Psychiatry & Psychotherapy Podcast - Q&A with Dr. Cummings Part 2

Episode Date: May 29, 2024

In this episode, we welcome back Dr. Michael Cummings to answer questions sent in by podcast listeners. Topics include Valproic Acid, Lithium, Treating Veterans, Restless Leg Syndrome, and much more.��   By listening to this episode, you can earn 1.25 Psychiatry CME Credits. Link to blog. Link to YouTube video.

All right, welcome back to the podcast. I am joined today with Dr. Michael Cummings. He is a psychopharmacologist, a regular contributor to this podcast. And today we are doing part two Q&A. We may just keep this going. We have too many questions to answer in part two. So we'll try our best. So the first one came from a listener who enjoyed an episode from Back from the Abyss. That's one of my friends' podcasts and uh craig dr craig covered if you were stuck on a desert island needing to treat you know people for the foreseeable future with only three psychiatric medications which three would you choose and why um i by the way i'm happy to be back i would probably choose um a dopamine antagonist anti-psychotic, it's a bit difficult to choose which one.

I might choose something like risperidone or haloperidol. I would also choose a mood stabilizer, the most versatile being lithium, although if I'm on a desert island, my ability to monitor lithium may be limited. So I would think about valproic acid, although it's coming up with a lot of issues now in terms of reproductive risk for both men and women,

to the point that in the EU it's severely restricted and in the UK, essentially women under 55 can't be prescribed of oproic acid unless they are on a permanent form of birth control. But mood stabilizer would certainly be the second category, and then I would likely think about an antidepressant, probably the most likely would be certuline among the SSRIs because it has the fewest interactions is fairly well tolerated by most people and can treat both depression and anxiety disorders.

Nice. Okay. So I, I'm curious, what is the research on valproc acid and min in pregnancy? Basically, as people are likely to recall, among its other properties, valproic acid is a histone deacetylase inhibitor, meaning that it blocks the acetylation of the protein that is involved in the winding and unwinding of DNA. As it turns out, one of the side effects of inhibiting the activity of the acetylation of histone is to increase methylation. in sperm DNA. First in animals they discovered that was related to neurocognitive, neurobehavioral problems in mice. Just recently, I believe it was Sweden, Finland, and Norway conducted a registry review

since they have birth to death registries and found indeed that there was an increase rate of neurobehavioral disorders in children born to men who were taking valproic acid within three months of their partner becoming pregnant. This is some good education here. Okay. So as of yet, the FDA has not moved on any of this data, but given that the European Union and the EU,

UK have, it's very likely the FDA will require restrictions or limitations in the use of alproic acid in the not too distant future, I would think. Okay. I think I would lean more towards lithium, personally, for the mood stabilizer. You know, level, I don't know, I usually get a pretty decent level at 900 to 1200. I think I would just look for side effects. Yeah, I mean, you can certainly do it without measuring levels. And I'm presuming on my desert island, I don't have a lab.

I think that was good. Yeah. I think I would go more for olanzapine for the antipsychotic just because, you know, you get the sleep aid as well. And I can use it for bipolar if you needed to. Well, I guess you could use other antipsychotics too, but it tends to be the one I go to for someone with bipolar. And I'd probably agree with you with the searcherlane for the antidepressant. So yeah, pretty similar. Yes.

Yeah, my hesitation with the olanzapine has to do with, of course, its metabolic side effects. Well, perhaps on a desert island, if we don't have a McDonald's, will be better. Yeah, so we're on a desert island. We're not eating very much, probably. So, you know. Okay, so if you had the choice, I guess this goes, into the last question as well, between depicote and lithium to treat bipolar, which would you choose? And is there any reason why you would choose depicote, I guess, because we've already

talked about mostly you would choose lithium? Yeah, I would choose lithium over depocote or divalprox if those were the only two mood stabilizers available. Lithium has a broader spectrum of activity, it is very good at treating mania and hypomania. It is moderately good at treating depression, which valproic acid is not especially antidepressant. It also reduces suicide risk and reduces violence risk better than valproic acid does. So in general, I see lithium as being the better mood stabilizer. Its caveats, of course, are that it has a narrow therapeutic index and also has a number of issues related to renal function. So we've had a couple of questions on this, so I may jump ahead here. What is Dr. Cummings take on the notion that lithium has less value effect

than previously thought on reducing suicidal risk in patients for the treatment of bipolar disorder and MDD. What's the current opinion about lithium's value in this regard? And they're referring to this article, which is Katz 2001 in JAMA, which looked at 519 veterans, and they were randomized to lithium or placebo. The mean lithium concentration at three months was about 0.54 mill equivalent per leader in the bipolar group, so a lower level than we might treat most bipolar patients. No overall difference in repeated suicide-related events between treatments were found. Hazard ratio was 1.10 and the confidence interval spanned past 1. Well, my comment would be my comment would be to one. One, they essentially,

