Insomnia meds

[Tangerine123]

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PGY-1 (Europe) having difficulties with patients with insomnia in the depression ward.

Currently I try with my patients the following order.
1) Sleep Hygiene
2) Baldrian and natural remedies
3) Zopiclon 3,75-7,5mg (only a few weeks)
4) Quetiapin (25mg)
4) Here is where I find it hard. Usually would go with Pipamperon 40mg.

I've seen colleagues go with Agomelatin, Mirtazapin, Amitriptyline, Imipramine. Yesterday I had a Patient requesting Trazodon, because she had it prescribed in the past.

Other meds that are approved for sleep disturbances here in are mutiple Benzos, Trazodon, Doxepin, Melperon, Olanzapin, Prothipendyl, Chlorprothixen, Levomeprozamin. I've also seen Antihistamines.

Every time I ask somebody, then answer tends to be that it's how they learned it from their Attendings and everybody has a "favorite" go-to med.

It seems that in the US many of these meds are not approved for sleep disturbances. So I've found little to no info. Pipamperon isn't even in my pharmacology book (Stahl's Prescriber's Guide).

Any tips would be appreciated, thanks

 

[Sikrouf]

I would try doxepine before quetiapine about every time i reckon

 

[jbomba]

I would try doxepine before quetiapine about every time i reckon

Is it fair to say seroquel at a low dose is just Benadryl with potential of more side effects?

 

[Taddy Mason]

If you dig into the lit for pharmacotherapy for insomnia the data really isn’t that great. The AASM guidelines basically admit this and even in their recs there appears to be some clear subjective bias. For acute hospitalization preaching good sleep hygiene can be limited as there are often a lot of factors beyond patients’ control but I’ll provide education on things that they can control. For outpatient I’ll push behavioral changes much harder and screen for potential underlying sleep disorders. As far as meds, I usually go with trazodone first and prescribe so patients can experiment with doses (e.g., 25-100mg). It gives patients a sense of control over managing their insomnia and minimizes them coming back with resistance to dose adjustments/continuing try it/approaching other options with preconceived notions because they had limited effect from too low a dose or side effects/morning sedation from too high a dose. Anecdotally, I’ve seen better results prescribing this way, though I highly suspect it’s largely placebo. Trazodone also has good data showing it prolongs stage 3 sleep, though there’s no good data demonstrating that this translates to clinical benefits. If there’s an indication for an antidepressant and ongoing sleep issues I’ll obviously skew towards something more sedating. I try to avoid GABAergic agents unless it’s a really reliable patient where I trust it will be short term and truly used as needed (…and GABAergic agents clearly disrupt sleep architecture as well). I pretty much refuse to consider quetiapine for insomnia unless someone is inpatient, prescribed it for insomnia outpatient, and continuing v. not isn’t a hill worth dying on in a given situation. As mentioned above, it’s purely acting as an antihistamine with way more long term side effects and I work in an area where there’s a higher prevalence of people misusing/diverting it (I realize there are much worse things to misuse, but it’s the principle of the matter and people tend to divert it in order to finance obtaining more problematic substances). If there’s limited benefit from pharmacotherapy and clearly behavioral and/or ongoing sleep hygiene issues I don’t feel obligated to keep prescribing or going down a rabbit hole of trying med after med or perpetually switching meds.

 

[michaelrack]

Will often prescribe trazodone for adults with MDD and insomnia. I try to avoid it in kids due to studies suggesting kids on a combination of SSRI and trazodone tend not to have their depression remit, especially for prozac and paxil (I believe, can't find the studies on my cell phone )

 

[happypsychmd]

Hi, absolutely agree with the response by @Taddy Mason. Sleep hygiene practices are #1 step (no screens one hour before bed, limit caffeine intake, exercise 30 minutes per day, use bed only for sleeping, etc). Next I try melatonin which is OTC and very safe (no more than 10 mg per day). Next we talk about hydroxyzine 50 mg nightly (like Benadryl but prescription and works fairly well for some folks for insomnia). Then we try Trazodone 25 mg to 100 mg as described above. I always avoid Z-drugs and medicines like Ambien given that they mess up sleep architecture, cause a lot of weird side effects (sleep walking), are addictive, you building a tolerance to them, and people often need increasing doses over time. Doxepin can be a good medicine for sleep, and I've seen it used in with success, especially an adult or geriatric psychiatry population. I agree with the rule of avoiding Seroquel if at all possible as it causes significant side effects and weight gain, and at doses lower then 50 mg is really just acting as an antihistamine.

 

[Stagg737]

If you dig into the lit for pharmacotherapy for insomnia the data really isn’t that great. The AASM guidelines basically admit this and even in their recs there appears to be some clear subjective bias. For acute hospitalization preaching good sleep hygiene can be limited as there are often a lot of factors beyond patients’ control but I’ll provide education on things that they can control. For outpatient I’ll push behavioral changes much harder and screen for potential underlying sleep disorders. As far as meds, I usually go with trazodone first and prescribe so patients can experiment with doses (e.g., 25-100mg). It gives patients a sense of control over managing their insomnia and minimizes them coming back with resistance to dose adjustments/continuing try it/approaching other options with preconceived notions because they had limited effect from too low a dose or side effects/morning sedation from too high a dose. Anecdotally, I’ve seen better results prescribing this way, though I highly suspect it’s largely placebo. Trazodone also has good data showing it prolongs stage 3 sleep, though there’s no good data demonstrating that this translates to clinical benefits. If there’s an indication for an antidepressant and ongoing sleep issues I’ll obviously skew towards something more sedating. I try to avoid GABAergic agents unless it’s a really reliable patient where I trust it will be short term and truly used as needed (…and GABAergic agents clearly disrupt sleep architecture as well). I pretty much refuse to consider quetiapine for insomnia unless someone is inpatient, prescribed it for insomnia outpatient, and continuing v. not isn’t a hill worth dying on in a given situation. As mentioned above, it’s purely acting as an antihistamine with way more long term side effects and I work in an area where there’s a higher prevalence of people misusing/diverting it (I realize there are much worse things to misuse, but it’s the principle of the matter and people tend to divert it in order to finance obtaining more problematic substances). If there’s limited benefit from pharmacotherapy and clearly behavioral and/or ongoing sleep hygiene issues I don’t feel obligated to keep prescribing or going down a rabbit hole of trying med after med or perpetually switching meds.

