“…This laterality effect has been also observed in an opposite correlation between acute symptom provocation (as emotional processes play a major role in OCD) and orbitofrontal perfusion in the right and left hemisphere [20], as well as symptom improvement and disruption of abnormal metabolic activity on the right hemisphere after cognitive behavioral therapy [21]. Additionally, symptomatic improvement was found in neurosurgery after right hemisphere anterior capsulotomy but not on left side [22,23]. Neuroimaging studies also found right hemisphere changes associated with therapeutic improvement after medication [24].…”
a b s t r a c tObsessive Compulsive Disorder (OCD) involves failures in two main inhibitory processes, namely cognitive (obsessions) and behavioral (compulsions). Recent research has supported two cortical-subcortical pathways on OCD pathogenesis: (a) the frontostriatal loop (dorsolateral-caudate-striatum-thalamus) responsible for impairments of behavioral inhibition; (b) the orbitofrontal loop (orbitofrontal, medial prefrontal and cingulate) responsible for impairments with cognitive inhibitory processes. These failures in both cognitive and motor inhibitory systems may mediate several neuropsychological deficits in these patients, namely memory, attention, planning and decision making. But are those deficits related to specific hemispheric effects, namely functional imbalance between hemispheres? In this article we hypothesize that: (1) OCD patients have an inter-hemispheric functional imbalance, probably due to inadequate filtering at the thalamic level; (2) the restoration of inter-hemispheric balance, will be correlative to symptomatic improvement.Ó 2011 Elsevier Ltd. All rights reserved.
IntroductionObsessive Compulsive Disorder (OCD) is one of the most debilitating psychiatric disorders. It has a cross cultural lifetime prevalence of 2.5% [1,2] being characterized by the presence of obsessions (intrusive, upsetting and unwanted thoughts and/or images) and/or compulsions (repetitive and stereotyped behavior or mental rituals) [3].Most prevailing evidences indicate that OCD is a biological disease. Functional brain imaging studies have converged in order to produce a model for pathophysiology of OCD which involves hyperactivity in certain cortical and subcortical regions [4]. Parallel and partially antagonistic information-processing pathways seem to be involved in order to appropriately create a balanced control of thought and movement. The initiation and sustainability of the repetitive behavior is thought to be modulated by the direct pathway. The completion of these behavioral routines will then be modulated by the indirect pathway. It is suggested that the OCD symptoms result of an hyperactivity in the direct pathway compare to the indirect one leading to a disinhibited thalamus and the creation of a self-perpetuating circuit between the thalamus and the orbital cortex [5,6]. Also, cortico-striatal projections are predominantly glutamatergic, thus excessive activity may contribute to the pathophysiology of OCD. Successful treatment is associated with a reduction in the CSTC hyperactivity.Thus, it has been thought that OCD involves failures in two main inhibitory processes, namely cognitive (responsible for the obsessions) and behavioral (responsible for the compulsions) [7]. Recent research has supported two cortical-subcortical pathways in OCD pathogenesis: (a) the frontostriatal loop (dorsolateral-caudate-striatum-thalamus) responsible for impairments of behavioral inhibition; (b) the orbitofrontal loop (orbitofrontal, medial prefrontal and cingulate) responsible for impairments with cognitive inhibi...
“…This laterality effect has been also observed in an opposite correlation between acute symptom provocation (as emotional processes play a major role in OCD) and orbitofrontal perfusion in the right and left hemisphere [20], as well as symptom improvement and disruption of abnormal metabolic activity on the right hemisphere after cognitive behavioral therapy [21]. Additionally, symptomatic improvement was found in neurosurgery after right hemisphere anterior capsulotomy but not on left side [22,23]. Neuroimaging studies also found right hemisphere changes associated with therapeutic improvement after medication [24].…”
a b s t r a c tObsessive Compulsive Disorder (OCD) involves failures in two main inhibitory processes, namely cognitive (obsessions) and behavioral (compulsions). Recent research has supported two cortical-subcortical pathways on OCD pathogenesis: (a) the frontostriatal loop (dorsolateral-caudate-striatum-thalamus) responsible for impairments of behavioral inhibition; (b) the orbitofrontal loop (orbitofrontal, medial prefrontal and cingulate) responsible for impairments with cognitive inhibitory processes. These failures in both cognitive and motor inhibitory systems may mediate several neuropsychological deficits in these patients, namely memory, attention, planning and decision making. But are those deficits related to specific hemispheric effects, namely functional imbalance between hemispheres? In this article we hypothesize that: (1) OCD patients have an inter-hemispheric functional imbalance, probably due to inadequate filtering at the thalamic level; (2) the restoration of inter-hemispheric balance, will be correlative to symptomatic improvement.Ó 2011 Elsevier Ltd. All rights reserved.