used what is a sub-therapeutic dose of lithium. And indeed, most studies have found that the optimal range for maintenance treatment with lithium and bipolar illness is in the range of 0.6 to 1.0 millimoles per liter, with the more severely ill or more frequently cycling patients doing somewhat better at 0.8 to 1.0. So my comment on that would be, yeah, if you give people subtherapeutic amounts of medication, it makes it less likely the medication will work. My other comment would be that is that there have been subsequent studies with much larger sample sizes. I believe the last one was published in 2017, and I can send you that to post,

which the subsequent studies have all found that lithium produced a significant. statistically significant decrease in suicide risk. Would you also look at like when you test veterans, sometimes it's harder to get findings that we might find elsewhere. I remember a TMS study, which was not very positive for veterans. Any thought on that population in general? Well, one, it's, of course, in most cases,

heavily skewed toward male patients. So it's not a good representation of the population as a whole. The other comment I would make, I worked in the VA for seven years, and a lot of the veteran patient population is fairly complexly ill much of the time. They often have, in addition to bipolar illness or other psychiatric illness issues with substance abuse as well as often multiple issues. intercurrent medical conditions. My main critique of this study would be, well, one, it's a fairly small sample size.

Most of the subsequent studies have had ends in the thousands and have been both genders and a much more community-based sample that use therapeutic doses. Okay. Is hydroxazine safer than diphenhydramine in terms of, anti-cholonergic burden? Yes. That one can give you an unequivocal answer. Diphon hydrogen was the very first antihistamine

to be produced, I believe, in 1946. It is highly anticholinergic. Hydroxazine was produced in the early 1950s. It was assumed to be anticholinergic because it was another antihistamine. However, subsequent KI studies, dissociation constant studies, have found that depending on species, the KI ranges from 600 to greater than 10,000. Affinity for a receptor is one over the KI, which means 1 over 600 to 1 over greater than 10,000.

Essentially, that means the drug has little affinity for acetylcholine receptors. Yeah, so it's... So hydroxazine in summary is a very good antihistamine and not very anticholundic at all. No. No, it's not very, in fact, one of the things I like about hydroxazine is that it is essentially purely antihistaminic. If your goal is to block H1 receptors to reduce anxiety or to sedate the person, it's a much cleaner approach than using drugs with receptor affinities that you may not want, like diphenhyrame or, for example, quixopine.

What's the top dose you could go up to on hydroxazine for sleep? Well, the daily maximum in Europe is set at 100 milligrams. It's set fairly low. it used to be 400 milligrams until they noticed that at higher doses in mice, it can prolong QT interval. There haven't been any human reports of QT prolongation with hydroxazine so that in a lot of registries, you'll still see the maximum listed as 400. Some systems like the California Department of State Hospitals lowered the daily maximum to 200 milligrams a day.

For most people, though, essentially, if you don't get good sedation at 50, well, 25 to 100 milligrams, you probably need to be looking at alternative sedative agents. And that's, you know, people vary hugely in terms of how sensitive they are to histamine blockade. There are some people who you give them 25 milligrams of, of hydroxazine and they may wake up tomorrow sometime.

There are other people who can easily swallow 100 milligrams and don't look as if they've taken anything. So it depends a lot on the individual. Okay, please explain how lithium can be used once a day at bed time for renal safety. Okay, basically, let's start with why you can use it once a day. the tissue half-life of lithium is longer than its plasma half-life. The brain half-life, meaning how long lithium stays in neurons, has a half-life of 28 hours.

So, greater than a day. So you really don't need to divide the dosing to have an adequate concentration in the brain. On the other hand, the shorter plasma half-life allows you to give the kidneys a rest between doses, lithium tends to accumulate in the distal principal cells of the nephron, where it interferes with protein kinasee and the formation of aquauporin 2 channels, and ultimately, if it accumulates to a high enough degree, it will actually interfere with mitochondrial function,

and you'll get essentially non-functional nephrons as a result. the more often you dose lithium, the more likely it is that the nephrons will suffer, basically. And there's no reason to divide the dosing, given the brain half-life. Excellent answer. Okay. This person said they have a patient with chronic catatonia that is really only responsive to ECT. is this sustainable long-term treatment? And how long, how often can they get this?

The answer is yes. How often they will need ECT will vary, depending on their catatonia. Unfortunately, there are some people who are pharmacoreistant, meaning that their catatonia does not respond to any medication, either benzodiazepine at robust doses or clozapine, has also been used to treat catatonia. And they require ECT.

Usually that's an acute course of two to three times per week until they are stable and then a gradual lengthening of the ECT interval until you find the longest period that can go without the catatonia beginning to reemerge. We have two patients at the hospital where I work who receive,

monthly ECT and both have been receiving monthly ECT for Catatonia. I believe one has been having ECT for five years and the other seven years. And rope by robust doses of lorazepam, we're talking about like what, 15, 18 milligrams sometimes per now? 15 up to, I think the largest dose we've given was 24 milligrams a day. Could you ever see it being stretched out ECT longer than one month? Could you stretch it out to two months or three months? Well, there aren't enough of these patients to know very well.