So my only critique(s) with this are that sleep hygiene has really poor data and IMO does jack squat unless a patient is actually motivated for specific change. I can count on one hand the number of my patients who have significantly benefited from education with sleep hygiene, and most people already know the majority of that info (most common thing they don't know is usually the bed is for sleep and sex rule). I'd also argue that the data is probably decent for the guidelines, and there are at least 5 groups internationally that have similar recommendations (did a major QI project on insomnia treatment), and the DOD/VA has a document that's around 140 pages that gets fairly comprehensive.

That being said, I generally agree with minimizing GABA meds (unless absolutely necessary) and that quetiapine is a hard no from me 99% of the time. I also use a similar approach with Trazodone, but do so with Doxepin doses 5-20mg. In my experience, most patients who are going to benefit do so with 10mg and usually don't need 20mg or 25mg doses.

Also agree 100% with ruling out other sleep disorders, especially OSA. I've "cured" a number of patients from their depression/anxiety just by sending them for a sleep study and getting this diagnosed. It's amazing how much people improve when they don't stop breathing in their sleep every 10 minutes...

 

[FlowRate]

Because you're on an inpatient unit, there's only so much you can do, although you did mention at times having multiple weeks of med trials. If you regularly have ~4-6 week inpatient admissions then it would be worth looking into having a staff person get trained up on CBTI and offering groups for that.

On an outpatient basis, I heavily emphasize CBTI and we have some good resources for it (an app called MyStrength has really well done modules for CBTI.)

CBTI is not just sleep hygiene. I often socialize patients a bit into the idea that the initial stages of CBTI may be counterintuitive or difficult (sleep phase restriction) but that it's worth it in the long run.

Agree with michaelrack that trazodone is common in US and especially good for situations where you want the antihistaminic effect for sleep but want to avoid the anticholinergic effect that some of the other common (antihistaminic and anticholinergic) options have.

If I offer a benzo or z drug it's usually with the understanding that it's a time limited treatment to kick start a second go at CBTI. It's generally not ideal since you want things as steady as possible w/r/t psychopharm before starting CBTI. Patients should slowly taper the med over the course of CBTI protocol.

There is the rare patient who may be a reasonable candidate to continue long term (otherwise well psychologically, tried multiple other treatments, gave CBTI a legitimate shot.)

I lean toward escitalopram when people have MDD/GAD with concurrent sleep onset/maintenance difficulty due to higher rate of sedation (usually mild) with that med. And away from fluoxetine (which can be more activating.)

 

[Stagg737]

Long post incoming:

Currently I try with my patients the following order.
1) Sleep Hygiene
2) Baldrian and natural remedies
3) Zopiclon 3,75-7,5mg (only a few weeks)
4) Quetiapin (25mg)
4) Here is where I find it hard. Usually would go with Pipamperon 40mg.

Yikes, not gonna lie I hate this algorithm and the only one I agree with is the zopiclone. EBM guidelines suggest the below as your treatment algorithm:

Always recommended:
1. CBT-i (BBT-i if CBT-i isn't realistic) as gold standard

Med options:
2. BZDr agonists or melatonin rec agonists (ramelteon, though VA/DOD is neutral here)
3. Orexin antagonists
4. Doxepin

Other options generally not recommended (weak recommendations against):
5. Trazodone
6. Benzos (some studies include Temazepam as a valid option, otherwise recommended against)
7. Mirtazapine/other sedating antidepressants
8. Antihistamines
9. Antipsychotics

--------

However, that is making sweeping generalizations, the reality of treating insomnia is much different. Identifying the TYPE of insomnia and the root etiology is essential. If it is truly a primary form of insomnia that needs to be directly treated then the above is more valid, but if it's secondary to anything else then obviously that should be addressed.

I always talk to patients about CBT-i and educate them on the CBT-i Coach app. I've heard some docs say they don't think it is worth it, but speaking with a specialist at APA last year there is actually data that using the app by itself without a counselor does still have positive evidence, and my patient population reflects that. If we're not talking to them about CBT-i, IMO we're failing to meet the standard of care.

If meds are necessary, then I look at whether it's acute or chronic insomnia. I'm more likely to try a short course of Ambien or even Temazepam if the insomnia is acute (new within the past 3-6 months) to try and re-initiate a more normal temporal sleep pattern. I always discuss with these patients that they will only get the 2-3 week supply and we will NOT be refilling the med. There are obvious exceptions, but I generally avoid GABA-ergic meds (other than occasionally gabapentin) for sleep, especially chronically.

If they're going to need something more long-term, I start with doxepin at 5-10mg and give the patients some room to adjust for themselves up to 20mg. I don't go above 25mg for insomnia alone, as I've found that if they're not having a decent effect at 25mg, increasing isn't likely to provide lasting benefits.

I think ramelteon and the orexin antagonists like Belsomra can be great options, but getting insurance to approve this in the US is often difficult and sometimes not possible, so those usually end up as later options d/t insurance dictating care and what patients can afford.

Trazodone is usually my second option. Despite the data being weak for it, it is generally very well tolerated and can be effective at very low doses. The guidelines even add an asterisk to trazodone and say "trazodone will likely continue to be regularly used due to its perceived efficacy and generally tolerable side effect profile".

