Psychiatric Annals

CME 

Outcomes with Neuromodulation in Obsessive-Compulsive Disorder

Stefano Pallanti, MD, PhD; Anna Marras, MSc; Giacomo Grassi, MD

Abstract

Neuromodulation is a new approach for mental disorders resistant to usual treatment that is network pathway-oriented and involves the use of several devices. It represents a promising tool in the quest for “precision medicine” and is aligned with the National Institute of Mental Health’s research domain criteria-based approach for the treatment of brain diseases. In this article, we review currently available data on neuromodulation approaches for obsessive-compulsive disorder (OCD). These approaches are repetitive transcranial magnetic stimulation, deep transcranial magnetic stimulation, and deep brain stimulation (DBS). DBS and, to a lesser degree, transcranial magnetic stimulation, seem to be promising tools for the treatment of resistant and refractory OCD. However, they both remain experimental, and further studies clarifying their long-term outcome and safety are needed. Biomarkers, more precise definitions, and response predictors are also needed and continue to be works-in-progress. [Psychiatr Ann. 2015;45(6):316–320.]


Abstract

Neuromodulation is a new approach for mental disorders resistant to usual treatment that is network pathway-oriented and involves the use of several devices. It represents a promising tool in the quest for “precision medicine” and is aligned with the National Institute of Mental Health’s research domain criteria-based approach for the treatment of brain diseases. In this article, we review currently available data on neuromodulation approaches for obsessive-compulsive disorder (OCD). These approaches are repetitive transcranial magnetic stimulation, deep transcranial magnetic stimulation, and deep brain stimulation (DBS). DBS and, to a lesser degree, transcranial magnetic stimulation, seem to be promising tools for the treatment of resistant and refractory OCD. However, they both remain experimental, and further studies clarifying their long-term outcome and safety are needed. Biomarkers, more precise definitions, and response predictors are also needed and continue to be works-in-progress. [Psychiatr Ann. 2015;45(6):316–320.]


Obsessive-compulsive disorder (OCD) is a pervasive and often chronic disorder associated with significant impairment of quality of life and social relationships. It has a lifetime prevalence of 1% to 3% in the general population.1

Structural and functional neuroimaging research has shown that the pathophysiology of OCD is associated with dysfunction of the orbitofronto-striato-pallido-thalamic circuitry, including several prefrontal and subcortical areas.2 More recently, the thinking about the neurobiology of OCD has shifted from the paradigm that it involves amygdala dysfunction in the prefrontal cortex to one that involves accumbens dysfunction in the prefrontal cortex.3 Part of the reason for this shift is that although anxiety is a core feature of OCD, several studies have shown that OCD patients exhibit a dysfunction in reward circuitry.4 Therefore, OCD and related conditions are now in their own section in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5).5

This network dysfunctions-based approach is a central objective of the National Institute of Mental Health’s research domain criteria (RDoC) project: Its ultimate goal is “precision medicine” for psychiatry, or, in other words, a diagnostic refinement based on a deeper understanding of the circuitries and networks of psychiatric disorders considered to be brain diseases.6

In this article, we review current data on neuromodulation approaches for OCD, focusing on deep brain stimulation (DBS), repetitive transcranial magnetic stimulation (rTMS), and deep transcranial magnetic stimulation (dTMS). These approaches are all being studied, and are also being used clinically in treatment-resistant OCD in some health care centers.

Neuromodulation Techniques for OCD

Resistance to usual treatments (40%–60% of OCD patients)7 has resulted in the search for effective, efficient, and safe treatment alternatives. Neuromodulation techniques have emerged as alternative treatments for refractory OCD because they have substantial advantages compared to ablative surgery. For example, neuromodulation techniques are adjustable, less invasive, and reversible.8

Deep Brain Stimulation

DBS is an approved therapy for movement disorders (dystonia, essential tremor, and Parkinson’s disease) that has been recently investigated in the treatment of refractory OCD. The first report of its use in OCD was in 1999.9 Although it is an invasive technique and not currently fully approved by the US Food and Drug Administration (it has a humanitarian device exemption in OCD), DBS has two main advantages: reversibility and adjustability.

