Hostname: page-component-586b7cd67f-2plfb Total loading time: 0 Render date: 2024-11-24T22:52:55.088Z Has data issue: false hasContentIssue false

Frontostriatal activation in patients with obsessive–compulsive disorder before and after cognitive behavioral therapy

Published online by Cambridge University Press:  18 March 2010

T. Freyer
Affiliation:
Department of Psychiatry and Psychotherapy, University Medical Center, Albert-Ludwigs-University Freiburg, Germany
S. Klöppel
Affiliation:
Department of Psychiatry and Psychotherapy, University Medical Center, Albert-Ludwigs-University Freiburg, Germany
O. Tüscher
Affiliation:
Department of Neurology, University Medical Center, Albert-Ludwigs-University Freiburg, Germany
A. Kordon
Affiliation:
Department of Psychiatry and Psychotherapy, University of Luebeck, Germany
B. Zurowski
Affiliation:
Department of Psychiatry and Psychotherapy, University of Luebeck, Germany
A.-K. Kuelz
Affiliation:
Department of Psychiatry and Psychotherapy, University Medical Center, Albert-Ludwigs-University Freiburg, Germany
O. Speck
Affiliation:
Department of Biomedical Magnetic Resonance, Institute for Experimental Physics, Otto-von-Guericke-University Magdeburg, Germany
V. Glauche
Affiliation:
Department of Neurology, University Medical Center, Albert-Ludwigs-University Freiburg, Germany
U. Voderholzer*
Affiliation:
Department of Psychiatry and Psychotherapy, University Medical Center, Albert-Ludwigs-University Freiburg, Germany Medical-Psychosomatic Hospital Roseneck, Prien, Germany
*
*Address for correspondence: Professor U. Voderholzer, M.D., Medical-Psychosomatic Clinic, Roseneck, Germany. (Email: [email protected])

Abstract

Background

Cognitive behavioral therapy (CBT) with exposure and response prevention (ERP) is the psychotherapeutic treatment of choice for obsessive–compulsive disorder (OCD). However, little is known about the impact of CBT on frontostriatal dysfunctioning, known to be the neuronal correlate of OCD.

Method

A probabilistic reversal learning (RL) task probing adaptive strategy switching capabilities was used in 10 unmedicated patients with OCD and 10 healthy controls during an event-related functional magnetic resonance imaging (fMRI) experiment. Patients were scanned before and after intensive CBT, controls twice at comparable intervals.

Results

Strategy change within the RL task involved activity in a broad frontal network in patients and controls. No significant differences between the groups or in group by time interactions were detected in a whole-brain analysis corrected for multiple comparisons. However, a reanalysis with a more lenient threshold revealed decreased responsiveness of the orbitofrontal cortex and right putamen during strategy change before treatment in patients compared with healthy subjects. A group by time effect was found in the caudate nucleus, demonstrating increased activity for patients over the course of time. Patients with greater clinical improvement, reflected by greater reductions in Yale–Brown Obsessive Compulsive Scale (YBOCS) scores, showed more stable activation in the pallidum.

Conclusions

Although these findings are preliminary and need to be replicated in larger samples, they indicate a possible influence of psychotherapy on brain activity in core regions that have been shown to be directly involved both in acquisition of behavioral rules and stereotypes and in the pathophysiology of OCD, the caudate nucleus and the pallidum.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2010

