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1.
Clin Drug Investig ; 37(8): 737-743, 2017 Aug.
Article in English | MEDLINE | ID: mdl-28432583

ABSTRACT

BACKGROUND AND OBJECTIVES: Generalized anxiety disorder (GAD) is a persistent anxiety disorder with a high rate of relapse. While several trials have demonstrated the efficacy of pharmacotherapy for GAD treatment, fewer studies have investigated its efficacy in preventing symptom relapse in long-term treatment. The aim of this study is to evaluate if long-term pharmacotherapy may prevent relapses in GAD patients. METHODS: This is a systematic review of the relapse prevention trials with GAD patients. RESULTS: Eight trials were included in this review with 5304 patients in total. All patients showed a higher risk of relapse if treatment was not maintained for at least 6 months after remission, with hazard ratios ranging from 0.12 to 0.58 and mostly moderate effect sizes (0.19-1.06). CONCLUSION: Long-term pharmacotherapy may prevent symptom relapse in GAD patients. As the relapse rate is very high, the data support the continuation of pharmacotherapy for as long as possible.


Subject(s)
Anxiety Disorders/drug therapy , Adult , Clinical Trials as Topic , Female , Humans , Male , Recurrence , Secondary Prevention
2.
J Affect Disord ; 167: 336-42, 2014.
Article in English | MEDLINE | ID: mdl-25020268

ABSTRACT

BACKGROUND: Generalized anxiety disorder (GAD) is a prevalent anxiety disorder, but its neurobiological basis has been poorly studied. A few cognitive models have been proposed for understanding GAD development and maintenance. The aim of this study is to review functional Magnetic Resonance Image (fMRI) studies conducted with GAD patients and evaluate if they support and underpin the theoretical cognitive models proposed for this anxiety disorder. METHODS: A literature systematic review was undertaken in PubMed and ISI databases with no time limits. RESULTS: From the studies included in this review, 10 explored the "emotional dysregulation model", showing, prefrontal cortex (PFC) and anterior cingulate cortex (ACC) hypofunction and deficient top-down control system during emotion regulation tasks, despite conflicting techniques and results. Only one study explored the "conditioned fear overgeneralization theory", other the "intolerance of uncertainty model" and two studies were unspecific (worry induction tasks). Between those, there were 4 studies evaluating pre- and post-treatment with antidepressants or "mindfulness". LIMITATIONS: The studies׳ methodologies differ between one another making it difficult to identify a common finding. CONCLUSION: Emotion dysregulation seems to be an important cognitive dysfunction in GAD patients and fMRI studies suggest that it is related to PFC and ACC hypofunction as well as a deficient cortex-amygdala functional connectivity.


Subject(s)
Anxiety Disorders/physiopathology , Cognition Disorders/physiopathology , Magnetic Resonance Imaging , Amygdala/physiopathology , Anxiety Disorders/psychology , Brain Mapping , Cerebral Cortex/physiopathology , Cognition Disorders/psychology , Humans , Nerve Net/physiopathology
3.
Cogn Behav Neurol ; 20(1): 11-4, 2007 Mar.
Article in English | MEDLINE | ID: mdl-17356338

ABSTRACT

OBJECTIVE: To describe the recurrent emergence of pathologic gambling (PG) during the sequential treatment of a patient with Juvenile Parkinson disease (PD) with different dopamine agonists. METHOD: Single case report. RESULTS: A patient with Juvenile PD developed PG soon after beginning treatment with pergolide, a mixed D1/D2 dopamine agonist that is also supposed to exhibit D3 activity. This behavior remitted upon the discontinuation of the drug. A subsequent therapeutic trial with pramipexole, a dopamine agonist with preferential D3 dopamine receptor activity, resulted in the recurrence of PG. Remarkably, previous treatment with levodopa was not associated with this side effect. CONCLUSIONS: These findings seem to confirm previous suggestions that dopaminergic hyperactivity plays an important role in the pathogenesis of PG. They further indicate that patients with PD may develop PG as a side effect of more than one dopamine agonist. There is still no consensus regarding the best strategy to deal with this potentially disturbing phenomenon.


Subject(s)
Antiparkinson Agents/adverse effects , Benzothiazoles/adverse effects , Gambling/psychology , Parkinsonian Disorders/complications , Pergolide/adverse effects , Adolescent , Adult , Antiparkinson Agents/therapeutic use , Benzothiazoles/therapeutic use , Disruptive, Impulse Control, and Conduct Disorders/chemically induced , Disruptive, Impulse Control, and Conduct Disorders/psychology , Dopamine Agonists/adverse effects , Dopamine Agonists/therapeutic use , Female , Humans , Levodopa/therapeutic use , Parkinsonian Disorders/drug therapy , Parkinsonian Disorders/psychology , Pergolide/therapeutic use , Pramipexole , Recurrence
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