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"Obsessive compulsive disorder"
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Deep brain stimulation for refractory obsessive-compulsive disorder (OCD): emerging or established therapy?
A consensus has yet to emerge whether deep brain stimulation (DBS) for treatment-refractory obsessive-compulsive disorder (OCD) can be considered an established therapy. In 2014, the World Society for Stereotactic and Functional Neurosurgery (WSSFN) published consensus guidelines stating that a therapy becomes established when “at least two blinded randomized controlled clinical trials from two different groups of researchers are published, both reporting an acceptable risk-benefit ratio, at least comparable with other existing therapies. The clinical trials should be on the same brain area for the same psychiatric indication.” The authors have now compiled the available evidence to make a clear statement on whether DBS for OCD is established therapy. Two blinded randomized controlled trials have been published, one with level I evidence (Yale-Brown Obsessive Compulsive Scale (Y-BOCS) score improved 37% during stimulation on), the other with level II evidence (25% improvement). A clinical cohort study (N = 70) showed 40% Y-BOCS score improvement during DBS, and a prospective international multi-center study 42% improvement (N = 30). The WSSFN states that electrical stimulation for otherwise treatment refractory OCD using a multipolar electrode implanted in the ventral anterior capsule region (including bed nucleus of stria terminalis and nucleus accumbens) remains investigational. It represents an emerging, but not yet established therapy. A multidisciplinary team involving psychiatrists and neurosurgeons is a prerequisite for such therapy, and the future of surgical treatment of psychiatric patients remains in the realm of the psychiatrist.
Journal Article
High-frequency neuromodulation improves obsessive–compulsive behavior
Nearly one billion people worldwide suffer from obsessive–compulsive behaviors
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,
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, yet our mechanistic understanding of these behaviors is incomplete, and effective therapeutics are unavailable. An emerging perspective characterizes obsessive–compulsive behaviors as maladaptive habit learning
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, which may be associated with abnormal beta–gamma neurophysiology of the orbitofrontal–striatal circuitry during reward processing
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,
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. We target the orbitofrontal cortex with alternating current, personalized to the intrinsic beta–gamma frequency of the reward network, and show rapid, reversible, frequency-specific modulation of reward- but not punishment-guided choice behavior and learning, driven by increased exploration in the setting of an actor-critic architecture. Next, we demonstrate that chronic application of the procedure over 5 days robustly attenuates obsessive–compulsive behavior in a non-clinical population for 3 months, with the largest benefits for individuals with more severe symptoms. Finally, we show that convergent mechanisms underlie modulation of reward learning and reduction of obsessive–compulsive symptoms. The results contribute to neurophysiological theories of reward, learning and obsessive–compulsive behavior, suggest a unifying functional role of rhythms in the beta–gamma range, and set the groundwork for the development of personalized circuit-based therapeutics for related disorders.
Selective and personalized neuromodulation of orbitofrontal beta–gamma rhythms in humans, achieved with an alternating current, robustly attenuates obsessive–compulsive behavior for 3 months.
Journal Article
Computational modelling reveals contrasting effects on reinforcement learning and cognitive flexibility in stimulant use disorder and obsessive-compulsive disorder: remediating effects of dopaminergic D2/3 receptor agents
RationaleDisorders of compulsivity such as stimulant use disorder (SUD) and obsessive-compulsive disorder (OCD) are characterised by deficits in behavioural flexibility, some of which have been captured using probabilistic reversal learning (PRL) paradigms.ObjectivesThis study used computational modelling to characterise the reinforcement learning processes underlying patterns of PRL behaviour observed in SUD and OCD and to show how the dopamine D2/3 receptor agonist pramipexole and the D2/3 antagonist amisulpride affected these responses.MethodsWe applied a hierarchical Bayesian method to PRL data across three groups: individuals with SUD, OCD, and healthy controls. Participants completed three sessions where they received placebo, pramipexole, and amisulpride, in a double-blind placebo-controlled, randomised design. We compared seven models using a bridge sampling estimate of the marginal likelihood.ResultsStimulus-bound perseveration, a measure of the degree to which participants responded to the same stimulus as before irrespective of outcome, was significantly increased in SUD, but decreased in OCD, compared to controls (on placebo). Individuals with SUD also exhibited reduced reward-driven learning, whilst both the SUD and OCD groups showed increased learning from punishment (nonreward). Pramipexole and amisulpride had similar effects on the control and OCD groups; both increased punishment-driven learning. These D2/3-modulating drugs affected the SUD group differently, remediating reward-driven learning and reducing aspects of perseverative behaviour, amongst other effects.ConclusionsWe provide a parsimonious computational account of how perseverative tendencies and reward- and punishment-driven learning differentially contribute to PRL in SUD and OCD. D2/3 agents modulated these processes and remediated deficits in SUD in particular, which may inform therapeutic effects.