After that it's really dependent on what else is going on with the patient. Other meds I'll sometimes use are mirtazapine, gabapentin, amitriptyline, or doxylamine. I generally avoid the other antihistamines as tolerance and need to increase dosing if scheduled is something I've seen a lot. I also NEVER start an antipsychotic medication for insomnia unless it's being used primarily to treat something else. Imo, the long-term metabolic side effects are just not worth the risk that comes with the sedating antipsychotics. However, you may be able to better justify this on an inpatient unit, especially if using an atypical to augment for depression.

I don't have experience with agomelatine, so I will not comment there. However, the data for valerian root for sleep is pretty terrible and ensuring product quality and dose consistency have repeatedly been pointed out as problems in pretty much every trial on valerian that's been put under the microscope. It might be a decent option for some people, but not something I actually recommend.

On the outpatient side there are more options (sleep restriction can be fantastic for some), but acutely you're going to be much more limited.

 

[Merovinge]

I think ramelteon and the orexin antagonists like Belsomra can be great options, but getting insurance to approve this in the US is often difficult and sometimes not possible, so those usually end up as later options d/t insurance dictating care and what patients can afford.

Curious how much these might change the game when readily available. Have a "classic" bipolar I patient that failed some sleep medications but has done amazingly on Dayvigo which I think is only being covered due to the repeated RTC/IP stays prior to it's initiation. They sleep 8 hours a night like clockwork since, only return of slight manic sx was a few day gap when the pharmacy didn't have it in stock.

 

[jbomba]

What are thoughts on the data for lunesta as a depression augmenter? The data I've seen suggests lunestas mechanism differs slightly from other z drugs in that it targets multiple sub units of the gaba-A receptor similar to that of benzo. In patients with mdd and insomnia and/or anxiety it might be a good option. The study I saw also saw improvements in depression scoring even when controlling for sleep which would suggest it's perhaps working independent of simply alleviating insomnia.

 

[tr]

I always avoid Z-drugs and medicines like Ambien given that they mess up sleep architecture, cause a lot of weird side effects (sleep walking), are addictive, you building a tolerance to them, and people often need increasing doses over time.

Say what. I thought the benefit of Z-drugs over benzos etc was that they maintain/improve sleep architecture

Effect of zolpidem on sleep architecture and its next-morning residual effect in insomniac patients: a randomized crossover comparative study with brotizolam - PubMed

This study was conducted to determine the effect of zolpidem (ZOL) 10 mg orally on the sleep architecture and the next-morning residual effect in patients with non-organic insomnia (ICD-10) as compared to the effect of brotizolam (BTM) 0.25 mg orally, a widely used short-acting benzodiazepine...

pubmed.ncbi.nlm.nih.gov

Effects of zolpidem on sleep parameters in patients with cirrhosis and sleep disturbances: A randomized, placebo-controlled trial - PubMed

Four weeks of 5 mg daily zolpidem in CTP class A or B cirrhosis patients with insomnia led to significant increases in TST and sleep efficiency and improvement in polysomnographic parameters of sleep initiation and maintenance without any significant change in sleep architecture.

pubmed.ncbi.nlm.nih.gov

Effects of zolpidem on cyclic alternating pattern, an objective marker of sleep instability, in Japanese patients with psychophysiological insomnia: a randomized crossover comparative study with placebo - PubMed

In Japanese patients with psychophysiological insomnia, zolpidem increased sleep stability by significantly improving the overnight CAP rate. Zolpidem also improved sleep depth and sleep quality, both subjectively and objectively.

pubmed.ncbi.nlm.nih.gov

So my only critique(s) with this are that sleep hygiene has really poor data and IMO does jack squat unless a patient is actually motivated for specific change

I don't know, I've seen a lot of improvement from basic sleep hygiene, but mainly the recs that have to do with circadian rhythm cues. I don't put much stock in the efficacy of lavender-scented-bath-before-bedtime recs, but modern life is basically a recipe for circadian dysrhythmia, especially in the winter. People stay indoors all day, get no natural light, and then spend their entire evening in front a screen that spews blue light and eliminates endogenous melatonin secretion. A lot of my patients who had no idea this pattern could contribute to their sleep woes report significant improvement once they make a small targeted effort to get some daytime sunlight and get rid of the bedtime TV/computer habit. You can't tell a depressed patient to get out there and exercise (they'll look at you like, if I could get up and exercise I wouldn't be coming to see you) but lots of them can manage sitting in a chair outdoors in their backyard or balcony for 20 minutes before noon, and that can jump-start a virtuous cycle of better sleep, improved energy, and the ability to engage in more behavioral activation.

Always recommended:
1. CBT-i (BBT-i if CBT-i isn't realistic) as gold standard

Agree if you're talking about chronic insomnia, but the OP is on an inpatient unit, where CBTi isn't a realistic intervention.
I love CBTi. I am trained to do it and I offer it myself. But for patients with short-term sleep disturbance related to psychiatric illness, it's overkill. Most of them are going to get better when their mood/anxiety episode resolves, which will come sooner if sleep is improved. Short-term use of sleepers is very helpful in this situation, in a much shorter timeframe than a 6 week course of CBTi. I always make sure patients know that pharmacological sleepers are intended for short-term use only.

CBTi-Coach, I have recommended a bunch but never had a patient actually follow up with it. I don't think they can really implement a lot of it without more direct therapist guidance.

 

[FlowRate]

Always recommended:
1. CBT-i (BBT-i if CBT-i isn't realistic) as gold standard

Med options:
2. BZDr agonists or melatonin rec agonists (ramelteon, though VA/DOD is neutral here)
3. Orexin antagonists
4. Doxepin

Other options generally not recommended (weak recommendations against):
5. Trazodone
6. Benzos (some studies include Temazepam as a valid option, otherwise recommended against)
7. Mirtazapine/other sedating antidepressants
8. Antihistamines
9. Antipsychotics

It's interesting to me how the EBM guidelines basically recommend Z-drugs yet a lot of institutional guidelines and individual practice/field of psychiatry generally shies away from those medications. I wonder if reflects common practice (starting something forever after an end-of-visit doorknob complaint or inbasket message) vs a more thorough/nuanced assessment of primary/secondary and onset/maintenance/midde-night, etc.