IntroductionObsessive Compulsive Disorder (OCD) is one of the most debilitating psychiatric disorders. It has a cross cultural lifetime prevalence of 2.5% [1,2] being characterized by the presence of obsessions (intrusive, upsetting and unwanted thoughts and/or images) and/or compulsions (repetitive and stereotyped behavior or mental rituals) [3].Most prevailing evidences indicate that OCD is a biological disease. Functional brain imaging studies have converged in order to produce a model for pathophysiology of OCD which involves hyperactivity in certain cortical and subcortical regions [4]. Parallel and partially antagonistic information-processing pathways seem to be involved in order to appropriately create a balanced control of thought and movement. The initiation and sustainability of the repetitive behavior is thought to be modulated by the direct pathway. The completion of these behavioral routines will then be modulated by the indirect pathway. It is suggested that the OCD symptoms result of an hyperactivity in the direct pathway compare to the indirect one leading to a disinhibited thalamus and the creation of a self-perpetuating circuit between the thalamus and the orbital cortex [5,6]. Also, cortico-striatal projections are predominantly glutamatergic, thus excessive activity may contribute to the pathophysiology of OCD. Successful treatment is associated with a reduction in the CSTC hyperactivity.Thus, it has been thought that OCD involves failures in two main inhibitory processes, namely cognitive (responsible for the obsessions) and behavioral (responsible for the compulsions) [7]. Recent research has supported two cortical-subcortical pathways in OCD pathogenesis: (a) the frontostriatal loop (dorsolateral-caudate-striatum-thalamus) responsible for impairments of behavioral inhibition; (b) the orbitofrontal loop (orbitofrontal, medial prefrontal and cingulate) responsible for impairments with cognitive inhibi...
“…Furthermore, larger right inferior frontal cortical volume was correlated with worse memory performance in patients [21]. In addition, topographic analysis of lesions following right hemisphere anterior capsulotomy were associated with good postoperative outcome in patients with OCD [22]. It is also noteworthy that functional MRI studies have shown that the rIFC and the subthalamic nucleus are involved in inhibition of prepotent or already initiated motor responses [23] and that patients with OCD have less activation compared with healthy volunteers in right hemisphere brain regions, including the inferior frontal gyrus, while performing such tasks [24].…”
Earlier studies are inconsistent regarding the structural basis of obsessive-compulsive disorder (OCD), and few studies have investigated whether patients with OCD have cortical thickness abnormalities compared with healthy volunteers. Using magnetic resonance imaging we compared regional differences in cortical thickness among 21 patients with OCD and 21 demographically matched healthy volunteers. Our findings indicate that the right inferior frontal cortex and posterior middle temporal gyrus are thicker in patients with OCD compared with healthy controls, which may contribute to response inhibition deficits and other aspects of phenomenology related to the disorder.
“…Leukotomies combined cingulotomy and subcaudate tractotomy. Different centers worldwide have established the efficacy of such surgical treatments, which are still proposed in cases of intractable OCD (7,8,11,20,29). In the past decade, the use of deep brain stimulation (DBS) has progressively replaced lesions and Bart Nuttin and his team (25) were the first to apply the concept of high frequency stimulation of a deep target, the anterior limb of the internal capsule, to treat patients suffering from severe OCD.…”
Section: Surgical Treatment For Ocd: From Lesions To Deep Brain Stimumentioning
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.