Accelerated neuromodulation therapy for Obsessive-Compulsive Disorder.
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ABSTRACT:
SUBMITTER: Williams NR
PROVIDER: S-EPMC8114181 | biostudies-literature | 2021 Mar-Apr
REPOSITORIES: biostudies-literature
Publications
Accelerated neuromodulation therapy for Obsessive-Compulsive Disorder.
Williams Nolan R NR Sudheimer Keith D KD Cole Eleanor J EJ Varias Andrea D AD Goldstein-Piekarski Andrea N AN Stetz Patrick P Lombardi Anthony A Filippou-Frye Maria M van Roessel Peter P Anderson Kelley K McCarthy Elizabeth A EA Wright Brianna B Sandhu Thasveen T Menon Sindu S Jo Booil B Koran Lorrin L Williams Leanne M LM Rodriguez Carolyn I CI
Brain stimulation 20210223 2
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Project description:Neuromodulation shows increasing promise in the treatment of psychiatric disorders, particularly obsessive-compulsive disorder (OCD). Development of tools and techniques including deep brain stimulation, transcranial magnetic stimulation, and electroconvulsive therapy may yield additional options for patients who fail to respond to standard treatments. This article reviews the motivation for and use of these treatments in OCD. We begin with a brief description of the illness followed by discussion of the circuit models thought to underlie the disorder. These circuits provide targets for intervention. Basal ganglia and talamocortical pathophysiology, including cortico-striato-thalamo-cortical loops is a focus of this discussion. Neuroimaging findings and historical treatments that led to the use of neuromodulation for OCD are presented. We then present evidence from neuromodulation studies using deep brain stimulation, electroconvulsive therapy, and transcranial magnetic stimulation, with targets including nucleus accumbens, subthalamic nucleus inferior thalamic peduncle, dorsolateral prefrontal cortex, supplementary motor area, and orbitofrontal cortex. Finally, we explore potential future neuromodulation approaches that may further refine and improve treatment.
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Project description:Nearly one billion people worldwide suffer from obsessive-compulsive behaviors1,2, yet our mechanistic understanding of these behaviors is incomplete, and effective therapeutics are unavailable. An emerging perspective characterizes obsessive-compulsive behaviors as maladaptive habit learning3,4, which may be associated with abnormal beta-gamma neurophysiology of the orbitofrontal-striatal circuitry during reward processing5,6. 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.
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Project description:Obsessive-compulsive disorder (OCD) is a highly prevalent and chronic condition that is associated with substantial global disability. OCD is the key example of the 'obsessive-compulsive and related disorders', a group of conditions which are now classified together in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, and the International Classification of Diseases, 11th Revision, and which are often underdiagnosed and undertreated. In addition, OCD is an important example of a neuropsychiatric disorder in which rigorous research on phenomenology, psychobiology, pharmacotherapy and psychotherapy has contributed to better recognition, assessment and outcomes. Although OCD is a relatively homogenous disorder with similar symptom dimensions globally, individualized assessment of symptoms, the degree of insight, and the extent of comorbidity is needed. Several neurobiological mechanisms underlying OCD have been identified, including specific brain circuits that underpin OCD. In addition, laboratory models have demonstrated how cellular and molecular dysfunction underpins repetitive stereotyped behaviours, and the genetic architecture of OCD is increasingly understood. Effective treatments for OCD include serotonin reuptake inhibitors and cognitive-behavioural therapy, and neurosurgery for those with intractable symptoms. Integration of global mental health and translational neuroscience approaches could further advance knowledge on OCD and improve clinical outcomes.
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Project description:Obsessive-compulsive disorder (OCD) is a prevalent and often severely disabling illness with onset generally in childhood or adolescence. Although white matter deficits have been implicated in the neurobiology of OCD, few studies have been conducted in pediatric patients when the brain is still developing and have examined their functional correlates. In this study, 23 pediatric OCD patients and 23 healthy volunteers, between the ages of 9 and 17 years, matched for sex, age, handedness, and IQ, received a diffusion tensor imaging exam on a 3T GE system and a brief neuropsychological battery tapping executive functions. Patient symptom severity was assessed using the Children's Yale-Brown Obsessive-Compulsive Scale (CY-BOCS). Patients with OCD exhibited significantly greater fractional anisotropy compared to matched controls in the left dorsal cingulum bundle, splenium of the corpus callosum, right corticospinal tract, and left inferior fronto-occipital fasciculus. There were no regions of significantly lower fractional anisotropy in patients compared to controls. Higher fractional anisotropy in the splenium was significantly correlated with greater obsession severity on the CY-BOCS in the subgroup of psychotropic drug-naïve patients. Among patients, there was a significant association between greater fractional anisotropy in the dorsal cingulum bundle and better performance on measures of response inhibition and cognitive control. The overall findings suggest a pattern of greater directional coherence of white matter tracts in OCD very early in the course of illness, which may serve a compensatory mechanism, at least for response inhibition functions typically subserved by the cingulum bundle.
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Project description:Metacognitive therapy (MCT) has been shown to be a promising treatment approach for obsessive-compulsive disorder (OCD). The changeability of metacognitions by (metacognitive) treatment and its relevance to treatment outcome is, however, still unclear. The current study investigates, (1) if treatment with MCT or exposure and response prevention (ERP) in a randomized-controlled pilot trial (n = 24 patients with OCD) changes OCD-specific metacognitions of thought fusion beliefs, beliefs about rituals and stop signals, and (2) if these changes are relevant for the treatment outcome in terms of patient- and therapist-rated OCD symptoms. ANOVA with pretest, posttest and follow-up scores could show that all three metacognitions significantly decreased during both treatments. Regarding thought fusion beliefs, a significant interaction effect indicated a higher decrease after MCT than ERP treatment. In hierarchical regression analyses, changes in stop signals from pre- to post-treatment significantly predicted patient-rating OCD symptoms at post-treatment and follow-up at 3 months after treatment. These changes were even predictive of post-treatment outcome after controlling for general metacognitions and dysfunctional cognitive beliefs. These findings support the assumption that metacognitions can change during both treatments and that changes in stop signals might be relevant for the treatment outcome on the symptom level in OCD.
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