Let's talk OCD alternative pharmacotherapies

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cbrons

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So as many of you know I've become somewhat of a pest with my frequent posting on the subject. However, I would like to know your thoughts on some alternatives to OCD treatment, aside from the typical SSRI or clomipramine trials. I've been reading that as many as 30% of OCD patients will not respond to a full trial of any of the SSRIs, and in my experience an even greater percentage will not experience significant symptomatic relief.

What is your most frustrating OCD case?

Have you tried some of the lesser known stuff? Ondansetron, memantine, or even inositol (been reading about this all morning). Any papers you can share with me? OCD has become a very fascinating illness to me, and I've been bothering my psychiatrist friends for a while with stories about their complex patients.

Additionally, do you recommend your patients undergo CBT/ERP? I.e. a program like Alexian Brothers Partial, Rogers Memorial Hospital Residential program (In Wisconsin) or other programs of high repute? For the more difficult patients, that is.

Thanks for your time, hope I am not becoming too much of a pest.

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So as many of you know I've become somewhat of a pest with my frequent posting on the subject. However, I would like to know your thoughts on some alternatives to OCD treatment, aside from the typical SSRI or clomipramine trials. I've been reading that as many as 30% of OCD patients will not respond to a full trial of any of the SSRIs, and in my experience an even greater percentage will not experience significant symptomatic relief.

What is your most frustrating OCD case?

Have you tried some of the lesser known stuff? Ondansetron, memantine, or even insotol (been reading about this all morning). Any papers you can share with me? OCD has become a very fascinating illness to me, and I've been bothering my psychiatrist friends for a while with stories about their complex patients.

Additionally, do you recommend your patients undergo CBT/ERP? I.e. a program like Alexian Brothers Partial, Rogers Memorial Hospital Residential program (In Wisconsin) or other programs of high repute? For the more difficult patients, that is.

Thanks for your time, hope I am not becoming too much of a pest.

My most frustrating OCD patient never did the CBT homework and never took the meds. She got better somehow though.
 
Have you tried some of the lesser known stuff? Ondansetron, memantine, or even inositol (been reading about this all morning). Any papers you can share with me? OCD has become a very fascinating illness to me, and I've been bothering my psychiatrist friends for a while with stories about their complex patients.
I've used memantine and, in fact, am in the process of submitting a paper on it. I haven't tried Ondansetron. Is there evidence for that? I have one patient using inositol, but I'm not sure it is really helping as he is on an SSRI and an atypical.

Additionally, do you recommend your patients undergo CBT/ERP? I.e. a program like Alexian Brothers Partial, Rogers Memorial Hospital Residential program (In Wisconsin) or other programs of high repute? For the more difficult patients, that is.

We sent one kid to the Mayo clinic's OCD inpatient program. He didn't do well, but that was less to do with the program and more to do with the patient's own struggles. I haven't personally sent anyone to Rogers, but one of the attendings has. It's supposed to be a very good program.
 
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Cingulotomy--yes brain surgery, and why me, I have a patient where every single med we tried didn't work or caused side effects to the degree where the patient didn't want it. E.g. we tried Tramadol (yes he's that treatment resistant) and it worked but he could not urinate while that medication.

Right now I've got him on SAM-E (yes we're that desperate), and if this doesn't work I'm thinking ECT or cingolotomy.

Tramadol does work for OCD and there's published information from Paul Keck supporting it's use.

Memantine, yes there's data supporting it as an augmentation agent.

There's also data that St. John's Wort could have benefits although the theory behind it is is mimcs the effect of an SSRI, is not as effective as an SSRI, is more expensive than teh $4/month antidepressants, and has more side effects than them so I tend not to recommend it.

If the SAM-E works, or if we pursue cingulotomy I'm thinking of writing a paper on this because so few doctors are thrust into this situation.
 
Cingulotomy--yes brain surgery, and why me, I have a patient where every single med we tried didn't work or caused side effects to the degree where the patient didn't want it. E.g. we tried Tramadol (yes he's that treatment resistant) and it worked but he could not urinate while that medication.

Right now I've got him on SAM-E (yes we're that desperate), and if this doesn't work I'm thinking ECT or cingolotomy.