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Abramowitz, JS (2006). The psychological treatment of obsessive-compulsive disorder. Canadian Journal of Psychiatry 51, 407416.CrossRefGoogle ScholarPubMed
Baxter, LR Jr., Phelps, ME, Mazziotta, JC, Guze, BH, Schwartz, JM, Selin, CE (1987). Local cerebral glucose metabolic rates in obsessive-compulsive disorder. A comparison with rates in unipolar depression and in normal controls. Archives of General Psychiatry 44, 211218.CrossRefGoogle ScholarPubMed
Baxter, LR Jr., Schwartz, JM, Bergman, KS, Szuba, MP, Guze, BH, Mazziotta, JC, Alazraki, A, Selin, CE, Ferng, HK, Munford, P, Phelps, ME (1992). Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive-compulsive disorder. Archives of General Psychiatry 49, 681689.CrossRefGoogle ScholarPubMed
Chamberlain, SR, Menzies, L, Hampshire, A, Suckling, J, Fineberg, NA, del Campo, N, Aitken, M, Craig, K, Owen, AM, Bullmore, ET, Robbins, TW, Sahakian, BJ (2008). Orbitofrontal dysfunction in patients with obsessive-compulsive disorder and their unaffected relatives. Science 321, 421422.CrossRefGoogle ScholarPubMed
Clarke, HF, Robbins, TW, Roberts, AC (2008). Lesions of the medial striatum in monkeys produce perseverative impairments during reversal learning similar to those produced by lesions of the orbitofrontal cortex. Journal of Neuroscience 28, 1097210982.CrossRefGoogle ScholarPubMed
Clarke, HF, Walker, SC, Dalley, JW, Robbins, TW, Roberts, AC (2007). Cognitive inflexibility after prefrontal serotonin depletion is behaviorally and neurochemically specific. Cerebral Cortex 17, 1827.CrossRefGoogle ScholarPubMed
Cools, R, Clark, L, Owen, AM, Robbins, TW (2002). Defining the neural mechanisms of probabilistic reversal learning using event-related functional magnetic resonance imaging. Journal of Neuroscience 22, 45634567.CrossRefGoogle ScholarPubMed
DeRubeis, RJ, Siegle, GJ, Hollon, SD (2008). Cognitive therapy versus medication for depression: treatment outcomes and neural mechanisms. Nature Reviews Neuroscience 9, 788796.CrossRefGoogle ScholarPubMed
Foa, EB, Liebowitz, MR, Kozak, MJ, Davies, S, Campeas, R, Franklin, ME, Huppert, JD, Kjernisted, K, Rowan, V, Schmidt, AB, Simpson, HB, Tu, X (2005). Randomized, placebo-controlled trial of exposure and ritual prevention, clomipramine, and their combination in the treatment of obsessive-compulsive disorder. American Journal of Psychiatry 162, 151161.CrossRefGoogle ScholarPubMed
Frank, MJ, Claus, ED (2006). Anatomy of a decision: striato-orbitofrontal interactions in reinforcement learning, decision making, and reversal. Psychological Review 113, 300326.CrossRefGoogle ScholarPubMed
Freyer, T, Valerius, G, Kuelz, AK, Speck, O, Glauche, V, Hull, M, Voderholzer, U (2009). Test–retest reliability of event-related functional MRI in a probabilistic reversal learning task. Psychiatry Research: Neuroimaging 174, 4046.CrossRefGoogle Scholar
Friston, KJ, Frith, CD, Turner, R, Frackowiak, RS (1995). Characterizing evoked hemodynamics with fMRI. NeuroImage 2, 157165.CrossRefGoogle ScholarPubMed
Goodman, WK, Price, LH, Rasmussen, SA, Mazure, C, Fleischmann, RL, Hill, CL, Heninger, GR, Charney, DS (1989). The Yale-Brown Obsessive Compulsive Scale. I. Development, use, and reliability. Archives of General Psychiatry 46, 10061011.CrossRefGoogle ScholarPubMed
Gottfried, JA, Smith, AP, Rugg, MD, Dolan, RJ (2004). Remembrance of odors past: human olfactory cortex in cross-modal recognition memory. Neuron 42, 687695.CrossRefGoogle ScholarPubMed
Hamilton, M (1960). A rating scale for depression. Journal of Neurology, Neurosurgery and Psychiatry 23, 5662.CrossRefGoogle ScholarPubMed
Hohagen, F, Winkelmann, G, Rasche-Ruchle, H, Hand, I, Konig, A, Munchau, N, Hiss, H, Geiger-Kabisch, C, Kappler, C, Schramm, P, Rey, E, Aldenhoff, J, Berger, M (1998). Combination of behaviour therapy with fluvoxamine in comparison with behaviour therapy and placebo. Results of a multicentre study. British Journal of Psychiatry. Supplement 35, 7178.CrossRefGoogle Scholar
