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What medication would best treat buspirone induced insomnia?

What medication would best treat buspirone induced insomnia?



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The anxiolytic buspirone causes insomnia in a small minority of patients. What existent medication would theoretically (or in practice) best treat this insomnia? Buspirone from my understanding is an agonist of the 5-HT1A autoreceptors, has very weak antagonism of the D2 receptors. There is also evidence that one of buspirone's metabolites increases plasma norepinephrine and epinephrine levels. I'm trying to think of a medication that would best block the effects of whatever it is that causes the insomnia. Buspirone is a tad "dirty" in that it and its metabolites affect many things so it's hard to say what causes the insomnia.


The Problem With Relying on Medicine

Medications should always be your last resort when it comes to treating your anxiety. The reason is not just because anxiety medications (known as anxiolytics) have side effects - although that is a problem with every mental health medication - but because medications prevent you from learning to cope without them.

That's the greatest issue with medication. All anxiety medications dull anxiety without teaching you how to control it. Anxiety isn't like getting an infection. You cannot simply take an antibiotic and have your anxiety go away. Those who rely too much on medication often find that they don't use or learn the skills necessary to cope with anxiety.

As soon as your stop taking any medicine your anxiety will most likely come back. And if you haven't learned any new coping skills, it may even be worse than before.


What Is Trazodone, Anyway?

Trazodone was first approved as an antidepressant by the Food and Drug Administration in 1981. Although doctors can legally prescribe trazodone (and all drugs, for that matter) for any reason, even if it’s not FDA-approved for that use, the drug has never been approved to treat insomnia.

A handful of studies have shown that trazodone may improve sleep during the first two weeks of treatment. But the drug hasn’t been well-studied for longer than six weeks for people whose primary problem is insomnia. As a result, little is known about how well it works or how safe it is past that point for the treatment of chronic insomnia. Also, an effective dose range has never been established for the drug when it’s being used to treat insomnia, although lower doses are typically given.

Updated treatment guidelines from the American Academy of Sleep Medicine published in 2021 recommend that doctors turn first to cognitive behavioral therapy (CBT) before drugs for most people suffering from insomnia. The AASM 2017 guidelines for doctors using medication to treat chronic insomnia do not recommend trazodone because there’s so little data to support its use. The American College of Physicians also does not recommend trazodone in its 2021 insomnia treatment guidelines. And a May 2018 Cochrane review found that there’s no good evidence to support the use of any antidepressant to treat insomnia, including trazodone.

Still, prescribing data suggests that some doctors remain convinced that trazodone is an appropriate sleep medication for many people, even those without depression. And it might be helpful for some people: A small “open label” study (participants are aware they are taking a specific drug) published in December 2020 in the Journal of Clinical Sleep Medicine involving people whose insomnia causes them to sleep less than 6 hours (as measured by a sleep test) once they do fall asleep, found that trazodone was helpful in keeping this small group of people asleep longer compared with people who received CBT.


Substance/Medication-Induced Sleep Disorder

Armeen Poor, MD, is a board-certified pulmonologist and intensivist. He specializes in pulmonary health, critical care, and sleep medicine.

Substance or medication-induced sleep disorder is the official diagnostic name for insomnia and other sleep problems which are caused by the use of alcohol, drugs, or taking certain medications. Roughly translated, that means that one of the effects of drinking alcohol, using a drug, or taking a medication, is having a problem with getting to sleep at the time you want to sleep, staying asleep at the time you want to sleep, excessive sleepiness during the day, or unusual behaviors when you do sleep.

Substance or medication-induced sleep disorder is different from the occasional difficulty with getting to sleep or staying asleep that is actually quite normal.

Substance or medication-induced sleep disorder is also different from the temporary insomnia or exhaustion that often affects people straight after alcohol or drug use, which is a normal response to the substance, or the activities of people who use alcohol or drugs, such as staying up later than your usual bedtime or participating in tiring activities during the time that alcohol or drugs are used (such as dancing). In contrast to these normal responses to alcohol or drugs, substance/medication-induced sleep disorder interferes with sleep more significantly, and the negative effects last for much longer.


