Neuroimaging and Anxiety: the Neural Substrates of Pathological and Non-pathological Anxiety

Taylor, James M.; Whalen, Paul J.

doi:10.1007/s11920-015-0586-9

Cited by 52 publications

(51 citation statements)

References 83 publications

(112 reference statements)

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“…The amygdala plays an essential role in orienting and processing threat and affect (Davis and Whalen, 2001), and is implicated in behavioral anxiety (Taylor and Whalen, 2015). Amygdala reactivity may underpin the disruption in mood, increased anxiety, biased emotional processing and preferential representation of negative information typical of depression (Price and Drevets, 2010).…”

Section: Introductionmentioning

confidence: 99%

Clinical neuroprediction: Amygdala reactivity predicts depressive symptoms 2 years later

Mattson

Hyde

Shaw

et al. 2016

Social Cognitive and Affective Neuroscience

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Depression is linked to increased amygdala activation to neutral and negatively valenced facial expressions. Amygdala activation may be predictive of changes in depressive symptoms over time. However, most studies in this area have focused on small, predominantly female and homogenous clinical samples. Studies are needed to examine how amygdala reactivity relates to the course of depressive symptoms dimensionally, prospectively and in populations diverse in gender, race and socioeconomic status. A total of 156 men from predominately low-income backgrounds completed an fMRI task where they viewed emotional facial expressions. Left and right amygdala reactivity to neutral, but not angry or fearful, facial expressions relative to a non-face baseline at age 20 predicted greater depressive symptoms 2 years later, controlling for age 20 depressive symptoms. Heightened bilateral amygdala reactivity to neutral facial expressions predicted increases in depressive symptoms 2 years later in a large community sample. Neutral facial expressions are affectively ambiguous and a tendency to interpret these stimuli negatively may reflect to cognitive biases that lead to increases in depressive symptoms over time. Individual differences in amygdala reactivity to neutral facial expressions appear to identify those at most risk for a more problematic course of depressive symptoms across time.

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Section: Introductionmentioning

confidence: 99%

Clinical neuroprediction: Amygdala reactivity predicts depressive symptoms 2 years later

Mattson

Hyde

Shaw

et al. 2016

Social Cognitive and Affective Neuroscience

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“…Decreased PFC‐amygdala connectivity is perhaps the most consistent FC abnormality reported for these regions in GAD (Hilbert et al., 2014; Mochcovitch et al., 2014; Taylor & Whalen, 2015). In HCs these regions are anticorrelated, which is often interpreted as PFC inhibiting amygdala (Banks, Eddy, Angstadt, Nathan, & Phan, 2007; Etkin, Egner, Peraza, Kandel, & Hirsch, 2006; Kim et al., 2011; Ochsner et al., 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Patients with GAD are characterized by abnormal neural activity , in prefrontal cortical (PFC) and limbic regions, including anterior cingulate cortex (ACC), anterior insula (AI) and amygdala (Hilbert, Lueken, & Beesdo‐Baum, 2014; Mochcovitch, da Rocha Freire, Garcia, & Nardi, 2014; Taylor & Whalen, 2015). PFC‐amygdala coupling (or functional connectivity (FC); Friston, 2011), has also been shown to be weaker in GAD, and has demonstrated association with symptom severity.…”

Section: Introductionmentioning

confidence: 99%

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Neural functional architecture and modulation during decision making under uncertainty in individuals with generalized anxiety disorder

et al. 2018

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BackgroundRecent evidence suggests that repetitive transcranial magnetic stimulation (rTMS) might be effective in treating generalized anxiety disorder (GAD). Cognitive models of GAD highlight the role of intolerance of uncertainty (IU) in precipitating and maintaining worry, and it has been hypothesized that patients with GAD exhibit decision‐making deficits under uncertain conditions. Improving understanding of the neural mechanisms underlying cognitive deficits associated with IU may lead to the identification of novel rTMS treatment targets and optimization of treatment parameters. The current report describes two interrelated studies designed to identify and verify a potential neural target for rTMS treatment of GAD.MethodsStudy I explored the integrity of prefrontal cortex (PFC) and amygdala neural networks, which underlie decision making under conditions of uncertainty, in GAD. Individuals diagnosed with GAD (n = 31) and healthy controls (n = 20) completed a functional magnetic resonance imaging (fMRI) gambling task that manipulated uncertainty using high versus low error rates. In a subsequent randomized‐controlled trial (Study II), a subset of the GAD sample (n = 16) completed the fMRI gambling task again after 30 sessions of active versus sham rTMS (1 Hz, right dorsolateral prefrontal cortex) to investigate the modulation of functional networks and symptoms.ResultsIn Study I, participants with GAD demonstrated impairments in PFC‐PFC and PFC‐amygdala functional connectivity (FC) mostly during the high uncertainty condition. In Study II, one region of interest pair, dorsal anterior cingulate (ACC) – subgenual ACC, showed “normalization” of FC following active, but not sham, rTMS, and neural changes were associated with improvement in worry symptoms.ConclusionsThese results outline a possible treatment mechanism of rTMS in GAD, and pave the way for future studies of treatment optimization.

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“…Whereas OCD is char-Archives of Psychiatry and Psychotherapy, 2017;3: 7-15 acterized by abnormalities in cortico-striatal neurocircuitry [14] and serotonin neurotransmission [15], the neurobiology of anxiety more characteristically involves abnormalities in frontal-limbic neurocircuitry [16]. OCD is also associated with a characteristic pattern of cognitive impairment in executive functioning, including reduced mental flexibility, deficits in response inhibition and reduced capacity for planning [17,18].…”

Section: Neurobiologymentioning

confidence: 99%

From anxiety to compulsivity – a review of changes to OCD classification in DSM-5 and ICD-11

Krzanowska¹,

Kuleta²

2017

Arch Psych Psych

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SummaryObsessive-compulsive disorder (OCD) is no longer classified as an anxiety disorder in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). It has become a flagship disorder of the new category of Obsessive Compulsive and Related Disorders (OCRDs) -a group of five disorders linked together by the core symptom of repetitive thoughts and behaviors and phenomenological and neurobiological similarity to OCD. Body dysmorphic disorder, hoarding disorder, trichotillomania, and skin picking disorder are the other disorders included in this group. In the upcoming eleventh edition of the International Classification of Diseases (ICD)-11, the World Health Organization (WHO) is planning to introduce similar changes to its own classification of OCD, further recommending the inclusion of olfactory reference disorder and hypochondriasis, in addition to the disorders listed in the DSM-5. In this article, we will review the classifications of OCD and OCDRs in the DSM-5 and the upcoming ICD-11, as well as describe the rationale and research leading to the creation of this new class of disorders.

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Neuroimaging and Anxiety: the Neural Substrates of Pathological and Non-pathological Anxiety

Cited by 52 publications

References 83 publications

Clinical neuroprediction: Amygdala reactivity predicts depressive symptoms 2 years later

Clinical neuroprediction: Amygdala reactivity predicts depressive symptoms 2 years later

Neural functional architecture and modulation during decision making under uncertainty in individuals with generalized anxiety disorder

From anxiety to compulsivity – a review of changes to OCD classification in DSM-5 and ICD-11

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