Use of Deep Brain Stimulation in OCD

The rationale for DBS in OCD involves the hyperactivity and hyperconnectivity within the cortico-striatum-thalamus-cortical circuit (CSTC).10 Therefore, five different regions that are hypothesized to be components of this circuitry2 have been tested as DBS targets in OCD: anterior limb of the internal capsule, nucleus accumbens (NAc), ventral capsule/ventral striatum, subthalamic nucleus (STN), and the inferior thalamic peduncle. Although the exact mechanism of DBS is unknown, it is hypothesized that DBS functionally overrides and modulates pathologic hyperactivity in disturbed networks.

Results obtained from 25 studies targeting the aforementioned five brain regions11 (Table 1) show high response rates for DBS treatment (approximately 50%), which appear to be similar for different target structures. This is consistent with the notion of a generalized dysfunction, particularly a hyperactivity, of the CSTC circuit that may be partially restored by targeting any of its components. This seems to be the case at least for the bilateral DBS of the NaC. Indeed, Figee et al.10 showed that this stimulation reduces hyperconnectivity while restoring the normal fronto-striatal connectivity in DBS-treated patients.

Deep Brain Stimulation Outcomes in Obsessive-Compulsive Disorder

Table 1.

Deep Brain Stimulation Outcomes in Obsessive-Compulsive Disorder

More recently, the Congress of Neurological Surgeons12 endorsed specific guidelines for DBS in OCD, classifying both levels of evidence and levels of recommendation. Only one study was classified as level I,13 providing evidence for the use of bilateral STN DBS. Two level II studies were included in this segment,14,15 and the latter provided level II evidence for the use of bilateral NaC DBS. Finally, three studies met criteria for level III.16–18 These results led the authors to conclude that there is insufficient evidence to make a recommendation for the use of unilateral DBS.

Transcranial Magnetic Stimulation

TMS is a noninvasive neuromodulation technique that is able to modulate cortical and subcortical function with the use of rapidly changing electromagnetic fields generated by a coil placed over the scalp. It has effects on brain plasticity, as documented by long-term potentiation and long-term depression at the cortical level.19

rTMS can either decrease or increase cortical excitability in relatively focal areas, with frequencies <1 Hz (low frequency rTMS) usually being inhibitory and frequencies >5 Hz (high-frequency rTMS) usually being excitatory.20 dTMS is a protocol of stimulation administered with a greater intracranial penetration coil that is able to reach deep limbic areas.

Use of Transcranial Magnetic Stimulation in OCD

rTMS has been employed in refractory OCD using both low-frequency and high-frequency stimulation. rTMS in OCD targets three main brain regions: the dorsolateral prefrontal cortex (DLPFC), the orbitofrontal cortex (OFC), and the supplementary motor area (SMA). The rationale of DLPFC stimulation is that this area may be a starting point to induce remote stimulation of regions involved in OCD, such as the anterior cingulate and OFC, that cannot be directly stimulated with current rTMS techniques.21 Only a few OFC trials have been conducted to date.22,23 The rationale for targeting this area is that OCD symptoms are associated with increased OFC activity and mediated by hyperactivity in orbito-frontal-subcortical circuits due to an imbalance of tone between direct and indirect striato-pallidal pathways.24 A combined positron emission tomography rTMS study25 clarified some neurobiologic effects of rTMS, such as focal dopamine changes in the ipsilateral anterior cingulate cortex and medial orbitofrontal cortex following DLPFC rTMS.

