scholarly journals Genetic and Neuroimaging Approaches to Understanding Post-Traumatic Stress Disorder

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.

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.


2021 ◽  
Author(s):  
Eline Voorendonk ◽  
Thomas Meyer ◽  
Sascha B. Duken ◽  
Vanessa van Ast

Intrusive and distressing memories are at the core of post-traumatic stress disorder (PTSD). Since cardiorespiratory fitness (CRF) has been linked with improved mental health, emotion regulation, and memory function, CRF may, by promoting these capabilities, protect against the development of intrusions after trauma. We investigated this idea in 115 healthy individuals, using a trauma film to induce intrusions. As potential mediators, we assessed indices of pre-trauma mental health such as heart rate variability, subjective and psychobiological peri-traumatic responses, and memory. Critically, results showed that higher CRF was related to fewer intrusions, but no mediators emerged of the CRF-intrusion relationship. These results indicate that individuals displaying higher CRF are less prone to develop traumatic memory intrusions. This suggests that promoting fitness prior to possible trauma exposure may provide a useful strategy to boost resilience against the development of debilitating re-experiencing symptoms of PTSD.


2009 ◽  
Vol 120 (6) ◽  
pp. 1096-1106 ◽  
Author(s):  
Melinda D. Veltmeyer ◽  
C. Richard Clark ◽  
Alexander C. McFarlane ◽  
Kathryn A. Moores ◽  
Richard A. Bryant ◽  
...  

Author(s):  
Jennifer Newman ◽  
Charles R. Marmar

This chapter discusses the role of executive function in post-traumatic stress disorder (PTSD), which is far from fully understood. Deficits are subtle and findings are often inconsistent. Impairments have been related to worsening of psychological symptoms, functioning, and quality of life. They can also negatively impact treatment. Functional imaging shows that neurocognitive deficits in PTSD may be related to an imbalance in brain connectivity, where emotion processing is enhanced and control is reduced. Structural findings show abnormalities in brain regions involved in higher-level functions. However, findings are often discrepant. Factors related to these inconclusive results are considered, including developmental course, premorbid functioning, and comorbidities such as traumatic brain injury, depression, substance use, attention deficit hyperactivity disorder, health behaviors, and medical concerns. Treatment implications, limitations of this work, and future directions are presented. The aim of future research is to advance scientific understanding of PTSD, neurocognitive impairments, and related conditions, with the goal of improving outcomes for those who encounter trauma.


2021 ◽  
Vol 22 (12) ◽  
pp. 6416
Author(s):  
Dor Danan ◽  
Doron Todder ◽  
Joseph Zohar ◽  
Hagit Cohen

Endocannabinoids play a role in adaptation to stress and regulate the release of glucocorticoids in stressed and unstressed conditions. We recently found that basal corticosterone pulsatility may significantly impact the vulnerability for developing post-traumatic-stress-disorder (PTSD), suggesting that the endocannabinoid system may contribute to its development. To examine this, we exposed rats to predator scent stress (PSS). Behavioral reactions were recorded seven days post-PSS. Cerebrospinal fluid (CSF) was collected from anesthetized rats shortly after PSS exposure to determine the levels of 2-arachidonoyl glycerol (2-AG) and anandamide (AEA). To correlate between endocannabinoids and corticosterone levels, rats were placed in metabolic cages for urine collection. To assess the levels of endocannabinoids in specific brain regions, rats’ brains were harvested one day after behavioral analysis for staining and fluorescence quantification. Moreover, 2-AG was elevated in the CSF of PTSD-phenotype rats as compared with other groups and was inversely correlated with corticosterone urinary secretion. Eight days post-PSS exposure, hippocampal and hypothalamic 2-AG levels and hippocampal AEA levels were significantly more reduced in the PTSD-phenotype group compared to other groups. We posit that maladaptation to stress, which is propagated by an abnormal activation of endocannabinoids, mediates the subsequent stress-induced behavioral disruption, which, later, reduces neuronal the expression of endocannabinoids, contributing to PTSD symptomology.


SLEEP ◽  
2020 ◽  
Vol 43 (7) ◽  
Author(s):  
Srinivas Laxminarayan ◽  
Chao Wang ◽  
Sridhar Ramakrishnan ◽  
Tatsuya Oyama ◽  
J David Cashmere ◽  
...  

Abstract Study Objectives We assessed whether the synchrony between brain regions, analyzed using electroencephalography (EEG) signals recorded during sleep, is altered in subjects with post-traumatic stress disorder (PTSD) and whether the results are reproducible across consecutive nights and subpopulations of the study. Methods A total of 78 combat-exposed veteran men with (n = 31) and without (n = 47) PTSD completed two consecutive laboratory nights of high-density EEG recordings. We computed a measure of synchrony for each EEG channel-pair across three sleep stages (rapid eye movement [REM] and non-REM stages 2 and 3) and six frequency bands. We examined the median synchrony in 9 region-of-interest (ROI) pairs consisting of 6 bilateral brain regions (left and right frontal, central, and parietal regions) for 10 frequency-band and sleep-stage combinations. To assess reproducibility, we used the first 47 consecutive subjects (18 with PTSD) for initial discovery and the remaining 31 subjects (13 with PTSD) for replication. Results In the discovery analysis, five alpha-band synchrony pairs during non-REM sleep were consistently larger in PTSD subjects compared with controls (effect sizes ranging from 0.52 to 1.44) across consecutive nights: two between the left-frontal and left-parietal ROIs, one between the left-central and left-parietal ROIs, and two across central and parietal bilateral ROIs. These trends were preserved in the replication set. Conclusion PTSD subjects showed increased alpha-band synchrony during non-REM sleep in the left frontoparietal, left centro-parietal, and inter-parietal brain regions. Importantly, these trends were reproducible across consecutive nights and subpopulations. Thus, these alterations in alpha synchrony may be discriminatory of PTSD.


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.


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