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ABSTRACT: Epidemiological studies have proposed that depression may increase the risk for Alzheimer's disease (AD), even in patients with early-onset depression. Although metabolism of amyloid β protein (Aβ) in elderly depression received attention in terms of their correlation, there is a serious heterogeneity in elderly depression in terms of age at onset of depression. Moreover, it is unknown whether early-onset major depressive disorder (MDD) has a long-term effect on the involvement of Aβ metabolism and later development of AD. Thus, we evaluated serum Aβ40 and Aβ42 levels, the Aβ40/Aβ42 ratio in 89 elderly (≥60 years of age) inpatients with MDD and 81 age-matched healthy controls, and compared them among patients with early-onset (<60 years) and late-onset (≥60 years) MDD and controls. The results showed that the serum Aβ40/Aβ42 ratio was significantly higher in patients with both early- and late-onset MDD than in controls (early-onset, p=0.010; late-onset, p=0.043), and it is of great interest that the serum Aβ40/Aβ42 ratio was negatively correlated with the age at MDD onset (R=-0.201, p=0.032). These results suggest that an earlier onset of MDD may have a more serious abnormality in Aβ metabolism, possibly explaining a biological mechanism underlying the link between depression and AD.
Progress in Neuro-Psychopharmacology and Biological Psychiatry 12/2012; · 3.25 Impact Factor
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ABSTRACT: Electroconvulsive therapy (ECT) has therapeutic effects on refractory depression and schizophrenia, although its biological mechanisms are still unclear. Recent studies in rodents suggest that electroconvulsive stimulation-induced seizures (ECSs) influence hippocampal adult neurogenesis, which has gained considerable traction as a possible cellular substrate for the treatment of depression. The aim of this study is to explore alteration of neurogenesis in the hippocampus following ECSs and the relationship between neurogenesis and behavior in rats. In the present study, we administered a single or 10-repeated application of electroconvulsive stimulations that reliably resulted in seizure (an animal model of electroconvulsive therapy) to rats. Then cell proliferation of newborn cells in the subgranular zone (SGZ) of the dentate gyrus (DG) was investigated 3 and 14 days after ECS treatments. Cell differentiation was also examined 4 weeks after newly formed cells were confirmed. As a result, ECS-induced cell proliferation in the hippocampus showed biphasic changes after ECS. The amount of cell proliferation at 3 days after the last ECS increased twice as much as the sham group. However, the number of proliferating cells at 14 days later decreased to a half of the sham level. Differentiation of newly formed cells was not influenced in ECS-treated groups compared with sham-treated groups. In addition, we investigated the effects of ECS on behavioral changes in rats by measuring locomotor activity in an open field test and spontaneous alteration behavior in a Y-maze test. Spontaneous behavior and memory function were not influenced by repeated ECSs. These results suggest that repeated ECSs affect progenitors that have a limited ability for cell proliferation, like amplifying progenitors, to increase newly generated neurons without negative behavioral change.