The SMA has been recently proposed as target area, with the rationale that premotor area hyperactivity (such as in SMA and dorsal anterior cingulate) is probably related to deficient inhibitory control.26 SMA dysfunction has been proposed as part of a candidate endophenotype of OCD because it has been proven to be hyperactive during response inhibition tasks.27

Recently, a meta-analysis assessing the efficacy of rTMS for OCD in 10 randomized-controlled trials (n = 282) showed a significant difference in outcome for active rTMS, with a 35% response rate versus a 13% response rate for sham intervention (odds ratio = 3.4, P = .002). Furthermore, protocols targeting the OFC or SMA appeared to be more effective compared to protocols that targeted the DLPFC28 (Table 2 and Table 3). This could be explained by the ability of rTMS to induce normalization of the hyperactivity of the OFC and SMA, which underlies deficient inhibition of irrelevant information and response control. This results in improved ability of OCD patients to inhibit intrusive thoughts, impulses, images, and repetitive motor responses.22,29 The clinical improvement seems to be correlated with the inhibitory effect of low-frequency rTMS on cortical excitability.30

rTMS Outcomes in Obsessive-Compulsive Disorder

Table 2.

rTMS Outcomes in Obsessive-Compulsive Disorder

dTMS Outcomes in Obsessive-Compulsive Disorder

Table 3.

dTMS Outcomes in Obsessive-Compulsive Disorder

However, these data are limited by the small sample sizes and by the heterogeneity of demographic/clinical variables (eg, degree of treatment resistance, response criteria), as well as by stimulation parameters.

Unanswered Questions and Future Research

Although promising, the neuromodulation techniques, including TMS and DBS, are still considered experimental in the treatment of refractory OCD.31

The exact neural mechanisms underlying OCD pathophysiology still remain unclear. Evidence regarding the most suitable treatment targets and the exact mechanisms through which current treatments improve OCD symptomatology is still missing.

With regard to DBS, its use is, as yet, more empirical than based on strong scientific explanation;32 neurofunctional studies leading to more precise targeting of key circuitries and brain areas are missing. Results obtained from the aforementioned studies have shown mean response rates of 50%, with similar response rates for different target areas, but Level I evidence is provided by only one study.13 Compared to classic ablative procedures, improvement rates appear to be similar if not higher, but direct comparison of therapeutic efficacies is necessary32 and the search for the most appropriate target areas and stimulation parameters continues.11 Future research is also needed to identify predictors of response. Haq et al.33 found that intraoperative smile and laughter induction may represent a long-term (2-year) predictor of DBS response in OCD patients. This is a preliminary hypothesis that needs to be examined in larger studies. Also, the identification of adequate biomarkers to determine the most suitable patient candidates for DBS is needed. Long-term data on DBS effectiveness and safety are very limited. Despite data from recent studies34 that showed effectiveness and safety of DBS 5 years after surgery, further studies on larger cohorts and different targets are needed to fully elucidate long-term outcomes and management.

Ethical concerns deriving from the potential cognitive and behavioral side effects of DBS have recently become the focus of medical discussion, as cognitive impairments have been shown in up to 33% of subjects.35 Given this evidence, as well as other potential psychiatric (depression, mania) and psychosocial (perception of self, familial problems) side effects, exclusion criteria must be clearly identified. However, some potential DBS-induced risks, such as personality changes, should not be considered as ethical criteria to decide against DBS surgery,36 as these modifications of mood, cognition, and behavior are often intended outcomes of this intervention.36,37

TMS represents a less invasive procedure, with adverse effects primarily consisting of potential seizures, mania, and hearing loss. Also possible are minor side effects such as transient headache, scalp discomfort, spasms, and twitching of facial muscles.38 On the other hand, unlike DBS, rTMS has shown the potential to induce long-term beneficial effects on cognition,39 which, at least in patients with depression, appear to be independent from clinical response.40 Targeting some areas, such as the OFC and SMA, has resulted in favorable results,22,23,29 but further studies are needed to confirm long-term efficacy. Moreover, recent guidelines for the therapeutic use of rTMS have been proposed,41 but for OCD, evidence is provided only by level II or level III studies. The authors of these studies conclude that there is no specific recommendation regarding the effect of high-frequency or low-frequency rTMS of the right or left DLPFC in OCD.41 Although TMS has been broadly investigated with electroencephalograms and resting-state functional magnetic resonance imaging to measure TMS-evoked responses directly from brain activity in patients with depression,42 similar studies are missing in patients with OCD. The latest contributions have focused on distinct interneuron circuits in the primary motor cortex (M1) underlying physiologic and behavioral plasticity,43 but neuroplasticity and long-term potentiation mechanisms in OCD remain inconclusive.

