Obsessive-compulsive disorder (OCD) is a relatively common, often chronic and disabling mental disorder associated to substantial impact on the quality of life.1 First-line treatments for OCD, cognitive behavioral therapy and selective serotonin reuptake inhibitors (SSRIs), produce significant improvement in only about 60% of patients. Moreover, many patients who are considered to be "responders" show significant residual symptoms and comorbidity.2 In cases of partial response to SSRIs, published expert guidelines recommend switching SSRIs and possibly augmenting with different medications, including atypical antipsychotic agents.3 Convergent evidence from genetic, neuroimaging, and open-label treatment studies supports a glutamatergic hyperactivity associated with OCD, which may represent the consequence of functional alterations of the glutamate transporter EAAC-1.4 Glutamate-modulating agents may therefore hold promise in treatment-refractory subjects.5 The new antiepileptic drug pregabalin (PGB) is a derivate of the inhibitory neurotransmitter [gamma]-aminobutyric acid; it modulates the synaptic release of glutamate and monoaminergic neurotransmitters via the [alpha]2d subunits of the voltage-gated Ca2+ channels and modulates the hippocampal theta oscillations.6 It has been shown to be particularly effective in several anxiety disorders, especially generalized anxiety disorder (GAD) and, to a lesser extent, social anxiety disorder and posttraumatic stress disorder, whereas few data are available on OCD.7,8 The aim of the present study was to assess the effectiveness of PGB augmentation in treatment-resistant OCD.

Di Nicola, M., Tedeschi, D., Martinotti, G., De Vita, O., Monetta, M., Pozzi, G., Janiri, L., Pregabalin augmentation in treatment-resistant obsessive-compulsive disorder: a 16-week case series, <<JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY>>, 2011; 31 (5): 675-677. [doi:10.1097/JCP.0b013e31822c29a8] [http://hdl.handle.net/10807/7536]

Pregabalin augmentation in treatment-resistant obsessive-compulsive disorder: a 16-week case series

Di Nicola, Marco;Tedeschi, Daniela;Martinotti, Giovanni;De Vita, Ofelia;Monetta, Marisa;Pozzi, Gino;Janiri, Luigi
2011

Abstract

Obsessive-compulsive disorder (OCD) is a relatively common, often chronic and disabling mental disorder associated to substantial impact on the quality of life.1 First-line treatments for OCD, cognitive behavioral therapy and selective serotonin reuptake inhibitors (SSRIs), produce significant improvement in only about 60% of patients. Moreover, many patients who are considered to be "responders" show significant residual symptoms and comorbidity.2 In cases of partial response to SSRIs, published expert guidelines recommend switching SSRIs and possibly augmenting with different medications, including atypical antipsychotic agents.3 Convergent evidence from genetic, neuroimaging, and open-label treatment studies supports a glutamatergic hyperactivity associated with OCD, which may represent the consequence of functional alterations of the glutamate transporter EAAC-1.4 Glutamate-modulating agents may therefore hold promise in treatment-refractory subjects.5 The new antiepileptic drug pregabalin (PGB) is a derivate of the inhibitory neurotransmitter [gamma]-aminobutyric acid; it modulates the synaptic release of glutamate and monoaminergic neurotransmitters via the [alpha]2d subunits of the voltage-gated Ca2+ channels and modulates the hippocampal theta oscillations.6 It has been shown to be particularly effective in several anxiety disorders, especially generalized anxiety disorder (GAD) and, to a lesser extent, social anxiety disorder and posttraumatic stress disorder, whereas few data are available on OCD.7,8 The aim of the present study was to assess the effectiveness of PGB augmentation in treatment-resistant OCD.
Inglese
Di Nicola, M., Tedeschi, D., Martinotti, G., De Vita, O., Monetta, M., Pozzi, G., Janiri, L., Pregabalin augmentation in treatment-resistant obsessive-compulsive disorder: a 16-week case series, <<JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY>>, 2011; 31 (5): 675-677. [doi:10.1097/JCP.0b013e31822c29a8] [http://hdl.handle.net/10807/7536]
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/10807/7536
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