I think basically you stretch the interval as long as you can, and it becomes fairly obvious when the person, you know, if you go from four weeks to five weeks and things are fine, good, then you go to six weeks. But at some point, you'll run into a time period where the catatonia begins to reemerge before the next DCT treatment. And, you know, so essentially it's a case of finding,

essentially a case of dose finding with respect to ECT. Okay, so an anonymous person asks, another doctor increased a patient Xanax when you, their provider, their psychiatrist, were trying to cut it down over months. What would you do? This is a recurring problem, sometimes known as the too many cooks in the kitchen problem.

I think the best you can do is indeed collaborate with your colleague and have a discussion with your colleague that you're attempting to reduce the use of El Prasalam Xanax and go over the reasons why and see if you can enlist their aid in letting you be the manager

for the El Prasalam dose. Most of the time people are cooperative, particularly if approached in a friendly, respectful manner. There's never a guarantee of that, of course, but the best initial approach is to try to work with your colleagues so that you can avoid the too many cooks problem. Okay.

So what are subtle signs of the Dark Triad, dark triad being Machiavellianism, psychopathy, narcissism? Basically, this is really a question about, in the psychopath, how can you tell if someone, somebody is headed down a psychopathic pathway. Most of the studies in children and adolescents show early evidence of indifference to the welfare of others and a tendency toward meeting the diagnostic criteria for conduct disorder. If those are occurring, certainly then an investigation of that person's, if you will,

psychological structure deserves further attention. All the way back to CLECLEC, he noted that many of the prisoners he interviewed who were psychopaths had histories, indeed dating back to childhood, suggesting that they were headed in that direction. Now, one of the findings he had that was very important was that 75% of those who were psychopathic and madden Invalescence went on to become adult criminals, but 25% did not.

So there is such a thing as a pro-social psychopath. What we have never figured out since then, however, is how to tilt the balance in the direction of making it more likely that people with the biological underpinning of psychopathy will become productive members of society rather than criminals. Okay, if you were to teach a child how to identify someone who is dark triad, how would you teach that child? Probably have a discussion with a child about does this person seem indifferent to others, meaning indifferent to the needs or cares of others? Do they ignore rules? Are they always breaking the rules? They don't care what happens to other people. Those are often, I think, the earliest signs of somebody

who's headed down the psychopathic pathway. Okay, so knowing all that you know about forensic psychopathology, and for those of you listening to the first time, Dr. Cummings is someone who works at a forensic hospital who has seen many violent sexual predators. How would you tell parents to teach their kids to not be groomed by a predator? Is there anything that you would teach the parents to do so as to make it more difficult for the child to be groomed.

Probably the most important element in preventing grooming is to be sure that there is an open communication channel between the child and the parents. Groomers are typically only successful when they can isolate the child from the parents. So, you know, teaching the child to look out for phrases like, well, why don't we talk with, don't tell your parents about this. That's been one of the unfortunate features of the internet is it has made it easier for some groomers to get children involved in a conversation online and move them further and further down the pathway of being groomed

while not telling their parents. So good open communication with the parents is vital to prevent that. Yeah, did you, let's see, did you hear about this, let's see, settlement for the Boy Scouts, sex abuse settlement, something like, I don't know, how many, I don't know, it seemed egregious the number of survivors. Yes, I heard about the settlement and the number of survivors who had been abused ran into the thousands, I believe.

Yeah, with more than 12. 12,000 survivors in the case. So I would say, to answer this myself, I would say, who are you being groomed by as the parent to trust with your child? Because usually there's a grooming of the parent as well to trust this person

in a way that you normally wouldn't trust a person, maybe. There's also that element of educating your children. children that you know about what is and is not appropriate interaction about touching and so forth. The other thing I would encourage parents to do is fairly early on teach their children the correct names of things related to their genitals so that, you know, they can come and accurately report. And if there is a violation and it goes to court, they make much better witnesses, if they can accurately describe what happened. Okay, so here's someone.

I want to ask if there are any clinical pearls for differentiating between restless leg syndrome and ecthesea? Yes, there are. Restless leg syndrome, of course, is a syndrome which occurs typically when the person lies down and is attempting to go to sleep. They have an uncomfortable feeling in the lower extremities,

it is relieved by they're getting up and walking around, but then tends to return when they get back in bed and try to go to sleep. In contrast with that, ectathiasia tends to be present throughout the day. It's not specifically associated with bedtime or attempting to go to sleep. It is a more generalized restlessness and may be much more, were associated with subjective feelings of anxiety as well, whereas the restless leg syndrome is more purely a physical sensation. With restless leg syndrome, an important feature for it is to check the person's iron status

because iron deficiency is a frequently overlooked cause of restless leg syndrome. Also, restless leg syndrome usually responds exceedingly well to either a low-dose benzodiazepine or to a small dose of dopamine agonist at bedtime, things like amantadine, for example. Very good. Another person asked, when do you check a lithium level

if you're giving once a night at bedtime dosing? They're confused about checking it at 24 hours or 12 hours. Okay. The standard and what all of the labs are using as their standard for lithium is a 12-hour trough. So that when you get back the lab report and it says the lithium level is this and this is the usual range. That usual range is based on a 12-hour trough. So for example, if the person takes their lithium at 8 p.m., then they need to get their blood drawn, at least reasonably close to 8 a.m.