Overall, neuromodulation techniques appear to be promising tools in the treatment of refractory OCD, and the development of more tailored protocols represents an intriguing future direction for research. A recent study44 employed alpha electroencephalogram (EEG)-guided TMS in OCD, with frequencies set at the individual’s intrinsic frequency of alpha EEG (usually ranging from 8 to 12 Hz). Even with the limitations of a small sample and uncontrolled medication treatment, significant Yale-Brown Obsessive Compulsive Scale score reductions in the alpha-TMS group were found. Finally, some issues pertaining to coil positioning over the targeted region need to be addressed. Coil positioning procedures are distinguished as “standard” (non-navigated) and “navigated.” The former are obtained by the means of a 10–20 EEG system, whereas the latter are obtained through a real-time frameless stereotaxic system to position the coil over the cortical target that was previously determined on neuroimaging data.45

Lastly, the combination of neuromodulation tools, mainly rTMS or dTMS and cognitive-behavioral therapy (CBT), could represent a new and interesting frontier. The rationale behind this approach would be to enhance the fear-extinction process and learning through long-term potentiation and neuroplasticity. Although data on this approach are still lacking, we recently described a successful case-report of rTMS as a CBT enhancer in a patient with treatment-resistant OCD.46 Further controlled studies are needed in an effort to evaluate this combination approach.

Conclusions

Neuromodulation is a network pathway-oriented treatment that represents a promising tool in the achievement of “precision medicine” and an RDoC-based approach to treatment-resistant OCD. DBS may ultimately be considered a “disease modifier” intervention and, although to a lesser degree, TMS also appears promising for the treatment of resistant and refractory OCD. However, several issues must be addressed in future studies, including clinical long-term outcomes and safety, neurobiological response predictors, and neuroplasticity phenomena related to neuromodulation.

