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November 5, 2013 at 5:37 am #3204doctordogMember
I wasn't really sure where to ask this, or if there's even an answer, but I was wondering if there was any relationship between my poor reactions to Memantine and Riluzole (more anxiety/agitation) and the fact that I react paradoxically to benzodiazepines? I've noticed a pattern with GABAerics ..
Is there anything that can be done? Is it possible the former might work better as augmentation (I only tried them as monotherapy)? I also have a history of being extremely sensitive to drugs, so was thinking about very low doses..
Running out of options for my severe anxiety and getting a little scared ..November 9, 2013 at 3:19 pm #3324Dr. Michael JenikeMember
Riluzole and Namenda has effects on the glutaminergic system and benzodiazepines on the GABA system. not sure if these side effects are related. the only way to know if augmentation of a SSRI with one of these agents will help is to give it a try. there are quite a few anti anxiety drugs; you could try buspirone. also, CBT has a lot to offer for anxiety. all best wishes,
Michael Jenike, MDNovember 10, 2013 at 5:47 am #3327doctordogMember
Thank you for your help, Dr Jenike. Unfortunately, I have tried buspirone but it increased my anxiety.
The only area I haven't really explored at this point is mood stabilizers like lithium.
Out of interest, is buprenorphine ever used for refractory OCD? I am aware of being used in depression, but there is only one very small OCD study on pubmed.December 8, 2013 at 10:26 am #3328Dr. Michael JenikeMember
here is a relevant article.
Michael Jenike, MD
Buprenorphine augmentation in the treatment of refractory OCD
- Malcolm B. Liddell email@example.com
- Victor Aziz
- Patrick Briggs
- Nimalee Kanakkehewa
- Omar Rawi
Background: OCD is often refractory to treatment. There is a need for the development of new, non-invasive treatments for severe OCD.
Rationale: There is evidence that opiates can be a useful adjunctive treatment in OCD. We summarise our experience with sublingual buprenorphine augmentation of standard pharmacological management of severe OCD.
Methods: Patients were recruited from a standard psychiatric outpatient clinic and gave their consent to the treatment trial. The severity of the OCD was rated with the Y-BOCS. The buprenorphine was introduced to their existing medication regime at a low dose and the dose increased according to response. In order to gauge the reproducibility of the response the buprenorphine was withdrawn and then reintroduced once symptoms had returned.
Results: 4 out of 7 patients with treatment resistant OCD showed a 30% reduction in the Y-BOCS score following buprenorphine augmentation. 3 of the responders were co-morbid for other Axis 1 diagnoses. All of the responders had shown some improvement with SSRIs or clomipramine. Non-responders had not shown any improvement with either antidepressant or antipsychotic drugs. Typically improvement appeared within 2 days of initiating buprenorphine and waned within 1 to 2 days of its discontinuation. The dose of buprenorphine required varied between 400 µg and 600 µg a day. One responder managed on alternate day dosing. Reintroduction of buprenorphine resulted in symptom control within 2 to 3 days. The buprenorphine treatment was not associated with significant side-effects and the improvement was maintained without progressive dose escalation.
Conclusions: Buprenorphine augmentation of standard treatment for OCD can result in clinically meaningful improvement in a proportion of refractory OCD cases. Further treatment trials are indicated.
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