Evidence-based pharmacological treatment of anxiety disorders, post-traumatic stress disorder and obsessive-compulsive disorder: A revision of the 2005 guidelines from the British Association for Psychopharmacology

Abstract Objective To assess whether diagnosed Obsessive Compulsive Disorder (OCD) and Post Traumatic Stress Disorder (PTSD) interactively alter brain activity, as measured by a Single Photon Emission Computed Tomography (SPECT) imaging. Method The sample included adults diagnosed with OCD (n = 915) with a mean age of 34.65 and predominantly male (68.6%) and adults with PTSD (n = 1,481) which had a mean age of 41.33 and was predominantly female (57.2%). Significant differences were observed for gender . Multiple ANCOVAs were conducted to determine differences between cerebral blood flow (CBF)in 17 different brain regions. Results Results showed hyper-perfusion in the PTSD group as compared to the OCD group in the pariental L/R[F(1,2393) = 6.47,p < 0.01/F(1,2393) = 12.31,p < .01], motor sensory L/R[F(1,2393) = 19.33,p < .001/F(1,2393) = 17.32,p < .01] and temporal left [F(1,2393) = 12.49,p < .01]. Conclusion Significantly higher rCBF in the pariental and motor sensory for OCD individuals may be due to visual-constructive and controlled fluency which are usually associated with compulsion. Due to the hyperalert nature related with OCD rituals, these areas are more active when compared to PTSD. Hyperfusion was reported for PTSD in the left temporal lobe compared to OCD, this region is usually associated with registering potential threasts in the environment. This can be explained by the hypervigilant conduct seen in individuals with PTSD. Overall, it appears that individuals with OCD struggle with continual inability to inhibit repetitive thoughts and behaviors due to the over activation in the motor sensory and parietal region. Alternatively, the activation in PTSD individuals can be a result of a way to help them cope with threats in the environment.

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Ketamine’s dose-related effects on anxiety symptoms in patients with treatment refractory anxiety disorders

Journal of Psychopharmacology ◽

10.1177/0269881117705089 ◽

2017 ◽

Vol 31 (10) ◽

pp. 1302-1305 ◽

Cited By ~ 36

Author(s):

Paul Glue ◽

Natalie J Medlicott ◽

Sarah Harland ◽

Shona Neehoff ◽

Bridie Anderson-Fahey ◽

...

Keyword(s):

Anxiety Disorder ◽

Anxiety Disorders ◽

Post Traumatic Stress Disorder ◽

Traumatic Stress ◽

Post Traumatic Stress ◽

Treatment Resistant ◽

Obsessive Compulsive ◽

Compulsive Disorder ◽

Post Traumatic ◽

Resistant Depression

The N-methyl-D-aspartate receptor antagonist ketamine has rapid onset activity in treatment-resistant depression, post-traumatic stress disorder and obsessive compulsive disorder. Due to similarities in brain network activity in depression and anxiety disorders, we hypothesized that ketamine might also be active in other refractory anxiety disorders. We evaluated the efficacy and safety of ketamine in 12 patients with refractory generalized anxiety disorder and/or social anxiety disorder who were not currently depressed, using an ascending single dose study design (0.25, 0.5, 1 mg/kg administered subcutaneously) at weekly intervals. Within 1 h of dosing, patients reported reduced anxiety, which persisted for up to seven days. A dose-response profile was noted for anxiolytic effects, dissociative side effects, and changes in blood pressure and heart rate, with minor changes at 0.25 mg/kg, and progressively greater and more durable changes at the higher doses. Ten of 12 patients were treatment responders at 0.5–1 mg/kg. Ketamine was safe and well tolerated in this population. Ketamine may be a potential therapeutic alternative for patients with refractory generalized anxiety disorder/social anxiety disorder. Along with its demonstrated effectiveness in patients with treatment-resistant depression, obsessive compulsive disorder and post-traumatic stress disorder, these data raise the intriguing possibility that ketamine may have broad efficacy in disorders characterized by negative emotional states, and that these disorders may share a common precipitating neurobiology.

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