Perceived intensity and unpleasantness of cutaneous and auditory stimuli: An evaluation of the generalized hypervigilance hypothesis

Department of Psychology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Pain (Impact Factor: 5.21). 02/2009; 141(3):215-21. DOI: 10.1016/j.pain.2008.10.003
Source: PubMed


According to the Generalized Hypervigilance Hypothesis (GHH) of McDermid et al., the unpleasantness of sensory stimuli, rather than their modality, determines whether they will be perceptually amplified in hypervigilant persons. In a test of this idea, ratings of the intensity of sensations evoked by cutaneous and auditory stimuli were obtained from individuals with chronic myofascial pain (fibromyalgia, temporomandibular disorders), and from (less hypervigilant) healthy control participants. In each modality, the stimuli spanned a wide intensity range, with the weakest stimuli being affectively neutral and the strongest being distinctly unpleasant, as determined by unpleasantness ratings. The pain patients showed robust perceptual amplification of the cutaneous pressure stimuli, and modest amplification of the auditory stimuli. In both cases, perceptual amplification extended to even the lowest stimulus intensities, a result that is not consistent with the predictions of the GHH. An alternative formulation, the attentional gain control model of hypervigilance, is proposed, according to which those types of stimuli that are associated with pain are amplified because of the attention that is habitually directed toward them.

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Available from: Mark Hollins, Sep 30, 2015
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    • "Our current findings and those from Napadow et al. [50] [51] both show a shift from negative to positive correlation in fibromyalgia as seen in the high attention states [27]. This alteration pattern may be relevant to the proposal of fibromyalgia as a hypervigilance condition with sustained attention to pain sensation [17] [32] [43]. A similar change in the coupling between the default network and anticorrelated networks was identified in chronic back pain, which was interpreted as a lasting effect of pain on brain function [3]. "
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    ABSTRACT: Fibromyalgia typically presents with spontaneous body pain with no apparent cause and is considered pathophysiologically to be a functional disorder of somatosensory processing. We have investigated potential associations between the degree of self-reported clinical pain and resting-state brain functional connectivity at different levels of putative somatosensory integration. Resting-state functional MRI was obtained in 40 women with fibromyalgia and 36 control subjects. A combination of functional connectivity-based measurements were used to assess (i) the basic pain signal modulation system at the level of the periaqueductal gray (PAG), (ii) the sensory cortex with an emphasis on the parietal operculum/secondary somatosensory cortex (SII) and (iii) the connectivity of these regions with the self-referential "default mode" network. Compared with control subjects, a reduction of functional connectivity was identified across the three levels of neural processing, each showing a significant and complementary correlation with the degree of clinical pain. Specifically, self-reported pain in fibromyalgia patients correlated with (i) reduced connectivity between PAG and anterior insula, (ii) reduced connectivity between SII and primary somatosensory, visual and auditory cortices, and (iii) increased connectivity between SII and the default mode network. The results confirm previous research demonstrating abnormal functional connectivity in fibromyalgia and show that alterations at different levels of sensory processing may contribute to account for clinical pain. Importantly, reduced functional connectivity extended beyond the somatosensory domain and implicated visual and auditory sensory modalities. Overall this study suggests that a general weakening of sensory integration underlies clinical pain in fibromyalgia.
    Pain 05/2014; 155(8). DOI:10.1016/j.pain.2014.04.028 · 5.21 Impact Factor
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    • "Thus, hypervigilance appears to be a cognitive, physiological, and behavioral pattern in which an individual either responds to neutral or ambiguous stimuli as if they were threatening or is enhanced in his or her detection and reaction to threatening or threat-related stimuli. Hypervigilance is present in a range of anxiety disorders (De Cort, Hermans, Spruyt, Griez, & Schuers, 2008; Freeman, Garety, & Phillips, 2000; Hollins et al., 2009; Sposari & Rapee, 2007), but is clearly prevalent in veterans and particularly those with PTSD. There is considerable evidence to support this claim from behavioral and electrophysiological studies that have demonstrated increased attentional bias toward ambiguous, potentially threatening , or trauma-relevant stimuli in combat veterans with PTSD (Buckley, Blanchard, & Neill, 2000; Kaspi, McNally, & Amir, 1995; Kimble, Fleming, Bandy, Kim, & Zambetti, 2010; Pineles, Shipherd, Mostoufi, Abramovitz, & Yovel, 2009; Stanford, Vasterling, Mathias, Constans, & Houston, 2001). "
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    ABSTRACT: Hypervigilance toward ambiguous or threatening stimuli is a prominent feature in many trauma survivors including active and returning soldiers. This study set out to investigate the factors that contribute to hypervigilance in a mixed sample. One hundred forty-five individuals, 50 of whom were war zone veterans, filled out a series of questionnaires including the Hypervigilance Questionnaire (HVQ; Kimble, Fleming, & Bennion, 2009). Other participants included military cadets, college undergraduates, and a traumatized community sample. In this sample, a history of military deployment and posttraumatic stress disorder symptoms independently predicted hypervigilance. The findings suggest that deployment to a war zone, in and of itself, can lead to hypervigilant behavior. Therefore, characterizing hypervigilance as pathological in a veteran sample must be done so with caution.
    Journal of Interpersonal Violence 01/2013; 28(8). DOI:10.1177/0886260512468319 · 1.64 Impact Factor
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    • "In both animal models and humans, this hypersensitivity manifests as increased sensitivity to normally painful stimuli (hyperalgesia) and/or pain in response to normally non-painful stimuli (allodynia) [2] [69]. In addition, patients demonstrate hypersensitivity to non-somatosensory stimuli, such as lights, noises, and odors [23] [24] [32]. The terms " central sensitization " or " central augmentation " are increasingly used to describe these phenomena of increased pain and sensory transmission that produce the common set of symptoms in the previously listed disorders [2] [68] [69] [71] [72]. "
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    ABSTRACT: Many service members and veterans report chronic unexplained symptoms such as pain, fatigue and memory complaints, which have most recently been characterized as post-deployment syndrome (PDS). Chronic widespread pain is a component of this syndrome, producing significant disability and considerable health care costs. The similarity between the nature of these complaints and other medically unexplained illnesses such as fibromyalgia, irritable bowel syndrome, and chronic fatigue syndrome suggest that they may share a common mechanism. Here, we provide support for PDS as a consequence of pain and sensory amplification secondary to neuroplastic changes within the central nervous system, a phenomenon often termed central sensitization. We also discuss how factors such as stress and genetics may promote chronic widespread pain in veterans and service members who develop PDS.
    Neurorehabilitation 12/2012; 31(4):367-72. DOI:10.3233/NRE-2012-00805 · 1.12 Impact Factor
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