 

[FlowRate]

avoid GABA-ergic meds (other than occasionally gabapentin)

Quick side-note, gabapentin probably has the worst generic name because it has no known direct effect on GABA or GABA receptors. It's a glutamate / voltage-gated Ca channel blocker.

 

[Merovinge]

Quick side-note, gabapentin probably has the worst generic name because it has no known direct effect on GABA or GABA receptors. It's a glutamate / voltage-gated Ca channel blocker.

This is crazy, I consider myself an above average psychopharmacologist and prescribe this medication semi-regularly and somehow this was completely lost upon me. Appreciate the pearl, definitely random humbling of the day.

 

[Wheatbread]

I generally do the Vistaril, Trazodone, Remeron, Seroquel algorithm. Seems that Doxepin is used quite a lot, used it a little in residency. I’ll have to try it more often. I’ve been generally avoidant of TCA due to s/e and OD risk. What dose do you feel comfortable going up to if patient is also on an SSRI/SNRI?

 

[jbomba]

I generally do the Vistaril, Trazodone, Remeron, Seroquel algorithm. Seems that Doxepin is used quite a lot, used it a little in residency. I’ll have to try it more often. I’ve been generally avoidant of TCA due to s/e and OD risk. What dose do you feel comfortable going up to if patient is also on an SSRI/SNRI?

Can I ask what is the purpose of Seroquel if vistaril isn't working? Aren't they hitting the same receptors (at sleep doses)? Not challenging you just genuinely curious.

 

[Wheatbread]

Can I ask what is the purpose of Seroquel if vistaril isn't working? Aren't they hitting the same receptors (at sleep doses)? Not challenging you just genuinely curious.

I don’t use it often and prefer not to, but will. Honestly nothing technical about mechanism, just seems to work with some folks.

 

[VA Hopeful Dr]

Quick side-note, gabapentin probably has the worst generic name because it has no known direct effect on GABA or GABA receptors. It's a glutamate / voltage-gated Ca channel blocker.

Its because its structurally similar to GABA

 

[FlowRate]

Can I ask what is the purpose of Seroquel if vistaril isn't working? Aren't they hitting the same receptors (at sleep doses)? Not challenging you just genuinely curious.

In my experience hydroxyzine is the mildest commonly used antihistamine sleep aid at typically used doses. So basically any other antihistamine option would be a step up in perceived potency/effect for most patients.

Its because its structurally similar to GABA

Right, understandable name in terms of origin, bad name in terms of remembering the mechanism.

 

[calvnandhobbs68]

I generally do the Vistaril, Trazodone, Remeron, Seroquel algorithm. Seems that Doxepin is used quite a lot, used it a little in residency. I’ll have to try it more often. I’ve been generally avoidant of TCA due to s/e and OD risk. What dose do you feel comfortable going up to if patient is also on an SSRI/SNRI?

Doses <25mg doxepin is basically a pure H1 antagonist. Very little risk at those doses when combining with an SSRI although I tell patients there’s some theoretical risk of course or if they decide 20mg isn’t enough, let me take 100mg.

I usually use 10-20mg since 3-6mg doses are way more expensive and you basically get the same effect at 10mg. If people really can’t tolerate the 10mg because it’s too sedating but helps with sleep maintenance, then I’ll sometimes try to use that to justify a prior auth for 3 or 6mg.

 

[clozareal]

Doses <25mg doxepin is basically a pure H1 antagonist. Very little risk at those doses when combining with an SSRI although I tell patients there’s some theoretical risk of course or if they decide 20mg isn’t enough, let me take 100mg.

I usually use 10-20mg since 3-6mg doses are way more expensive and you basically get the same effect at 10mg. If people really can’t tolerate the 10mg because it’s too sedating but helps with sleep maintenance, then I’ll sometimes try to use that to justify a prior auth for 3 or 6mg.

There's a liquid formulation that is generic that I prescribe to get to 3-6mg without having to use the more expensive 3mg and 6mg pills.

 

[Taddy Mason]

So my only critique(s) with this are that sleep hygiene has really poor data and IMO does jack squat unless a patient is actually motivated for specific change. I can count on one hand the number of my patients who have significantly benefited from education with sleep hygiene…

I always talk to patients about CBT-i and educate them on the CBT-i Coach app. I've heard some docs say they don't think it is worth it, but speaking with a specialist at APA last year there is actually data that using the app by itself without a counselor does still have positive evidence, and my patient population reflects that. If we're not talking to them about CBT-i, IMO we're failing to meet the standard of care.

These statements are a bit incongruent.

 

[splik]

These statements are a bit incongruent.

Not really. CBTi ≠ sleep hygiene. Sleep hygiene is not a treatment for insomnia in and of itself. CBTi is effective for insomnia.

 

[Taddy Mason]

Not really. CBTi ≠ sleep hygiene. Sleep hygiene is not a treatment for insomnia in and of itself. CBTi is effective for insomnia.

Sleep hygiene is a component of CBTi and it was never suggested that education on sleep hygiene alone was adequate treatment for insomnia.

 

[clausewitz2]

Sleep hygiene is a component of CBTi and it was never suggested that education on sleep hygiene alone was adequate treatment for insomnia.

But plenty of folks do seem to think sleep hygiene education is a meaningful intervention, and that what @Stagg737 was reacting to, I imagine. Handing someone a sheet with sleep hygiene tips is CBTi in just the same way that handing someone a sheet of cognitive distortions is the same as CBT.

Perhaps you would never just provide sleep hygiene education alone, but I promise that this is not an uncommon approach in practice.

 

[deleted1100659]

1. I hate medications for sleep. They don't work well long term quite often. I think of insomnia as a symptom rather than a disease, I want to treat the root of the problem.