Ho Pian, KL, van Megen, HJ, Ramsey, NF, Mandl, R, van Rijk, PP, Wynne, HJ, Westenberg, HG (2005). Decreased thalamic blood flow in obsessive-compulsive disorder patients responding to fluvoxamine. Psychiatry Research 138, 8997.CrossRefGoogle ScholarPubMed
Huey, ED, Zahn, R, Krueger, F, Moll, J, Kapogiannis, D, Wassermann, EM, Grafman, J (2008). A psychological and neuroanatomical model of obsessive-compulsive disorder. Journal of Neuropsychiatry and Clinical Neuroscience 20, 390408.CrossRefGoogle ScholarPubMed
Linden, DE (2006). How psychotherapy changes the brain – the contribution of functional neuroimaging. Molecular Psychiatry 11, 528538.CrossRefGoogle ScholarPubMed
Maia, TV, Cooney, RE, Peterson, BS (2008). The neural bases of obsessive-compulsive disorder in children and adults. Development and Psychopathology 20, 12511283.CrossRefGoogle ScholarPubMed
Menzies, L, Chamberlain, SR, Laird, AR, Thelen, SM, Sahakian, BJ, Bullmore, ET (2008). Integrating evidence from neuroimaging and neuropsychological studies of obsessive-compulsive disorder: the orbitofronto-striatal model revisited. Neuroscience and Biobehavioral Reviews 32, 525549.CrossRefGoogle ScholarPubMed
Nabeyama, M, Nakagawa, A, Yoshiura, T, Nakao, T, Nakatani, E, Togao, O, Yoshizato, C, Yoshioka, K, Tomita, M, Kanba, S (2008). Functional MRI study of brain activation alterations in patients with obsessive-compulsive disorder after symptom improvement. Psychiatry Research 163, 236247.CrossRefGoogle ScholarPubMed
Nakao, T, Nakagawa, A, Yoshiura, T, Nakatani, E, Nabeyama, M, Yoshizato, C, Kudoh, A, Tada, K, Yoshioka, K, Kawamoto, M, Togao, O, Kanba, S (2005). Brain activation of patients with obsessive-compulsive disorder during neuropsychological and symptom provocation tasks before and after symptom improvement: a functional magnetic resonance imaging study. Biological Psychiatry 57, 901910.CrossRefGoogle ScholarPubMed
Nakatani, E, Nakgawa, A, Ohara, Y, Goto, S, Uozumi, N, Iwakiri, M, Yamamoto, Y, Motomura, K, Iikura, Y, Yamagami, T (2003). Effects of behavior therapy on regional cerebral blood flow in obsessive-compulsive disorder. Psychiatry Research 124, 113120.CrossRefGoogle ScholarPubMed
Remijnse, PL, Nielen, MM, van Balkom, AJ, Cath, DC, van Oppen, P, Uylings, HB, Veltman, DJ (2006). Reduced orbitofrontal-striatal activity on a reversal learning task in obsessive-compulsive disorder. Archives of General Psychiatry 63, 12251236.CrossRefGoogle ScholarPubMed
Remijnse, PL, Nielen, MM, van Balkom, AJ, Hendriks, GJ, Hoogendijk, WJ, Uylings, HB, Veltman, DJ (2009). Differential frontal-striatal and paralimbic activity during reversal learning in major depressive disorder and obsessive-compulsive disorder. Psychological Medicine 39, 15031518.CrossRefGoogle ScholarPubMed
Saxena, S, Brody, AL, Maidment, KM, Dunkin, JJ, Colgan, M, Alborzian, S, Phelps, ME, Baxter, LR (1999). Localized orbitofrontal and subcortical metabolic changes and predictors of response to paroxetine treatment in obsessive-compulsive disorder. Neuropsychopharmacology 21, 683693.CrossRefGoogle ScholarPubMed
Schwartz, JM, Stoessel, PW, Baxter, LR Jr., Martin, KM, Phelps, ME (1996). Systematic changes in cerebral glucose metabolic rate after successful behavior modification treatment of obsessive-compulsive disorder. Archives of General Psychiatry 53, 109113.CrossRefGoogle ScholarPubMed
Valerius, G, Lumpp, A, Kuelz, AK, Freyer, T, Voderholzer, U (2008). Reversal learning as a neuropsychological indicator for the neuropathology of obsessive compulsive disorder? A behavioral study. Journal of Neuropsychiatry and Clinical Neuroscience 20, 210218.CrossRefGoogle ScholarPubMed
van den Heuvel, OA, Veltman, DJ, Groenewegen, HJ, Cath, DC, van Balkom, AJ, van Hartskamp, J, Barkhof, F, van Dyck, R (2005). Frontal-striatal dysfunction during planning in obsessive-compulsive disorder. Archives of General Psychiatry 62, 301309.CrossRefGoogle ScholarPubMed
Whiteside, SP, Port, JD, Abramowitz, JS (2004). A meta-analysis of functional neuroimaging in obsessive-compulsive disorder. Psychiatry Research 132, 6979.CrossRefGoogle ScholarPubMed