Brain research 11/2012; · 2.46 Impact Factor
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ABSTRACT: BACKGROUND: There is accumulating evidence regarding gender differences in clinical symptoms or response to antidepressants in patients with depression. However, less attention has been given to sex differences in the underlying biological mechanisms of depression. The adrenal androgens, dehydroepiandrosterone (DHEA) and its sulfate derivative (DHEA-S), play a critical role in controlling affect, mood, and anxiety. Changes in serum adrenal androgen levels have been reported in conditions pertaining to stress as well as in psychiatric disorders. The objective of the present study was to investigate differences in serum levels of adrenal androgens in male and female patients with major depressive disorder (MDD). METHODS: Participants included 90 inpatients with MDD at the psychiatric ward of Juntendo University Koshigaya Hospital who were receiving antidepressants. Serum levels of DHEA and DHEA-S were assessed at the time of admission. Matched controls (based on sex and age) included 128 healthy individuals. First, data from male and female MDD patients and controls were compared. Second, correlations between serum hormone levels and scores on the Hamilton Rating Scale for Depression (HAM-D) of patients with MDD were assessed by gender. In addition, effects of various factors on adrenal androgens were analyzed using multiple regression analysis. RESULTS: Serum DHEA levels were significantly increased in both male and female MDD patients compared with controls. Serum levels of DHEA-S in male patients were significantly decreased compared with male controls, whereas no significant differences were seen in female patients and controls. No significant correlations among adrenal androgens were observed in male patients with MDD, whereas significant positive correlations were found in both male and female controls. No significant correlations were seen between adrenal androgens and HAM-D scores in male or female patients. Multiple regression analysis showed that both hormones were affected by the age at onset of depression. LIMITATIONS: All subjects in the present study were on antidepressant medications. CONCLUSIONS: Elevated levels of serum DHEA may be associated with the biological pathophysiology of depression, as DHEA administration has been found to be effective for the treatment of depression. Findings of differential changes in DHEA-S levels in men compared with women may suggest distinct characteristics of these hormones between men and women with depression. However, DHEA/DHEA-S may be a poor indicator for evaluating severity of depression.
Journal of affective disorders 10/2012; · 3.76 Impact Factor
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ABSTRACT: BACKGROUND: Depression may increase the risk of developing Alzheimer's disease. Large cohort studies have shown that recurrent depression is associated with a risk of developing dementia. Other studies have documented smaller hippocampal volume in patients with recurrent depression. It is speculative that a greater risk of developing dementia may result from a higher number of previous depressive episodes. This study compared patients with recurrent and single-episode depression in the remitted stage, and healthy controls to elucidate the impact of the number of depressive episodes on memory. METHODS: Logical memory and visual reproduction subtests of the Wechsler Memory Scale-Revised were given to 68 patients with major depressive disorder (MDD) (30 patients with a single episode and residual 38 patients with recurrent multiple episodes) and 57 healthy controls. The patients with MDD received memory assessment at the time of initial remission and at the follow-up period 3 years after remission. RESULTS: At the time of initial remission, scores of both logical memory and visual reproduction subtests were significantly lower in both patient groups compared with healthy controls. At follow-up, memory dysfunction of the single-episode group disappeared, whereas scores in the recurrent group remained significantly lower than those of the single-episode group and controls. LIMITATIONS: All patients in the present study were on antidepressant medications. CONCLUSIONS: Patients with recurrent MDD with multiple depressive episodes showed residual memory dysfunction even after 3 years of remission. Persistence of memory deficits in the recurrent depression may be a risk factor for developing dementia.
Journal of affective disorders 07/2012; · 3.76 Impact Factor
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ABSTRACT: Brain-derived neurotrophic factor (BDNF) may have an important role in the pathophysiology of depression. Previous studies indicate that serum BDNF levels were lower in patients with depression and increased after treatment with antidepressants. However, results of studies on serum BDNF levels in remitted patients with depression have been inconsistent. The purpose of the present study was to determine which factors influence the alteration of serum BDNF levels in depression in the remitted state.
Serum BDNF levels were evaluated in 75 remitted inpatients with major depressive disorder (MDD) and 108 controls. Multiple regression analyses were conducted using serum BDNF levels as the dependent variable; and the number of episodes, Hamilton Rating Scale for Depression score at admission, or duration of last depressive episode as independent variables.
Serum BDNF levels were lower in remitted patients with MDD than in controls (P < .001). Multiple regression analysis showed a significant effect between the duration of the last depressive episode and serum BDNF levels (P < .022).
Serum BDNF levels in remitted patients with MDD did not recover to the level of healthy controls, and lower serum BDNF levels were influenced by a longer duration of last depressive episode. It is possible that persistent hippocampal reduction in remitted depression may be caused by lower BDNF levels associated with a longer duration of the last depressive episode.
