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
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
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.
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.
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Deep Brain Stimulation Outcomes in Obsessive-Compulsive Disorder
||Response Rates (mean)
||Y-BOCS Decrease (mean)
rTMS Outcomes in Obsessive-Compulsive Disorder
||Response Rates (mean)
||38% (19 of 50)
||24% (6 of 25)
||52% (11 of 21)
dTMS Outcomes in Obsessive-Compulsive Disorder
||Response Rates (mean)
||25% (4 of 16)