2. In addition to the above, why arent they sleeping? Anxiety at night? Using large amounts of caffeine before bed? Doing stuff they shouldnt be doing? Usually theres a reason behind it. I want to treat the reason ideally

3. If I do sleep medications would generally be trazodone>vistaril or gabapentin (depending on cause of the insomnia)>remeron scheduled (if they have depression and no major metabolic issues)> doxepin (if <65 years old). Ramelteon is an option too. I never do controlled substances for sleep. Hate seroquel for sleep but see it used quite often. I never use it for sleep if I can avoid it unless they actually have comorbid bipolar depression

 

[happypsychmd]

Say what. I thought the benefit of Z-drugs over benzos etc was that they maintain/improve sleep architecture

Effect of zolpidem on sleep architecture and its next-morning residual effect in insomniac patients: a randomized crossover comparative study with brotizolam - PubMed

This study was conducted to determine the effect of zolpidem (ZOL) 10 mg orally on the sleep architecture and the next-morning residual effect in patients with non-organic insomnia (ICD-10) as compared to the effect of brotizolam (BTM) 0.25 mg orally, a widely used short-acting benzodiazepine...

pubmed.ncbi.nlm.nih.gov

Effects of zolpidem on sleep parameters in patients with cirrhosis and sleep disturbances: A randomized, placebo-controlled trial - PubMed

Four weeks of 5 mg daily zolpidem in CTP class A or B cirrhosis patients with insomnia led to significant increases in TST and sleep efficiency and improvement in polysomnographic parameters of sleep initiation and maintenance without any significant change in sleep architecture.

pubmed.ncbi.nlm.nih.gov

Effects of zolpidem on cyclic alternating pattern, an objective marker of sleep instability, in Japanese patients with psychophysiological insomnia: a randomized crossover comparative study with placebo - PubMed

In Japanese patients with psychophysiological insomnia, zolpidem increased sleep stability by significantly improving the overnight CAP rate. Zolpidem also improved sleep depth and sleep quality, both subjectively and objectively.

pubmed.ncbi.nlm.nih.gov

I don't know, I've seen a lot of improvement from basic sleep hygiene, but mainly the recs that have to do with circadian rhythm cues. I don't put much stock in the efficacy of lavender-scented-bath-before-bedtime recs, but modern life is basically a recipe for circadian dysrhythmia, especially in the winter. People stay indoors all day, get no natural light, and then spend their entire evening in front a screen that spews blue light and eliminates endogenous melatonin secretion. A lot of my patients who had no idea this pattern could contribute to their sleep woes report significant improvement once they make a small targeted effort to get some daytime sunlight and get rid of the bedtime TV/computer habit. You can't tell a depressed patient to get out there and exercise (they'll look at you like, if I could get up and exercise I wouldn't be coming to see you) but lots of them can manage sitting in a chair outdoors in their backyard or balcony for 20 minutes before noon, and that can jump-start a virtuous cycle of better sleep, improved energy, and the ability to engage in more behavioral activation.



Agree if you're talking about chronic insomnia, but the OP is on an inpatient unit, where CBTi isn't a realistic intervention.
I love CBTi. I am trained to do it and I offer it myself. But for patients with short-term sleep disturbance related to psychiatric illness, it's overkill. Most of them are going to get better when their mood/anxiety episode resolves, which will come sooner if sleep is improved. Short-term use of sleepers is very helpful in this situation, in a much shorter timeframe than a 6 week course of CBTi. I always make sure patients know that pharmacological sleepers are intended for short-term use only.

CBTi-Coach, I have recommended a bunch but never had a patient actually follow up with it. I don't think they can really implement a lot of it without more direct therapist guidance.

I think you are right and I stand corrected! I was looking up more studies because I previously carried in my head that zolpidem decreases restful deep sleep (NREM or N3) sleep time. However, it looks like that N3 and REM sleep are unaffected and N2 stage sleep is increased in patients taking zolpidem. I did find one older study that looked at healthy 21–35 yr olds, and found that zolpidem 0–20 mg did not affect stage 1 or stage 3–4. The high dose reduced REM sleep. (Merlotti L, Roehrs T, Koshorek G, Zorick F, Lamphere J, Roth T. The dose effects of zolpidem on the sleep of healthy normals. J Clin Psychopharm. 1989;1:9–14). I agree that benzodiazepines are more harmful to sleep architecture than zolpidem.

However, I still stand by my earlier point that I am very hesitant to use zolpidem as a medicine to treat insomnia because I do think there is evidence that it is habit-forming, can cause rebound insomnia, has been linked to cognitive side effects (poor focus, lethargy, disorientation), parasomnias, and increased risk of falls. Side effect profile makes me worried to use this medication when there are others that seem to have less risks and potentially more benefit for patients.

 

[deleted1100659]

I think you are right and I stand corrected! I was looking up more studies because I previously carried in my head that zolpidem decreases restful deep sleep (NREM or N3) sleep time. However, it looks like that N3 and REM sleep are unaffected and N2 stage sleep is increased in patients taking zolpidem. I did find one older study that looked at healthy 21–35 yr olds, and found that zolpidem 0–20 mg did not affect stage 1 or stage 3–4. The high dose reduced REM sleep. (Merlotti L, Roehrs T, Koshorek G, Zorick F, Lamphere J, Roth T. The dose effects of zolpidem on the sleep of healthy normals. J Clin Psychopharm. 1989;1:9–14). I agree that benzodiazepines are more harmful to sleep architecture than zolpidem.

However, I still stand by my earlier point that I am very hesitant to use zolpidem as a medicine to treat insomnia because I do think there is evidence that it is habit-forming, can cause rebound insomnia, has been linked to cognitive side effects (poor focus, lethargy, disorientation), parasomnias, and increased risk of falls. Side effect profile makes me worried to use this medication when there are others that seem to have less risks and potentially more benefit for patients.

