The involvement of distinct neural systems in patients with obsessive–compulsive disorder with autogenous and reactive obsessions

Beşiroğlu, Lütfullah; Sözen, Mehmet A.; Ozbebit, Ozgur; Avcu, Serhat; Selvı, Yavuz; Bora, Aydın; Atlı, Abdullah; Ünal, Özkan; Bulut, Mahmut

doi:10.1111/j.1600-0447.2011.01726.x

Cited by 29 publications

(30 citation statements)

References 56 publications

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“…22, 23, 24, 26, 27, 28, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51 Of these, three studies were excluded because they did not compare metabolites between OCD patients and HC subjects. 44, 45, 46 Another study was excluded because it was a review article.…”

Section: Resultsmentioning

confidence: 99%

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Reduction of N-acetylaspartate in the medial prefrontal cortex correlated with symptom severity in obsessive-compulsive disorder: meta-analyses of 1H-MRS studies

Aoki

Suwa

2012

Transl Psychiatry

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Structural and functional neuroimaging findings suggest that disturbance of the cortico–striato–thalamo–cortical (CSTC) circuits may underlie obsessive-compulsive disorder (OCD). However, some studies with 1H-magnetic resonance spectroscopy (1H-MRS) reported altered level of N-acetylaspartate (NAA), they yielded inconsistency in direction and location of abnormality within CSTC circuits. We conducted a comprehensive literature search and a meta-analysis of 1H-MRS studies in OCD. Seventeen met the inclusion criteria for a meta-analysis. Data were separated by frontal cortex region: medial prefrontal cortex (mPFC), dorsolateral prefrontal cortex, orbitofrontal cortex, basal ganglia and thalamus. The mean and s.d. of the NAA measure were calculated for each region. A random effects model integrating 16 separate datasets with 225 OCD patients and 233 healthy comparison subjects demonstrated that OCD patients exhibit decreased NAA levels in the frontal cortex (P=0.025), but no significant changes in the basal ganglia (P=0.770) or thalamus (P=0.466). Sensitivity analysis in an anatomically specified subgroup consisting of datasets examining the mPFC demonstrated marginally significant reduction of NAA (P=0.061). Meta-regression revealed that NAA reduction in the mPFC was positively correlated with symptom severity measured by Yale–Brown Obsessive Compulsive Scale (P=0.011). The specific reduction of NAA in the mPFC and significant relationship between neurochemical alteration in the mPFC and symptom severity indicate that the mPFC is one of the brain regions that directly related to abnormal behavior in the pathophysiology of OCD. The current meta-analysis indicates that cortices and sub-cortices contribute in different ways to the etiology of OCD.

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Section: Resultsmentioning

confidence: 99%

“…Thus, 17 studies were included in the final meta-analysis. 22, 23, 24, 26, 27, 28, 31, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43 …”

Section: Resultsmentioning

confidence: 99%

Reduction of N-acetylaspartate in the medial prefrontal cortex correlated with symptom severity in obsessive-compulsive disorder: meta-analyses of 1H-MRS studies

Aoki

Suwa

2012

Transl Psychiatry

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“…Effects of OCD on Glu or Glx were noted in prior studies in caudate, white matter, or posterior middle cingulate (Yücel et al, 2008; Whiteside et al, 2006, 2012; Rosenberg et al, 2000, 2004). Of studies of pACC or aMCC, some (Kitamura et al, 2006; Ebert et al, 1997; Sumitani et al, 2007) did not quantify Glu or Glx; others (Yalçın et al, 2011; Bédard et al, 2011; Besiroglu et al, 2011; Fan et al, 2010) expressed results as ratios (e.g., Glx/Cr). Two studies of pACC using absolute metabolites (Lázaro et al, 2012; Simpson et al, 2012) found no effects of OCD on Glx.…”

