The Relative Efficacy of Current Medication and Therapy for OCD

January 14, 2014
H. Blair Simpson, MD, PhD

What do we know about the relative efficacy of current medication and therapy for OCD? This question answered and highlights of recent studies, future directions, and causes are summarized in this video.

What do we know about the relative efficacy of current medication and [cognitive-behavioral] therapy (CBT) for OCD? Dr H. Blair Simpson answers that question and discusses future directions and causes in the study of OCD.

Dr Simpson is funded by the National Institute of Mental Health (NIMH).

Her team is recruiting adults for an OCD treatment study. Information can be found at:
http://www.ocdtreatmentstudy.comhttp://www.columbia-ocd.org

Transcript

In collaboration with Dr Edna Foa at the University of Pennsylvania, our clinic did a study to exactly answer the question. The data from that study showed very clearly that the therapy-when delivered by highly trained therapists and well supervised with patients who adhere to the treatment-is at least as good if not better than the medication. So that is surprising for psychiatrists to know. That's why either the medication or the therapy are first-line treatments for OCD.

Many people make the assumption [and ask] what happens when you put [medication and therapy] together [and wonder if] that [would be] better still. The interesting thing about that first study is that's not what we found. We found that the medication and the therapy together were no better than the therapy alone. There are a couple of important caveats. In that study, the medication and the therapy were started at the same time [and medication can take up to 6 weeks to work]. The therapy in that study was delivered not twice weekly, but 5 days a week for 3 weeks within a week of home visits so the therapy [was intensive over a month's duration]. So that combination cell in essence was like a month of intensive therapy and the ["rocket booster" at the end] was medication. So what I would say is that no, you do not need to start people . . . all people do not need to start on combination. They can start with medication, or start with the therapy.

If people get a partial response to medication, we have now done 2 studies, again in collaboration with Dr Edna Foa at the University of Pennsylvania that show definitively that adding CBT on top of people who have gotten the most that they are going to get out of their medication will help more people get well. In those subsequent studies, everyone came in on a stable dose of their serotonin reuptake inhibitor (SRI) medication. They had been on it for at least 12 weeks on the maximum dose. They weren't going to get anything more from their medication.

One study randomized them to exposure and ritual prevention (ERP) treatment versus a control therapy where we were able to control for attention and support and coming to our clinic with a research staff. We could show clearly that the control therapy didn't do much. By adding ERP treatment on top of the medication, many people (70%) responded and a third got well. That study was comparing adding exposure therapy versus adding antipsychotic medication, which is right now the only other treatment we have for people who have a partial response to SRI medication. Again, people came in on their SRI medication; all of them had been in on their highest dose for at least 12 weeks and they weren't going to get anything more from their SRI. This is the situation that psychiatrists are going to [encounter].

The question becomes what do you do? This was a study where we compared adding ERP treatment versus adding antipsychotic medication-in the study we used risperidone because the evidence was best for risperidone in OCD-versus a placebo. What we found in that study is that once again with ERP treatment 80% of people responded and 43% were well after 17 sessions. Moreover, we have also shown that if you get well, you are very likely to maintain your response out to 6 months if you have gotten well from ERP.

The big picture is there are SRI medications as a first-line treatment. There is this very particular type of CBT as a first-line treatment. When you get a partial response to SRI medication, the first thing you should be thinking about is adding the CBT on top. With all the caveats I've given you, that if you have a patient who cannot adhere to the treatment, then you're not going to get the good results that we can get in our studies. If the therapist isn't giving the right treatment, you're not going to get the good results that you get in our studies. That's where as a psychiatrist, once you've tried those options, you [use treatments] that are less evidence-based to try to help your patients.

Future directions
We [are] interested in who the people are who get well once they have been given an SRI medication and then CBT/ERP added on top? As I said, about 70% to 80% of people will respond to that combination and about 35% to 40% of people will get well at the end of that added-on 17 sessions. And if you give some people a little bit more, maybe as high as 60% will get well.

