Psychiatry and Clinical Neurosciences

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Regional cerebral blood flow abnormalities in late‐life depression:Relation to refractoriness and chronification
Psychiatry and Clinical Neurosciences - Tập 52 Số 1 - Trang 97-105 - 1998
Shuichi Awata, Hiroshi Itoh, Michiko Konno, Shuichi Ono, Ryuta Kawashima, Hiroshi Fukuda, M Sato
Abstract We examined patterns of regional cerebral blood flow (rCBF) abnormalities in 18 patients with major depressive disorder in late life using single photon emission computed tomography (SPECT) and (99mTc‐hexamethyl‐propylenamine oxime (99mTc‐HMPAO). Compared with 13 age‐matched controls, relative rCBF was significantly decreased bilaterally in the anterior cingulate gyrus, the prefrontal cortex, the temporal cortex, the parietal cortex, the hippocampus and the caudate nucleus. However, it was not correlated with the severity of depression or global cognitive dysfunction. In 10 patients with a prolonged depressive episode or prolonged residual symptoms (the refractory subgroup), robust and extensive decreases in rCBF were found compared with controls and the rCBF decreased significantly in the anterior cingulate gyrus and the prefrontal cortex compared with that in the non‐refractory subgroup. In the non‐refractory subgroup, rCBF decreased significandy in the caudate nucleus and tended to decrease in the anterior cingulate gyrus compared with controls. These findings indicate that dysfunction of the limbic system, the cerebral association cortex and the caudate nucleus may be implicated in late‐life depression and that robust and extensive hypoperfusion, especially in the anterior cingulate and the prefrontal regions, may relate to refractoriness or chronification of depression.
Cross‐cultural adaptation and psychometric properties of the Social Capital Questionnaire for Adolescent Students among preadolescents and adolescents in Japan
Psychiatry and Clinical Neurosciences - Tập 73 Số 9 - Trang 601-602 - 2019
Tomoya Hirota, Masaki Adachi, Michio Takahashi, Kazuhiko Nakamura
Comorbid substance use disorder in schizophrenia: A selective overview of neurobiological and cognitive underpinnings
Psychiatry and Clinical Neurosciences - Tập 67 Số 6 - Trang 367-383 - 2013
Patrizia Thoma, Irene Daum
Although individuals with schizophrenia show a lifetime prevalence of 50% for suffering from a comorbid substance use disorder, substance abuse usually represents an exclusion criterion for studies on schizophrenia. This implies that surprisingly little is known about a large group of patients who are particularly difficult to treat. The aim of the present work is to provide a brief and non‐exhaustive overview of the current knowledgebase about neurobiological and cognitive underpinnings for dual diagnosis schizophrenia patients. Studies published within the last 20 years were considered using computerized search engines. The focus was on nicotine, caffeine, alcohol, cannabis and cocaine being among the most common substances of abuse. All drugs of abuse target dopaminergic, glutamatergic and GABAergic transmission which are also involved in the pathophysiology of schizophrenia. Current literature suggests that neurocognitive function might beless disrupted in substance‐abusing compared to non‐abusing schizophrenia patients, but in particular the neuroimaging database on this topic is sparse. Detrimental effects on brain structure and function were shown for patients for whom alcohol is the main substance of abuse. It is as yet unclear whether this finding might be an artifact of age differences of patient subgroups with different substance abuse patterns. More research is warranted on the specific neurocognitive underpinnings of schizophrenia patients abusing distinct psychoactive substances. Treatment programs might either benefit from preserved cognitive function as a resource or specifically target cognitive impairment in different subgroups of addicted schizophrenia patients.
Resting state default‐mode network connectivity in early depression using a seed region‐of‐interest analysis: Decreased connectivity with caudate nucleus
Psychiatry and Clinical Neurosciences - Tập 63 Số 6 - Trang 754-761 - 2009
Robyn Bluhm, Peter Williamson, Ruth A. Lanius, Jean Théberge, Maria Densmore, Robert Bartha, Richard W. J. Neufeld, Elizabeth Osuch
Aim:  Reports on resting brain activity in healthy controls have described a default‐mode network (DMN) and important differences in DMN connectivity have emerged for several psychiatric conditions. No study to date, however, has investigated resting‐state DMN in relatively early depression before years of medication treatment. The objective of the present study was, therefore, to investigate the DMN in patients seeking help from specialized mental health services for the first time for symptoms of depression.Methods:  Fourteen depressed subjects and 15 matched controls were scanned using 4‐T functional magnetic resonance imaging while resting with eyes closed. All but one subject was medication free. A precuneus/posterior cingulate cortex (P/PCC) seed‐region connectivity analysis was used to identify the DMN and compare study groups in regions of relevance to depression.Results:  The P/PCC analysis identified the DMN well in both study groups, consistent with prior literature. Direct comparison showed significantly reduced correlation between the P/PCC and the bilateral caudate in depression compared with controls and no areas of increased connectivity in the depressed group.Conclusions:  The present study is the first to investigate resting‐state DMN in the early stages of treatment‐seeking for depression. Depressed subjects had decreased connectivity between the P/PCC and the bilateral caudate, regions known to be involved in motivation and reward processing. Deficits in DMN connectivity with the caudate may be an early manifestation of major depressive disorder.