Or if they go, you know, if they take it at 10 p.m., then aim for around 10 a.m. Although the question was about lithium, there is a difference for valproic acid extended release. As you know, there's most common forms are valproic acid, depakene, divalprox, DR, which the delay is only a few minutes, just to get it to the distal stomach. And then there's the extended release, which has a very slow release. For the extended release, unlike 12 hours for the other two,

you need to either measure it at 24 hours, or if you have a 12-hour measurement, you can estimate the 24-hour trough by dividing it by 1.3. Hmm. That's good. I like that. Okay, what's your best advice for treating dementia patients with behavioral disturbances in the long-term care setting.

Okay. The dementia patient with behavioral disturbance, the medications that have been, that have data to support their effectiveness include Mementine in combination with the acetylcholineostase inhibitors, the SSRIs, and tracidone when given in small doses multiple times per day. Trazidone 12.5 to 25 milligrams, two or three times a day to decrease psychomotor agitation. The antipsychotics do work for those people who are demented

and suffer from psychotic signs and symptoms. However, the antipsychotics increase mortality rates, in the elderly demented coming back to the Veterans Administration. The Maust study was the largest study done in this area. And they calculated number needed harm, which they calculated harm as death and extra death in the next six months.

Halloparadol, for example, had a number needed harm of eight. So if you treat eight patients, you'll kill one of them with Halthol. The mood stabilizers also had problems. I think Valproic acid had a number needed to harm of 26. Resperidone was in the low 20s around 22. The best of the dopamine antagonist was quatyapine

with a number needed to harm of 32. In contrast to that, the number needed harm with the SSRIs was right around 150, which is actually close to the non-medicated mortality rate in people of similar age. I was looking at a study, this was a antipsychotic drugs use and risk of stroke and myocardio infarction. A systematic review and meta-analysis is published in 2019. In this study, they were looking at 7,08 articles, and, you know, and, you know, and, you And what they found was that with patients with dementia, the risk of issues was much lower.

So in the cohort general population without dementia, without psychiatric illness, the risk increased twofold for stroke, hazard ratio, 2.3. however the risk among patients with dementia was much lower at 1.16 and they also found there was no clear association among studies of psychiatric populations has a ratio 1.44 and across the confidence interval across one any thoughts on treating different populations like it seems like there's a lower risk of treating people in the psychiatric population, in the dementia population, with antipsychotics. There does seem to be, it's not very clear why this group is different, although a number of researchers have found very similar numbers, it may be that having, particularly a long-term psychotic illness, may in some way be protective, perhaps by long-term psychotic illness, may in some way be protective,

perhaps by long-term exposure to antipsychotic medications. We don't frankly know that very well, however. It's certainly clear, for example, that in people with schizophrenia spectrum disorders, they actually have a lesser risk of things like tardide dyskinesia than, say, people with an anxiety disorder or a mood disorder who are exposed to a dopamine antagonist antipsychotic. why they are at lower risk. Frankly, I don't think anyone knows the answer to that.

Okay, here's the next one. What are your thoughts on co-prescribing benzodiazepines and stimulants? How problematic is this? And I can remember one time I got probably the most upset at any resident moonlighting that I'd ever been upset at. And if you're listening to this, I'm not going to. to give away your identity to anyone, so don't worry. But this resident was

moonlighting and treating someone with the Xanax, two, TID, and concerta, like, or like, no, I think it was it was Adderall, like 60 milligrams a day. I'm like, what are you doing? You've never learned this from anyone here. Anyways. In general, my comment would be

pharmacologically, that makes very little sense since you're treating the person with medications that are directly opposing each other. You're giving the person the stimulant, hoping to target in particular the cortical D1 receptors in the frontal lobe, and you're also giving them a drug that increases gabaergic effects at GABAA receptors,

which are also most plentiful in cortical regions in the frontal lobe. So you're trying to turn up the activity of those neurons and turn it down at the same time, which makes, frankly, very little sense. Now, I would admit there can be subtleties if someone, for example, is on a routine dose of stimulant and takes an occasional dose of benzodiazepine for acute anxiety. For example, might also suffer from social anxiety disorder, something like that. that, you know, their stimulus will be less effective when they take the benzodiazepine,

but if it's limited, that may be not entirely unreasonable given the clinical circumstances, but from a pharmacological standpoint, it makes no sense to give somebody a drug to increase neuronal activity and a drug to decrease neuronal activity at the same time. It kind of reminds me of patients who have a history of using methamphetamines, and alcohol heavily at the same time? Yes. And the reason they do that is because, indeed, the alcohol does take the edge off of the methamphetamine.

