Neuroimaging of the periaqueductal gray: State of the field

Linnman, Clas; Moulton, Eric A.; Barmettler, Gabi; Becerra, Lino; Borsook, David

doi:10.1016/j.neuroimage.2011.11.095

Cited by 333 publications

(357 citation statements)

References 299 publications

(393 reference statements)

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“…PAG activity correlated with stimulationinduced change in the rating of neutral faces. The PAG region is previously implicated in the coupling of peripheral arousal state to emotional processing and expression of fear (Mobbs et al, 2009;Gray et al, 2012;Linnman et al, 2012). Consistently with these previous studies, our data show that a modulation of the neural activity in the PAG area caused by CS results in an increased evaluation of the emotional intensity in neutral faces.…”

Section: Discussionsupporting

confidence: 92%

Effect of Parasympathetic Stimulation on Brain Activity During Appraisal of Fearful Expressions

Makovac

Garfinkel

Bassi

et al. 2015

Neuropsychopharmacol

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Autonomic nervous system activity is an important component of human emotion. Mental processes influence bodily physiology, which in turn feeds back to influence thoughts and feelings. Afferent cardiovascular signals from arterial baroreceptors in the carotid sinuses are processed within the brain and contribute to this two-way communication with the body. These carotid baroreceptors can be stimulated non-invasively by externally applying focal negative pressure bilaterally to the neck. In an experiment combining functional neuroimaging (fMRI) with carotid stimulation in healthy participants, we tested the hypothesis that manipulating afferent cardiovascular signals alters the central processing of emotional information (fearful and neutral facial expressions). Carotid stimulation, compared with sham stimulation, broadly attenuated activity across cortical and brainstem regions. Modulation of emotional processing was apparent as a significant expression-by-stimulation interaction within left amygdala, where responses during appraisal of fearful faces were selectively reduced by carotid stimulation. Moreover, activity reductions within insula, amygdala, and hippocampus correlated with the degree of stimulationevoked change in the explicit emotional ratings of fearful faces. Across participants, individual differences in autonomic state (heart rate variability, a proxy measure of autonomic balance toward parasympathetic activity) predicted the extent to which carotid stimulation influenced neural (amygdala) responses during appraisal and subjective rating of fearful faces. Together our results provide mechanistic insight into the visceral component of emotion by identifying the neural substrates mediating cardiovascular influences on the processing of fear signals, potentially implicating central baroreflex mechanisms for anxiolytic treatment targets.

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Section: Discussionsupporting

confidence: 92%

Effect of Parasympathetic Stimulation on Brain Activity During Appraisal of Fearful Expressions

Makovac

Garfinkel

Bassi

et al. 2015

Neuropsychopharmacol

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“…However, the PAG has bidirectional connections to a wide range of cortical and subcortical structures (42), and the modulation of sensory circuitry may be entirely central in origin. For example, bidirectional modulation of one central region by another region has been reported in studies of reappraisal of negative affect (43).…”

Section: Common Emotion Appraisal Circuitry Mediated Behavioral and Boldmentioning

confidence: 99%

Placebo improves pleasure and pain through opposite modulation of sensory processing