Effects of maternal separation and antidepressant drug on epigenetic regulation of the brain‐derived neurotrophic factor exon I promoter in the adult rat hippocampus
Psychiatry and Clinical Neurosciences - Tập 72 Số 4 - Trang 255-265 - 2018
Sung Woo Park, Mi Kyoung Seo, Jung Goo Lee, Lê Thị Thu Hiền, Young Hoon Kim
AimEarly life stress can induce epigenetic changes through genetic and environmental interactions and is a risk factor for depression. Brain‐derived neurotrophic factor (BDNF) has been implicated in the pathophysiology of depression and antidepressant drug action. We investigated epigenetic changes at the BDNF exon I promoter in the hippocampus of adult rats subjected to maternal separation (MS) during early life and treated with an antidepressant drug as adults.MethodsRat pups were subjected to MS from postnatal day 1 to 21 and received chronic escitalopram (ESC) as adults. We assessed the effects of MS and ESC on BDNF exon I and DNA methyltransferases (DNMT) mRNA levels (quantitative reverse‐transcription polymerase chain reaction), acetylated histone H3, and MeCP2 binding to the BDNF promoter I (chromatin immunoprecipitation followed by real‐time polymerase chain reaction), and BDNF protein levels (enzyme‐linked immunosorbent assay).ResultsThe levels of BDNF protein, exon I mRNA, histone H3 acetylation, and DNMT1 and DNMT3a mRNA were altered in the MS group compared with the control group. Significant decreases were observed in the BDNF protein, exon I mRNA, and histone H3 acetylation levels and there were significant increases in DNMT1 and DNMT3a mRNA levels. The comparison between the MS + ESC and MS groups revealed significant increases in BDNF protein, exon I mRNA, and histone H3 acetylation levels and significant decreases in MeCP2 and DNMT1 and DNMT3a mRNA levels.ConclusionThese findings indicate that MS induced epigenetic changes at the BDNF exon I promoter and these changes were prevented by antidepressant drug treatment during adulthood.
Cognitive and symptom profiles in Asperger’s syndrome and high‐functioning autism
Psychiatry and Clinical Neurosciences - Tập 61 Số 1 - Trang 99-104 - 2007
Tomonori Koyama, Hisateru Tachimori, Hideo Osada, Toshinobu Takeda, Hiroshi Kurita
Abstract  Asperger syndrome (AS) and autistic disorder are two subtypes of pervasive developmental disorders (PDD), but there has been considerable debate over whether AS and autistic disorder without mental retardation (IQ ≥ 70), called high‐functioning autism (HFA), are distinct conditions or not. The aim of the present paper was to clarify this issue through a comparison of cognitive function and autistic symptom profiles. Based on the DSM‐IV and ICD‐10 definitions of language acquisition, 36 age‐ and IQ‐balanced subjects with AS (mean age, 12.8 years; mean full‐scale IQ, 98.3) were compared with 37 subjects with HFA (mean age, 12.6 years; mean full‐scale IQ, 94.6) on the Japanese version of the Wechsler Intelligence Scales and the Childhood Autism Rating Scale‐Tokyo Version (CARS‐TV). Compared with the HFA subjects, the AS subjects scored significantly higher on Verbal IQ, Vocabulary, and Comprehension, but scored significantly lower on Coding. Although the total CARS‐TV score did not differ significantly between the two groups, AS subjects scored significantly lower (i.e. less abnormal) on Verbal communication and Non‐verbal communication than did the HFA subjects. A history of normal language acquisition in early childhood could predict his/her better verbal ability in mid‐childhood or later. Autistic cognitive characteristics shared by both AS and HFA subjects appear to support the validity of the current diagnostic classification of PDD.
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