protein phosphatase 2A activity was significantly decreased. Together, these data indicate that insulin dysfunction induced abnormal tau hyperphosphorylation through two distinct mechanisms: one was consequent to hypothermia; the other was temperature-independent, inherent to insulin depletion, and probably caused by inhibition of phosphatase activity.

Failure of neuronal maturation in Alzheimer disease dentate gyrus.

The dentate gyrus, an important anatomic structure of the hippocampal formation, is one of the major areas in which neurogenesis takes place in the adult mammalian brain. Neurogenesis in the dentate gyrus is thought to play an important role in hippocampus-dependent learning and memory. Neurogenesis has been reported to be increased in the dentate gyrus of patients with Alzheimer disease, but it is not known whether the newly generated neurons differentiate into mature neurons. In this study, the expression of the mature neuronal marker high molecular weight microtubule-associated protein (MAP) isoforms MAP2a and b was found to be dramatically decreased in Alzheimer disease dentate gyrus, as determined by immunohistochemistry and in situ hybridization. The total MAP2, including expression of the immature neuronal marker, the MAP2c isoform, was less affected. These findings suggest that newly generated neurons in Alzheimer disease dentate gyrus do not become mature neurons, although neuroproliferation is increased.

c-jun N-terminal kinase hyperphosphorylates R406W tau at the PHF-1 site during mitosis.

Tauopathies such as Alzheimer disease (AD) probably involve a type of phosphorylation imbalance causing the accumulation of abnormally hyperphosphorylated tau in neurons and/or glias. Investigation of R406W tau mutation may provide insight into such abnormal tau hyperphosphorylation, since this mutation causes AD-like dementia and tauopathy in humans and because it has the unique ability to reduce tau phosphorylation in vitro and in cultured cells. Here we show that R406W mutation primarily disrupts tau phosphorylation at Ser404, a priming phosphorylation site of glycogen synthase kinase-3beta (GSK-3beta), thereby reducing subsequent GSK-3beta-mediated phosphorylation at the PHF-1 site (mostly Ser396). In contrast, c-jun N-terminal kinase (JNK) as activated in the mitotic phase directly hyperphosphorylates R406W tau at the PHF-1 site. This was confirmed by PHF-1 hyperphosphorylation of R406W tau in mitotic cells, its association with cytoplasmic JNK activation, and its inhibition by a JNK inhibitor, SP600125. These data unveil the unknown mechanisms of physiological tau phosphorylation at the PHF-1 site and suggest that cytoplasmic JNK activation may play an important role in the abnormal tau hyperphosphorylation associated with R406W tau mutation and in AD.

[Perimenopausal and late life depression].

This article reviews recent evidence related to perimenopausal and late life depression. Transition to menopause and its changing hormonal milieu are associated with higher risk for mood disorders in some women. Several randomized placebo-controlled trials reveal the antidepressant efficacy of the hormone replacement therapy in depressed perimenopausal women but caution is still required for its use on perimenopausal depression due to the side effects. In the elderly populations, both major and minor depressions are frequent and their natural histories in the community are poor. From the public health perspective of Japan where aging is progressing most rapidly among the world, depression prevention may be imperative, but requires accurate assessment of not only depression but also vascular, Alzheimer dementia and suicide in the elderly.

Motivation factors for suicidal behavior and their clinical relevance in admitted psychiatric patients.

BACKGROUND: Suicidal behavior (SB) is a major, worldwide health concern. To date there is limited understanding of the associated motivational aspects which accompany this self-initiated conduct. AIMS: To develop a method for identifying motivational features associated with SB by studying admitted psychiatric patients, and to examine their clinical relevance. METHODS: By performing a factor analytic study using data obtained from a patient sample exhibiting high suicidality and a variety of SB methods, Motivations for SB Scale (MSBS) was constructed to measure the features. Data included assessments of DSM-IV psychiatric and personality disorders, suicide intent, depressive symptomatology, overt aggression, recent life events (RLEs) and methods of SB, collated from structured interviews. Association of identified features with clinical variables was examined by correlation analyses and MANCOVA. RESULTS: Factor analyses elicited a 4-factor solution composed of Interpersonal-testing (IT), Interpersonal-change (IC), Self-renunciation (SR) and Self-sustenance (SS). These factors were classified according to two distinctions, namely interpersonal vs. intra-personal directedness, and the level of assumed influence by SB or the relationship to prevailing emotions. Analyses revealed meaningful links between patient features and clinical variables. Interpersonal-motivations (IT and IC) were associated with overt aggression, low suicidality and RLE discord or conflict, while SR was associated with depression, high suicidality and RLE separation or death. Borderline personality disorder showed association with IC and SS. When self-strangulation was set as a reference SB method, self-cutting and overdose-taking were linked to IT and SS, respectively. CONCLUSIONS: The factors extracted in this study largely corresponded to factors from previous studies, implying that they may be useful in a wider clinical context. The association of these features with SB-related factors suggests that they constitute an integral part of the process leading to SB. These results provide a base for further research into clinical strategies for patient management and therapy.