Abstract:
BACKGROUND:Recent evidence from clinical studies and animal models of traumatic brain injury (TBI) suggest that neuronal and glial loss might progress after the initial insult in selectively vulnerable regions of the brain such as the hippocampus. There is also evidence that hippocampal dysfunction plays a role in the pathogenesis of mood disorders. We examined the relationship between hippocampal damage and mood disorders after TBI and the effect of hippocampal atrophy on the outcome of TBI patients. METHODS:The study group consisted of 37 patients with closed head injury who were evaluated at baseline and at 3, 6, and 12 months after trauma. Psychiatric diagnosis was made with a structured clinical interview and DSM-IV criteria. Quantitative magnetic resonance imaging scans were obtained at 3-months follow-up. RESULTS:Patients with moderate to severe head injury had significantly lower hippocampal volumes than patients with mild TBI. Patients who developed mood disorders had significantly lower hippocampal volumes than patients without mood disturbance. Furthermore, there was a significant interaction between mood disorders diagnosis and severity of TBI, by which patients with moderate to severe TBI who developed mood disorders had significantly smaller hippocampal volumes than patients with equivalent severe TBI who did not develop mood disturbance. Finally, reduced hippocampal volumes were associated with poor vocational outcome at 1-year follow-up. CONCLUSIONS:Our findings are consistent with a "double-hit" mechanism by which neural and glial elements already affected by trauma are further compromised by the functional changes associated with mood disorders (e.g., the neurotoxic effects of increased levels of cortisol or excitotoxic damage resulting from overactivation of glutaminergic pathways). Finally, patients with greater hippocampal damage were less likely to return to a productive life 1 year after trauma.
journal_name
Biol Psychiatryjournal_title
Biological psychiatryauthors
Jorge RE,Acion L,Starkstein SE,Magnotta Vdoi
10.1016/j.biopsych.2006.07.024subject
Has Abstractpub_date
2007-08-15 00:00:00pages
332-8issue
4eissn
0006-3223issn
1873-2402pii
S0006-3223(06)00935-8journal_volume
62pub_type
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journal_title:Biological psychiatry
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journal_title:Biological psychiatry
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章
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journal_title:Biological psychiatry
pub_type: 杂志文章,评审
doi:10.1016/j.biopsych.2018.01.014
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pub_type: 临床试验,杂志文章
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journal_title:Biological psychiatry
pub_type: 杂志文章,评审
doi:10.1016/s0006-3223(98)00287-x
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/0006-3223(86)90163-0
更新日期:1986-04-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章
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更新日期:1996-01-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
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journal_title:Biological psychiatry
pub_type: 杂志文章
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/s0006-3223(00)01127-6
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journal_title:Biological psychiatry
pub_type: 杂志文章
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更新日期:1988-02-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2009.01.001
更新日期:2009-08-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2008.03.019
更新日期:2008-09-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2006.04.023
更新日期:2006-09-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章
doi:10.1016/s0006-3223(01)01133-7
更新日期:2001-07-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章
doi:10.1016/s0006-3223(03)00699-1
更新日期:2003-12-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2011.03.026
更新日期:2011-08-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
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更新日期:1996-07-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 临床试验,杂志文章
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journal_title:Biological psychiatry
pub_type: 杂志文章
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journal_title:Biological psychiatry
pub_type: 杂志文章
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更新日期:2017-06-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2008.08.019
更新日期:2009-01-15 00:00:00
abstract::Delirium, also known as acute confusional state, is a common reversible organic psychiatric syndrome. This paper focuses on toxic delirium associated with prominent paroxysmal electroencephalogram (EEG) dysfunction occurring in nonepileptic patients. Our data derive from observations in two conditions, viz., delirium ...
journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/0006-3223(89)90198-4
更新日期:1989-02-15 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/0006-3223(91)90222-8
更新日期:1991-02-15 00:00:00
abstract:BACKGROUND:A variety of immunologic alterations have been observed in patients with schizophrenia. These findings have lent support to theories that autoimmune mechanisms may be important in some patients with the illness. The CD5+ B lymphocyte, a B-cell subset associated with autoimmune disease, has been the subject o...
journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/s0006-3223(98)00307-2
更新日期:1999-07-01 00:00:00
abstract::Serum free thyroxine (FT4), total thyroxine (TT4), and Brief Psychiatric Rating Scale (BPRS) measurements were obtained following hospital admission and at 2-week intervals during hospitalization in 80 male psychiatric inpatients with a variety of major psychotic and affective disorders. A strong correlation between t...
journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/0006-3223(89)90148-0
更新日期:1989-01-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/0006-3223(85)90098-8
更新日期:1985-06-01 00:00:00
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journal_title:Biological psychiatry
pub_type: 杂志文章
doi:10.1016/j.biopsych.2019.02.011
更新日期:2019-06-15 00:00:00
abstract::Despite recognition that schizophrenia must have syndrome status in the absence of proof of a single etiopathophysiologic process, a century of work has been based on designs that conceptualize schizophrenia as a single disease entity. Reducing heterogeneity at several levels of functioning is desirable. In this artic...
journal_title:Biological psychiatry
pub_type: 杂志文章,评审
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更新日期:1999-08-01 00:00:00