Local Cerebral Glucose Metabolic Rates in Obsessive-Compulsive Disorder

Benkelfat, Chawki; Nordahl, Thomas E.; Semple, William E.; King, Anna C.; Murphy, Dennis L.; Cohen, Robert M.

doi:10.1001/archpsyc.1990.01810210048007

Cited by 383 publications

(153 citation statements)

References 41 publications

(7 reference statements)

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“…36,37 Taken together, the results of these studies suggest that reduction of thalamic activity, and a resultant decrease in thalamocortical excitation, 18 may represent a final common pathway to response to a variety of different treatments in nondepressed OCD patients. 19,38 As in many prior studies, 5,[8][9][10]12,17,36 the magnitude of change in thalamic metabolism did not correlate with the degree of response of OCD symptoms to intensive CBT. This suggests that while decreasing thalamic activity may be a marker of response to treatment in OCD it is not specifically related to the extent of symptom improvement.…”

Section: Discussionsupporting

confidence: 47%

“…Thus, decreasing cingulate activity may sometimes be associated with improvement in OCD symptoms but does not appear to be a necessary mechanism of action for treatment response. Instead, the functional changes most strongly associated with treatment response in OCD are decreases in activity in the right OFC, 8,[10][11][12][13]36,37,42,43 right caudate 9,11,12,14,16,17,36,37,42 and thalamus. 9,11,15,36,37 In contrast to the effects of pharmacotherapy on brain function, enhancement of dACC activity may be a primary mechanism of action of CBT for OCD.…”

Section: Discussionmentioning

confidence: 99%

“…Functional brain imaging studies of patients with obsessive-compulsive disorder (OCD) have repeatedly found elevated cerebral glucose metabolism and blood flow in the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), basal ganglia and thalamus [1][2][3][4][5][6][7] that decrease with response to treatment with serotonin reuptake inhibitor (SRI) medications 5,[8][9][10][11][12][13][14][15] or cognitive-behavioral therapy (CBT). 9,16,17 These findings and others have led to the theory that the symptomatic expression of OCD is mediated by hyperactivity along frontal-subcortical circuits connecting the OFC, caudate, globus pallidus and the medial dorsal nucleus of the thalamus.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Rapid effects of brief intensive cognitive-behavioral therapy on brain glucose metabolism in obsessive-compulsive disorder

Saxena

Gorbis²,

O’Neill³

et al. 2008

Mol Psychiatry

124

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Brief intensive cognitive-behavioral therapy (CBT) using exposure and response prevention significantly improves obsessive-compulsive disorder (OCD) symptoms in as little as 4 weeks. However, it has been thought that much longer treatment was needed to produce the changes in brain function seen in neuroimaging studies of OCD. We sought to elucidate the brain mediation of response to brief intensive CBT for OCD and determine whether this treatment could induce functional brain changes previously seen after longer trials of pharmacotherapy or standard CBT. [ 18 F]-fluorodeoxyglucose positron emission tomography brain scans were obtained on 10 OCD patients before and after 4 weeks of intensive individual CBT. Twelve normal controls were scanned twice, several weeks apart, without treatment. Regional glucose metabolic changes were compared between groups. OCD symptoms, depression, anxiety and overall functioning improved robustly with treatment. Significant changes in normalized regional glucose metabolism were seen after brief intensive CBT (P = 0.04). Compared to controls, OCD patients showed significant bilateral decreases in normalized thalamic metabolism with intensive CBT but had a significant increase in right dorsal anterior cingulate cortex activity that correlated strongly with the degree of improvement in OCD symptoms (P = 0.02). The rapid response of OCD to intensive CBT is mediated by a distinct pattern of changes in regional brain function. Reduction of thalamic activity may be a final common pathway for improvement in OCD, but response to intensive CBT may require activation of dorsal anterior cingulate cortex, a region involved in reappraisal and suppression of negative emotions.

