Effects of cognitive-behavioral therapy on brain activation in specific phobia

Straube, Thomas; Glauer, Madlen; Dilger, Stefan; Mentzel, Hans‐Joachim; Miltner, Wolfgang H. R.

doi:10.1016/j.neuroimage.2005.07.007

Cited by 234 publications

(181 citation statements)

References 80 publications

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“…Thus, another ROI and inter-regional connection were added to the model in an attempt to better approximate the neural network of fear extinction. The anterior cingulate was included in the model because of recent work suggesting that this region may play an important role in memory for footshock (Malin and McGaugh, 2006), extinction of specific phobias (Straube et al, 2006), and gating among external sensory and internally driven stimuli and limbic structures involved in emotional and behavioral responses to CSs (Hamner et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…Brain lesion, stimulation, recording and metabolic mapping studies have addressed the question of which brain areas are important in fear extinction learning and memory in both animals and humans (Quirk et al, 2000, Davis, 2002, Garcia, 2002, Barrett et al, 2003, Quirk et al, 2003, Phelps et al, 2004, Straube et al, 2006. From these findings, an emerging picture has developed, implicating an interaction between prefrontal and subcortical output regions as contributing to conditioned fear extinction (Quirk et al, 2006).…”

mentioning

confidence: 99%

“…Since then, other brain mapping studies utilized structural equation modeling to analyze functional neural networks related to behavior in both animals and humans (McIntosh and Gonzalez-Lima, 1992, McIntosh and Gonzalez-Lima, 1993, Buchel and Friston, 1997, Seminowicz et al, 2004, Grady et al, 2005, Horwitz et al, 2005 validating the combined use of functional brain mapping and anatomically based structural equation modeling as an analytical tool for advancing our understanding of brain-behavior relations at the systems level. In the present study, brain regions of interest were defined based on previous findings (Davis et al, 1982, Ledoux et al, 1984, Quirk et al, 2000, Maren, 2001, Davis, 2002, Quirk et al, 2003, Maren and Quirk, 2004, Pare et al, 2004, Phelps et al, 2004, Maren, 2005, Quirk et al, 2006, Straube et al, 2006, and, in particular, structural equation modeling nodes (ROIs) were selected based on the cortical and hippocampal circuitry model of fear extinction proposed by Maren (2005). Maren's model (Fig.…”

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confidence: 99%

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Network model of fear extinction and renewal functional pathways

2007

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The objective of this study was to examine the opposite behavior responses of conditioned fear extinction and renewal and how they are represented by network interactions between brain regions. This work is a continuation of a series of brain mapping studies of various inhibitory phenomena, including conditioned inhibition, blocking and extinction. A tone-footshock fear conditioning paradigm in rats was used, followed by extinction and testing in two different contexts. Fluorodeoxyglucose autoradiography was used to compare mean regional brain activity and interregional correlations resulting from the presentation of the extinguished tone in or out of the extinction context. A confirmatory structural equation model, constructed from a neural network proposed to underlie fear extinction, showed a reversal from negative regional interactions during extinction recall to positive interactions during fear renewal. Additionally, the magnitude of direct effects was different between groups, reflecting a change in the strength of the influences conveyed through those pathways. The results suggest that the extinguished tone encountered outside of the extinction context recruits auditory and limbic areas, which in turn influence the interactions of the infralimbic cortex with the amygdala and ventrolateral periaqueductal gray. Interestingly, the results also suggest that two independent pathways influence conditioned freezing: one from the central amygdaloid nucleus and the other from the infralimbic cortex directly to the ventrolateral periaqueductal gray. KeywordsPath analysis; Structural equation modeling; Brain mapping; Prefrontal cortex; Hippocampus; AmygdalaIn the past few years, there has been increased interest in the neural substrates of fear extinction, partly due to the relevance of fear extinction to the treatment of anxiety disorders (Craske, 1999). Brain lesion, stimulation, recording and metabolic mapping studies have addressed the question of which brain areas are important in fear extinction learning and memory in both animals and humans (Quirk et al.,

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Network model of fear extinction and renewal functional pathways

2007

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“…75 Research has also shown the effects of psychotherapeutic intervention on CBF in depression, 76 obsessive-compulsive disorder, 77 panic disorder, 78 social phobia 79 and spider phobia. 80,81 In unipolar depression, 82 a prospective PET study revealed comparative results for psychotherapeutic (cognitive behavioural therapy) and pharmacologic (venlafaxine) treatment. Both treatments yielded a significant increase in glucose metab olism in the right occipital-temporal cortex and significant decreases in the orbitofrontal cortex and left medial prefrontal cortex.…”

Section: Should Neuroimaging Studies Include Ptsd Patients Receiving mentioning

confidence: 99%

Does neuroimaging research examining the pathophysiology of posttraumatic stress disorder require medication-free patients?

