A PET Study of Tiagabine Treatment Implicates Ventral Medial Prefrontal Cortex in Generalized Social Anxiety Disorder

Evans, Karleyton C.; Simon, Naomi M.; Dougherty, Darin D.; Hoge, Elizabeth A.; Worthington, John J.; Chow, Candice; Kaufman, Rebecca E.; Gold, Andrea L.; Fischman, Alan J.; Pollack, Mark H.; Rauch, Scott L.

doi:10.1038/npp.2008.69

Cited by 59 publications

(37 citation statements)

References 47 publications

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“…One study reported greater orbitofrontal cortex activation to angry vs neutral prosody (Quadflieg et al, 2008). In contrast, other studies have found decreased activation (Van Ameringen et al, 2004) and decreased glucose metabolic rates in the ventromedial prefrontal cortex (Evans et al, 2009), which increased following treatment with tiagabine (Evans et al, 2009). Glutamate/creatine and NAA/creatine ratios appear to be elevated in the rACC and are correlated with symptom severity .…”

Section: Social Phobiamentioning

confidence: 83%

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

Shin

Liberzon

2009

Neuropsychopharmacol

1,741

927

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Anxiety disorders are a significant problem in the community, and recent neuroimaging research has focused on determining the brain circuits that underlie them. Research on the neurocircuitry of anxiety disorders has its roots in the study of fear circuits in animal models and the study of brain responses to emotional stimuli in healthy humans. We review this research, as well as neuroimaging studies of anxiety disorders. In general, these studies have reported relatively heightened amygdala activation in response to disorder-relevant stimuli in post-traumatic stress disorder, social phobia, and specific phobia. Activation in the insular cortex appears to be heightened in many of the anxiety disorders. Unlike other anxiety disorders, post-traumatic stress disorder is associated with diminished responsivity in the rostral anterior cingulate cortex and adjacent ventral medial prefrontal cortex. Additional research will be needed to (1) clarify the exact role of each component of the fear circuitry in the anxiety disorders, (2) determine whether functional abnormalities identified in the anxiety disorders represent acquired signs of the disorders or vulnerability factors that increase the risk of developing them, (3) link the findings of functional neuroimaging studies with those of neurochemistry studies, and (4) use functional neuroimaging to predict treatment response and assess treatment-related changes in brain function.

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Section: Social Phobiamentioning

confidence: 83%

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

Shin

Liberzon

2009

Neuropsychopharmacol

1,741

927

View full text Add to dashboard Cite

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“…Na maior parte dos estudos, foram utilizadas amostras clínicas 18,19,[27][28][29][30][31][32][33] ou amostras provenientes da população geral 23,[34][35][36][37][38][39][40][41] , e em quatro estudos 9,42-44 foram incluídas amostras mistas. Os demais estudos 20,[45][46][47][48][49][50] não descreveram a procedência da amostra utilizada.…”

Section: Resultsunclassified

“…Cinco estudos utilizaram também exames de neuroimagem como parâmetro de comparação, quatro optaram pela tomografia por emissão de pósitrons (PET) 19,27,45,47 e um, por tomografia computadorizada por emissão de fóton único (SPECT) 18 . A duração dos diferentes ensaios clínicos variou de 1 (N = 1) a 28 semanas (N = 1), tendo a maioria duração de 12 semanas (N = 8).…”

Section: Resultsunclassified

“…Conforme apresentado na tabela 5, foram localizados cinco estudos que usaram anticonvulsivantes no tratamento do TAS, sendo três com o levetiracetam 24,41,43 e dois com a tiagabina 46,47 . A tiagabina apresentou-se eficaz quanto à melhora dos sintomas de ansiedade social em relação ao placebo.…”

Section: Anticonvulsivantesunclassified

“…Os resultados relativos aos exames de neuroimagem 47 , por meio de PET, apontaram para o aumento no metabolismo da glicose no córtex pré-frontal, medial e ventral, áreas relacionadas à resposta de medo condicionado, entre os sujeitos que fizeram uso de tiagabina em relação ao placebo.…”

Section: Anticonvulsivantesunclassified

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Tratamentos farmacológicos para o transtorno de ansiedade social: existem novos parâmetros na atualidade?

Santos¹,

Osório²,

Loureiro³

et al. 2011

Rev. psiquiatr. clín.

