The Neurobiological Basis of Anxiety and Fear: Circuits, Mechanisms, and Neurochemical Interactions (Part II)

1998 ◽  
Vol 4 (2) ◽  
pp. 122-132 ◽  
Author(s):  
Dennis S. Charney ◽  
Christian C. G. Grillon ◽  
J. Douglas Bremner

This article is Part II of a review of the neuronal circuits, neural mechanisms, and neuromodulators that seem to be involved in anxiety and fear states. Part I focused on the specific brain structures, including the roles of the amygdala, locus coeruleus, hippocampus, and various cortical regions and the neural mechanisms of fear conditioning, extinction, and behavioral sensitization in mediating the signs and symptoms of anxiety and fear. Part II attempts to develop a better understanding of neurochemical mediation of traumatic remembrance and the neurobiological consequences of stress, particularly when experienced early in life. Finally, the data is synthesized to provide a basis for understanding the pathophysiology of anxiety disorders, such as Panic disorder and Posttraumatic Stress Disorder. NEUROSCIENTIST 4:122–132, 1998

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuanchao Zheng ◽  
Melanie E. Garrett ◽  
Delin Sun ◽  
Emily K. Clarke-Rubright ◽  
Courtney C. Haswell ◽  
...  

AbstractThe volume of subcortical structures represents a reliable, quantitative, and objective phenotype that captures genetic effects, environmental effects such as trauma, and disease effects such as posttraumatic stress disorder (PTSD). Trauma and PTSD represent potent exposures that may interact with genetic markers to influence brain structure and function. Genetic variants, associated with subcortical volumes in two large normative discovery samples, were used to compute polygenic scores (PGS) for the volume of seven subcortical structures. These were applied to a target sample enriched for childhood trauma and PTSD. Subcortical volume PGS from the discovery sample were strongly associated in our trauma/PTSD enriched sample (n = 7580) with respective subcortical volumes of the hippocampus (p = 1.10 × 10−20), thalamus (p = 7.46 × 10−10), caudate (p = 1.97 × 10−18), putamen (p = 1.7 × 10−12), and nucleus accumbens (p = 1.99 × 10−7). We found a significant association between the hippocampal volume PGS and hippocampal volume in control subjects from our sample, but was absent in individuals with PTSD (GxE; (beta = −0.10, p = 0.027)). This significant GxE (PGS × PTSD) relationship persisted (p < 1 × 10−19) in four out of five threshold peaks (0.024, 0.133, 0.487, 0.730, and 0.889) used to calculate hippocampal volume PGSs. We detected similar GxE (G × ChildTrauma) relationships in the amygdala for exposure to childhood trauma (rs4702973; p = 2.16 × 10−7) or PTSD (rs10861272; p = 1.78 × 10−6) in the CHST11 gene. The hippocampus and amygdala are pivotal brain structures in mediating PTSD symptomatology. Trauma exposure and PTSD modulate the effect of polygenic markers on hippocampal volume (GxE) and the amygdala volume PGS is associated with PTSD risk, which supports the role of amygdala volume as a risk factor for PTSD.


2018 ◽  
Vol 54 (5) ◽  
pp. 639-647 ◽  
Author(s):  
Erin C. Berenz ◽  
Timothy P. York ◽  
Hanaan Bing-Canar ◽  
Ananda B. Amstadter ◽  
Briana Mezuk ◽  
...  

2012 ◽  
Vol 25 (5) ◽  
pp. 541-551 ◽  
Author(s):  
Adam Michael Spaulding

Due to relatively recent and ongoing world events (eg, terrorist attacks, wars, and natural disasters), there has been a shift in attention from some of the more common psychiatric illnesses to one of the more elusive, namely, posttraumatic stress disorder (PTSD). PTSD is a severe, and often chronic, condition that can lead to significant morbidity and mortality. Although originally a condition seen primarily among war veterans, PTSD is now becoming more prevalent in the general community. PTSD often presents concurrently with other conditions, such as depression, bipolar, anxiety/panic disorders, and alcohol and drug abuse. Because of this, PTSD often goes unrecognized and is underdiagnosed in clinical practice. Thus, an opportunity for pharmacist intervention exists, both in the institution and in the community. With proper education and training, pharmacists can be efficient in screening for signs and symptoms of PTSD, triaging appropriate patients, and can play an integral role in managing the diverse array of drug therapy options for PTSD.


2019 ◽  
Author(s):  
Jonathan Wendall Reeves ◽  
Aaron Jason Fisher ◽  
Steven Woodward

Research on the link between respiratory sinus arrhythmia (RSA) and posttraumatic stress disorder (PTSD) has largely focused on average levels of RSA. However, given that rapid shifts in parasympathetic tone are necessary to maintain adaptive cardiac variability, the exclusive focus on these tonic estimates provides an incomplete quantification of parasympathetic cardiac regulation. The present study is a secondary analysis of previously published data. This analysis aimed to address this limitation by examining the dynamic regulatory effect of the parasympathetic nervous system on heart rate. As such, we examined epoch-to-epoch parasympathetic cardiac regulation – operationalized as the lagged relationship between RSA and heart rate (HR) across consecutive 30-s epochs – across a single night in participants with PTSD, panic disorder (PD), comorbid PTSD and PD (PTSD+PD), and healthy controls. Electrocardiogram and respiratory signals were continuously recorded from 23 participants with PTSD, 14 with PD, 16 with PTSD+PD, and 16 control participants over a single night of sleep in a laboratory setting. No group differences in tonic RSA were observed; however, participants with PTSD only and PTSD+PD exhibited significantly greater epoch-to-epoch parasympathetic cardiac regulation over the night than those with PD only and control participants. Moreover, greater severity of hyperarousal symptoms was significantly associated with increased epoch-to-epoch parasympathetic cardiac regulation among participants with PTSD only and PTSD+PD. These data provide preliminary evidence for an upregulatory parasympathetic response to self-reported hyperarousal in participants with PTSD only and PTSD+PD reflected by increased epoch-to-epoch parasympathetic cardiac regulation.


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