Tramadol does work for OCD and there's published information from Paul Keck supporting it's use.

Memantine, yes there's data supporting it as an augmentation agent.

There's also data that St. John's Wort could have benefits although the theory behind it is is mimcs the effect of an SSRI, is not as effective as an SSRI, is more expensive than teh $4/month antidepressants, and has more side effects than them so I tend not to recommend it.

If the SAM-E works, or if we pursue cingulotomy I'm thinking of writing a paper on this because so few doctors are thrust into this situation.

Interesting. I see a lot of OCD and have done research in the area. However, I work with kids and typically they move on from our clinic after they're 18. So, I haven't seen anyone with things so bad to try cingulotomy. If you think of it, let us know how that goes. Have you tried Riluzole?
 
Nope but maybe I should. I think it'd be reasonable to try that before ECT or cingulotomy.

We're at the point where we're trying meds he was already on and couldn't tolerate but on the premise that perhaps if I start at a lower dosage and very very slowly titrate up he might be able to tolerate them. I restarted him on Zoloft 25 mg Q daily instead of 50 and within 3 days he had panic attacks from Zoloft and called me at 3AM, apologizing for the call, but telling me he was in the middle of a panic attack, crying and he didn't know what to do.

This is a seriously desperate case. A person at the Lindner Center, known as a top person in the field already saw him and he's still got OCD as bad as it was at that time.

And I did bring up cingulotomy as an option and this guy is so desperate he's open to trying it.
 
Nope but maybe I should. I think it'd be reasonable to try that before ECT or cingulotomy.

We're at the point where we're trying meds he was already on and couldn't tolerate but on the premise that perhaps if I start at a lower dosage and very very slowly titrate up he might be able to tolerate them. I restarted him on Zoloft 25 mg Q daily instead of 50 and within 3 days he had panic attacks from Zoloft and called me at 3AM, apologizing for the call, but telling me he was in the middle of a panic attack, crying and he didn't know what to do.

This is a seriously desperate case. A person at the Lindner Center, known as a top person in the field already saw him and he's still got OCD as bad as it was at that time.

And I did bring up cingulotomy as an option and this guy is so desperate he's open to trying it.

Yeah, that is sad and I hate to see people suffer like that. You might want to try Riluzole. From what I know of you, I'm assuming he failed ERP/CBT. Sounds like cingulotomy might be a good way to go. Just curious, do you have places near you that do that?
 
Cingulotomy--yes brain surgery, and why me, I have a patient where every single med we tried didn't work or caused side effects to the degree where the patient didn't want it. E.g. we tried Tramadol (yes he's that treatment resistant) and it worked but he could not urinate while that medication.

Right now I've got him on SAM-E (yes we're that desperate), and if this doesn't work I'm thinking ECT or cingolotomy.

Tramadol does work for OCD and there's published information from Paul Keck supporting it's use.

Memantine, yes there's data supporting it as an augmentation agent.

There's also data that St. John's Wort could have benefits although the theory behind it is is mimcs the effect of an SSRI, is not as effective as an SSRI, is more expensive than teh $4/month antidepressants, and has more side effects than them so I tend not to recommend it.

If the SAM-E works, or if we pursue cingulotomy I'm thinking of writing a paper on this because so few doctors are thrust into this situation.

Horrible. Did he fail a good ERP program?
 
Yes.

Another problem is he has PTSD. This is a patient where psychotherapy can help, but given his GAF, and the severity of his PTSD along with OCD, psychotherapy is one of those things where I'm wondering if he's well enough for another try of it. He's scared leaving his home. As he's said it, something to the effect of -years have gone by and I don't get better, what do I do?-
He's in his late 20s and has had this problem since his teens.

I just talked to the guy in the university who specializes in ECT and he told me he'd wouldn't recommend it.

I know only a few people do cingulotomies in the country. Deep Brain Stimulation may also work and I know for a fact that is a possibility in the Cleveland Clinic, though I don't know the closest person that can do cingulotomy in the country and I'm looking into it.