But, you know, compared to reasonable levels of treatment with, say, methylfinidate or mixed amphetamine salts like Adderall, at clinical doses, people who abuse methamphetamine are using gigantic doses of methamphetamine typically. and that's why the high can take on a very harsh edge or characteristic in terms of paranoia, jitteriness, anxiety. And then indeed people will attempt to soften that by co-administering alcohol or other sedative hypnotics. Okay, here's the next one. From a patient who says,

The knowledge I've gained from Dr. Cummings in these episodes has greatly shaped the way I practice and education. patients. I'm so grateful for every episode he does with you. Thank you. This person goes on to say, I'm seeing many patients in practice who are taking crantum capsules and drinking crantam tea daily, attempts to decrease or cease use result in severe withdrawal symptoms. I was wondering if you had any guidance on using Suboxone to taper or any pearls regarding management of these patients. Like most addictions, it can be difficult to get the person off of the thing they have become addicted to. Drugs like buprenorphine have been used usually in a time-limited fashion, although time-limited in this context usually means a year or two, while the person is gradually tapered off of the crantum.

It's not a very common addiction, but it does seem to be one of the more stubborn addictions when people become addicted. Okay, here's the next person. I inherited several patients from another provider on high doses of daily benzodiazepines, especially Alprazolam. What are your thoughts on management and tapering these individuals? Do you feel as though the pendulum has swung too far? far in the direction of demonizing benzodiazepines?

I think benzodiazepines have reasonable uses, albeit they're fairly limited. Certainly if you have somebody who is acutely agitated or is in need of an acute muscle relaxant, for example, or who needs to have a seizure stopped, those are perfectly appropriate uses of benzodiazepines. Interestingly, most of the studies looking at longer-term efficacy has found that, and I know there are exceptions, everyone has one or two patients who swear by their benzodiazepine. But for the most part, when people have looked at efficacy over the long-haul, benzodiazepines are not very effective in the long term for much of anything.

Now, do I believe that means that their demonic drugs well know. But I think we should indeed encourage people not to use them except as essentially brief rescue medications because they create more problems than they fix for most individuals. And now in terms of tapering somebody who's been on a benzodiazepine for a long time, be prepared for it to be a very long and slow process. The problem most clinicians have is they want to go too fast. When I've had patients who've been on a benzodiazepine for decades, the taper and withdrawal often takes one to two years.

Another person asks, like, okay, do you, how do you taper? Like, let's say someone's on one milligram of clonopin per day, how would you just decrease it by 0.25 every couple months or would you work with a compounding pharmacist? What's your thoughts? Most of the people I've seen who are truly having problems with, for example, clonazepam, their dose is typically much higher than one milligram a day. It is a very slow process. I typically don't taper people from, for example, from clenazepam faster than, a quarter to a half milligram per month. And I work with the patient to find the rate that is comfortable for them.

The exception of that is people who've only been on a benzodiazepine for a very short time. It takes about 30 days for somebody to become tolerant of a benzodiazepine. So if the person's only on it for a short period of time, taper becomes much less of an issue because they have not become tolerant of the pencypine. Okay, so Dr. Pearson asks for patient who benefited from clozapine but cannot continue

due to inability to follow up with regular labs, for whom single antipsychotics are ineffective, what is the best combination of antipsychotics you would recommend? Probably the very next best would be a combination of olanzapine, and a potent D2 antagonist. Although having said that, the response numbers for somebody who has truly treatment-resistant schizophrenia via the

housed data, which were based on the older cane criteria, the response rate to all of the antipsychotics other than olanzapine is 0% to 5%. It's not very impressive. So as monotherapy, those drugs have a 95% failure rate.

Olanzapine at concentrations of 120 to 150 nanograms per milliliter, where you get a little bit of glutamate modulation has a success rate of 7%. I haven't seen very good numbers on the combination, but my guess would be you do get some additive effect, so you may be looking at a response rate of more in the 9%. to 12% range. Still not very impressive. I mean, I wouldn't want to go to my doctor and say,

well, you're proposing treating me with something that has an 88 to 91% probability of failure. But sometimes that's the best we can do. Is there any ability with this type of patient to get approval do the risk factor of them not being compliant with labs maybe, but is there any way to bypass Clozapine REMs or to write the letter and say, hey, I have a patient who will die if they don't continue this, they're not going to monitor, but they really need to be on this. And they've been safe on it for years, so the risk of developing any side effects is pretty low. Presently, there is no way around the Closopine Rims program.