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ResumoContexto: O transtorno de ansiedade social (TAS), apesar da baixa taxa de detecção e do alto índice de comorbidades associadas, é considerado uma condição tratável. Apesar da resposta estabelecida a diversas classes de medicamentos, os algoritmos para o tratamento do TAS necessitam de atualização constante. Objetivo: Realizar revisão sistemática da literatura no que diz respeito à eficácia dos tratamentos farmacológicos relativos ao TAS, a partir de estudos controlados, conduzidos no período de 2005 a 2010. Método: Foram utilizados os indexadores eletrônicos PsycoInfo, Lilacs e Medline, utilizando-se as palavras-chave: "social phobia or social anxiety and treatment". Resultados: De acordo com critérios de inclusão adotados, 29 artigos foram incluídos e analisados. Mostram-se eficazes para o tratamento do TAS as seguintes drogas, de acordo com a classe: a) ISRSs: escitalopram, fluvoxamina, citalopram, GR205171 e sertralina; b) ISRSN: venlafaxina; c) IMAOs: fenelzina, moclobemina; d) aminoácidos: d-cicloserina; f) anticonvulsivantes: tiagabina. Conclusão: Os ISRSs e os ISRSNs têm seu uso estabelecido e ainda continuam sendo considerados primeira opção de tratamento. Porém, destaca-se o potencial futuro da d-cicloserina e dos anticonvulsivantes, com necessidade de um número maior de estudos controlados que confirmem os achado iniciais. A ação das diferentes drogas em nível neurobiológico, bem como dos tratamentos associados, necessita ainda ser mais explorada.Forni- Santos L, et al. / Rev Psiq Clín. 2011;38(6):238-46 Palavras-chave: Transtorno de ansiedade, tratamento, psicofarmacologia, fobia social, resposta ao tratamento. AbstractBackground: Social anxiety disorder (SAD), despite its low detection rates and high level of associated comorbidities, is considered a treatable condition. Although the condition's response to several drug classes is well established, the algorithms for the treatment of SAD require regular updating. Objective: To perform a systematic literature review on the efficacy of pharmacological treatments for SAD based on controlled trials published between 2005 and 2010. Method: Searches were performed in the electronic databases PsycInfo, Lilacs, and Medline using the search terms "social phobia or social anxiety and treatment". Results: In accordance with the inclusion criteria adopted, 29 articles were included and analyzed. The following drugs, grouped according to class, proved efficient to treat SAD: a) SSRIs: escitalopram, fluvoxamine, citalopram, GR205171, and sertraline; b) SNRI: venlafaxine; c) MAOIs: phenelzine, moclobemide; d) amino acids: f-cycloserine; and (e) anticonvulsants: tiagabine. Discussion: The use of SSRIs and SNRIs to treat SAD is well established and these are still considered the firstline treatment for the condition; however, evidence suggests the future potential of D-cycloserine and anticonvulsants, whose efficacy must be confirmed by further controlled trials. The action profiles of the different medications used to treat SAD at the neurobiological level,...

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Toward the Application of Functional Neuroimaging to Individualized Treatment for Anxiety and Depression

2014

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Functional neuroimaging has led to significant gains in understanding the biological bases of anxiety and depressive disorders. However, the ability of functional neuroimaging to directly impact clinical practice is unclear. One important method by which neuroimaging could impact clinical care is to generate single patient level predictions that can guide clinical decision-making. The present review summarizes published functional neuroimaging studies of predictors of medication or psychotherapy outcome in major depressive disorder, obsessive-compulsive disorder (OCD), posttraumatic stress disorder, generalized anxiety disorder, panic disorder, and social anxiety disorder. In major depressive disorder and OCD, there is converging evidence of specific brain circuitry that has both been implicated in the disordered state itself, and where pretreatment activation levels have been predictive of treatment response. Specifically, in major depressive disorder, greater pretreatment ventral and pregenual anterior cingulate cortex (ACC) activation may predict better antidepressant medication outcome but poorer psychotherapy outcome. In OCD, activation in the ACC and orbitofrontal cortex has been inversely associated with pharmacological treatment response. In other anxiety disorders, research in this area is just beginning, with the ACC potentially implicated. However, the question of whether these results can directly translate to clinical practice remains open. In order to achieve the goal of single patient level prediction and individualized treatment, future research should strive to establish replicable models with good predictive performance and clear incremental validity.

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A PET Study of Tiagabine Treatment Implicates Ventral Medial Prefrontal Cortex in Generalized Social Anxiety Disorder

Cited by 59 publications

References 47 publications

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

Tratamentos farmacológicos para o transtorno de ansiedade social: existem novos parâmetros na atualidade?

Toward the Application of Functional Neuroimaging to Individualized Treatment for Anxiety and Depression

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