I agree, its still acts on the GABA receptor ultimately. People often get reliant on sleep medications whether its physiologic or a mental thing, or combination of both.

Also im very hesitant on studies of sleep medications decreasing or increasing REM sleep, just because trazodone for example, if you look at the studies there you can find some studies saying it increases REM sleep and vice versa.

 

[jbomba]

In my experience hydroxyzine is the mildest commonly used antihistamine sleep aid at typically used doses. So basically any other antihistamine option would be a step up in perceived potency/effect for most patients.

Right, understandable name in terms of origin, bad name in terms of remembering the mechanism.

When you talk about vistaril being more mild/less potent are we talking about receptor binding affinity vs that of Seroquel as in this example?

 

[FlowRate]

When you talk about vistaril being more mild/less potent are we talking about receptor binding affinity vs that of Seroquel as in this example?

Perceived sedating effect as reported by patients. I haven't kept objective numbers but these are some of the most common meds we prescribe. Hydroxyzine is consistently the weakest or most likely to be assessed as "no effect." Trazodone, quetiapine, and mirtazapine are sufficiently close together. I've occasionally heard patients report specifically finding unisom better tolerated and more effective than other antihistaminic meds but not often enough to specifically rank or favor it one way or the other.

 

[Stagg737]

Curious how much these might change the game when readily available. Have a "classic" bipolar I patient that failed some sleep medications but has done amazingly on Dayvigo which I think is only being covered due to the repeated RTC/IP stays prior to it's initiation. They sleep 8 hours a night like clockwork since, only return of slight manic sx was a few day gap when the pharmacy didn't have it in stock.

I also find them to be pretty interesting and would be interested to see how they work for various sleep issues. I'm sure we'll have a better idea 10 years from now, lol. The few patients who I have gotten approved for Belsomra have actually done pretty well with it, though I have noted several of them feeling like it was "wearing off" after several months.

It's interesting to me how the EBM guidelines basically recommend Z-drugs yet a lot of institutional guidelines and individual practice/field of psychiatry generally shies away from those medications. I wonder if reflects common practice (starting something forever after an end-of-visit doorknob complaint or inbasket message) vs a more thorough/nuanced assessment of primary/secondary and onset/maintenance/midde-night, etc.

I think a lot of it is practical. The first person the patient is going to see for sleep is the PCP, who I think are less likely to start with the big guns like Ambien and more likely to try something more benign. I think part of this is the backlash that's come from the opioid epidemic and fears a lot of PCPs have about prescribing controlled substances. I think PCPs are also more likely to just prescribe something to help with sleep that will help the patient "right now" instead of recommending several weeks of therapy that may take a few months to get into. Plus, I think most physicians are probably unaware that CBT-i is the first-line therapy or just disregard therapy is a legitimate treatment option for insomnia.

Quick side-note, gabapentin probably has the worst generic name because it has no known direct effect on GABA or GABA receptors. It's a glutamate / voltage-gated Ca channel blocker.

Yes, I typically just think of it as the GABA system in general, but probably should separate GABA and glutamate as it's fairly unique in regards to it's MOA and variety of receptors it is associated with. I kind of think of it as a "simpler" form of topiramate in some ways, given it's likely narrower MOA as well as the more straightforward bioavailability, lack of significant metabolism, and straightforward excretion.

I generally do the Vistaril, Trazodone, Remeron, Seroquel algorithm. Seems that Doxepin is used quite a lot, used it a little in residency. I’ll have to try it more often. I’ve been generally avoidant of TCA due to s/e and OD risk. What dose do you feel comfortable going up to if patient is also on an SSRI/SNRI?

Agree 100% with C&H. At 25mg and lower it's basically an antihistamine, I kind of look at it as a cleaner version of Mirtazapine at the low doses.

Can I ask what is the purpose of Seroquel if vistaril isn't working? Aren't they hitting the same receptors (at sleep doses)? Not challenging you just genuinely curious.

When you talk about vistaril being more mild/less potent are we talking about receptor binding affinity vs that of Seroquel as in this example?

Hydroxyzine is pretty specific for the H1 receptor (cetirizine is its active metabolite, if that provides any context). Meanwhile, quetiapine also has a fair amount of action at alpha-adrenergic (mostly 1B) receptors as well. Additionally, norquetiapine has some fairly significant muscarinic effects which may also contribute to it's sedative effects.

 

[tr]

It's interesting to me how the EBM guidelines basically recommend Z-drugs yet a lot of institutional guidelines and individual practice/field of psychiatry generally shies away from those medications. I wonder if reflects common practice (starting something forever after an end-of-visit doorknob complaint or inbasket message) vs a more thorough/nuanced assessment of primary/secondary and onset/maintenance/midde-night, etc.

I actually use zolpidem a lot but that is because it has characteristics that suit it uniquely to my patient population. I treat a lot of perinatal women and zolpidem has a short half life, is undetectable in breast milk, and does not cause AM grogginess, so a nursing mother can use it to get a 5h block of sleep while spouse/partner feeds baby, then be clearheaded enough to take her shift when it's time.

But anecdotally a lot of patients report subjectively better quality sleep and I think the next-day clearheadedness really sets it apart from a lot of antihistaminic sleepers that leave people feeling groggy the next morning. Doxepin and trazodone are awful for this. (Side note, antihistamines also bad for nursing moms because drying effect can reduce milk supply.)

I'm not bothered about the long-term issues with cognitive impairment or dependence/rebound insomnia because I don't use any sleep meds long term, they're always a short term component of an intervention for a mood/anxiety episode, and I tell patients up front to expect to wean off the sleeper as their mood improves. I don't find that most patients have trouble giving up the sleeper once they feel better. If the issue is chronic insomnia I go direct to CBTi.

Somnambulism, definitely an issue but I view it like any other bothersome side effect. Warn that it's a possibility, and if it occurs, stop that med and try something else. I'm not sure why this particular side effect gives everyone the willies.