Lanius

Brewin

Bremner

et al. 2010

jpn

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Background:In an attempt to avoid unknown influence, most neuroimaging studies examining the pathophysiology of posttraumatic stress disorder (PTSD) exclude patients taking medications. Here we review the empirical evidence for relevant medications having a confounding effect on task performance or cerebral blood flow (CBF) in this population. The evidence for potentially confounding effects of psychotherapy in PTSD are also discussed. Methods: The literature that we reviewed was obtained through a PubMed search from 1980 to 2009 using the search terms posttraumatic stress disorder, PTSD, psychotropic medications, neuroimaging, functional magnetic res onance imaging, positron emission tomography, cerebral blood flow, CBF, serotonin-specific reuptake blocker, benzodiazepine, ketamine, methamphetamine, lamotrigine and atypical antipsychotic agents. Results: The empirical evidence for relevant medications having a confounding effect on task performance or CBF in relevant areas remains sparse for most psychotropic medications among patients with PTSD. However, considerable evidence is accumulating for 2 of the most commonly prescribed medication classes (serotonin-specific reuptake inhibitors and benzodiazepines) in healthy controls. Compelling data for the potentially confounding effects on brain areas relevant to PTSD for psychotherapeutic interventions are also accumulating. Conclusion: Neuroimaging studies examining the pathophysiology of PTSD should ideally recruit both medicated (assuming that the medication treatment has not resulted in the remission of symptoms) and unmedicated participants, to allow the findings to be generalized with greater confidence to the entire population of patients with PTSD. More research is needed into the independent effects of medications on task performance and CBF in regions of interest in PTSD. Neuroimaging studies should also take into account whether patients are currently engaged in psychotherapeutic treatment.

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“…Modulation of brain activity with cognitive behavioral therapy (CBT) has been reported in panic disorder using a variety of neuroscience methods (Kircher et al, 2013;Prasko et al, 2004;Sakai et al, 2006;Seo, Choi, Chung, Rho, & Chae, 2014;Straube, Glauer, Dilger, Mentzel, Miltner, 2006;Mansson et al, 2016-for a review of studies completed through 2014 see Yang, Kircher, & Straube 2014). Three studies using resting state paradigms found converging evidence that CBT modulates brain activity in frontal regions in individuals with panic disorder (Prasko et al, 2004;Sakai et al, 2006;Seo et al, 2014).…”

Section: Anxiety Disordersmentioning

confidence: 99%

Using neuroscience as an outcome measure for behavioral interventions in Autism spectrum disorders (ASD): A review

Stavropoulos

2017

Research in Autism Spectrum Disorders

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A B S T R A C TThough medications have proven effective in improving associated symptoms of autism spectrum disorder (ASD), behavioral interventions remain the most effective method of improving core symptoms (e.g. social communication, restricted and repetitive behaviors) in this population. Although the cause remains unknown, research provides evidence that ASD is a neurologically based disorder, with differences in brain activity contributing to observed social difficulties. Given the above, along with recent publications underscoring the importance of utilizing neuroscience to measure changes associated with intervention in ASD, it is surprising that studies that measure neurological changes in response to behavioral interventions remain quite rare. Using systematic searches of the PsychINFO and MEDLINE databases, the current review summarizes the extant literature on neural changes in response to behavioral interventions in ASD, and compares the state of the literature in ASD with other disorders such as anxiety, depression, and schizophrenia. We conclude that research utilizing neuroscience to measure changes in response to behavioral interventions in ASD is lacking, and suggest that future research make integrating these two lines of research a priority.

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Effects of cognitive-behavioral therapy on brain activation in specific phobia

Cited by 234 publications

References 80 publications

Network model of fear extinction and renewal functional pathways

Network model of fear extinction and renewal functional pathways

Does neuroimaging research examining the pathophysiology of posttraumatic stress disorder require medication-free patients?

Using neuroscience as an outcome measure for behavioral interventions in Autism spectrum disorders (ASD): A review

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