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: 13.75). 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
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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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    Human Brain Mapping 11/2014; 35(11). DOI:10.1002/hbm.22574 · 6.92 Impact Factor
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    • "Accordingly, as shown in Fig. 4, the typical patterns of stimulation processing in the Apprehension Type of anxiety are associated with (a) reduced attentional control and related impaired effectiveness of stimulation processing and avoidance of threatening stimuli (in clinical and nonclinical groups and trait anxiety); (b) reduction in autonomic reactivity; (c) impairment/inhibition of emotional processing, both on an attentional and physiological level; and (d) left-hemisphere involvement in processing stimulation (cf. Baxter et al., 1987; Borkovec, Ray, & Stober, 1998; Eysenck, 2006; Fletcher & Henson, 2001; Hoehn-Saric, MacLeod, & Zimmerli, 1989; Hofmann et al., 2005; Laguna, Ham, Hope, & Bell, 2004; Nitschke & Heller, 2002; Stober, 1998; Swedo et al., 1989; Thayer, Friedman, & Borkovec, 1996; Tucker, Antes, Stenslie, & Barnhardt, 1978; Wagner, 1999; Wu et al., 1991). It seems probable that the role of anxiety in direct modulation of stimulation processing is associated with specific patterns of stimulation processing formed by dominant controlling functions. "
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