 

[Stagg737]

Sleep hygiene is a component of CBTi and it was never suggested that education on sleep hygiene alone was adequate treatment for insomnia.

You may not have suggested it, but it is used as the sole "treatment" for insomnia enough that it was seen as its own intervention in pretty much every set of insomnia guidelines I encountered. When it gets brought up I generally assume people are talking about sleep hygiene by itself.

1. I hate medications for sleep. They don't work well long term quite often. I think of insomnia as a symptom rather than a disease, I want to treat the root of the problem.

2. In addition to the above, why arent they sleeping? Anxiety at night? Using large amounts of caffeine before bed? Doing stuff they shouldnt be doing? Usually theres a reason behind it. I want to treat the reason ideally

That can be a pretty dangerous way to look at it if they have primary insomnia. However, that just highlights how important it is to have an accurate picture of what is happening with their sleep to treat it properly. If sleep hygiene like you mention is legitimately the cause, then it's an easy fix. If it's secondary to another condition (medical or psych), work schedule, or other social factors then meds are just a band-aid for the real problem. If they don't have any of those situations and they have true primary insomnia like paradoxical insomnia, then it warrants direct attention.

 

[Merovinge]

Somnambulism, definitely an issue but I view it like any other bothersome side effect. Warn that it's a possibility, and if it occurs, stop that med and try something else. I'm not sure why this particular side effect gives everyone the willies.

Mostly because of lawsuits over this I think, there's a lot of lore about docs being sued based on some lighting striking a unicorn level of frequency negative events (e.g. dying or killing someone during somnambulism). I have no idea how much this is a real concern but I sure heard about it in residency.

 

[Stagg737]

Somnambulism, definitely an issue but I view it like any other bothersome side effect. Warn that it's a possibility, and if it occurs, stop that med and try something else. I'm not sure why this particular side effect gives everyone the willies.

I think it's because of how severe some cases become. I had a lady come to us who said Ambien was the only thing that helped her for sleep, but that she'd gained 80 pounds in the past year because she would sleep eat very frequently with it. I also had a guy that said he woke up in his car several miles from his house and couldn't remember anything. Whether this was actual somnambulism or he just couldn't remember a brief period of being awake doesn't matter to me, that guy won't be getting Ambien from me ever, and thankfully he never wanted to take it again.

 

[tr]

I think it's because of how severe some cases become. I had a lady come to us who said Ambien was the only thing that helped her for sleep, but that she'd gained 80 pounds in the past year because she would sleep eat very frequently with it. I also had a guy that said he woke up in his car several miles from his house and couldn't remember anything. Whether this was actual somnambulism or he just couldn't remember a brief period of being awake doesn't matter to me, that guy won't be getting Ambien from me ever, and thankfully he never wanted to take it again.

Wow that's bad. I will say that I don't give Ambien to people who live alone because of the possibility that they may have sleep behaviors and not detect them. (Wondering how come lady #1 continued to take Ambien regularly for a *year* even though she knew it was making her raid the fridge every night?)

 

[Stagg737]

Wow that's bad. I will say that I don't give Ambien to people who live alone because of the possibility that they may have sleep behaviors and not detect them. (Wondering how come lady #1 continued to take Ambien regularly for a *year* even though she knew it was making her raid the fridge every night?)

From what I recall she didn't figure it out for 6-8 months, but when she tried to stop she was only getting like 2-4 hours per night (mostly d/t severe PTSD) and ended up restarting it. As much as I disliked PGY-3, I had some very interesting patient experiences that I'd probably never see or address in the settings I actually enjoy.

 

[deleted1100659]

You may not have suggested it, but it is used as the sole "treatment" for insomnia enough that it was seen as its own intervention in pretty much every set of insomnia guidelines I encountered. When it gets brought up I generally assume people are talking about sleep hygiene by itself.



That can be a pretty dangerous way to look at it if they have primary insomnia. However, that just highlights how important it is to have an accurate picture of what is happening with their sleep to treat it properly. If sleep hygiene like you mention is legitimately the cause, then it's an easy fix. If it's secondary to another condition (medical or psych), work schedule, or other social factors then meds are just a band-aid for the real problem. If they don't have any of those situations and they have true primary insomnia like paradoxical insomnia, then it warrants direct attention.

paradoxical insomnia..isnt the treatment for this cbt i with associated sleep hygiene regardless? Also thats a pretty subjective disorder if I remember correctly. Trouble falling asleep generally some kind of cause, whether its medical or bad habits. I think you missed my point though- you want to understand why someone isnt sleeping rather than just giving a medication for insomnia

 

[randomdoc1]

From my understanding, the non-pharmacologic interventions have a larger effect size than pharm interventions assuming the diagnosis is primary insomnia. Secondary insomnia is another story and is insomnia well....secondary to something. Obviously, treat underling causes such as psychiatric disorders, non-psychiatric disorders, substance intoxication or withdrawal (including ongoing effects of caffeine, etc.). If causal factors are controlled for, regulating the circadian rhythm and promoting the drive to sleep is what works. CBTi as well as sleep restriction therapy. Our sleep cycle primarily functions on a sleep deficit model. And if I remember correctly, our circadian rhythms tend to not line up perfectly with a 24 hour day which means, it is NORMAL to cyclically have bad nights of sleep. The trick is to not fall into the temptation of napping/sleeping too early/etc. Or else the circadian rhythm will get dysregulated as you've reset the clock to a different schedule. What I found helpful is when patients wore something that has some actigraphy function which many sleep specialists use to look at their sleep schedule when assessing continued reports of insomnia. Guess what? I have *never* seen an abnormal one. Patient says they only sleep 2 hours a night? Well, that's not what the graph shows exactly. Yes, they slept two hours in a night and took a 5 hour nap in the day. Once the schedule is reconsolidated back into the night, very minimal if any pharmacology is needed.

