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Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond.

ABSTRACT: The study of inflammation in fear- and anxiety-based disorders has gained interest as growing literature indicates that pro-inflammatory markers can directly modulate affective behavior. Indeed, heightened concentrations of inflammatory signals, including cytokines and C-reactive protein, have been described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.). However, not all reports indicate a positive association between inflammation and fear- and anxiety-based symptoms, suggesting that other factors are important in future assessments of inflammation's role in the maintenance of these disorders (ie, sex, co-morbid conditions, types of trauma exposure, and behavioral sources of inflammation). The most parsimonious explanation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the stress response and central and peripheral immune cells to release cytokines. Dysregulation of the stress axis in the face of increased sympathetic tone and decreased parasympathetic activity characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Taken together, the available data suggest that targeting inflammation may serve as a potential therapeutic target for treating these fear- and anxiety-based disorders in the future. However, the field must continue to characterize the specific role pro-inflammatory signaling in the maintenance of these unique psychiatric conditions.

SUBMITTER: Michopoulos V

PROVIDER: S-EPMC5143487 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature

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Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond.

Michopoulos Vasiliki V Powers Abigail A Gillespie Charles F CF Ressler Kerry J KJ Jovanovic Tanja T

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 20160811 1

The study of inflammation in fear- and anxiety-based disorders has gained interest as growing literature indicates that pro-inflammatory markers can directly modulate affective behavior. Indeed, heightened concentrations of inflammatory signals, including cytokines and C-reactive protein, have been described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.). However, not all reports indicate a positive ...[more]

PMID: 27510423

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Project description:BACKGROUND:The WHO reports that anxiety disorders are the most common mental disorders worldwide. Most people who experience such events recover from it; however, people with post-traumatic stress disorder (PTSD) continue to be severely depressed and anxious for several months or even years following the event. Palestinians are particularly at a higher risk for developing anxiety disorders and PTSD due to the continuous exposure to political violence, prolonged displacement, and other limitation on professional, educational, financial opportunities, and mental health services. This paper aims to provide a systematic review of the literature and established studies concerning Anxiety disorders besides PTSD in Palestine. METHODS:PubMed, Science Direct, Google Scholar was used to search for materials for the critical analysis of empirical articles. The following aspects were taken into consideration: study type, sample, and key findings. RESULTS:In this review, we included about twenty-four studies from Palestine (West Bank and Gaza). Five studies relate to children, five relate to adolescents, three relate to women, three relate to physical diseases, and four relate to gender and age differences. Results show that anxiety disorders and PTSD are one of the most common mental disorders in Palestine. Anxiety and PTSD develop from a complex set of risk factors, including genetics, personality, and life events. They are mostly associated with low quality of life and disability. The results indicate that a significant proportion of Palestinian experiencing serious issues that deal with several challenges, distinct barriers including; inconsistent availability of medications, absence of multidisciplinary teamwork, insufficient specialists, fragmented mental health system, and occupation. CONCLUSION:As primary prevention, the occupation has to have considered as the main source of anxiety and other mental health disorders in Palestine. Besides, there is a need to implement a mental health care system through multidisciplinary work and raising awareness regarding the prevalence of mental disorders.

Project description:Pathological fear and anxiety are highly debilitating and, despite considerable advances in psychotherapy and pharmacotherapy they remain insufficiently treated in many patients with PTSD, phobias, panic and other anxiety disorders. Increasing preclinical and clinical evidence indicates that pharmacological treatments including cognitive enhancers, when given as adjuncts to psychotherapeutic approaches [cognitive behavioral therapy including extinction-based exposure therapy] enhance treatment efficacy, while using anxiolytics such as benzodiazepines as adjuncts can undermine long-term treatment success. The purpose of this review is to outline the literature showing how pharmacological interventions targeting neurotransmitter systems including serotonin, dopamine, noradrenaline, histamine, glutamate, GABA, cannabinoids, neuropeptides (oxytocin, neuropeptides Y and S, opioids) and other targets (neurotrophins BDNF and FGF2, glucocorticoids, L-type-calcium channels, epigenetic modifications) as well as their downstream signaling pathways, can augment fear extinction and strengthen extinction memory persistently in preclinical models. Particularly promising approaches are discussed in regard to their effects on specific aspects of fear extinction namely, acquisition, consolidation and retrieval, including long-term protection from return of fear (relapse) phenomena like spontaneous recovery, reinstatement and renewal of fear. We also highlight the promising translational value of the preclinial research and the clinical potential of targeting certain neurochemical systems with, for example d-cycloserine, yohimbine, cortisol, and L-DOPA. The current body of research reveals important new insights into the neurobiology and neurochemistry of fear extinction and holds significant promise for pharmacologically-augmented psychotherapy as an improved approach to treat trauma and anxiety-related disorders in a more efficient and persistent way promoting enhanced symptom remission and recovery.

Project description:The fear conditioning and extinction neurocircuitry has been extensively studied in healthy and clinical populations, with a particular focus on posttraumatic stress disorder. Despite significant overlap of symptoms between posttraumatic stress disorder and anxiety disorders, the latter has received less attention. Given that dysregulated fear levels characterize anxiety disorders, examining the neural correlates of fear and extinction learning may shed light on the pathogenesis of underlying anxiety disorders.To investigate the psychophysiological and neural correlates of fear conditioning and extinction recall in anxiety disorders and to document how these features differ as a function of multiple diagnoses or anxiety severity.This investigation was a cross-sectional, case-control, functional magnetic resonance imaging study at an academic medical center. Participants were healthy controls and individuals with at least 1 of the following anxiety disorders: generalized anxiety disorder, social anxiety disorder, specific phobia, and panic disorder. The study dates were between March 2013 and May 2015.Two-day fear conditioning and extinction paradigm.Skin conductance responses, blood oxygenation level-dependent responses, trait anxiety scores from the State Trait Anxiety Inventory-Trait Form, and functional connectivity.This study included 21 healthy controls (10 women) and 61 individuals with anxiety disorders (36 women). P values reported for the neuroimaging results are all familywise error corrected. Skin conductance responses during extinction recall did not differ between individuals with anxiety disorders and healthy controls (?p2?=?0.001, P?=?.79), where ?p2 is partial eta squared. The anxiety group had lower activation of the ventromedial prefrontal cortex (vmPFC) during extinction recall (?p2?=?0.178, P?=?.02). A similar hypoactive pattern was found during early conditioning (?p2?=?0.106, P?=?.009). The vmPFC hypoactivation was associated with anxiety symptom severity (r?=?-0.420, P?=?.01 for conditioning and r?=?-0.464, P?=?.004 for extinction recall) and the number of co-occuring anxiety disorders diagnosed (?p2?=?0.137, P?=?.009 for conditioning and ?p2?=?0.227, P?=?.004 for extinction recall). Psychophysiological interaction analyses revealed that the fear network connectivity differed between healthy controls and the anxiety group during fear learning (?p2 range between 0.088 and 0.176 and P range between 0.02 and 0.003) and extinction recall (?p2 range between 0.111 and 0.235 and P range between 0.02 and 0.002).Despite no skin conductance response group differences during extinction recall, brain activation patterns between anxious and healthy individuals differed. These findings encourage future studies to examine the conditions longitudinally and in the context of treatment trials to improve and guide therapeutics via advanced neurobiological understanding of each disorder.

Dataset Information

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond.

Publications

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond.

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