scholarly journals Post-traumatic stress disorder and declarative memory functioning: a review

2011 ◽  
Vol 13 (3) ◽  
pp. 346-351 ◽  

Declarative memory dysfunction is associated with post-traumatic stress disorder (PTSD). This paper reviews this literature and presents two frameworks to explain the nature of this dysfunction: that memory deficits are a product of neurobiological abnormalities caused by PTSD and/or that pre-existing memory deficits serve as a risk factor for the development of PTSD following trauma exposure. Brain regions implicated in declarative memory deficits include the hippocampus and prefrontal cortex, and imaging and biochemistry studies as they relate to memory dysfunction are described. Prospective and twin studies provide support for a risk factor model.

2020 ◽  
Vol 21 (12) ◽  
pp. 4503
Author(s):  
Sabah Nisar ◽  
Ajaz A. Bhat ◽  
Sheema Hashem ◽  
Najeeb Syed ◽  
Santosh K. Yadav ◽  
...  

Post-traumatic stress disorder (PTSD) is a highly disabling condition, increasingly recognized as both a disorder of mental health and social burden, but also as an anxiety disorder characterized by fear, stress, and negative alterations in mood. PTSD is associated with structural, metabolic, and molecular changes in several brain regions and the neural circuitry. Brain areas implicated in the traumatic stress response include the amygdala, hippocampus, and prefrontal cortex, which play an essential role in memory function. Abnormalities in these brain areas are hypothesized to underlie symptoms of PTSD and other stress-related psychiatric disorders. Conventional methods of studying PTSD have proven to be insufficient for diagnosis, measurement of treatment efficacy, and monitoring disease progression, and currently, there is no diagnostic biomarker available for PTSD. A deep understanding of cutting-edge neuroimaging genetic approaches is necessary for the development of novel therapeutics and biomarkers to better diagnose and treat the disorder. A current goal is to understand the gene pathways that are associated with PTSD, and how those genes act on the fear/stress circuitry to mediate risk vs. resilience for PTSD. This review article explains the rationale and practical utility of neuroimaging genetics in PTSD and how the resulting information can aid the diagnosis and clinical management of patients with PTSD.


2007 ◽  
Vol 38 (4) ◽  
pp. 533-542 ◽  
Author(s):  
S. B. Norman ◽  
M. B. Stein ◽  
J. E. Dimsdale ◽  
D. B. Hoyt

BackgroundIdentifying risk factors for the development of post-traumatic stress disorder (PTSD) is important for understanding and ultimately preventing the disorder. This study assessed pain shortly after traumatic injury (i.e. peritraumatic pain) as a risk factor for PTSD.MethodParticipants (n=115) were patients admitted to a Level 1 Surgical Trauma Center. Admission to this service reflected a severe physical injury requiring specialized, emergent trauma care. Participants completed a pain questionnaire within 48 h of traumatic injury and a PTSD diagnostic module 4 and 8 months later.ResultsPeritraumatic pain was associated with an increased risk of PTSD, even after controlling for a number of other significant risk factors other than acute stress disorder symptoms. An increase of 0.5 s.d. from the mean in a 0–10 pain rating scale 24–48 h after injury was associated with an increased odds of PTSD at 4 months by more than fivefold, and at 8 months by almost sevenfold. A single item regarding amount of pain at the time of hospital admission correctly classified 65% of participants.ConclusionsIf these findings are replicated in other samples, high levels of peritraumatic pain could be used to identify individuals at elevated risk for PTSD following traumatic injury.


Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 107 ◽  
Author(s):  
Tammy D. Kim ◽  
Suji Lee ◽  
Sujung Yoon

Post-traumatic stress disorder (PTSD) is a chronic condition characterized by symptoms of physiological and psychosocial burden. While growing research demonstrated signs of inflammation in PTSD, specific biomarkers that may be representative of PTSD such as the detailed neural correlates underlying the inflammatory responses in relation to trauma exposure are seldom discussed. Here, we review recent studies that explored alterations in key inflammatory markers in PTSD, as well as neuroimaging-based studies that further investigated signs of inflammation within the brain in PTSD, as to provide a comprehensive summary of recent literature with a neurological perspective. A search was conducted on studies published from 2009 through 2019 in PubMed and Web of Science. Fifty original articles were selected. Major findings included elevated levels of serum proinflammatory cytokines in individuals with PTSD across various trauma types, as compared with those without PTSD. Furthermore, neuroimaging-based studies demonstrated that altered inflammatory markers are associated with structural and functional alterations in brain regions that are responsible for the regulation of stress and emotion, including the amygdala, hippocampus, and frontal cortex. Future studies that utilize both central and peripheral inflammatory markers are warranted to elucidate the underlying neurological pathway of the pathophysiology of PTSD.


