Neuroscience Bulletin

, 27:215 | Cite as

Review of structural neuroimaging in patients with refractory obsessivecompulsive disorder



The notion that some special brain regions may be involved in the pathogenesis of obsessive-compulsive disorder (OCD) dates back to the beginning of the twentieth century. Structural neuroimaging studies in the past 2 decades have revealed important findings that facilitate understanding of OCD pathogenesis. Current knowledge based on functional and structural neuroimaging investigations largely emphasizes abnormalities in fronto-striatal-thalamic-cortical and orbitofronto-striato-thalamic circuits in the pathophysiology of OCD. However, these neuroimaging studies did not focus on refractory OCD. The present review mainly focused on structural neuroimaging performed in OCD, which had been ignored previously, and highlighted current evidence supporting that orbito-frontal cortex and thalamus are key brain regions, and that the hippocampus-amygdala complex is associated with refractoriness to the available treatment strategies. However, to fully reveal the neuroanatomy of refractoriness, longitudinal studies with larger samples are required.


structural neuroimaging refractory obsessive-compulsive disorder orbito-frontal cortex thalamus 



关于某些脑区参与强迫症的说法可追溯至20世纪初。 在过去20年间, 结构神经影像研究得到了很多重大发现, 大大促进了对强迫症病因的了解。 目前的功能和结构神经影像研究主要强调了额叶—纹状体—视丘—皮层和眶额—纹状体—视丘回路异常在强迫症中的作用。 然而, 难治性强迫症在研究中常常被忽略。 本综述主要回顾了强迫症结构神经影像的一些发现, 提示眶额皮层和丘脑是参与强迫症的关键区域, 而且杏仁海马复合体也与该病的难治性有关。 未来的研究只有增大样本量才能更全面地揭示难治性强迫症的神经结构学基础。