However, there may be in the near future a number of people in psychopharmacology, including myself, have been lobbying the FDA to drop the monitoring requirement at some point. The most aggressive recommendation has been 18 weeks, meaning stopping monitoring after 18 weeks, because that's when you start to see it very large falloff in the rate of severe neutropenia, all the way out to most conservatively about two years and then not monitoring beyond that. Probably the strongest data in this area comes from the Europeans for a number of decades now. The Europeans have not required A and C monitoring beyond 12 months.

their mortality rate from severe neutropenia does not differ from ours. It's about one per 10,000 cases, arguing that all of the additional monitoring we're doing is not moving the needle and therefore has no reason to exist. We'll see what the FDA does, but I know the FDA is actually contemplating maybe scrapping the RIMS program altogether, which I have to say I don't think would be such a bad thing.

Now, the other thing about labs these days is we have gone to the point where there is now technology available where you can obtain an ANC count by finger stick rather than by venipuncture. It is not quite as accurate as venipunction,

but it's typically within five of the vina puncture value, which is adequate for monitoring purposes. For a lot of patients, that removes the barrier because you can actually set up one of the finger stick machines in a clinic. I know in San Bernardino County, the county clinic is working toward having a couple of their clinics actually have the monitoring device in the clinic. it's basically a finger stick the person puts a drop of blood on essentially a strip you put the

strip into the machine and about two minutes later you get an ANC value I'm going to look into that I have a couple of patients that have been hesitant well the family would like to do it but the patients are completely unwilling yeah the I think there is more than one device on the market. Now the very first one that came out was made by Athelis. And the machines, I think, are around $1,000. And the test strips are around $35. Doable.

Doable. Okay, I'm going to look into that. Really cool. Okay, so Trichotillomania. Hmm. How do you treat patients with trichotillomania? Trichotillomania, in terms of theory, fits into what has become known as sort of an extended version of obsessive, compulsive disorder, leading people to try SSRIs and other serotonergic agents to decrease it, frankly with somewhat mixed results in number of studies indicate a decrease.

there's also been some evidence to support use of naltrexone for trichetillomania, as well as for things like drinking and kleptomania. These appear to be tricketillomania fits into a category of compulsive behaviors, essentially being driven by the dorsal striatum, which of course is the same area that does give rise to obsessive-compulsive disorder, people are looking for ways to target that area. Okay, from a clinical psychiatrist who has listened to Dr. Cummings, many times, asks, what is your opinion of research efficacy of TMS versus ECT?

Any update on the availability of St. TMS in the general population? Basically, ECT remains our most effective treatment, if you're talking about treating major depressive disorder, psychotic disorders, catatonia, bipolar illness. TMS has more modest efficacy, however, it can be quite effective as either a primary or adjunctive treatment in major depressive disorder. It's also shown efficacy in suppressing auditory hallucinations. It, probably it's the main thing that makes it attractive of course is it is easier to administer than the ct is very good uh any thoughts on the saint tms protocol this is uh for those of you don't know it's a lot of tms uh i haven't seen much data to suggest that it is qualitatively better

than other forms of TMS. People have tried very frequent, frontal, and frequent bilateral TMS. And there are some indications of improved efficacy when you do that, but it's not, you know, it's not a day and night difference between that and the more standard TMS protocols.

The initial studies, to me, look very positive. So are you seeing something that I'm not seeing. I'm seeing that it's, well, it can be effective. It's not like, oh, this is now going to cure mood disorders across the board. They're expensive, too, for the centers that I know about. I mean, we're talking about, you know, over a week of TMS, which, you know, they give the TMS throughout the day, eight hours a day. It could be $20,000 for a week treatment.

So, yeah. The private pay TMS centers are very expensive. So you're not as excited about the same protocol. No. There's often at the initial outset of something like the St. TMS or ketamine's another example, a lot of very positive excitement, and there's also often at the beginning a very huge placebo effect. Okay, ketamine versus es ketamine. The person says, I have numerous ECT referrals for young clients being prescribed and failed.

S ketamine, I can't find evidence to support this kind of es ketamine use, and I'm wondering if there's research information I missed. No, basically, es ketamine is a viable treatment for some people with. depression but it is not in most patients as effective as infusion of ketamine but even infusion of ketamine is is limited it's very rapid in effect but it's effect is fairly short-lived and the more you give it the shorter its antidepressant benefits become so it can my own view of ketamine is it can be an excellent treatment for somebody with severe depression who's at suicide risk and you're needing to get them to a more euthymic state quickly and then transition them to a more long term treatment. I don't think either ketamine infusion or as ketamine is very viable as an ongoing treatment for mood disorder. There are some other uses that people have been putting it to. People have been indeed looking at.

at a number of psychedelics including ketamine to see if it would enhance some forms of psychotherapy. Early indications are fairly positive, but indeed they're just that. They're early indications. Yeah. When I look at the effect size, even for those studies, they're not larger than partial. Partial for me, for a depressed patient is like, you know, effect size of two to three is what Loma Linda partial is getting. We monitor patients on a regular basis. So for me, when I think about if someone's not being treated effectively in the outpatient, I think partial first. They get to partial and there's, you know, in partial for a couple months, they're still not doing well. sometimes we think about

ECT. What's your thoughts on borderline personality disorder and the effectiveness of ketamine and ECT? I'm not sure I've seen much solid data to support ECT for either

of those indications. Certainly somebody who develops a concurrent major depressive episode who might be an ECT candidate or a ketamine candidate, but I don't see borderline personality disorder as, well, it doesn't have a primary pharmacological treatment, really.

