In the US, OCD affects about 4 million people.1 Compared with schizophrenia, which is notoriously disabling, OCD causes similar degrees of serious impairment in social relationships and daily living, but we often do not consider OCD in this light because effective treatments are available. However, up to half of patients do not respond to first-line treatments and traditional pharmacological approaches are often associated with difficult adverse effects. In fact, even when patients do “respond,” it is rare to see true symptom remission.
Unlike depression studies, which often measure the percentage of “responders” and “remitters,” many OCD studies only measure “responders” and “partial responders.” For these reasons, it is essential to develop a more effective treatment algorithm that can help patients who do not respond to first-line options.
Current OCD treatment
OCD is characterized by uncontrollable, recurring thoughts or images (obsessions) accompanied by the urge to repeat specific behaviors (compulsions) to alleviate these intrusive thoughts. Effective treatments reduce symptoms and help patients cope with the anxiety surrounding these obsessions and compulsions. The American Psychiatric Association implemented an OCD treatment algorithm that designates a specific type of cognitive behavioral therapy (CBT)—exposure-response prevention (ERP)—and SSRIs as first-line treatments [PDF].
ERP involves patients working with their therapist to actively expose themselves in increasing degrees to the very things that elicit their fears. The process reduces anxiety surrounding the various triggers that induce the obsessive thoughts and compulsions. This form of CBT is effective in patients who complete a full course of treatment; however, some patients may have difficulty fully committing to the therapy as it can be extremely anxiety inducing. Ultimately, 45% of OCD patients either quit ERP because of the difficult treatment process or fail to respond to this treatment to a satisfactory degree.2 One option is to introduce a pharmacological treatment in parallel with ERP.
The first pharmacological option for patients with OCD is an SSRI. These agents work by blocking the reuptake of serotonin from neurons, increasing the amount of serotonin available in the synaptic cleft. This leads to a variety of downstream effects throughout the brain and has been associated with altering brain activity at various locations associated with OCD symptoms.3 Based on this finding, SSRIs are considered the first-choice pharmacological treatment for OCD. They are effective in about 50% to 70% of patients.4,5 However, because the effects of SSRIs are not localized only to OCD brain regions, they can have significant negative adverse effects in other parts of the body.
Further exacerbating this issue is the fact that patients with OCD often require higher doses of SSRIs than those effective in treating depression. Research has shown that increasing the dose of SSRIs in this manner can lead to increased adverse effects, which can often be severe enough that patients choose to stop their medications.6,7 Moreover, because we do not fully understand how SSRIs work in the brain to reduce OCD symptoms, we have not yet found methods for predicting who will respond to the treatment in any reliable, affordable, or clinically feasible way.
Options after first-line treatment
After non-response to ERP and/or initial doses of SSRIs, psychiatrists have only a few validated options. Clinicians will often escalate the dose of SSRIs, try multiple different SSRIs, or switch to or add clomipramine, an older, but sometimes more effective SRI, but which unfortunately can often have more serious adverse effects. Next, atypical antipsychotics such as risperidone or aripiprazole are added to the patients’ treatment regimen.
Again, the adverse effects associated with adding an antipsychotic are often worse than those associated with treatment with an SSRI alone. This process of escalating doses and testing different medications and combinations can often take several months to years.
When all the treatment options are exhausted, the next option in the treatment algorithm is surgical implantation of a deep brain stimulator (DBS) or a procedure known as a ventral capsulotomy, which creates a lesion in part of the brain implicated in OCD.8 While surgery has been proven effective in treatment-resistant patients, there are risks, costs, and complications associated with the procedures.9
Furthermore, brain surgery can be particularly anxiety-provoking for patients with severe OCD, and many are not willing to proceed with surgery. This leaves clinicians in a difficult position, and other non-invasive treatment options are needed. Recently, a new, non-invasive treatment was cleared by the FDA, offering psychiatrists another neurocircuitry-based tool with far fewer risks compared with surgical options.
Transcranial magnetic stimulation
Recently, the FDA cleared the Brainsway H7 deep transcranial magnetic stimulation (dTMS) device that works by directing electromagnetic fields that generate excitation or inhibition of neurons deep inside the brain. It is completely noninvasive and performed in an outpatient setting, with no need for hospital gowns or anesthesia. Patients receive stimulation through a helmet with a built-in magnetic coil (Figure 1).
Treatment is well tolerated, usually with only mild discomfort due to sensations on the scalp sometimes described as feeling like a woodpecker tapping on the head; however, with increasing treatments, the scalp desensitizes to this sensation, and most patients report it to be less bothersome with each treatment.
Unlike SSRIs, this treatment is localized, more precisely targeting specific brain regions—the medial prefrontal cortex and the anterior cingulate cortex (Figure 2)—that play an essential role in regulating OCD symptoms.10 This localized specificity means that the rest of the body is spared adverse effects.
Clinical trial results show that daily dTMS treatment for a 6-week period results in a statistically significant 30% reduction in symptom severity as measured by the Yale-Brown Obsessive-Compulsive Scale.11 This magnitude of response is on par with responses seen in SSRI treatment; however, dTMS may achieve these results faster. Many SSRI studies demonstrate similar responses but only after 8 to 12 weeks.12
At the 10-week follow up, the response rate to dTMS increased further. This increase demonstrated a positive treatment effect over time, even once the stimulation had ceased. Overall, 38.1% of patients in the dTMS group showed a response, compared with 11.1% of patients in the sham treatment group.11 Adverse effects were limited; the most frequent adverse reaction was headache, which resolved shortly after treatment.
This clinical trial was especially unique, because prior to each treatment session, OCD symptoms were provoked in each patient. This provocation of symptoms was personalized, based on a fear hierarchy created between patients and their clinician before the start of treatment. For example, immediately before undergoing dTMS treatment, patients with obsessions related to contamination fears may have been presented with a dirty sponge to touch, or perhaps they brought triggering items from home.
This idea of provoking symptoms and activating trigger-specific circuity stems from earlier studies in PTSD, addiction, and smoking cessation that have shown greater improvement in groups that had provocation protocols.13,14 The sham group also received the brief “exposure” or “provocation” protocol but did not see the same results.11
He reports that he is employed by TMS Health Solutons, an insurance-based, group psychiatric private practice that offers rTMS and dTMS as one of many various treatment modalities.
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