This group supposedly has a list of providers that do cingolotomies.
http://www.ocfoundation.org/
 
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That's what I was wondering about - I would think DBS would be a nice thing to try before resorting to a cingulotomy. On that note, would a cingulotomy even be indicated anymore or would failure to respond to DBS rule it out? And is there insurance coverage for either?
 
I don't know. Whenever you try experimental interventions, insurance companies don't want to pay for it. I know of only one insurance provider (forgot which one but it's a one hardly anyone carries) that'll pay for TMS.

Sometimes the institution will pay for it if the patient agrees to be a subject in their research. I just looked it up on Medscape and it stated that DBS had some bad outcomes while cingulotomies had no bad outcomes whatsoever but didn't work all the time.
 
Atypicals at low dosages do have some benefits in augmentation but that's it for OCD. I'd consider them in treatment resistant cases if someone found a med that benefited the OCD but didn't get the patient symptom-free (then again how often do we ever get someone with OCD completely symptom-free?)

Anytime a patient appears to have OCD one should at least run the possiblity this is psychosis in the differential.

With regards to my specific patient, this guy experiences inability to urinate with several meds, even meds not known to cause this problem. Given that several of the antipsychotics have anticholinergic properties, I'm staying away from them on this guy.
 
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Interesting. No one even raised the idea of antipsychotics, especially for those whose obsessive thoughts can border on psychosis.

I learned about the management of OCD from some of big players in OCD research who also saw the treatment-refractory patients in their tertiary clinics. They tended to stress that although comorbidity between OCD and schizophrenia is high (33%) the phenomenology of obsessionality without insight is different to the primary delusions of schizophrenia and should not be treated as such. conventional antipsychotics tend to have no effect on OCD symptoms, though atypicals are often added for augmentation. I questioned this contradiction. Theoretically, it is suggested that atypicals are used not because of the delusional-like nature of severe OCD but because of the 5-HT1a action of the atypicals. There are apparently animal studies suggesting that 5-HT1a agonism reduced compulsive behavior.
 
Right now I've got him on SAM-E (yes we're that desperate), and if this doesn't work I'm thinking ECT or cingolotomy.

There is no evidence of ECT in OCD, it doesn't make sense why you would suggest this. TMS and deep TMS have been floated about as possibilities, again the evidence base is weak but at least you are not broadly attacking the brain. I would never refer a patient for anterior cingulotomy the side effects are so severe they are worse than OCD itself. I am not too keen on functional neurosugery for epilepsy either the patients never seem to do better and often complex psychological overlay. DBS on the other hand I think could be promising. It doesnt appear to have the side effects of chopping out important bits of people's brains and definitely helps for movement disorders. I've often thought OCD is like a movement disorder and certainly the basal ganglia appears to be involved so it would make sense DBS so applied would help for OCD as well as movement d/o.
 
Theoretically, it is suggested that atypicals are used not because of the delusional-like nature of severe OCD but because of the 5-HT1a action of the atypicals

Yep, that's the reasoning. D2 blockage apparently offers no benefit.

There is no evidence of ECT in OCD, it doesn't make sense why you would suggest this
I wouldn't say no data, but the data is weak. The reasoning is we're scooping down to the treatment choices of desperation. While a cingolotomy may or may not work, some people would reasonably want to give ECT a try before their brains are sliced and diced. That's the reasoning. A good physician's job is to offer treatment options and have the patient make informed decisions, not decide for them.

I'm thinking of trying inositol, haven't given that a try yet.

SAM-E, inositol, fish oil. plus maybe combining Tramadol (that did work for the patient) along with a med that would help him urinate such as perhaps Prazosin are considerations I got for this guy. The Prazosin may help out well with urinating, but also with PTSD related nightmares the patient suffers. If I find anything that works on this guy to some degree that he is willing to take indefinitely then I'll try augmentation treatment with Namenda and maybe an atypical. Believe me I don't want this guy to be my first OCD-brain surgery patient.

The only thing I think I'm missing from publishing this case is I want a happy ending and I ought to start having the guy fill out a YBOCS to gauge his improvement.
 
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Why can't he urinate? Insufficient production, lack of urge, can't contract?
 
I'm really not sure.