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Section: Discussionsupporting

confidence: 47%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Rapid effects of brief intensive cognitive-behavioral therapy on brain glucose metabolism in obsessive-compulsive disorder

Saxena

Gorbis²,

O’Neill³

et al. 2008

Mol Psychiatry

124

View full text Add to dashboard Cite

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“…Baxter et al 48,53 observed a relation between decreased metabolic activity of the caudate nucleus and improvement of symptoms after treatment, and showed later that this decrease in metabolic activity of the head of the caudate nucleus occurred not only after pharmacologic treatment, but also after behavioral psychotherapeutic treatment. Benkelfat et al 54 found a decrease of metabolism of the left caudate after treatment with clomipramine. Swedo et al 55 , also assessing patients pre-and post-treatment, showed a correlation between an increase in activity in the right orbitofrontal region and improvement in symptoms after drug therapy.…”

Section: The Basal Ganglia and The Pathophysiology Of Ocdmentioning

confidence: 97%

Relationship between obsessive-compulsive disorders and diseases affecting primarily the basal ganglia

et al. 1999

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Obsessive-compulsive disorder (OCD) has been reported in association with some neurological diseases that affect the basal ganglia such as Tourette's syndrome, Sydenham's chorea, Parkinson's disease, and Huntington's disease. Furthermore, studies such as neuroimaging, suggest a role of the basal ganglia in the pathophysiology of OCD. The aim of this paper is to describe the association of OCD and several neurologic disorders affecting the basal ganglia, report the existing evidences of the role of the basal ganglia in the pathophysiology of OCD, and analyze the mechanisms probably involved in this pathophysiology.

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“…In parallel, the results of neuroimaging studies in OCD patients have implicated dysfunction of the OFC and of the striatum in the pathophysiology of OCD (for review see Saxena et al, 1998;Stein, 2000). The metabolic activity of these two regions was found to be higher in OCD patients compared to healthy controls, to increase during symptom provocation, and to decrease after a successful treatment with selective serotonin reuptake inhibitors (SSRIs; Baxter et al, 1992;Benkelfat et al, 1990;Breiter et al, 1996;Cottraux et al, 1996;Insel, 1992;McGuire et al, 1994;Rauch et al, 1994;Saxena et al, 1999;Swedo et al, 1992). Although the serotonergic system, the OFC, and the striatum are interconnected, the specific abnormality of these regions, as well as the ways in which they interact to produce obsessions and compulsions, is unknown.…”

Section: Introductionmentioning

confidence: 99%

The Role of the Striatum in Compulsive Behavior in Intact and Orbitofrontal-Cortex-Lesioned Rats: Possible Involvement of the Serotonergic System

Schilman

Klavir

Winter

et al. 2010

Neuropsychopharmacol

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In the signal attenuation rat model of obsessive-compulsive disorder (OCD), 'compulsive' behavior is induced by attenuating a signal indicating that a lever-press response was effective in producing food. We have recently found that lesions to the rat orbitofrontal cortex (OFC) led to an increase in compulsive lever-pressing that was prevented by systemic administration of the selective serotonin reuptake inhibitor paroxetine, and paralleled by an increase in the density of the striatal serotonin transporter. This study further explored the interaction between the OFC, the striatum, and the serotonergic system in the production of compulsive lever-pressing. Experiment 1 revealed that OFC lesions decrease the content of serotonin, dopamine, glutamate, and GABA in the striatum. Experiment 2 showed that intrastriatal administration of paroxetine blocked OFC lesion-induced increased compulsivity, but did not affect compulsive responding in intact rats. Experiments 3 and 4 found that pre-training striatal lesions had no effect on compulsive lever-pressing, whereas post-training striatal inactivation exerted an anticompulsive effect. These results strongly implicate the striatum in the expression of compulsive lever-pressing in both intact and OFC-lesioned rats. Furthermore, the results support the possibility that in a subpopulation of OCD patients a primary pathology of the OFC leads to a dysregulation of the striatal serotonergic system, which is manifested in compulsive behavior, and that antiobsessional/anticompulsive drugs exerts their effects, in these patients, by normalizing the dysfunctional striatal serotonergic system.

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Local Cerebral Glucose Metabolic Rates in Obsessive-Compulsive Disorder

Cited by 383 publications

References 41 publications

Rapid effects of brief intensive cognitive-behavioral therapy on brain glucose metabolism in obsessive-compulsive disorder

Rapid effects of brief intensive cognitive-behavioral therapy on brain glucose metabolism in obsessive-compulsive disorder

Relationship between obsessive-compulsive disorders and diseases affecting primarily the basal ganglia

The Role of the Striatum in Compulsive Behavior in Intact and Orbitofrontal-Cortex-Lesioned Rats: Possible Involvement of the Serotonergic System

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