Depression and Anxiety 03/2012; 29(9):775-9. · 4.18 Impact Factor
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ABSTRACT: Epidemiologic studies have demonstrated that a history of depression increases the risk of developing Alzheimer's disease, particularly among individuals with early-onset depression. On the other hand, recent studies have suggested that a higher amyloid-β protein (Aβ)40 to Aβ42 ratio may be associated with the future onset of Alzheimer's disease. Our objective was to assess whether the pathophysiology of early-onset depression may involve or affect Aβ metabolism.
In this extension of a case-control pilot study, 193 inpatients with DSM-IV major depressive disorder (MDD) (mean age = 55.9 years) from the Juntendo Koshigaya Hospital, Saitama, Japan, and 413 healthy controls from the community (mean age = 56.6 years) were recruited between May 2004 and April 2009. Serum Aβ40 and Aβ42 levels, Aβ40/Aβ42 ratio, and other clinical and biological factors were compared between controls and patients in 3 age groups: young (< 40 years), middle-aged (≥ 40 to < 65 years), and elderly (≥ 65 years). Depressive symptoms were assessed with the Hamilton Depression Rating Scale. All patients were receiving antidepressant medication at the time of the study, and doses of current antidepressants were converted to an equivalent imipramine dose.
The serum Aβ40/Aβ42 ratio was significantly higher in MDD patients than controls in all age groups (young: P = .003; middle-aged: P < .001; elderly: P = .006). These differences were also observed in noncarriers of the apolipoprotein E ε4 allele.
Our findings suggest that Aβ metabolism may be affected in depression; these findings also possibly answer the question of why even early-onset depression is a risk factor for developing Alzheimer's disease.
The Journal of Clinical Psychiatry 11/2011; 73(1):115-20. · 5.80 Impact Factor
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ABSTRACT: Brain-derived neurotrophic factor (BDNF) is a member of the nerve growth factor family and plays a critical role in growth, differentiation, maintenance and synaptic plasticity of neuronal systems. Previous studies have demonstrated lower serum BDNF concentrations in major depressive disorder (MDD), with concentrations negatively correlating with the severity of the disease. However, few investigations have examined the relationship between serum BDNF and detailed clinical symptoms. The aim of present study was to clarify the magnitudes of the relationships between various depressive symptom and serum BDNF.
Serum BDNF concentrations were evaluated from 109 inpatients with MDD and 163 healthy controls. Depressive symptoms were assessed using the Hamilton rating scale for depression (HAM-D), and symptoms were categorized into four groups: "anxiety somatization"; "cognitive disturbance"; "retardation"; and "sleep disturbance".
Serum BDNF concentration was significantly lower in patients with MDD compared to controls (p<0.001). We identified significant negative correlations between serum BDNF concentration and both total score (R=-0.19, p=0.044) and "anxiety somatization" sub-score (R=-0.32, p=0.001) from the HAM-D in patients with MDD.
All patients in the present study were on antidepressant medications.
These results suggest that serum BDNF level may offer a biological marker for anxiety symptoms in medicated patients with MDD.