Every single medication with any hint of anticholinergic properties always stopped him from urinating but even ones that aren not known to cause this problem.

The problem here is the only meds that ever worked for him also prevented him from urinating too. His other doctors were never able to isolate a cause.
 
Just throwing something weird out with minimal knowledge base. My assumption would be that the brain in general has a higher level of ach activity than the detrussor, just given how infrequently it is contracted. Could an ach agonist at a certain dose cause central insensitivity to ach and leave the detrussor responsive?

This is probably contraindicated for a few reasons, but this will be my last dumb question 😉
 
One would have to wonder, what are the chances of having such severe OCD and PTSD? I would assume that some psychological testing be completed prior to anything extreme (surgery) being discussed with the patient. The statement that he made to you seems very provocative and sets my "male borderline" alarm off. In any case, I highly respect your ability to sniff out PD. Another issue that I have been finding is that a number of my bipolar patients (pure mood and schizoaffective types) take on many OCD traits at times.
 
Oh he actually is a male borderline, but the borderline has largely improved with DBT therapy. Pretty sharp!

The odds of having OCD and PTSD are rare, but they are not mutually exclusive. His borderline sx are actually very much under control. No self mutilation for several months, he does not suffer emotional dysregulation more than I'd expect that someone with his other conditions, and he is very polite and cooperative.

When he called me 3AM, no I didn't interpret that as a borderline manipulative thing. He apologized during the call, and that was the only time he ever called the servicelate at night,...actually ever. He is always respect, calm, and insightful. E.g. the guy's kept a journal of every single med that's been tried on him, he regularly practices CBT skills, and he's been a model patient in inpatient when I had him on one occasion.

When I first saw him, the only thing that tipped me off to possible borderline was he had his PTSD trauma as a child so I asked him about borderline symptoms then asked to see his forearms that were heavily scarred.
 
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We have a practicioner up here who is an OCD specialist and sends tough cases to Sweden, I think, for anterior cingulotomies. (I guess it's cheaper there? Maybe you can get a Volvo too? 😛) These have been for severe cases and he reports good outcomes (including one IM physician who returned to practice).
 
The only thing I think I'm missing from publishing this case is I want a happy ending and I ought to start having the guy fill out a YBOCS to gauge his improvement.

Even if you don't get a happy ending isn't it still worthy of publishing?
 
Atypicals at low dosages do have some benefits in augmentation but that's it for OCD. I'd consider them in treatment resistant cases if someone found a med that benefited the OCD but didn't get the patient symptom-free (then again how often do we ever get someone with OCD completely symptom-free?)

Anytime a patient appears to have OCD one should at least run the possiblity this is psychosis in the differential.

With regards to my specific patient, this guy experiences inability to urinate with several meds, even meds not known to cause this problem. Given that several of the antipsychotics have anticholinergic properties, I'm staying away from them on this guy.

Oh, didn't realize you hadn't tried an atypical and just assumed you had. That is really one of the first line augmentations strategies after an SSRI and SNRI. You might have a hard time getting someone to do cingulotomy without trying this first.
 
Even if you don't get a happy ending isn't it still worthy of publishing?

IMHO not really because it won't add something. All of us had patients where treatments didn't work (or you will).

Chimed-you're right about atypicals being done as a first-line augmentation strategy. Problem here is we haven't yet established a foundation medication for him to be on. The only things that worked for him also forced him to catheterizing himself, and he doesn't like that.
 
I haven't tried Memantine for OCD. I have used it for pseudobulbar palsey and it worked. There's now several studies showing Memantine could be of benefit in OCD though not to the degree where even if one read all the articles I'd think they'd use it early on.

Could an ach agonist at a certain dose cause central insensitivity to ach and leave the detrussor responsive?

Sorry, didn't get to this one yet. This is a theory. This case certainly is weird.
 
New to me pt, would love some input: 30 yo CF with 10 yr hx of picking (legs-->lips-->eyebrow), has a very excoriated patch in R lateral eyebrow which she insists began with a superficial skin infxn (d/t overplucking), but now has insight into the fact that while she *feels* the picking will improve its appearance, she now knows it makes it worse and wants to stop. Remote hx of eating d/o behaviors, none active now, but a lot of body image distortions/loathing.