结构神经影像 难治性 强迫症 眶额皮层 丘脑 


  1. [1]
    Robins LN, Hezler JE, Orvaschel C, Anthony JC, Blazer DG, Burnham A, et al. The diagnostic interview schedule. In: Eaton WW and Kessler LG (Eds). Epidemiologic field methods in psychiatry: the NIMH epidemiologic catchment area program. Orlando: Academic Press, 1985: 143–168.Google Scholar
  2. [2]
    Whiteside SP, Port JD, Abramowitz JS. A meta-analysis of functional neuroimaging in obsessive-compulsive disorder. Psychiatry Res 2004, 132: 69–79.PubMedCrossRefGoogle Scholar
  3. [3]
    Perse T. Obsessive-compulsive disorder: a treatment review. J Clin Psychiatry 1988, 49: 48–55.PubMedGoogle Scholar
  4. [4]
    Jenike MA, Rauch SL. Managing the patient with treatment-resistant obsessive compulsive disorder: current strategies. J Clin Psychiatry 1994, 55: 11–17.PubMedGoogle Scholar
  5. [5]
    Rasmussen SA, Eisen JL. Treatment strategies for chronic and refractory obsessive-compulsive disorder. J Clin Psychiatry 1997, 58: 9–13.PubMedGoogle Scholar
  6. [6]
    Pallanti S, Hollander E, Bienstock C, Koran L, Leckman J, Marazziti D, et al. Treatment non-response in OCD: methodological issues and operational definitions. Int J Neuropsychopharmacol 2002, 5: 181–191.PubMedCrossRefGoogle Scholar
  7. [7]
    Whiteside SP, Port JD, Abramowitz JS. A meta-analysis of functional neuroimaging in obsessive-compulsive disorder. Psychiatry Res 2004, 132: 69–79.PubMedCrossRefGoogle Scholar
  8. [8]
    Baxter LR. Neuroimaging studies of obsessive-compulsive disorders. Psychiatr Clin North Am 1992, 15: 871–884.PubMedGoogle Scholar
  9. [9]
    Saxena S, Brody AL, Maidment KM, Dunkin JJ, Colgan M, Alborzian S, et al. Localized orbitofrontal and subcortical metabolic changes and predictors of response to paroxetine treatment in obsessive-compulsive disorder. Neuropsychopharmacology 1999, 21: 683–693.PubMedCrossRefGoogle Scholar
  10. [10]
    Saxena S, Bota RG, Brod AL. Brain-behavior relationships in obsessive-compulsive disorder. Semin Clin Neuropsychiatry 2001, 6: 82–101.PubMedCrossRefGoogle Scholar
  11. [11]
    Insel TR. Toward a neuroanatomy of obsessive-compulsive disorder. Arch Gen Psychiatry 1992, 49: 739–744.PubMedGoogle Scholar
  12. [12]
    Scarone S, Colombo C, Livian S, Abbruzzese M, Ronchi P, Locatelli M, et al. Increased right caudate nucleus size in obsessive-compulsive disorder: detection with magnetic resonance imaging. Psychiatr Res 1992, 45: 115–121.CrossRefGoogle Scholar
  13. [13]
    Atmaca M, Yildirim H, Ozdemir H, Aydin A, Tezcan E, Ozler S. Volumetric MRI assessment of brain regions in patients with refractory obsessive-compulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2006, 30: 1051–1057.PubMedCrossRefGoogle Scholar
  14. [14]
    Atmaca M, Yildirim H, Ozdemir H, Tezcan E, Poyraz AK. Volumetric MRI study of key brain regions implicated in obsessive-compulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2007, 31: 46–52.PubMedCrossRefGoogle Scholar
  15. [15]
    Rosenberg DR, Benazon NR, Gilbert A, Sullivan A, Moore GJ. Thalamic volume in pediatric obsessive-compulsive disorder patients before and after cognitive behavioral therapy. Biol Psychiatry 1995, 48: 294–300.CrossRefGoogle Scholar
  16. [16]
    Szeszko PR, Robinson D, Alvir JM, Bilder RM, Lencz T, Ashtari M, et al. Orbital frontal and amygdala volume reductions in obsessive-compulsive disorder. Arch Gen Psychiatry 1999, 56: 913–919.PubMedCrossRefGoogle Scholar
  17. [17]
    O’sullivan RL, Rauch SL, Breiter HC, Grachev ID, Baer L, Kennedy DN, et al. Reduced basal ganglia volumes in trichotillomania measured via morphometric magnetic resonance imaging. Biol Psychiatry 1997, 42: 39–45.PubMedCrossRefGoogle Scholar
  18. [18]
    Bartha R, Stein MB, Williamson PC, Drost DJ, Neufeld RW, Carr TJ, et al. A short echo 1H spectroscopy and volumetric MRI study of the corpus striatum in patients with obsessive-compulsive disorder and comparison subjects. Am J Psychiatry 1998, 155: 1584–1591.PubMedGoogle Scholar
  19. [19]
    Riffkin J, Yucel M, Maruff P, Wood SJ, Soulsby B, Olver J, et al. A manual and automated MRI study of anterior cingulate and orbitofrontal cortices, and caudate nucleus in obsessive-compulsive disorder: comparison with healthy controls and patients with schizophrenia. Psychiatry Res 2005, 138: 99–113.PubMedCrossRefGoogle Scholar
  20. [20]
    Pujol J, Soriano-Mas C, Alonso P, Cardoner N, Menchen JM, Deus J, et al. Mapping structural brain alterations in obsessive-compulsive disorder. Arch Gen Psychiatry 2004, 61: 720–730.PubMedCrossRefGoogle Scholar
  21. [21]
    Choi JS, Kang DH, Kim JJ, Ha TH, Lee JM, Youn T, et al. Left anterior subregion of orbitofrontal cortex volume reduction and impaired organizational strategies in obsessive-compulsive disorder. J Psychiatr Res 2004, 38: 193–199.PubMedCrossRefGoogle Scholar
  22. [22]
    Radua J, Mataix-Cols D. Voxel-wise meta-analysis of grey matter changes in obsessive-compulsive disorder. Br J Psychiatry 2009, 195: 393–402.PubMedCrossRefGoogle Scholar
  23. [23]
    Rotge JY, Guehl D, Diharreguy B, Tignol J, Bioulac B, Allard M, et al. Meta-analysis of brain volume changes in obsessive-compulsive disorder. Biol Psychiatry 2009, 65: 75–83.PubMedCrossRefGoogle Scholar
  24. [24]