Journal of affective disorders 07/2011; 135(1-3):332-5. · 3.76 Impact Factor
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Yuri Hotta,
Tohru Ohnuma,
Ryo Hanzawa,
Nobuto Shibata,
Hitoshi Maeshima,
Hajime Baba,
Tokiko Hatano,
Yuto Takebayashi,
Maiko Kitazawa,
Motoyuki Higa, Toshihito Suzuki,
Heii Arai
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ABSTRACT: Treating the 20-30% of patients with schizophrenia whose symptoms are resistant to antipsychotic treatment, a condition known as treatment-resistant schizophrenia (TRS), can be problematic. Recently, an association between Disrupted-in-Schizophrenia-1 (DISC1), a candidate susceptibility gene for schizophrenia, and TRS was reported. Associations between three missense SNPs, rs3738401 (Q264R), rs6675281 (L607F), and rs821616 (S704C) in DISC1, especially rs3738401, showed strong significance. Thus, the main aim of our current study was to examine if the reported possible functional polymorphisms in DISC1 were related to Japanese TRS. First, DISC1 was re-investigated in 485 Japanese patients with schizophrenia and 660 healthy controls with a case-control study using four candidate SNPs, rs751229, rs3738401, rs821597, and rs821616. DISC1 was not associated with schizophrenia in the Japanese population. Second, we investigated whether these SNPs contributed to TRS in 127 inpatients with schizophrenia (35 patients; TRS and 92 patients; non-TRS). The genotypic distributions of these four SNPs were not significantly different between TRS and non-TRS in either genotypic or recessive models of minor alleles. In addition, clinical variables, such as improvement in clinical symptoms, duration of hospitalization, and total antipsychotics dose amounts, were not different among the genotypes of these SNPs. Taken together, results showed that DISC1 had no apparent degree of association with Japanese patients with schizophrenia as a candidate susceptibility gene for disease per se or TRS.
Progress in Neuro-Psychopharmacology and Biological Psychiatry 01/2011; 35(2):636-9. · 3.25 Impact Factor
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ABSTRACT: Background: Depression may increase the risk of developing Alzheimer's disease (AD). Recent large cohort studies have also shown that a low plasma amyloid β (Aβ)-42 level combined with a high Aβ40 level increases the risk of developing AD, suggesting plasma Aβ42/40 ratio as useful for identifying risk of developing mild cognitive impairment and AD. Although several studies have examined Aβ levels in the peripheral blood of elderly individuals with depression, results have been inconsistent. Furthermore, no results have been described for younger depression.Methods: Serum Aβ40, Aβ42 level and Aβ40/42 ratio were evaluated using enzyme-linked immunosorbent assay in 60 patients with major depressive disorder (MDD) and 60 healthy controls. The results were analyzed in two age groups (young, <60 years; elderly, ≥60 years).Results: Serum Aβ40 level was significantly higher in young MDD patients compared to young controls (P < 0.001), but it was not significantly deferent in the elderly group. Serum Aβ42 level did not differ significantly in both young and elderly groups. Aβ40/42 ratio was significantly higher in both young (P < 0.001) and elderly (P < 0.001) patients with MDD compared to controls.Conclusions: Serum Aβ40/42 ratio was significantly higher in MDD patients than in controls, and this difference was seen for both elderly and young subjects. This may suggest that even young subjects with MDD undergo pathological changes in the very early stage of amyloid deposition.
Psychogeriatrics 03/2010; 9(4):180 - 185. · 1.21 Impact Factor
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ABSTRACT: Since oral administration of d-alanine, an agonist that binds to the glycine site of N-methyl-d-aspartate (NMDA) receptors, improves the positive and cognitive symptoms of patients with schizophrenia, measurement of endogenous plasma alanine levels could serve as a clinical marker for schizophrenia severity and improvement. Mean plasma alanine levels were compared in healthy controls and patients with schizophrenia during the clinical course of the disease. Methods: eighty-one Japanese patients with schizophrenia and 50 age- and gender-matched healthy controls were studied. Plasma alanine levels were measured twice, during the acute stage and during the remission stage, using high-performance liquid chromatography. On admission, lower plasma alanine levels in patients with schizophrenia were accompanied by more severe schizophrenic symptoms, especially positive symptoms. The plasma alanine levels in patients with schizophrenia increased significantly from the time of admission to discharge, when they were significantly higher than control levels. An increase in plasma alanine levels from the acute stage to the remission stage of schizophrenia was correlated with improvement in symptoms. Drug-naïve patients did not show a significant difference in plasma alanine levels when compared with healthy controls. The measurement of plasma alanine levels may be a therapeutic marker for schizophrenia.