Or we can always use the highly efficacious 10mg xanax + 300mg seroquel + 3mg clonazepam qhs regimen? lmao xD

 

[jbomba]

Thoughts on using z-drugs in patient with mild-moderate OSA? Is this a big no no? Any specific drugs you might recommend over another if going the z drug route?

 

[Merovinge]

Or we can always use the highly efficacious 10mg xanax + 300mg seroquel + 3mg clonazepam qhs regimen? lmao xD

At that point, may as well MJ it and shot Propofol straight into the veins.

 

[mistafab]

3 points.

1. A quick few questions from STOP-BANG is worth asking when people complain about poor sleep, especially sleep maintenance problems.

2. Melatonin type meds (either otc or ramelteon type) work better as a daily regimen, rather than PRN for circadian disturbance and sleep onset problems

3. Lots of sleep maintenance insomnia folks withdraw from nicotine in the middle of the night. And worse, they regularly smoke upon awakening before going back to bed creating an ingrained pattern.

I find discussing their tobacco/nicotine use pattern especially pre/during bed can be very helpful for improving their sleep quality and pattern. I have even used patches at night in people not wanting to quit as a way to improve sleep, and as a side effect it lowered their NUD burden. Really good angle to bring up IMO for nicotine users with sleep problems. They use stimulants right before bed and wonder why it’s hard to sleep. Or they get up and hit the stim and find it hard to get back to sleep. No duh.

 

[birchswing]

At that point, may as well MJ it and shot Propofol straight into the veins.

I'm not sure how reliable the source is because this comes from the person who was found guilty for his death, but his doctor (the one his touring company hired to treat him and forced him under contract to have ironically to ensure his health) claimed to police that Michael Jackson's benzodiazepine tolerance is what necessitated his use of propofol. That the combo mentioned above (Xanax etc) is what caused it to get to that point.

He was on Ativan, Valium, Versed, and Propofol at the time of his death—for the medical procedure of . . . sleep. And a physician was present. And didn't call 911 for over a half hour after finding him non-responsive (he says he was alive at the time he found him, but the EMTs said he was in cardiac arrest already).

The physician has a credibility issue, but at least according to him the benzodiazepine tolerance was so great it required propofol.

 

[Merovinge]

I'm not sure how reliable the source is because this comes from the person who was found guilty for his death, but his doctor (the one his touring company hired to treat him and forced him under contract to have ironically to ensure his health) claimed to police that Michael Jackson's benzodiazepine tolerance is what necessitated his use of propofol. That the combo mentioned above (Xanax etc) is what caused it to get to that point.

He was on Ativan, Valium, Versed, and Propofol at the time of his death—for the medical procedure of . . . sleep. And a physician was present. And didn't call 911 for over a half hour after finding him non-responsive (he says he was alive at the time he found him, but the EMTs said he was in cardiac arrest already).

The physician has a credibility issue, but at least according to him the benzodiazepine tolerance was so great it required propofol.

It's actually worse than you are saying since said physician was a cardiologist and practicing entirely out of the scope of their practice, at least from my cursory recollection of the issue. But yes, the understanding was he was using such escalating sleep medications that at some point someone made the horrible decision to start propofol for something it is never used or indicated for.

 

[Sikrouf]

Is it fair to say seroquel at a low dose is just Benadryl with potential of more side effects?

Not quite based on my experience and receptor profile

 

[Sikrouf]

Thoughts on using z-drugs in patient with mild-moderate OSA? Is this a big no no? Any specific drugs you might recommend over another if going the z drug route?

Last time ive checked we had at least enough studies to justify a trial - assuming the zdrugs are justified for the reasons already adressed

 

[Malecha1990]

Quick side-note, gabapentin probably has the worst generic name because it has no known direct effect on GABA or GABA receptors. It's a glutamate / voltage-gated Ca channel blocker.

Probably one of the few favorite questions attendings would ask while in training. In the words of one notable admiral, “It’s a trap!”

 

[hallowmann]

I think it's because of how severe some cases become. I had a lady come to us who said Ambien was the only thing that helped her for sleep, but that she'd gained 80 pounds in the past year because she would sleep eat very frequently with it. I also had a guy that said he woke up in his car several miles from his house and couldn't remember anything. Whether this was actual somnambulism or he just couldn't remember a brief period of being awake doesn't matter to me, that guy won't be getting Ambien from me ever, and thankfully he never wanted to take it again.

I have actually seen quite a bit of disorientation, delirium, sleepwalking, and parasomnias that are very severe associated with Z-drugs, and it has certainly affected my prescribing of them. I will also say that the people who have been on zolpidem longterm, have had so much trouble even reducing doses very slowly that it competes with my patients on long-term alprazolam in terms of difficulty of deprescribing.

That said, I would agree that the the perinatal and post-partum population are one of the few that actually get zolpidem from me with some regularity, because of said benefits. OBs here love it too.

 

[Stagg737]

paradoxical insomnia..isnt the treatment for this cbt i with associated sleep hygiene regardless? Also thats a pretty subjective disorder if I remember correctly. Trouble falling asleep generally some kind of cause, whether its medical or bad habits. I think you missed my point though- you want to understand why someone isnt sleeping rather than just giving a medication for insomnia

Yes, but like all primary insomnias if first line doesn't work then medications are suggested as above. Sleep hygiene should be part of CBT-i anyway. I understood your point, but if the problem is a primary insomnia, the cause of their sleep problems is not an external factor, it's the insomnia itself. If there is an external factor then we're talking about secondary insomnia (insomnia d/t med condition, psych disorder, SUD, other sleep d/o, etc) then yes, you treat the causal factor. Here's a link to the AASM insomnia guidelines. Only 19 pages, so more digestible than the other guidelines. Medication treatment for primary insomnias starts on page 498:

https://aasm.org/resources/clinicalguidelines/040515.pdf