I think even a really good ketamine outpatient provider, I know, he tends to stay away from treating patients with borderline personality disorder with ketamine. Well, these are people who are already more prone than the average person. to dissociative states. And of course, ketamine is a dissociative anesthetic. So I would have some prepudiation for that reason. The other thing is I haven't seen very good outcome data suggesting that any medication is, if you will,

greatly effective for treating borderline personality disorder. medications in that context seem to be mostly useful in targeting specific symptoms so that the person can manage their life better and make progress in something like dialectical behavioral therapy yeah and i would i would also um today i'm released in an episode today as in May 17th when we're recording this, me and Dr. Cummings are recording this May 17th, on reflective function, which is probably one of the coolest assessment tools I've seen on attachment and also on the capacity to really understand borderline per size disorder. So essentially, what?

reflective function scale is, is they measure the adult attachment interview, and then they look at certain questions that gauge your internal reflectiveness of yourself and other people as you do the adult attachment interview. And they gauge this on an 11-point scale, negative 1 to 9, and 9 being the highest. And most patients with borderline a size sort of score around a three. In one good study by Levy et al, they found that reflective function increased from three to four. Five is average, so three to four is a big jump. With a year of transference focus therapy, interestingly, in this specific study, dialectical behavioral therapy showed no increase, and supportive psychotherapy should no increase.

Transferred's focus therapy is very much based on the relationship with the patient and the therapist. And so it's thought that this could help potentially your understanding of your early life attachments. So that's maybe why your reflectiveness would increase. So yeah, I would say that is kind of for me like this new like pinnacle of understanding because when you measure therapists reflective function, you're going to find this really interesting. We think about common factors, right? And like, what makes one therapist better than another, better than another therapist? So common factors have been kind of the buzzword for that. Empathy, therapy, Theoretical Alliance, everyone will say that kind of stuff. There was a new study that I stumbled

upon. It was, if you look at the difference between one, the best therapist and the worst therapist, 70.5% of it could be made sense of by the reflective function. score of the therapist. So the therapist is talking about their childhood, age zero to 12. You're gauging their ability to reflect deeply, meaningfully. That predicted actually the best versus the worst therapist and the outcomes. And 70.5% though, I was like blown away, right? So that's what I think about when I think of borderline precise order and I think of the effective treatments that may be coming in the horizon, what we need to do is we need high reflective function therapists working with these types of clients, whether that's DBT mentalization-based

therapy, transforms-focused therapy. There needs to be some emphasis on the interpersonal relationship with the therapist. Yeah, any thoughts on that? Yeah, I think that's a very promising area. And I, again, the psychotherapies that have shown good outcomes with borderline personality disorder are much more effective than medications are in treating the underlying disorder. Medications are largely useful for helping the patient manage some of the more intense symptoms. But that's about it. Medications are a much more symptomatic treatment in this context rather than addressing the underlying disorder. Now, I think that a lot of people have an unrealistically negative view of borderline personality disorder.

I've always been impressed by the fact that if you wait long enough, meaning till the borderline person is middle age, because they've done these sorts of studies, typically by the time the person reaches their 40s, half of those people who were once met the diagnostic criteria no longer do. Yeah, and I would say in the mentalization-based study, which I know probably the best, did they meet the criteria anymore, the vast majority of them, after treatment, who were followed for, I think, five years afterwards, they did not meet the criteria. I think 85% did not meet the criteria. And so, you know, when we think about personality disorder, it's a little bit,

a misnomer because personality seems like it's forever. It's like never changing. And we've talked about this, Dr. Cummings and I before. It's affect dysregulation is the primary thing underlying it that may be, you know, maybe there's better names for it. Yeah. Well, indeed, I know there has to be a better name out there because borderline is a complete misnomer in the sense that these people are.

not bordering on anything, they are what they are. And what they are, are people who have a difficult time modulating their mood state, their affective state. Okay. So, let's see, well, we are at about an hour. And yeah, anything that you are, that's still on your mind that you wanted to kind of teach the audience here, teach the next generation of providers. Maybe we could go to a fun question. Okay. Or just like a Dr. Cummings question. Someone was interested, like, here you go. What is your story, Dr. Cummings? Can you tell us about your training pathway and how you ended up where you are? Okay. I can in brief. I was actually as an undergraduate, I was a history major and physics minor, and a odd combination to begin with.