Psychiatry Research 03/2010; 177(1-2):27-31. · 2.52 Impact Factor
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ABSTRACT: Electroconvulsive therapy (ECT) is known as a successful treatment for severe depression. Despite great efforts, the biological mechanisms underlying the beneficial effects of ECT remain largely unclear. In this study, animals received a single, 10, or 20 applications of electroconvulsive seizure (ECS), and then cell proliferation and apoptosis were investigated in the subgranular zone (SGZ) of the dentate gyrus. We analyzed whether a series of ECSs could induce changes in the dentate gyrus in a dose-response fashion. A single-ECS seizure significantly increased cell proliferation in the SGZ by ∼2.3-fold compared to sham treatment. After 10 ECSs, a significant increase in cell proliferation was observed in the SGZ by ∼2.4-fold compared to sham treatment. Moreover, 10 ECSs induced a significant increase in cell proliferation by 1.3-fold compared to a single-ECS group. However, cell proliferation did not differ between the group with 20 ECSs and sham group. In addition, a significant increase in the number of apoptotic cells was found in the group with 10 ECSs, whereas no significant change in it was found in either a single ECS or 20 ECSs group compared to sham treatment. These findings indicate that the optimal number of treatments and duration of stimulation requires investigation. Further studies are needed to elucidate the intracellular mechanisms underlying both effective and excessive ECT.
Synapse 03/2010; 64(11):814-21. · 2.94 Impact Factor
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ABSTRACT: The authors aimed to investigate whether remitted adult and elderly major depressive disorder patients show different patterns of executive dysfunction. Executive functions of 20 euthymic major depressive disorder patients and 29 healthy comparison subjects were evaluated using the Behavioral Assessment of the Dysexecutive Syndrome. Relative to adult patients and healthy comparison subjects, euthymic elderly patients were more impaired in the subtest of Modified Six Elements. Since the regions most implicated in this subtest are the medial prefrontal, the anterior cingulate, and the dorsolateral prefrontal areas, the authors conclude that dysfunctions of such frontal neural networks remain unresolved even in the remission phase of late-life depression.
The Journal of neuropsychiatry and clinical neurosciences 01/2010; 22(1):70-4. · 2.34 Impact Factor
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ABSTRACT: Depression may increase the risk of developing Alzheimer's disease (AD). Recent large cohort studies have also shown that a low plasma amyloid beta (Abeta)-42 level combined with a high Abeta40 level increases the risk of developing AD, suggesting plasma Abeta42/40 ratio as useful for identifying risk of developing mild cognitive impairment and AD. Although several studies have examined Abeta levels in the peripheral blood of elderly individuals with depression, results have been inconsistent. Furthermore, no results have been described for younger depression.
Serum Abeta40, Abeta42 level and Abeta40/42 ratio were evaluated using enzyme-linked immunosorbent assay in 60 patients with major depressive disorder (MDD) and 60 healthy controls. The results were analyzed in two age groups (young, <60 years; elderly, >or=60 years).
Serum Abeta40 level was significantly higher in young MDD patients compared to young controls (P < 0.001), but it was not significantly deferent in the elderly group. Serum Abeta42 level did not differ significantly in both young and elderly groups. Abeta40/42 ratio was significantly higher in both young (P < 0.001) and elderly (P < 0.001) patients with MDD compared to controls.
Serum Abeta40/42 ratio was significantly higher in MDD patients than in controls, and this difference was seen for both elderly and young subjects. This may suggest that even young subjects with MDD undergo pathological changes in the very early stage of amyloid deposition.