Section: Discussionmentioning

confidence: 99%

Cingulate and thalamic metabolites in obsessive-compulsive disorder

O’Neill¹,

Lai²,

Sheen³

et al. 2016

Psychiatry Research: Neuroimaging

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Focal brain metabolic effects detected by proton magnetic resonance spectroscopy (MRS) in obsessive-compulsive disorder (OCD) represent prospective indices of clinical status and guides to treatment design. Sampling bilateral pregenual anterior cingulate cortex (pACC), anterior middle cingulate cortex (aMCC), and thalamus in 40 adult patients and 16 healthy controls, we examined relationships of the neurometabolites glutamate+glutamine (Glx), creatine+phosphocreatine (Cr), and choline-compounds (Cho) with OCD diagnosis and multiple symptom types. The latter included OC core symptoms (Yale-Brown Obsessive-Compulsive Scale--YBOCS), depressive symptoms (Montgomery-Åsberg Depression Rating Scale--MADRS), and general functioning (Global Assessment Scale--GAS). pACC Glx was 9.7% higher in patients than controls. Within patients, Cr and Cho correlated negatively with YBOCS and MADRS, while Cr correlated positively with the GAS. In aMCC, Cr and Cho correlated negatively with MADRS, while Cr in thalamus correlated positively with GAS. These findings present moderate support for glutamatergic and cingulocentric perspectives on OCD. Based on our prior metabolic model of OCD, we offer one possible interpretation of these group and correlational effects as consequences of a corticothalamic state of elevated glutamatergic receptor activity alongside below-normal glutamatergic transporter activity.

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“…In a study using proton magnetic resonance spectroscopy, patients with autogenous obsessions, which do not emerge in response to identifiable external stimuli, had elevated NAA/CR ratios in the amygdala and hippocampus. This increase was not observed in the same brain regions of healthy controls or patients with reactive obsessions, a subtype of OCD in which obsessions are evoked by specific external stimuli (Besiroglu et al, 2011). In contrast, altered energy metabolism was found in the ACC, a commonly implicated brain region in the pathology of OCD, in patients with either subtype of OCD.…”

Section: Pathology Of Ocdmentioning

confidence: 93%

Mechanisms of deep brain stimulation for obsessive compulsive disorder: effects upon cells and circuits

Bourne¹,

Eckhardt²,

Sheth³

et al. 2012

Front. Integr. Neurosci.

117

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Deep brain stimulation (DBS) has emerged as a safe, effective, and reversible treatment for a number of movement disorders. This has prompted investigation of its use for other applications including psychiatric disorders. In recent years, DBS has been introduced for the treatment of obsessive compulsive disorder (OCD), which is characterized by recurrent unwanted thoughts or ideas (obsessions) and repetitive behaviors or mental acts performed in order to relieve these obsessions (compulsions). Abnormal activity in cortico-striato-thalamo-cortical (CSTC) circuits including the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), ventral striatum, and mediodorsal (MD) thalamus has been implicated in OCD. To this end a number of DBS targets including the anterior limb of the internal capsule (ALIC), ventral capsule/ventral striatum (VC/VS), ventral caudate nucleus, subthalamic nucleus (STN), and nucleus accumbens (NAc) have been investigated for the treatment of OCD. Despite its efficacy and widespread use in movement disorders, the mechanism of DBS is not fully understood, especially as it relates to psychiatric disorders. While initially thought to create a functional lesion akin to ablative procedures, it is increasingly clear that DBS may induce clinical benefit through activation of axonal fibers spanning the CSTC circuits, alteration of oscillatory activity within this network, and/or release of critical neurotransmitters. In this article we review how the use of DBS for OCD informs our understanding of both the mechanisms of DBS and the circuitry of OCD. We review the literature on DBS for OCD and discuss potential mechanisms of action at the neuronal level as well as the broader circuit level.

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The involvement of distinct neural systems in patients with obsessive–compulsive disorder with autogenous and reactive obsessions

Abstract: While disturbed energy metabolism in ACC might reflect a common pathology in patients with OCD regardless of symptom dimension, alterations in mesiotemporal lobe are more likely for autogenous obsessions.

Cited by 29 publications

References 56 publications

Reduction of N-acetylaspartate in the medial prefrontal cortex correlated with symptom severity in obsessive-compulsive disorder: meta-analyses of 1H-MRS studies

Reduction of N-acetylaspartate in the medial prefrontal cortex correlated with symptom severity in obsessive-compulsive disorder: meta-analyses of 1H-MRS studies

Cingulate and thalamic metabolites in obsessive-compulsive disorder

Mechanisms of deep brain stimulation for obsessive compulsive disorder: effects upon cells and circuits

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