On stimulants for yrs (terrible historian for drugs/doses) (ADHD dx'd in teens), has been on Vyvanse 100 mg/d for "a long time". Has had therapeutic trials of prozac, celexa, wellbutrin, effexor--currently on zoloft, 200 mg for past 3 months. No noticeable improvement in picking behaviors (spends 1.5 hrs/day on them, hides it from her fiance, but the disfigurement is quite obvious). Hx PSA, sober from heavy EtOH & rec MJ x several weeks. No real obsessional thoughts endorsed, no hx of any psychotic behavior. No hx any atypicals.

Is there any evidence to support either an increase in picking behaviors with stimulant use OR efficacy for atypicals in decreasing picking behaviors? Doing the pubmed search now, but thought I'd check in with my expert colleagues 😉
 

Yeah, that's what I thought. I think getting her to go off the Vyvanse will be a hard sell. My sense is that she's less ADHD than the offspring of high-achieving high-income parents (atty & MD), and that the stimulant use is more reflective of sub abusing tendencies than true ADHD. Anyway, she's engaging poorly here in tx, so I'm not even sure I'll have the opportunity to have the conversation about stimulants with her.
 
an increase in picking behaviors with stimulant use

Yes, very yes, particularly in someone with underlying compulsive skin picking or even trichotillomania behaviors. Talking to patients, the enhanced focus of stimulant use seems to be allocated to the minutiae that are picked. And I assume we were mainly talking about vyvanse, prescriptions stimulants, what have you - but note that it is similar to the skin-picking behaviors that are seen with crystal meth and sometimes cocaine.
 
Anyone ever give this? Have papers on it? I know of 3 people (one using Memantine as monotherapy) and they claim their compulsions are much better controlled.

Yep. (think I already replied above to you...) I'm in the process of submitting a case report on it right now. There aren't that many papers on it, mostly just case reports. Although I typically keep up more with pediatric OCD, so you might want to do a pubmed search for adult cases.

Here are some references:
Aboujaoude, E., Barry, J. J., & Gamel, N. (2009): Memantine augmentation in treatment-resistant obsessive-compulsive disorder: an open-label trial. Journal of Clinical Psychopharmacology, 29(1), 51–55. doi:10.1097/JCP.0b013e318192e9a4

Hezel, D. M., Beattie, K., & Stewart, S. E. (2009): Memantine as an augmenting agent for severe pediatric OCD. The American Journal of Psychiatry, 166(2), 237. doi:10.1176/appi.ajp.2008.08091427

Pasquini, M., & Biondi, M. (2006): Memantine augmentation for refractory obsessive-compulsive disorder. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 30(6), 1173–1175. doi:10.1016/j.pnpbp.2006.04.013

Stewart, S. E., Jenike, E. A., Hezel, D. M., Stack, D. E., Dodman, N. H., Shuster, L., & Jenike, M. A. (2010): A single-blinded case-control study of memantine in severe obsessive-compulsive disorder. Journal of Clinical Psychopharmacology, 30(1), 34–39. doi:10.1097/JCP.0b013e3181c856de







 
Yep. (think I already replied above to you...) I'm in the process of submitting a case report on it right now. There aren't that many papers on it, mostly just case reports. Although I typically keep up more with pediatric OCD, so you might want to do a pubmed search for adult cases.

Here are some references:
Aboujaoude, E., Barry, J. J., & Gamel, N. (2009): Memantine augmentation in treatment-resistant obsessive-compulsive disorder: an open-label trial. Journal of Clinical Psychopharmacology, 29(1), 51–55. doi:10.1097/JCP.0b013e318192e9a4

Hezel, D. M., Beattie, K., & Stewart, S. E. (2009): Memantine as an augmenting agent for severe pediatric OCD. The American Journal of Psychiatry, 166(2), 237. doi:10.1176/appi.ajp.2008.08091427

Pasquini, M., & Biondi, M. (2006): Memantine augmentation for refractory obsessive-compulsive disorder. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 30(6), 1173–1175. doi:10.1016/j.pnpbp.2006.04.013

Stewart, S. E., Jenike, E. A., Hezel, D. M., Stack, D. E., Dodman, N. H., Shuster, L., & Jenike, M. A. (2010): A single-blinded case-control study of memantine in severe obsessive-compulsive disorder. Journal of Clinical Psychopharmacology, 30(1), 34–39. doi:10.1097/JCP.0b013e3181c856de







Looking forward to seeing your case report. Just read the study out of the McLean residential OCD program, and I really hope larger studies begin soon.
 