So now [a patent is] well. They have been on the medication for a long time, they received the CBT added on top . . . the first thing those patients ask us is, "Do I still need my medication?" That is an important clinical question and we're really thrilled. Edna Foa and I are funded by the National Institute of Mental Health to answer that exact question. We're currently both at our site and at the University of Pennsylvania doing a study where people on SRIs who are at their maximum dose and have been there for 12 weeks (they're not going to get more from their medication) come to us. They get this very specific therapy added on top first and with the people are well, we then are going to randomize to half of them (not known to them and not known to us) will stay on their medication for the next 6 months and half of them will be tapered to a pill placebo . . . our sense of it is that some people may actually be able to come off their medication but at this moment we don't know who can do that. Hopefully another study to really look at . . . who gets well with this combination of treatment and who doesn't, who gets well enough that actually it's safe and good for them to slowly taper off their SRI, and who should not come off their SRI medication-that's the point of the study.

If there are people who are watching this video or you have patients who think might be appropriate for the study, please go to our study website. Again, the study is being run in both Philadelphia and New York. We think it's a great study and frankly for patients who haven't had this combination, here is how you can get treatment you should be getting at no cost to you as well as you can help us advance the field and [potentially] help a much broader population of patients.

Causes of OCD
There are 2 ways to think about this. Any behavior I have is because my brain is causing that behavior. I'm talking to you now because I have circuits in my brain that allow me to speak, that move my tongue. In that sense, if I have obsessions and compulsions, my brain is causing me to have obsessions and compulsions.

We can study that by doing brain imaging studies of people who have OCD and people who don't and look for what is different about how their brain is functioning. What we know from human imaging studies is that there is a hyperactive brain circuit in people with OCD that is not present in people without OCD and it includes brain regions called the orbital frontal cortex, the striatum, and the thalamus. These brain areas are connected to each other in a loop. The working model of OCD is that there is a hyperactive brain circuit and that is what is contributing to the symptoms of obsessions and compulsions.

That's what I would call pathophysiology: how does the brain produce a behavior. But it's a completely different question to ask, "How did my brain get like that in the first place?" That's a different way to look at cause. That's what I call etiology, which we know much less about.

The current thinking and there's some data to suggest some people have certain genes that may make people vulnerable. There are certain problems that may happen as your brain is getting set up during development. There are certain infections and post-infection syndromes that may lead in some people to OCD symptoms. There are case examples of people who had a neurological stroke or have a brain tumor in that brain circuit that can lead to OCD. So that's an area that's harder to study and that we know less about, but if you take what causes obsessions and compulsions is that abnormal circuit, then anything that can disrupt the normal circuit potentially could lead to OCD symptoms. That's a way to think about pathophysiology and etiology of what causes OCD.

Studies discussed in this video:
Foa EB, Liebowitz MR, Kozak MJ, et al. Randomized, placebo-controlled trial of exposure and ritual prevention, clomipramine, and their combination in the treatment of obsessive-compulsive disorder. Am J Psychiatry. 2005;162:151-161.

Simpson HB, Foa EB, Liebowitz MR, et al. A randomized, controlled trial of cognitive-behavioral therapy for augmenting pharmacotherapy in obsessive-compulsive disorder.  Am J Psychiatry. 2008;165:621-630.

Simpson HB, Foa EB, Liebowitz MR, et al. Cognitive-behavioral therapy vs risperidone for augmenting serotonin reuptake inhibitors in obsessive-compulsive disorder a randomized clinical trial serotonin reuptake inhibitor augmentation serotonin reuptake inhibitor augmentation. JAMA Psychiatry. 2013.

Disclosures:

Dr Simpson is Professor of Clinical Psychiatry, Columbia University, and Director of the Anxiety Disorders Clinic and the Center for OCD and Related Disorders at New York State Psychiatric Institute in New York City,