I went to grad school in physics, and in the process of doing that, I worked as a teacher's assistant, TA, and was in charge of a couple of classes for pre-med students and pre-nursing students, who needed to get their, if you will, their non-heavy-duty calculus physics prerequisite. So I spent a lot of time teaching them, got interested in medicine, and from that, went from grad school in physics to medicine. It was actually intending originally

to pursue a career in neurosurgery, but became blind, because I was so very interested in the brain, switched to psychiatry, went to Loma Linda University for Psychiatry Residency, and then I went to an NIH extramural program located at UC San Diego. At that time, it was termed a fellowship

in psychobiology and psychopharmacology, which got me into research and information interest in medications, then worked for the VA for seven years, and then migrated from the VA to the California Department of State Hospitals, which is a roundabout way of saying I don't think I've ever been quite able to make up my mind what I want to do when I grow up. Well, I'm like very curious, like, if you don't mind telling the story of how you lost your site? Yeah, I was serving in the U.S. Navy, and I came down with a viral infection, which was, the viral infection itself was fairly ordinary, upper respiratory infection, except that it caused a lot of

oral nasal ulceration. The infection died down after about 10 days, but then subsequent to that, I developed a corioretinitis, which basically resulted in the death and rupture of retinal blood vessels. Awful. Awful. It's like, I'm like, I'm in awe that you have been able to gain the level of knowledge that you have. Despite that setback, you just kept going. psychologically what was that like like it was difficult of course because I got you know I had I frankly had intended to make a career of the Navy perhaps

aiming for aerospace medicine of course I got discharged from the Navy and then had to figure out well now what luckily I had good relationships with a couple of the people in the Department of Psychiatry at Loma Linda, and they were open to the idea of my pursuing psychiatry residency, which I did, and with some technical aides along the way, I've gained a lot of information education by using computers and screen readers, which I have to say the screen readers fortunately have improved

the very early one sounded a lot like a Norwegian with a very bad head cold and they actually now have fairly pleasant relatively human sounding voices which are much easier

to listen to when you're reading something what what advice would you give to your younger self like let's say the younger self that was just starting or somewhere in their psychiatry residency probably the best piece of advice I could give people is to always

read, be curious and read. You know, as Osler at the beginning of the 20th century, end of the 19th century, made the comment that it's amazing, how many psychiatrists, or not psychiatrists, physicians practice without reading. Of course, it's also amazing how badly they practice.

Physicians and psychiatrists need to remain curious. We need to be educating ourselves. There's an awful lot we still don't know. And frankly, we owe it to our patients to educate ourselves as much as we can, and then to attempt to apply that to helping our patients. Okay, so someone's hearing this like, yes, I would like to read. We have, of course, on our website, Psychiatrapodcast.com, we have a lot of this stuff for free.

You can go on there. You can download PDFs of any of Dr. Cummys episodes. And in those episodes, we hyperlink a ton of articles that Dr. Cummys has recommended over the year. So that's one place you could start. Are there any other books that are your like maybe like top three? pharmacotherapy books that you recommend at this point? Yeah, certainly, as you know, this is a somewhat biased answer, and it's because I work quite a bit with Steve Stahl.

I would say his essentials of psychopharmacology is an excellent beginning for most people. It's readable, it's of sufficiently short length that it's not quite the tome that the comprehensive textbook of psychiatry is even a little shorter than the synopsis of that book, although that also is an excellent general background reference for psychiatry. I think probably the most important thing, though, about reading is to develop the habit of spending 30 minutes a day reading, whatever you're interested in, but reading. reading. Pick your favorite journals and just the typical you know typical journal article is about 3,500 to 3,500 words. If you're a fairly fast reader, you can easily read that in 30 minutes.

And the main trap I see most people fall into is they see things they want to read, but they're busy, we're all busy, and they go, well, I'll get to it later. Well, unfortunately, often later never comes. If you can basically rigidly set aside some quiet period of around 30 minutes, you know, have a cup of tea, a cup of coffee, read an article.

Okay. And, you know, if you do that every day, that's 365 articles a year. Well, I think that's excellent advice. And I would say if you're trying to get through one of those big textbooks, what I used to do is I would just say, okay, I'm going to try to read 15 pages a day or 10 pages a day, depending on what rotation I was in,

and then just clip through them. And, you know, if you commit to that, you'll get through 100 pages, 10 days. and, you know, it's a good way to get through a big book. So, awesome. Well, thank you, Dr. Cummys. Really appreciate it. Okay.

I'm coming on. Appreciate it. I know, I mean, I wasn't able to read all of these questions. We'll get to some more. If you're part of the email list, if you go on the psychiatry, psychotherapy, or sorry, psychiatrypodcast.com. And you look at our resources. You'll be on our list automatically. And we'll do this again.

I think this could be like a 20-part series. and 200-part series. The endless question. The endless questions. All right, take care. Okay, thanks.