Ellingsen

Wessberg

Eikemo

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Placebo analgesia is often conceptualized as a reward mechanism. However, by targeting only negative experiences, such as pain, placebo research may tell only half the story. We compared placebo improvement of painful touch (analgesia) with placebo improvement of pleasant touch (hyperhedonia) using functional MRI and a crossover design. Somatosensory processing was decreased during placebo analgesia and increased during placebo hyperhedonia. Both placebo responses were associated with similar patterns of activation increase in circuitry involved in emotion appraisal, including the pregenual anterior cingulate, medial orbitofrontal cortex, amygdala, accumbens, and midbrain structures. Importantly, placebo-induced coupling between the ventromedial prefrontal cortex and periaqueductal gray correlated with somatosensory decreases to painful touch and somatosensory increases to pleasant touch. These findings suggest that placebo analgesia and hyperhedonia are mediated by activation of shared emotion appraisal neurocircuitry, which down-or upregulates early sensory processing, depending on whether the expectation is reduced pain or increased pleasure.expectancy | neuroimaging | hedonic feelings M edical treatments aim to provide relief from pain and aversive states. Consequently, research on placebo effects has focused on relief of negative hedonic feelings, like pain and displeasure (1). In contrast, placebo improvement of positive hedonics has received little attention. However, pain and pleasure processes are tightly linked. Relief from pain can induce a pleasant experience underpinned by activation of reward neurocircuitry (2-4). Moreover, a painful stimulus can even be perceived as pleasant when it represents relief from a more severe outcome (5). In line with this pain-pleasure link, placebo analgesia can be conceptualized as a type of reward mechanism; pain relief is a better outcome than the alternative (6-8) and is typically framed as a gain (improvement of pain) (9).Like pain, pleasure is greatly affected by context and expectation (10). Manipulation of people's beliefs about the price of a wine (11), the amount of fruit in a sweet drink (12), the richness of a skin cream (13), and who is caressing them (14) alters the experienced pleasantness of these stimuli.Placebo-induced improvement of aversive experiences (e.g., pain, anxiety, unpleasant taste) is often underpinned by a decrease in central sensory processing. Placebo analgesia is characterized by decreases in the thalamus, posterior insula (pINS), and primary and secondary somatosensory areas (SI and SII) (15)(16)(17). Placebo reduction of affective responses to unpleasant visual stimuli is similarly underpinned by suppression of visual processing (8). It is not, however, known whether placeboenhanced pleasantness (i.e., hyperhedonia) also alters early stages of sensory processing, or if this change is encoded in higher-level valuation areas.Functional neuroimaging studies have revealed that the ventromedial prefrontal cortex (vmPFC), amygdala, ventral...

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“…The amygdala is the point of convergence from higher hierarchical networks that assess safety and threat (45), the central nucleus of the amygdala then projects appropriately selected responses to the periaqueductal gray (PAG), hypothalamus, and brainstem, expressed as various orchestrated defensive programs (45). The ventrolateral PAG (vlPAG) is the most caudal and ventral (hence the most primitive), expressing a passive coping strategy comprising quiescence, hyporeactivity, hypotension, and bradycardia (46). This is also described as a "co-ordinated immobilization and dissociation defence response" (47), akin to the primitive reptilian defense response (48).…”

Section: Hypothesized Mechanism For Sids Protection By Supine Sleepmentioning

confidence: 99%

Proposal for mechanisms of protection of supine sleep against sudden infant death syndrome: an integrated mechanism review

Bergman

2014

Pediatr Res

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Supine sleep decreases sudden infant death syndrome (SIDS) incidence, however the mechanisms for this are unclear. The triple risk model for SIDS requires that one or more underlying abnormalities of breathing or autonomic control are present; these are rare, but brainstem defects are found in most SIDS cases. Supine sleep increases sympathetic nervous system tone, and level of state organization, and may therefore act as a stressor. This is evidenced by physiological arousal, and by delayed neurodevelopment in supine compared to prone sleepers. It is argued here that prone sleep position is the biological normative standard in healthy infants, supporting autonomic regulation. During rapid eye movement (REM) sleep (and other circumstances), a parasympathetic-mediated adverse autonomic event (AAE) may be spontaneously triggered. In healthy infants, gasping initiates autoresuscitation and recovery. Hypothesis: the underlying vulnerability to SIDS is specific to autoresuscitation from an AAE, the initial serotonin-dependent gasp is commonly compromised. Serotonin metabolism defects also influence sleep architecture, increasing the likelihood of AAE. The mechanism whereby supine sleep decreases SIDS may therefore be a stressor effect, disturbing sleep architecture to decrease REM and AAEs, and increasing sympathetic tone, which may prevent and counteract the purely parasympathetic-mediated AAE, thereby decreasing the risk of SIDS.

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Neuroimaging of the periaqueductal gray: State of the field

Cited by 333 publications

References 299 publications

Effect of Parasympathetic Stimulation on Brain Activity During Appraisal of Fearful Expressions

Effect of Parasympathetic Stimulation on Brain Activity During Appraisal of Fearful Expressions

Placebo improves pleasure and pain through opposite modulation of sensory processing

Proposal for mechanisms of protection of supine sleep against sudden infant death syndrome: an integrated mechanism review

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