    Cecconi JP, Lopes AC, Duran FL, Santos LC, Hoexter MQ, Gentil AF, et al. Gamma ventral capsulotomy for treatment of resistant obsessive-compulsive disorder: a structural MRI pilot prospective study. Neurosci Lett 2008, 447: 138–142.PubMedCrossRefGoogle Scholar
  25. [25]
    Lawrence AD, Sahakian BJ, Robbins TW. Cognitive functions and corticostriatal circuits: insights from Huntington’s disease. Trend Cogn Sci 1998, 2: 379–388.CrossRefGoogle Scholar
  26. [26]
    Phillips ML, Drevets WC, Rauch SL, Lane R. Neurobiology of emotion perception I: the neural basis of normal emotion perception. Biol Psychiatry 2003, 54: 504–514.PubMedCrossRefGoogle Scholar
  27. [27]
    McGuire PK, Bench CJ, Frith CD, Marks IM, Frackowiak RS, Dolan RJ. Functional anatomy of obsessive-compulsive phenomena. Br J Psychiatry 1994, 164: 459–468.PubMedCrossRefGoogle Scholar
  28. [28]
    Adler CM, McDonough-Ryan P, Sax KW, Holland SK, Arndt S, Strakowski SM. fMRI of neuronal activation with symptom provocation in unmedicated patients with obsessive compulsive disorder. J Psychiatr Res 2000, 34: 317–324.PubMedCrossRefGoogle Scholar
  29. [29]
    Szeszko PR, MacMillan S, McMeniman M, Lorch E, Madden R, Ivey J, et al. Amygdala volume reductions in pediatric patients with obsessive-compulsive disorder treated with paroxetine: preliminary findings. Neuropsychopharmacology 2004, 29: 826–832.PubMedCrossRefGoogle Scholar
  30. [30]
    Nagy J, Zambo K, Decsi L. Anti-anxiety action of diazepam after intra-amygdaloid application in the rat. Neuropharmacology 1979, 18: 573–576.PubMedCrossRefGoogle Scholar
  31. [31]
    Gonzalez LE, Andrews N, File SE. 5-HT1A and benzodiazepine receptors in the basolateral amygdala modulate anxiety in the social interaction test, but not in the elevated plus-maze. Brain Res 1996, 732: 145–153.PubMedCrossRefGoogle Scholar
  32. [32]
    Zangrossi H Jr, Viana MB, Graeff FG. Anxiolytic effect of intraamygdala injection of midazolam and 8-hydroxy-2-(di-n-propylamino) tetralin in the elevated T-maze. Eur J Pharmacol 1999, 369: 267–270.PubMedCrossRefGoogle Scholar
  33. [33]
    Gray JA. The neuropsychology of anxiety: An enquiry into the functions of the septo-hippocampal system. Oxford, England: Oxford University Press, 1982.Google Scholar
  34. [34]
    Pitman RK. A cybernetic model of obsessive-compulsive psychopathology. Compr Psychiatry 1987, 28: 334–343.PubMedCrossRefGoogle Scholar
  35. [35]
    Van Laere K, Nuttin B, Gabriels L, Dupont P, Rasmussen S, Greenberg BD, et al. Metabolic imaging of anterior capsular stimulation in refractory obsessive-compulsive disorder: a key role for the subgenual anterior cingulate and ventral striatum. J Nucl Med 2006, 47: 740–747.PubMedGoogle Scholar
  36. [36]
    Atmaca M, Yildirim H, Ozdemir H, Ozler S, Kara B, Ozler Z, et al. Hippocampus and amygdalar volumes in patients with refractory obsessive-compulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2008, 32: 1283–1286.PubMedCrossRefGoogle Scholar
  37. [37]
    Nuttin B, Cosyns P, Demeulemeester H, Gybels J, Meyerson B. Electrical stimulation in anterior limbs of internal capsules in patients with obsessive-compulsive disorder. Lancet 1999, 354: 1526.PubMedCrossRefGoogle Scholar
  38. [38]
    Mian MK, Campos M, Sheth SA, Eskandar EN. Deep brain stimulation for obsessive-compulsive disorder: past, present, and future. J Neurosurgery 2010, 29: 1–9.Google Scholar
  39. [39]
    Greenberg BD, George MS, Martin JD, Beniamin J, Schlaepfer TE, Altemus M, et al. Effect of prefrontal repetitive transcranial magnetic stimulation in obsessive-compulsive disorder: a preliminary study. Am J Psychiatry 1997, 154: 867–869.PubMedGoogle Scholar
  40. [40]
    Alonso P, Pujol J, Cardoner N, Benlloch L, Deus J, Menchón JM, et al. Right prefrontal repetitive transcranial magnetic stimulation in obsessive-compulsive disorder: a double blind, placebo-controlled study. Am J Psychiatry 2001, 58: 1143–1145.CrossRefGoogle Scholar
  41. [41]
    Sachdev PS, McBride R, Loo CK, Mitchell PB, Malhi GS, Croker VM. Right versus left prefrontal transcranial stimulation for obsessive-compulsive disorder: a preliminary investigation. J Clin Psychiatry 2001, 62: 981–984.PubMedCrossRefGoogle Scholar
  42. [42]
    Mantovani A, Lisanby SH, Pieraccini F, Ulivelli M, Castrogiovanni P, Rossi S. Repetitive transcranial magnetic stimulation (rTMS) in the treatment of obsessive-compulsive disorder (OCD) and Tourette’s syndrome (TS). Int J Neuropsychopharmacol 2006, 9: 95–100.PubMedCrossRefGoogle Scholar
  43. [43]
    Prasko J, Pasková B, Záleský R, Novák T, Kopecek M, Bares M, et al. The effect of repetitive transcranial magnetic stimulation (rTMS) on symptoms in obsessive-compulsive disorder: a randomized, double-blind, sham-controlled study. Neuro Endocrinol Lett 2006, 27: 327–332.PubMedGoogle Scholar
  44. [44]
    Ruffini C, Locatelli M, Lucca A, Benedetti F, Insacco C, Smeraldi E. Augmentation effect of repetitive transcranial magnetic stimulation over the orbitofrontal cortex in drug-resistant obsessive-compulsive disorder patients: A controlled investigation. Prim Care Companion J Clin Psychiatry 2009, 11: 226–230.PubMedCrossRefGoogle Scholar

Copyright information

© Shanghai Institutes for Biological Sciences, CAS and Springer-Verlag Berlin Heidelberg 2011

Authors and Affiliations

  1. 1.Department of PsychiatryFirat University School of MedicineElazigTurkey

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