Dopamine reuptake site densities in patients with social phobia

doi:10.1176/ajp.154.2.239

Cited by 173 publications

(18 citation statements)

References 24 publications

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“…This association is supported by findings that individuals with social phobia have lower levels of both DA re-uptake [159] and D2-like DA receptor binding in striatum [136] than healthy individuals. In addition, the Met allele of the COMT gene has been associated with the failure to extinguish the response to conditioned fear stimuli [90], a common characteristic of patients with anxiety disorders [89].…”

Section: Pain Cognitive Deficits and Affective Dysregulation In mentioning

confidence: 72%

“…DA neurotransmission has an important influence on outcome prediction, attention, response inhibition, and motivation [109], as well as affective symptoms associated with anxiety [136, 159] and depression [37]. While many of these factors also relate to the subjective experience of pain in healthy individuals [103, 166], alterations in the same functions are common in patients with chronic pain syndromes [5, 35, 63].…”

Section: Evidence Linking the Dopamine System And Painmentioning

confidence: 99%

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Pain, affective symptoms, and cognitive deficits in patients with cerebral dopamine dysfunction

Jarcho

Mayer

Jiang

et al. 2012

Pain

137

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Converging preclinical, and human epidemiological, neuroimaging and genetic evidence suggests a central role for dopamine neurotransmission in modulating pain perception and analgesia. Dysregulation in dopamine signaling may modulate the experience of pain both directly, by enhancing or diminishing the propagation of nociceptive signals, and indirectly, by influencing affective and cognitive processes, which affect the expectation, experience and interpretation of nociceptive signals. Hypersensitivity to pain, and high rates of comorbid chronic pain, are common in disorders linked with deficits in dopamine system function, including disorders of mood and affect, substance abuse, and Parkinson’s disease. Hyposensitivity to pain, however, is common in patients with schizophrenia, which has been linked with excessive dopamine neurotransimssion. Although patients are typically affected most by the primary symptoms of their disorders, alterations in pain perception may further increase the burden of their illness, compromising their quality of life. The present review focuses on this relationship, and discusses clinical and potential therapeutic implications both for patients with dopamine-related disorders, and those with chronic pain syndromes.

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Section: Pain Cognitive Deficits and Affective Dysregulation In mentioning

confidence: 72%

Section: Evidence Linking the Dopamine System And Painmentioning

confidence: 99%

Pain, affective symptoms, and cognitive deficits in patients with cerebral dopamine dysfunction

Jarcho

Mayer

Jiang

et al. 2012

Pain

137

View full text Add to dashboard Cite

show abstract

“…Consistent with this conceptualization, relatively early PET imaging studies demonstrated altered striatal functions in SAD, which may be rooted in abnormal central dopamine function, linked to dopamine D2 receptor and dopamine transporter (DAT) availability in the striatum (Tiihonen et al , 1997; Schneier et al , 2000; Schneier et al , 2008) (also see Schneier et al , 2009). In behavioral terms, when compared with non-anxious counterparts, adults with SAD report that positive events are less likely to occur (Gilboa-Schechtman et al , 2000), report greater difficulty expressing positive emotions (Turk et al , 2005) and demonstrate a reduced tendency to sustain or savor positive affect once experienced (Eisner et al , 2009).…”

Section: Introductionmentioning

confidence: 85%

Spatiotemporal dissociation of brain activity underlying threat and reward in social anxiety disorder

Richey

Ghane

Valdespino

et al. 2016

Social Cognitive and Affective Neuroscience

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Social anxiety disorder (SAD) involves abnormalities in social motivation, which may be independent of well-documented differences in fear and arousal systems. Yet, the neurobiology underlying motivational difficulties in SAD is not well understood. The aim of the current study was to spatiotemporally dissociate reward circuitry dysfunction from alterations in fear and arousal-related neural activity during anticipation and notification of social and non-social reward and punishment. During fMRI acquisition, non-depressed adults with social anxiety disorder (SAD; N = 21) and age-, sex- and IQ-matched control subjects (N = 22) completed eight runs of an incentive delay task, alternating between social and monetary outcomes and interleaved in alternating order between gain and loss outcomes. Adults with SAD demonstrated significantly reduced neural activity in ventral striatum during the anticipation of positive but not negative social outcomes. No differences between the SAD and control groups were observed during anticipation of monetary gain or loss outcomes or during anticipation of negative social images. However, consistent with previous work, the SAD group demonstrated amygdala hyper-activity upon notification of negative social outcomes. Degraded anticipatory processing in bilateral ventral striatum in SAD was constrained exclusively to anticipation of positive social information and dissociable from the effects of negative social outcomes previously observed in the amygdala. Alterations in anticipation-related neural signals may represent a promising target for treatment that is not addressed by available evidence-based interventions, which focus primarily on fear extinction and habituation processes.

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“…A later study showed striatal hyperactivation in behaviorally inhibited adolescents, specifically when anticipated incentives were contingent on participants’ choices (21). Consistent with these data, research in adult social phobia has found altered striatal dopamine function (25, 26) and task-elicited striatal perturbations (27); no such work has examined striatal function in adolescent social phobia. These findings suggest that striatal hyperactivation may manifest in adolescent social phobia and raise questions about the specificity of this functional alteration in social phobia relative to generalized anxiety disorder.…”

mentioning

confidence: 91%

Striatal Functional Alteration During Incentive Anticipation in Pediatric Anxiety Disorders

Guyer

Choate

Detloff

et al. 2012

AJP

154

156

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Objective Behavioral inhibition is an early childhood temperament recently associated with altered striatal response in adolescence to incentives of increasing magnitudes. Since early childhood behavioral inhibition is also associated with risk for adolescent social phobia, a similar pattern of striatal activation may manifest in social phobia. The present study compares striatal function in healthy adolescents, adolescents with social phobia, and adolescents with generalized anxiety disorder. Method Blood-oxygen-level-dependent signal in striatal regions was examined in 58 medication-free adolescents—14 with social phobia, 18 with generalized anxiety disorder but not social phobia, and 26 with no psychiatric disorder—matched on sex, age, puberty, IQ, and socioeconomic status. During functional magnetic resonance imaging, participants responded to incentive cues depicting potential monetary gains or losses of varying magnitudes. Results While anticipating incentives of increasing magnitude, adolescents with social phobia showed increasingly heightened caudate and putamen activation at a level greater than that seen in the healthy comparison and generalized anxiety disorder groups. The generalized anxiety disorder group showed a unique valence-specific putamen response relative to the healthy comparison or social phobia group. Both patient groups displayed more complex patterns in the nucleus accumbens than in the caudate or putamen. Conclusions Caudate and putamen hypersensitivity to incentives of increasing magnitudes characterizes adolescent social phobia, relative to activation in this region in adolescents with generalized anxiety disorder as well as healthy adolescents. Thus, these findings resemble the pattern previously found in adolescents with early childhood behavioral inhibition, thereby implicating similar neural responses to anticipation of incentives in both early childhood behavioral inhibition and adolescent social phobia.

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Dopamine reuptake site densities in patients with social phobia

Cited by 173 publications

References 24 publications

Pain, affective symptoms, and cognitive deficits in patients with cerebral dopamine dysfunction

Pain, affective symptoms, and cognitive deficits in patients with cerebral dopamine dysfunction

Spatiotemporal dissociation of brain activity underlying threat and reward in social anxiety disorder

Striatal Functional Alteration During Incentive Anticipation in Pediatric Anxiety Disorders

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