Journal Article
Deep brain stimulation for psychiatric disorders: From focal brain targets to cognitive networks
•DBS is a promising therapy for OCD and MDD but still has variable clinical outcomes.•We propose that a sharper focus on network effects of DBS may improve response rates.•Objective measures of cognitive/emotional deficits may lead to a network biomarker for psychiatric diseases
Deep brain stimulation (DBS) is a promising intervention for treatment-resistant psychiatric disorders, particularly major depressive disorder (MDD) and obsessive-compulsive disorder (OCD). Up to 90% of patients who have not recovered with therapy or medication have reported benefit from DBS in open-label studies. Response rates in randomized controlled trials (RCTs), however, have been much lower. This has been argued to arise from surgical variability between sites, and recent psychiatric DBS research has focused on refining targeting through personalized imaging. Much less attention has been given to the fact that psychiatric disorders arise from dysfunction in distributed brain networks, and that DBS likely acts by altering communication within those networks. This is in part because psychiatric DBS research relies on subjective rating scales that make it difficult to identify network biomarkers. Here, we overview recent DBS RCT results in OCD and MDD, as well as the follow-on imaging studies. We present evidence for a new approach to studying DBS’ mechanisms of action, focused on measuring objective cognitive/emotional deficits that underpin these and many other mental disorders. Further, we suggest that a focus on cognition could lead to reliable network biomarkers at an electrophysiologic level, especially those related to inter-regional synchrony of the local field potential (LFP). Developing the network neuroscience of DBS has the potential to finally unlock the potential of this highly specific therapy.
Journal Article
Error-related brain activity as a transdiagnostic endophenotype for obsessive-compulsive disorder, anxiety and substance use disorder
Increased neural error-signals have been observed in obsessive-compulsive disorder (OCD), anxiety disorders, and inconsistently in depression. Reduced neural error-signals have been observed in substance use disorders (SUD). Thus, alterations in error-monitoring are proposed as a transdiagnostic endophenotype. To strengthen this notion, data from unaffected individuals with a family history for the respective disorders are needed.
The error-related negativity (ERN) as a neural indicator of error-monitoring was measured during a flanker task from 117 OCD patients, 50 unaffected first-degree relatives of OCD patients, and 130 healthy comparison participants. Family history information indicated, that 76 healthy controls were free of a family history for psychopathology, whereas the remaining had first-degree relatives with depression (n = 28), anxiety (n = 27), and/or SUD (n = 27).
Increased ERN amplitudes were found in OCD patients and unaffected first-degree relatives of OCD patients. In addition, unaffected first-degree relatives of individuals with anxiety disorders were also characterized by increased ERN amplitudes, whereas relatives of individuals with SUD showed reduced amplitudes.
Alterations in neural error-signals in unaffected first-degree relatives with a family history of OCD, anxiety, or SUD support the utility of the ERN as a transdiagnostic endophenotype. Reduced neural error-signals may indicate vulnerability for under-controlled behavior and risk for substance use, whereas a harm- or error-avoidant response style and vulnerability for OCD and anxiety appears to be associated with increased ERN. This adds to findings suggesting a common neurobiological substrate across psychiatric disorders involving the anterior cingulate cortex and deficits in cognitive control.
Journal Article