Combat veterans with posttraumatic stress disorder exhibit decreased habituation of the P1 midlatency auditory evoked potential

Gillette, Gregory M.; Skinner, R.D.; L, Rasco; Fielstein, Elliot M.; Davis, Doyle H.; Pawelak, James E.; Freeman, Thomas; Karson, Craig N.; Boop, Frederick A.; García‐Rill, Edgar

doi:10.1016/s0024-3205(97)00688-7

Cited by 74 publications

(43 citation statements)

References 37 publications

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“…PTSD patients also exhibit deficient P1 suppression, another measure of inhibitory or gating processes (Gillette et al, 1997;Skinner et al, 1999). One study found negative correlations between PPI and PTSD symptoms, however, this was not replicated in a subsequent study (Grillon et al, 1998a(Grillon et al, ,b,1996.…”

Section: Startle Abnormalities In Anxiety Disordersmentioning

confidence: 99%

“…Interestingly, panic disorder and PTSD patients exhibit mild but significant disruptions in PPI (Grillon et al, 1998bLudewig et al, 2005Ludewig et al, ,2002Ornitz and Pynoos, 1989). PTSD patients also exhibit deficient P1 suppression, another measure of inhibitory or gating processes (Gillette et al, 1997;Skinner et al, 1999). One study found negative correlations between PPI and PTSD symptoms, however, this was not replicated in a subsequent study (Grillon et al, 1998a(Grillon et al, ,b,1996.…”

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confidence: 99%

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Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

Risbrough

Stein

2006

Hormones and Behavior

211

139

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Anxiety disorders are a group of mental disorders that include generalized anxiety disorder (GAD), panic disorder, phobic disorders (e.g., specific phobias, agoraphobia, social phobia) and posttraumatic stress disorder (PTSD). Anxiety disorders are among the most common of all mental disorders and, when coupled with an awareness of the disability and reduced quality of life they convey, they must be recognized as a serious public health problem. Over 20 years of preclinical studies point to a role for the CRF system in anxiety and stress responses. Clinical studies have supported a model of CRF dysfunction in depression and more recently a potential contribution to specific anxiety disorders (i.e., panic disorder and PTSD). Much work remains in both the clinical and preclinical fields to inform models of CRF function and its contribution to anxiety. First, we will review the current findings of CRF and HPA axis abnormalities in anxiety disorders. Second, we will discuss startle reflex measures as a tool for translational research to determine the role of the CRF system in development and maintenance of clinical anxiety. KeywordsCRH; CRF; Posttraumatic stress disorder; Anxiety; Panic disorder; Startle Overview of CRF neuroendocrine effects and its effects on G-protein-coupled receptorsCorticotropin releasing factor (CRF; also termed "CRH" for corticotropin releasing hormone) was first described in Science by Vale et al. (1981). They reported the discovery of a hypothesized hypothalamic factor, CRF, a 41 amino acid peptide which selectively and potently activated pituitary corticotropin (or adrenal corticotropin releasing hormone, ACTH) secretion. They predicted that this peptide could be "a key signal in mediating and integrating an organism's endocrine, visceral and behavioral response to stress" (Vale et al., 1981(Vale et al., p. 1397). More than 20 years of subsequent animal research and clinical studies have confirmed this hypothesis, supporting a role for CRF, and its more recently discovered ligand family Urocortin 1, 2 and 3, in anxiety and stress responses Reyes et al., 2001;Spina et al., 1996). In this review, we will focus on the current state of knowledge of CRF system dysregulation in clinical anxiety and discuss future avenues of translational research on the role of CRF in startle phenotypes observed in some anxiety disorders. CRF mediation of the neuroendocrine response to stressIn response to stress, CRF is released from the median eminence of the hypothalamus, where it subsequently binds to receptors at the anterior pituitary and increases ACTH release into the * Corresponding author. 8950 Villa La Jolla Drive, Suite B-218, La Jolla, CA 92037, USA. E-mail address: mstein@ucsd.edu (M.B. Stein). bloodstream. ACTH consequently acts at the adrenal cortex to facilitate release of glucocorticoids such as cortisol. This system, known as the hypothalamic-pituitary-adrenal axis (HPA), is an important component of the response to stress and has been shown to be dysregulated in both anxiety and de...

