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"Compulsive behavior"
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High-frequency neuromodulation improves obsessive–compulsive behavior
Nearly one billion people worldwide suffer from obsessive–compulsive behaviors
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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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. 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
Probing Compulsive and Impulsive Behaviors, from Animal Models to Endophenotypes: A Narrative Review
Failures in cortical control of fronto-striatal neural circuits may underpin impulsive and compulsive acts. In this narrative review, we explore these behaviors from the perspective of neural processes and consider how these behaviors and neural processes contribute to mental disorders such as obsessive–compulsive disorder (OCD), obsessive–compulsive personality disorder, and impulse-control disorders such as trichotillomania and pathological gambling. We present findings from a broad range of data, comprising translational and human endophenotypes research and clinical treatment trials, focussing on the parallel, functionally segregated, cortico-striatal neural projections, from orbitofrontal cortex (OFC) to medial striatum (caudate nucleus), proposed to drive compulsive activity, and from the anterior cingulate/ventromedial prefrontal cortex to the ventral striatum (nucleus accumbens shell), proposed to drive impulsive activity, and the interaction between them. We suggest that impulsivity and compulsivity each seem to be multidimensional. Impulsive or compulsive behaviors are mediated by overlapping as well as distinct neural substrates. Trichotillomania may stand apart as a disorder of motor-impulse control, whereas pathological gambling involves abnormal ventral reward circuitry that identifies it more closely with substance addiction. OCD shows motor impulsivity and compulsivity, probably mediated through disruption of OFC-caudate circuitry, as well as other frontal, cingulate, and parietal connections. Serotonin and dopamine interact across these circuits to modulate aspects of both impulsive and compulsive responding and as yet unidentified brain-based systems may also have important functions. Targeted application of neurocognitive tasks, receptor-specific neurochemical probes, and brain systems neuroimaging techniques have potential for future research in this field.
Journal Article
New developments in human neurocognition: clinical, genetic, and brain imaging correlates of impulsivity and compulsivity
Impulsivity and compulsivity represent useful conceptualizations that involve dissociable cognitive functions, which are mediated by neuroanatomically and neurochemically distinct components of cortico-subcortical circuitry. The constructs were historically viewed as diametrically opposed, with impulsivity being associated with risk-seeking and compulsivity with harm-avoidance. However, they are increasingly recognized to be linked by shared neuropsychological mechanisms involving dysfunctional inhibition of thoughts and behaviors. In this article, we selectively review new developments in the investigation of the neurocognition of impulsivity and compulsivity in humans, in order to advance our understanding of the pathophysiology of impulsive, compulsive, and addictive disorders and indicate new directions for research.
Journal Article
Prevalence, comorbidity, and breed differences in canine anxiety in 13,700 Finnish pet dogs
Behaviour problems and anxieties in dogs decrease their quality of life and may lead to relinquishment or euthanasia. Considering the large number of pet dogs and the commonness of these problematic behaviours, a better understanding of the epidemiology and related molecular and environmental factors is needed. We have here studied the prevalence, comorbidity, and breed specificity of seven canine anxiety-like traits: noise sensitivity, fearfulness, fear of surfaces and heights, inattention/impulsivity, compulsion, separation related behaviour and aggression with an online behaviour questionnaire answered by dog owners. Our results show that noise sensitivity is the most common anxiety-related trait with a prevalence of 32% in 13,700 Finnish pet dogs. Due to the high prevalence of noise sensitivity and fear, they were the most common comorbidities. However, when comparing the relative risk, the largest risk ratios were seen between hyperactivity/inattention, separation related behaviour and compulsion, and between fear and aggression. Furthermore, dog breeds showed large differences in prevalence of all anxiety-related traits, suggesting a strong genetic contribution. As a result, selective breeding focusing on behaviour may reduce the prevalence of canine anxieties. Anxious animals may suffer from chronic stress and thus, modified breeding policies could improve the welfare of our companion dogs.
Journal Article
Why can't I stop? : reclaiming your life from a behavioral addiction
\"Addictions to drugs or alcohol are usually apparent, but what about behavioral addictions? A person addicted to shoplifting or gambling, for example, or picking at their skin, may suffer in the shadows while their behavior consumes their time and energy--and disrupts their life. Legal, medical, and financial troubles are common for such a person and their loved ones, as are social and family conflicts. Behavioral addictions are serious illnesses and usually do not go away on their own--telling the loved one to simply stop doing the behavior will not work. This book is for anyone who has a behavioral addiction, and for their families and friends. It describes what a behavioral addiction is, what causes it, and how it can be diagnosed and treated. It takes an in-depth look at seven specific addictions: to gambling, stealing, sex, internet use, shopping and buying, hair pulling and skin picking, and food. Behavioral addictions have a physical basis in the brain and are addictive because, like alcohol and narcotics, they are rewarding. The addicted person spends enormous amounts of time preparing for or engaging in the habit, and in the process neglects other areas of life. He or she may also be convicted of a crime, put their sexual partner at risk of infection, lose their job due to negligence and their home due to debt. These repetitive habits persist despite negative consequences so that, ultimately, the person loses all conscious control over the behavior. The guidance provided here helps readers deal with the complicated issues surrounding these addictions, including how family members can help the addicted person while helping themselves. Dr. Grant has published many books and has appeared on CNN, BBC, GMA, The Early Show, and elsewhere\"-- Provided by publisher.
Book
Central norepinephrine transmission is required for stress-induced repetitive behavior in two rodent models of obsessive-compulsive disorder
RationaleObsessive-compulsive disorder (OCD) is characterized by repetitive behaviors exacerbated by stress. Many OCD patients do not respond to available pharmacotherapies, but neurosurgical ablation of the anterior cingulate cortex (ACC) can provide symptomatic relief. Although the ACC receives noradrenergic innervation and expresses adrenergic receptors (ARs), the involvement of norepinephrine (NE) in OCD has not been investigated.ObjectiveTo determine the effects of genetic or pharmacological disruption of NE neurotransmission on marble burying (MB) and nestlet shredding (NS), two animal models of OCD.MethodsWe assessed NE-deficient (Dbh −/−) mice and NE-competent (Dbh +/−) controls in MB and NS tasks. We also measured the effects of anti-adrenergic drugs on NS and MB in control mice and the effects of pharmacological restoration of central NE in Dbh −/− mice. Finally, we compared c-fos induction in the locus coeruleus (LC) and ACC of Dbh −/− and control mice following both tasks.ResultsDbh −/− mice virtually lacked MB and NS behaviors seen in control mice but did not differ in the elevated zero maze (EZM) model of general anxiety-like behavior. Pharmacological restoration of central NE synthesis in Dbh −/− mice completely rescued NS behavior, while NS and MB were suppressed in control mice by anti-adrenergic drugs. Expression of c-fos in the ACC was attenuated in Dbh −/− mice after MB and NS.ConclusionThese findings support a role for NE transmission to the ACC in the expression of stress-induced compulsive behaviors and suggest further evaluation of anti-adrenergic drugs for OCD is warranted.
Journal Article