2008 ◽  
Vol 193 (3) ◽  
pp. 254-255 ◽  
Author(s):  
Jennifer Wild ◽  
Ruben C. Gur

SummaryPost-traumatic stress disorder (PTSD) is often associated with verbal memory deficits, which could influence treatment outcome. We assessed neuropsychological functioning in individuals with PTSD and their response to cognitive– behavioural therapy (CBT). Treatment non-responders had significantly poorer performance on measures of verbal memory compared with responders and demonstrated narrative encoding deficits. Differences were not explained by IQ, performance on tasks of attention, initial PTSD severity, depression, time since trauma, or alcohol/substance misuse. Verbal memory deficits seem to diminish the effectiveness of CBT and should be considered in its implementation.


2015 ◽  
Vol 45 (13) ◽  
pp. 2737-2746 ◽  
Author(s):  
S. J. H. van Rooij ◽  
M. Kennis ◽  
R. Sjouwerman ◽  
M. P. van den Heuvel ◽  
R. S. Kahn ◽  
...  

BackgroundSmaller hippocampal volume has often been observed in patients with post-traumatic stress disorder (PTSD). However, there is no consensus whether this is a result of stress/trauma exposure, or constitutes a vulnerability factor for the development of PTSD. Second, it is unclear whether hippocampal volume normalizes with successful treatment of PTSD, or whether a smaller hippocampus is a risk factor for the persistence of PTSD.MethodMagnetic resonance imaging (MRI) scans and clinical interviews were collected from 47 war veterans with PTSD, 25 healthy war veterans (combat controls) and 25 healthy non-military controls. All veterans were scanned a second time with a 6- to 8-month interval, during which PTSD patients received trauma-focused therapy. Based on post-treatment PTSD symptoms, patients were divided into a PTSD group who was in remission (n = 22) and a group in whom PTSD symptoms persisted (n = 22). MRI data were analysed with Freesurfer.ResultsSmaller left hippocampal volume was observed in PTSD patients compared with both control groups. Hippocampal volume of the combat controls did not differ from healthy controls. Second, pre- and post-treatment analyses of the PTSD patients and combat controls revealed reduced (left) hippocampal volume only in the persistent patients at both time points. Importantly, hippocampal volume did not change with treatment.ConclusionsOur findings suggest that a smaller (left) hippocampus is not the result of stress/trauma exposure. Furthermore, hippocampal volume does not increase with successful treatment. Instead, we demonstrate for the first time that a smaller (left) hippocampus constitutes a risk factor for the persistence of PTSD.


2021 ◽  
Author(s):  
David S. Krantz ◽  
Lisa M. Shank ◽  
Jeffrey L. Goodie

Evidence indicates that post-traumatic stress disorder (PTSD) is a significant risk factor for the development and progression of cardiovascular disease (CVD). Most explanations for PTSD-CVD associations conceptualize PTSD as a stress-related mental health disorder that elicits physiological, behavioral, and psychological responses that are causal factors in the development of cardiovascular disorders. This article reviews evidence for the broader physical health consequences of PTSD, and presents a conceptual model based on research suggesting that PTSD is a systemic disorder. Specifically, research findings indicate that diagnostic criteria are just the “tip of the iceberg” of a broader systemic disorder with elements that are cardiovascular risk factors. These systemic physiological and behavioral elements therefore should not be regarded as accompanying but unrelated diseases or comorbidities, but as inherent components of PTSD that directly impact the development of CVD. The systemic disorder approach has implications for the conceptualization of PTSD as a cardiovascular risk factor, needed research on PTSD and CVD, and clinical efforts to reduce PTSD-associated cardiovascular risk. It is suggested that treatments that aim to reduce cardiovascular disease risk need to address both the PTSD diagnostic components and its associated cardiovascular risk factors. Further research is needed to test the applicability and implications of the systemic disorder perspective.


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