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Section: Startle Abnormalities In Anxiety Disordersmentioning

confidence: 99%

mentioning

confidence: 99%

Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

Risbrough

Stein

2006

Hormones and Behavior

211

139

View full text Add to dashboard Cite

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“…A number of studies reported P 50 sensitivity to reticular formation non-specific cholinergic activation (Buchwald et al, 1991) and consequently to levels of arousal (Erwin and Buchwald, 1986;de Lugt et al, 1996), sensory activation and a variety of disorders. Sensory gating (Skinner et al, 1999) and habituation (Gillette et al, 1997;Pitman et al, 1999) of P 50 was found impaired in subjects with Post-Traumatic Stress Disorder (PTSD) compared to controls, indicating dysregulation of sensory processing in PTSD. Such decreased gating was also observed in normal adolescents compared to normal older subjects (Rasco et al, 2000).…”

Section: Earlier Studies On P 50mentioning

confidence: 99%

The auditory P50 component to onset and offset of sound

Pratt

Starr

Michalewski

et al. 2008

Clinical Neurophysiology

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Objective: The auditory Event-Related Potentials (ERP) of component P 50 to sound onset and offset have been reported to be similar, but their magnetic homologue has been reported absent to sound offset. We compared the spatio-temporal distribution of cortical activity during P 50 to sound onset and offset, without confounds of spectral change. Methods: ERPs were recorded in response to onsets and offsets of silent intervals of 0.5 s (gaps) appearing randomly in otherwise continuous white noise and compared to ERPs to randomly distributed click pairs with half second separation presented in silence. Subjects were awake and distracted from the stimuli by reading a complicated text. Measures of P 50 included peak latency and amplitude, as well as source current density estimates to the clicks and sound onsets and offsets. Results: P 50 occurred in response to noise onsets and to clicks, while to noise offset it was absent. Latency of P 50 was similar to noise onset (56 ms) and to clicks (53 ms). Sources of P 50 to noise onsets and clicks included bilateral superior parietal areas. In contrast, noise offsets activated left inferior temporal and occipital areas at the time of P 50 . Source current density was significantly higher to noise onset than offset in the vicinity of the temporo-parietal junction. Conclusions: P 50 to sound offset is absent compared to the distinct P 50 to sound onset and to clicks, at different intracranial sources. P 50 to stimulus onset and to clicks appears to reflect preattentive arousal by a new sound in the scene. Sound offset does not involve a new sound and hence the absent P 50 . Significance: Stimulus onset activates distinct early cortical processes that are absent to offset.

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“…The failure of patients with PTSD to inhibit negative emotion and memories of traumatic experiences may imply a defect in PPI. They may suffer impairment of intra-attention and be unable to restrain the onset or recall of negative information, suggesting that PPI dysfunction is a component of the pathophysiologic mechanism of PTSD [9,10,11,12]. This idea is further supported by animal studies.…”

Section: Discussionmentioning

confidence: 85%

“…By regulating motor and pre-motor systems, PPI reduces responses toward irrelevant information, which is recognized as an operational measurement of SG [8]. Increasing evidence indicates that PPI dysfunction positively correlates with PTSD [9,10,11]. Recently, a clinical study also suggested disrupted sensory filtering in PTSD [12].…”

Section: Introductionmentioning

confidence: 99%

Repetitive transcranial magnetic stimulation ameliorates anxiety-like behavior and impaired sensorimotor gating in a rat model of post-traumatic stress disorder

et al. 2017

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Combat veterans with posttraumatic stress disorder exhibit decreased habituation of the P1 midlatency auditory evoked potential

Cited by 74 publications

References 37 publications

Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

Role of corticotropin releasing factor in anxiety disorders: A translational research perspective

The auditory P50 component to onset and offset of sound

Repetitive transcranial magnetic stimulation ameliorates anxiety-like behavior and impaired sensorimotor gating in a rat model of post-traumatic stress disorder

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