I learned about the management of OCD from some of big players in OCD research who also saw the treatment-refractory patients in their tertiary clinics. They tended to stress that although comorbidity between OCD and schizophrenia is high (33%) the phenomenology of obsessionality without insight is different to the primary delusions of schizophrenia and should not be treated as such. conventional antipsychotics tend to have no effect on OCD symptoms, though atypicals are often added for augmentation. I questioned this contradiction. Theoretically, it is suggested that atypicals are used not because of the delusional-like nature of severe OCD but because of the 5-HT1a action of the atypicals. There are apparently animal studies suggesting that 5-HT1a agonism reduced compulsive behavior.

Could you please clarify the contraindication?

Re: 5-HT1A--are you referring to partial agonism actions of Geodon and Abilify? Could you please elaborate?
 
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I learned about the management of OCD from some of big players in OCD research who also saw the treatment-refractory patients in their tertiary clinics. They tended to stress that although comorbidity between OCD and schizophrenia is high (33%) the phenomenology of obsessionality without insight is different to the primary delusions of schizophrenia and should not be treated as such. conventional antipsychotics tend to have no effect on OCD symptoms, though atypicals are often added for augmentation. I questioned this contradiction. Theoretically, it is suggested that atypicals are used not because of the delusional-like nature of severe OCD but because of the 5-HT1a action of the atypicals. There are apparently animal studies suggesting that 5-HT1a agonism reduced compulsive behavior.

I'd clarify the difference between "OCD" sx's in schizophrenia (aka schizo-obsessive d/o) and traditional OCD. I remember learning that the compulsive behaviors were ego-syntonic in schizo-obsessive, rather than ego-dystonic in traditional OCD. Bu tI haven't reviewed the literature in some time.
 
Yep, that's the reasoning. D2 blockage apparently offers no benefit.


I wouldn't say no data, but the data is weak. The reasoning is we're scooping down to the treatment choices of desperation. While a cingolotomy may or may not work, some people would reasonably want to give ECT a try before their brains are sliced and diced. That's the reasoning. A good physician's job is to offer treatment options and have the patient make informed decisions, not decide for them.

I'm thinking of trying inositol, haven't given that a try yet.

SAM-E, inositol, fish oil. plus maybe combining Tramadol (that did work for the patient) along with a med that would help him urinate such as perhaps Prazosin are considerations I got for this guy. The Prazosin may help out well with urinating, but also with PTSD related nightmares the patient suffers. If I find anything that works on this guy to some degree that he is willing to take indefinitely then I'll try augmentation treatment with Namenda and maybe an atypical. Believe me I don't want this guy to be my first OCD-brain surgery patient.

The only thing I think I'm missing from publishing this case is I want a happy ending and I ought to start having the guy fill out a YBOCS to gauge his improvement.

Please help me out here. Is it that 5-HT2a antagonism may have therapeutic effectiveness in OCD and that D2 blockade does not? Are atypicals superior to typicals in OCD?

Any relevance of 5-HT1a?
 
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Please help me out here. Is it that 5-HT2a antagonism may have therapeutic effectiveness in OCD and that D2 blockade does not? Are atypicals superior to typicals in OCD?

Yes. This benefit was only seen in atypicals and at low dosages. At higher dosages, there was no more benefit. There apparently is no benefit with D2 blockage.
 
Well, my 100mg/day of Vyvanse faux-ADHD pt (with hx of PSA, including meth & cocaine) balked when I told her to stop it (mind you, she looks like she's taken a potato peeler to her eyebrow... and is planning a July wedding). Tried to get her on Abilify too. Dropped out of tx. Not a shocker. Ah well.
 
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