References

  1. Ruscio AM, Stein DJ, Chiu WT, Kessler RC. The epidemiology of obsessive-compulsive disorder in the National Comorbidity Survey Replication. Mol Psychiatry. 2010;15:53–63. doi:10.1038/mp.2008.94 [CrossRef]
  2. Menzies L, Chamberlain SR, Laird AR, Thelen SM, Sahakian BJ, Bullmore ET. Integrating evidence from neuroimaging and neuropsychological studies of obsessive-compulsive disorder: the orbitofronto-striatal model revisited. Neurosci Biobehav Rev. 2008;32(3):525–549. doi:10.1016/j.neubiorev.2007.09.005 [CrossRef]
  3. Pallanti S, Hollander E. Pharmacological, experimental therapeutic, and transcranial magnetic stimulation treatments for compulsivity and impulsivity. CNS Spectr. 2013;19(1):50–61. doi:10.1017/S1092852913000618 [CrossRef]
  4. Figee M, Vink M, de Geus F, et al. Dysfunctional reward circuitry in obsessive-compulsive disorder. Biol Psychiatry. 2011;69(9):867–874. doi:10.1016/j.biopsych.2010.12.003 [CrossRef]
  5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.
  6. Insel TR. The NIMH Research Domain Criteria (RDoC) Project: precision medicine for psychiatry. Am J Psychiatry. 2014;171(4):395–397. doi:10.1176/appi.ajp.2014.14020138 [CrossRef]
  7. Pallanti S, Hollander E, Goodman WK: A qualitative analysis of nonresponse: management of treatment-refractory obsessive-compulsive disorder. J Clin Psychiatry. 2004;65:6–10.
  8. Lipsman N, Neimat JS, Lozano AM. Deep brain stimulation for treatment-refractory obsessive-compulsive disorder: the search for a valid target. Neurosurgery. 2007;61:1–11. doi:10.1227/01.neu.0000279719.75403.f7 [CrossRef]
  9. 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(9189):1526. doi:10.1016/S0140-6736(99)02376-4 [CrossRef]
  10. Figee M, Luigjes J, Smolders R, et al. Deep brain stimulation restores frontostriatal network activity in obsessive-compulsive disorder. Nat Neurosci. 2013;16(4):386–387. doi:10.1038/nn.3344 [CrossRef]
  11. Kohl S, Schönherr DM, Luigjes J, et al. Deep brain stimulation for treatment-refractory obsessive compulsive disorder: a systematic review. BMC Psychiatry. 2014;14(1):214. doi:10.1186/s12888-014-0214-y [CrossRef]
  12. Hamani C, Pilitsis J, Rughani AI, et al. Deep brain stimulation for obsessive-compulsive disorder: systematic review and evidence-based guideline sponsored by the American Society for Stereotactic and Functional Neurosurgery and the Congress of Neurological Surgeons (CNS) and endorsed by the CNS and American Association of Neurological Surgeons. Neurosurgery. 2014;75(4):327–333. doi:10.1227/NEU.0000000000000499 [CrossRef]
  13. Mallet L, Polosan M, Jaafari N, et al. Subthalamic nucleus stimulation in severe obsessive-compulsive disorder. N Engl J Med. 2008;359(20):2121–2134. doi:10.1056/NEJMoa0708514 [CrossRef]
  14. Denys D, Mantione M, Figee M, et al. Deep brain stimulation of the nucleus accumbens for treatment-refractory obsessive-compulsive disorder. Arch Gen Psychiatry. 2010;67(10):1061–1068. doi:10.1001/archgenpsychiatry.2010.122 [CrossRef]
  15. Huff W, Lenartz D, Schormann M, et al. Unilateral deep brain stimulation of the nucleus accumbens in patients with treatment-resistant obsessive-compulsive disorder: outcomes after one year. Clin Neurol Neurosurg. 2010;112(2):137–143. doi:10.1016/j.clineuro.2009.11.006 [CrossRef]
  16. Greenberg BD, Gabriels LA, Malone DA Jr, et al. Deep brain stimulation of the ventral internal capsule/ventral striatum for obsessive-compulsive disorder: worldwide experience. Mol Psychiatry. 2010;15(1):64–79. doi:10.1038/mp.2008.55 [CrossRef]
  17. Goodman WK, Foote KD, Greenberg BD, et al. Deep brain stimulation for intractable obsessive compulsive disorder: pilot study using a blinded, staggered-onset design. Biol Psychiatry. 2010;67(6):535–542. doi:10.1016/j.biopsych.2009.11.028 [CrossRef]
  18. Jimenez-Ponce F, Velasco-Campos F, Castro-Farfan G, et al. Preliminary study in patients with obsessive-compulsive disorder treated with electrical stimulation in the inferior thalamic peduncle. Neurosurgery. 2009;65(6):203–209. doi:10.1227/01.NEU.0000345938.39199.90 [CrossRef]
  19. George MS, Post RM. Daily left prefrontal repetitive transcranial magnetic stimulation for acute treatment of medication-resistant depression. Am J Psychiatry. 2011;168(4):356–364. doi:10.1176/appi.ajp.2010.10060864 [CrossRef]
  20. Rosa MA, Lisanby SH. Somatic treatments for mood disorders. Neuropsychopharmacology. 2011;37(1):102–116. doi:10.1038/npp.2011.225 [CrossRef]
  21. Alonso P, Pujol J, Cardoner N, et al. Right prefrontal repetitive transcranial magnetic stimulation in obsessive-compulsive disorder: a double-blind, placebo-controlled study. Am J Psychiatry. 2001;158(7):1143–1145. doi:10.1176/appi.ajp.158.7.1143 [CrossRef]
  22. 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(5):226–230. doi:10.4088/PCC.08m00663 [CrossRef]
  23. Nauczyciel C, Le Jeune F, Naudet F, et al. Repetitive transcranial magnetic stimulation over the orbitofrontal cortex for obsessive-compulsive disorder: a double-blind, crossover study. Transl Psychiatry. 2014;4(9):e436. doi:10.1038/tp.2014.62 [CrossRef]
  24. Baxter LR Jr, Schwartz JM, Mazziotta JC, et al. Cerebral glucose metabolic rates in non-depressed patients with obsessive-compulsive disorder. Am J Psychiatry. 1988;145(12):1560–1563. doi:10.1176/ajp.145.12.1560 [CrossRef]
