Cerebral glucose metabolic in childhood-onset obsessive-compulsive disorder

Child Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892.
Archives of General Psychiatry (Impact Factor: 14.48). 07/1989; 46(6):518-23. DOI: 10.1001/archpsyc.1989.01810060038007
Source: PubMed

ABSTRACT The cerebral metabolic rate for glucose was studied in 18 adults with childhood-onset obsessive-compulsive disorder (OCD) and in age- and sex-matched controls using positron emission tomography and fludeoxyglucose F 18. Both groups were scanned during rest, with reduced auditory and visual stimulation. The group with OCD showed an increased glucose metabolism in the left orbital frontal, right sensorimotor, and bilateral prefrontal and anterior cingulate regions as compared with controls. Ratios of regional activity to mean cortical gray matter metabolism were increased for the right prefrontal and left anterior cingulate regions in the group with OCD as a whole. Correlations between glucose metabolism and clinical assessment measures showed a significant relationship between metabolic activity and both state and trait measurements of OCD and anxiety as well as the response to clomipramine hydrochloride therapy. These results are consistent with the suggestion that OCD may result from a functional disturbance in the frontal-limbic-basal ganglia system.

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    • "Numerous functional neuroimaging studies show CSTC circuit dysfunction to be a crucial pathophysiological feature of OCD (Saxena & Rauch, 2000). In individuals with OCD, hyperactivity during neutral or resting states has been observed in the key nodes in this CSTC circuitry, which include the OFC, ACC, and striatum (e.g., Nordahl et al., 1989; Swedo et al., 1989), which is heightened during the symptom provocation paradigm (e.g., Adler et al., 2000; Breiter et al., 1996). Despite recent studies identifying the importance of a variety of brain areas underlying OCD such as the amygdala (van den Heuvel et al., 2004) and the hippocampus (Kwon et al., 2003), among other areas, the predominant research focus is on the CSTC circuit (Brennan et al., 2013). "
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    ABSTRACT: This article will explore recent studies that have identified alterations in brain regions in individuals with obsessive–compulsive disorder (OCD). Specifically, alterations have been found in the cortical surface anatomy, the white matter, the gray matter, the cerebellum, the olfactory-processing structures, the temporal lobe, the prefrontal cortex, and the amygdala. Although some emerging data implicate these brain regions in OCD, the cortico–striatal–thalamic–cortical circuitry remains the prime focus of research. This article will also give an overview of studies that have found different symptom dimensions in individuals with OCD to have distinct neural correlates.
    Brain Mapping An Encyclopedic Reference, Edited by Editor-in-Chief: Arthur W. Toga, 02/2015: chapter Volume 3: Social Cognitive Neuroscience, Cognitive Neuroscience, Clinical Brain Mapping: pages Pages 993–1000; Elsevier Inc.., ISBN: ISBN: 978-0-12-397316-0
    • "To further elucidate the functional and neurochemical abnormalities in the rACC in OCD, we combined an fMRI probe of rACC function, the emotional counting Stroop paradigm (ecStroop) (Whalen et al, 1998), with J-resolved 1 H-MRS to measure rACC Glu and Gln levels in patients with OCD versus individuals without OCD. Given evidence of ACC hyperactivation in OCD from studies using functional neuroimaging both at rest (Baxter et al, 1987; Machlin et al, 1991; Perani et al, 1995; Swedo et al, 1989) and "
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    ABSTRACT: The anterior cingulate cortex is implicated in the neurobiology of obsessive-compulsive disorder (OCD). However, few studies have examined functional and neurochemical abnormalities specifically in the rostral subdivision of the ACC (rACC) in OCD patients. We used functional magnetic resonance imaging (fMRI) during an emotional counting Stroop task and single-voxel J-resolved proton magnetic resonance spectroscopy ((1)H-MRS) in the rACC to examine the function and neurochemistry of the rACC in individuals with OCD and comparison individuals without OCD. Between-group differences in rACC activation and glutamine/glutamate ratio (Gln/Glu), Glu, and Gln levels as well as associations between rACC activation, Gln/Glu, Glu, Gln, behavioral, and clinical measures were examined using linear regression. In a sample of 30 participants with OCD and 29 age- and sex-matched participants without OCD, participants with OCD displayed significantly reduced rACC deactivation compared to those without OCD in response to OCD-specific words versus neutral words on the emotional counting Stroop task. However, Gln/Glu, Glu, and Gln in the rACC did not differ between groups nor was there an association between reduced rACC deactivation and Gln/Glu, Glu, or Gln in the OCD group. Taken together, these findings strengthen the evidence for rACC dysfunction in OCD, but weigh against an underlying association with abnormal rACC glutamatergic neurotransmission.Neuropsychopharmacology accepted article preview online, 09 February 2015. doi:10.1038/npp.2015.36.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 02/2015; 40(8). DOI:10.1038/npp.2015.36 · 7.05 Impact Factor
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    • "Convergent experimental evidence from neuroimaging and neuropsychological studies associated the orbitofrontal cortex (OFC), the anterior cingulate cortex (ACC), and basal ganglia (BG) with the pathophysiology of OCD. PET studies at rest and PET/fMRI studies during symptom provocation consistently found hypermetabolism in these brain regions [Baxter et al., 1987, 1988, 1990; Rauch et al., 1994; Simon et al., 2010; Swedo et al., 1989]. These findings suggested dysfunctional cortico-striato-thalamo-cortical (CSTC) pathways to be involved in this disorder which led to the formulation of a fronto-striatal model of OCD [Chamberlain et al., 2008; Menzies et al., 2008; Saxena et al., 1999; Saxena et al., 1998; Saxena and Rauch, 2000]. "
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    ABSTRACT: Obsessive-compulsive disorder (OCD) is characterized by recurrent intrusive thoughts and ritualized, repetitive behaviors, or mental acts. Convergent experimental evidence from neuroimaging and neuropsychological studies supports an orbitofronto-striato-thalamo-cortical dysfunction in OCD. Moreover, an over excitability of the amygdala and over monitoring of thoughts and actions involving the anterior cingulate, frontal and parietal cortex has been proposed as aspects of pathophysiology in OCD. We chose a data driven, graph theoretical approach to investigate brain network organization in 17 unmedicated OCD patients and 19 controls using resting-state fMRI. OCD patients showed a decreased connectivity of the limbic network to several other brain networks: the basal ganglia network, the default mode network, and the executive/attention network. The connectivity within the limbic network was also found to be decreased in OCD patients compared to healthy controls. Furthermore, we found a stronger connectivity of brain regions within the executive/attention network in OCD patients. This effect was positively correlated with disease severity. The decreased connectivity of limbic regions (amygdala, hippocampus) may be related to several neurocognitive deficits observed in OCD patients involving implicit learning, emotion processing and expectation, and processing of reward and punishment. Limbic disconnection from fronto-parietal regions relevant for (re)-appraisal may explain why intrusive thoughts become and/or remain threatening to patients but not to healthy subjects. Hyperconnectivity within the executive/attention network might be related to OCD symptoms such as excessive monitoring of thoughts and behavior as a dysfunctional strategy to cope with threat and uncertainty. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 11/2014; 35(11). DOI:10.1002/hbm.22574 · 5.97 Impact Factor
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