Psychogeriatrics 12/2009; 9(4):180-5. · 1.21 Impact Factor
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ABSTRACT: Antipsychotic-induced extrapyramidal symptoms (AIEPSs) are commonly recognized side effects of typical 1st generation antipsychotics, and considerable variability is seen in the susceptibility of individual patients to AIEPSs. Regulator of G-protein signaling 2 (RGS2) proteins regulate intracellular signaling and second messenger activation of molecules including dopamine, serotonin, and acetylcholine receptors, all of which appear to be involved in the pathophysiology of AIEPSs. Previous studies have shown an association between AIEPSs in schizophrenia and RGS2, especially the minor G allele of single nucleotide polymorphism (SNP) rs4606 (+2971C>G) in RGS2, and have suggested a possible protective effect by the G allele on AIEPSs. In this study, we investigated whether the rs4606 SNP in RGS2 alone also showed an effect on AIEPSs by utilizing the Drug-Induced Extrapyramidal Symptom Scale (DIEPSS) in 103 Japanese patients with schizophrenia. In the assumed G allele recessive model, sialorrhea and total Parkinsonism scores were significantly higher in subjects with the GG genotype than in subjects with other genotypes. Other clinical variables were not significantly different among the various genotype groups. Controlling for clinical variables as covariates, a one-way analysis of covariance found no association between rs4606 genotypes and DIEPSS scores. Taken together, these results, although preliminary, suggest that rs4606 does not affect AIEPSs in Japanese subjects.
Neuroscience Letters 11/2009; 469(1):55-9. · 2.11 Impact Factor
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ABSTRACT: Multiple case reports have described pregnancy in phencyclidine hydrochloride (PCP) abusers. Characteristic clinical symptoms of PCP-exposed infants have revealed neurobehavioral or physical abnormalities. We designed this study to evaluate whether chronic prenatal exposure to PCP during the last 2 weeks of gestation in rats produces alterations of hippocampal neurogenesis in offspring. Rats received repeated subcutaneous injection of PCP (5 mg/kg) once daily during the last 2 weeks of gestation. Control animals received subcutaneous injection of physiological saline during gestation. Dams receiving repeated PCP administrations showed markedly increased locomotor activities on days 1, 5, and 10 during the last 2 weeks of gestation. At 21 days after birth, 5-bromo-2'-deoxyuridine (BrdU)-positive cells of offspring were counted in the granule cell layer (GCL) and subgranular zone of the dentate gyrus. The numbers of BrdU-positive cells in the GCL in male and female offspring of the PCP-treated group were significantly increased by approximately 77% compared with those from the control group. At 56 days, the number of surviving BrdU-positive cells also remained to be increased by 74% in the GCL in PCP-treated group. At 21 days, locomotor activities of offspring in the PCP-treated group were significantly decreased by approximately 30% compared with those in the control group. However, neuronal differentiation of newly formed cells and cell survival were not influenced at 5 weeks after BrdU injections. Some altered biochemical or physiological conditions of offspring from dams receiving repeated PCP injections during pregnancy could influence changes in cell proliferation in the GCL of offspring during early development. Changes to cell proliferation in the hippocampus may affect behavioral abnormalities during infancy in offspring.
Synapse 06/2009; 63(9):729-36. · 2.94 Impact Factor
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ABSTRACT: An autopsy case of a 37 year old man with mitochondrial encephalomyopathy is reported. Ragged red fibers and crystalline inclusions in mitochondria were revealed by biopsy of the striated muscle of the patient. Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) was diagnosed clinically. In addition to severe atrophy and degeneration of the generalized striated muscles and many foci of laminar necrosis of the cerebral cortex, the following abnormalities were observed: 1) hypertrophy of the myocardium, 2) fatty change of the liver, 3) focal sclerosis of the glomeruli and dilatation of the tubules of the kidneys, 4) hyalinous degeneration of the Langerhans' islands of the pancreas and 5) wavy change of the smooth muscle fibers of the muscularis propria of the gastrointestinal tract. We suggest that mitochondrial encephalomyopathy affects various organs and tissues, among which susceptibility of the muscular tissues —skeletal muscle, myocardium and smooth muscle—is high. Acta Pathol Jpn 42: 818–825, 1992.