  25. Cho SS, Strafella AP. rTMS of the left dorsolateral prefrontal cortex modulates dopamine release in the ipsilateral anterior cingulate cortex and orbitofrontal cortex. PloS One. 2009;4(8):e6725. doi:10.1371/journal.pone.0006725 [CrossRef]
  26. Yücel M, Harrison BJ, Wood SJ, et al. Functional and biochemical alterations of the medial frontal cortex in obsessive-compulsive disorder. Arch Gen Psychiatry. 2007;64(8):946–955. doi:10.1001/archpsyc.64.8.946 [CrossRef]
  27. de Wit SJ, de Vries FE, van der Werf YD, et al. Presupplementary motor area hyperactivity during response inhibition: a candidate endophenotype of obsessive-compulsive disorder. Am J Psychiatry. 2012;169(10):1100–1108. doi:10.1176/appi.ajp.2012.12010073 [CrossRef]
  28. Berlim MT, Neufeld NH, Van den Eynde F. Repetitive transcranial magnetic stimulation (rTMS) for obsessive–compulsive disorder (OCD): an exploratory meta-analysis of randomized and sham-controlled trials. J Psychiatr Res. 2013;47(8):999–1006. doi:10.1016/j.jpsychires.2013.03.022 [CrossRef]
  29. Mantovani A, Simpson HB, Fallon BA, Rossi S, Lisanby SH. Randomized sham-controlled trial of repetitive transcranial magnetic stimulation in treatment-resistant obsessive-compulsive disorder. Int J Neuropsychopharmacol. 2010;13:217–227. doi:10.1017/S1461145709990435 [CrossRef]
  30. Mantovani A, Rossi S, Bassi BD, Simpson HB, Fallon BA, Lisanby SH. Modulation of motor cortex excitability in obsessive-compulsive disorder: an exploratory study on the relations of neurophysiology measures with clinical outcome. Psychiatry Res. 2013;210(3):1026–1032. doi:10.1016/j.psychres.2013.08.054 [CrossRef]
  31. Morishita T, Fayad SM, Goodman WK, et al. Surgical neuroanatomy and programming in deep brain stimulation for obsessive compulsive disorder. Neuromodulation. 2014;17(4):312–319. doi:10.1111/ner.12141 [CrossRef]
  32. Haynes WI, Mallet L. High-frequency stimulation of deep brain structures in obsessive-compulsive disorder: the search for a valid circuit. Eur J Neurosci. 2010;32(7):1118–1127. doi:10.1111/j.1460-9568.2010.07418.x [CrossRef]
  33. Haq IU, Foote KD, Goodman WG, et al. Smile and laughter induction and intraoperative predictors of response to deep brain stimulation for obsessive-compulsive disorder. Neuroimage. 2011;54(1):S247–255. doi:10.1016/j.neuroimage.2010.03.009 [CrossRef]
  34. Ooms P, Mantione M, Figee M, Schuurman PR, van den Munckhof P, Denys D. Deep brain stimulation for obsessive-compulsive disorders: long-term analysis of quality of life. J Neurol Neurosurg Psychiatry. 2014;85(2):153–158. doi:10.1136/jnnp-2012-302550 [CrossRef]
  35. Clausen J. Ethical brain stimulation–neuroethics of deep brain stimulation in research and clinical practice. Eur J Neurosci. 2010;32(7):1152–1162. doi:10.1111/j.1460-9568.2010.07421.x [CrossRef]
  36. Schlaepfer TE, Lisanby SH, Pallanti S. Separating hope from hype: some ethical implications of the development of deep brain stimulation in psychiatric research and treatment. CNS Spectr. 2010;15(5):285–287.
  37. Synofzyk M, Schlaepfer TE. Stimulating personality: ethical criteria for deep brain stimulation in psychiatric patients and for enhancement purposes. J Biotechnol. 2008;3:1511–1520. doi:10.1002/biot.200800187 [CrossRef]
  38. Rossi S, Hallett M, Rossini PM, Pascual-Leone A. Safety, ethical considerations, and application guidelines for the use of transcranial magnetic stimulation in clinical practice and research. Clin Neurophysiol. 2009;120(12):2008–2039. doi:10.1016/j.clinph.2009.08.016 [CrossRef]
  39. Guse B, Falkai P, Wobrock T. Cognitive effects of high-frequency repetitive transcranial magnetic stimulation: a systematic review. J Neural Transm. 2010;117(1):105–122. doi:10.1007/s00702-009-0333-7 [CrossRef]
  40. Pallanti S, Di Rollo A, Antonini S, Cauli G, Hollander E, Quercioli L. Low-frequency rTMS over right dorsolateral prefrontal cortex in the treatment of resistant depression: cognitive improvement is independent from clinical response, resting motor threshold is related to clinical response. Neuropsychobiology. 2012;65(4):227–235. doi:10.1159/000336999 [CrossRef]
  41. Lefaucheur JP, André-Obadia N, Antal A, et al. Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS). Clin Neurophysiol. 2014;125(11):2150–2206. doi:10.1016/j.clinph.2014.05.021 [CrossRef]
  42. Ziemann U, Reis J, Schwenkreis P, et al. TMS and drugs revisited 2014. Clin Neurophysiol. 2014;S1388-2457(14)00837-2. [Epub ahead of print]. doi:10.1016/j.clinph.2014.08.028 [CrossRef]
  43. Hamada M, Galea JM, Di Lazzaro V, Mazzone P, Ziemann U, Rothwell JC. Two distinct interneuron circuits in human motor cortex are linked to different subsets of physiological and behavioral plasticity. J Neurosci. 2014;34(38):12837–12849. doi:10.1523/JNEUROSCI.1960-14.2014 [CrossRef]
  44. Xiaoyan M, Yueqin H, Liwei L, Yi J. A randomized double-blinded sham-controlled trial of α electroencephalogram-guided transcranial magnetic stimulation for obsessive-compulsive disorder. Chin Med J (Engl). 2014;127(4):601–616.
  45. Lefaucheur JP. Why image-guided navigation becomes essential in the practice of transcranial magnetic stimulation. Neurophysiol Clin. 2010;40(1):1–5. doi:10.1016/j.neucli.2009.10.004 [CrossRef]
  46. Grassi G, Godini L, Grippo A, Piccagliani D, Pallanti S. Enhancing cognitive-behavioral therapy with repetitive transcranial magnetic stimulation in refractory obsessive-compulsive-disorder: a case report. Brain Stimul. 2015;8(1):160–161. doi:10.1016/j.brs.2014.10.007 [CrossRef]