Pathology International 12/2008; 42(11):818 - 825. · 1.62 Impact Factor
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ABSTRACT: Based on the hypothesis of NMDA receptor hypofunction in schizophrenia, plasma glycine, L-serine, and D-serine levels have been studied, since they could serve as biological markers. However, changes over time in the levels of these amino acids in schizophrenic patients have not been investigated. To clarify the mean plasma glycine, L-serine, and D-serine levels in patients with schizophrenia, levels of these amino acids were compared between healthy controls and patients with schizophrenia. The plasma levels of these amino acids during the clinical course of schizophrenia were also compared.
Eighty-nine Japanese patients with schizophrenia and 50 age- and gender-matched healthy controls were studied. Plasma glycine, L-serine, and D-serine levels and their ratios were measured twice, during the acute stage and during the remission stage, using high-performance liquid chromatography.
The admission plasma glycine, L-serine, and D-serine levels of schizophrenic patients were higher than those of healthy controls. There were no significant differences between drug-naïve patients and healthy controls in the admission levels of the plasma amino acids, but chronically medicated patients had higher admission plasma glycine and D-serine levels. Only the D-serine level and the D-/L-serine ratio were markedly significantly increased in schizophrenic patients from the time of admission to the time of discharge as their clinical symptoms improved. In addition, the increase in the plasma D-serine levels of drug-naïve patients was correlated with improvements in positive symptoms.
Plasma amino acid levels, especially D-serine levels, could be useful as a "therapeutic" or "clinical state" marker in patients with acute schizophrenia.
Progress in Neuro-Psychopharmacology and Biological Psychiatry 10/2008; 32(8):1905-12. · 3.25 Impact Factor
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ABSTRACT: Five cases with eating disorders (one case with anorexia nervosa alone, 4 cases with anorexia nervosa and bulimia nervosa) complicated with schizophrenia and 3 cases of bulimia nervosa complicated with schizophrenia were reported. The eating disorders and schizophrenia were diagnosed according to the diagnostic criteria of DSM-III-R. As to the type of schizophrenia, 4 patients were of an undifferentiated type and 4 cases were of a disorganized type. Regarding the prepsychotic personality, 6 of the 8 cases showed schizothyme personality traits. All the patients showed depressive symptoms which are relatively common in eating disorders. In all the patients, significant social or school life difflculties persisted and a resumption of premorbid functioning was not seen. The possibility of an afflnity between anorexia nervosa and schizophrenia was discussed.
Psychiatry and Clinical Neurosciences 06/2008; 46(4):859 - 868. · 2.13 Impact Factor
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ABSTRACT: Past neuropsychological studies on depression have documented executive dysfunction and it has been reported that some dysfunction persists even after depressive symptoms disappear. Studies have shown a correlation between cerebrovascular lesions and executive dysfunction in depression among the elderly. The aim of the present study was to focus on executive functions in remitted major depressive disorder (MDD) patients, and to investigate whether remitted young and elderly patients show different patterns of executive dysfunction, and to ascertain the relationships with vascular lesions.
Subjects were 79 inpatients with MDD and 85 healthy controls. Each subject received Wisconsin Card Sorting Test (WCST), Stroop test, and Verbal Fluency Test (VFT) in a remitted state. Both the MDD and control groups were divided into young and elderly groups, and the performances between 4 groups were compared.
For Stroop test, the scores of the MDD group were significantly lower than controls. In addition, as for VFT, the scores for the elderly MDD group were significantly lower than the other groups. Multiple regression analysis showed that VFT scores were affected by the presence of vascular lesions.
The results of the present study demonstrated that executive dysfunction remained even in a remitted state in MDD patients, but the patterns of impairment were different between young and elderly patients. The results also suggested that vascular lesions affect executive dysfunction, particularly in elderly depressive patients.
Journal of Affective Disorders 03/2008; 111(1):46-51. · 3.52 Impact Factor
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Journal of Clinical Psychopharmacology 01/2008; 27(6):727-8. · 4.10 Impact Factor