Deep Brain Stimulation Outcomes in Obsessive-Compulsive Disorder

Target Patients (n) Response Rates (mean) Y-BOCS Decrease (mean)
ALIC 18 75% 46.5%
NaC 37 45.5% 37.8%
VC/VS 44 50% 41.5%
STN 25 57.1% 45.3%
ITP 11 100% 82.5%

rTMS Outcomes in Obsessive-Compulsive Disorder

Target Patients (n) Response Rates (mean)
Left DLPFC 70 38% (19 of 50)
Right DLPFC 54 24% (6 of 25)
Pre-SMA 31a 52% (11 of 21)

dTMS Outcomes in Obsessive-Compulsive Disorder

Target Patients (n) Response Rates (mean)
OFC 35 25% (4 of 16)
Authors

Stefano Pallanti, MD, PhD, is a Professor, Department of Psychiatry and Behavioral Sciences, UC Davis School of Medicine; a Visiting Professor, Albert Einstein College of Medicine and Montefiore Medical Center; and an Associate Professor of Psychiatry, Department of Neuroscience, University of Florence. Anna Marras, MSc, is a Doctoral Student in Neuroscience, University of Florence. Giacomo Grassi, MD, is a Resident in Psychiatry, University of Florence.

Address correspondence to Stefano Pallanti, MD, PhD, Largo Brambilla, 3, 50134 Firenze, Italy; email: stefanopallanti@yahoo.it.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/00485713-20150602-07

Sign up to receive

Journal E-contents