How Does Sleep Impact ADHD — and Vice Versa?

Few things impact mental health more than sleep. Poor or insufficient sleep makes almost every psychological problem worse. In extreme cases, it can be the cause of the problem. With attention deficit disorder (ADHD or ADD), that link is obvious and complicated, because there are several ways sleep and ADHD affect each other.

Poor sleep can lead to ADHD-like symptoms and complicate a diagnosis. A few years ago, some researchers joined the “ADHD Is a Myth” crowd and declared all people with ADHD to be victims of chronic insomnia. That’s an overreach, but their findings did support the idea that quality of sleep must be considered in making an ADHD diagnosis. This is why you should start your teen’s diagnostic journey at the door of a qualified professional, and why you should study your child’s sleep patterns to answer the provider’s questions.

Are Sleep Problems Misdiagnosed as ADHD?

In my experience, insomnia-induced ADHD isn’t common, but I have referred two dozen teens and young adults for sleep studies to avoid misdiagnosing them. Some were found to have sleep apnea, narcolepsy, or primary insomnia, and treatment improved sleep and reduced symptoms. But those teens also wound up being treated at our clinic for ADHD. Nevertheless, I believe that severe sleep deprivation can present with ADHD-like symptoms, but most of such cases should be screened out from an ADHD diagnosis with an evaluation.

Poor sleep can result from ADHD, complicating diagnosis. This condition is common but under-recognized. Both of my children have what I call “ADHD-related insomnia.” I made up this name for it because I saw it so often among my clients, whose active minds didn’t shut down just because it was 10:30 p.m. It’s hard to know if this condition describes your child because you can’t easily separate this kind of insomnia from the one previously described. Which comes first: the chicken or the egg? The best solution the prescriber at our clinic has found is to begin treatment with stimulant medication, and follow the case closely for a month. Some teens will sleep better after beginning stimulants. A few will have daytime sleepiness despite taking them. That generally proves the diagnosis, but it also suggests it’s time to try a different stimulant or to pursue a sleep study.

How Can You Treat ADHD-Related Sleep Problems?

Sleep problems sometimes improve by treating the ADHD. More often, the insomnia remains but doesn’t worsen on stimulants, just as it has for my kids. In such cases, the prescriber may consider sleep medication as an adjunct. This is a complex decision, but our experience has been that, even when ADHD symptoms are improved by stimulants, ADHD-related insomnia will limit the effectiveness of treatment unless it too is addressed.

How Does ADHD Medication Impact Sleep?

Poor sleep can result from taking ADHD medication, complicating treatment. The point of stimulant medication is to stimulate the part of the brain that focuses attention. That’s the opposite of what we need when it’s time to hit the hay. However, for some people with ADHD, stimulants help sleep. For many others, insomnia predates stimulant use, which is another reason to assess sleep problems before any medication is prescribed. Figuring this out is subject to the “Hawthorne Effect.” If one is warned that sleep may be impaired by a stimulant, one gets worried about sleep, and may notice it isn’t very good. That makes it easy to blame the stimulant, rather than a chronic sleep impairment. Many teens compensate for poor sleep by taking naps. After starting a stimulant, one may not be able to nap as easily or as deeply.

On the other hand, if the teen hasn’t had sleep problems before, hasn’t over-used napping, begins to lose sleep after starting on medication, and doesn’t revert to better sleep in two or three weeks, a decision must be made. A common strategy is to discontinue stimulants and/or switch to a non-stimulant for ADHD. If the stimulants are working, we prefer to tinker with their timing and release to improve sleep. We find the Daytrana patch helpful for those with stimulant-induced insomnia, because it’s the only medication that can be shut off early (by removing the patch). In other cases, we find that treating the sleep problem directly is a better long-term solution than eliminating the stimulant.

Poor sleep reflects an unregulated life. Poor sleep may be the result of a dysregulated sleep-wake cycle and poor sleep hygiene. The worst thing about bad sleep is that it is self-perpetuating. The worse a teen sleeps, the more out of rhythm he will become. When he tries to compensate, the sleep gets worse. Good sleep hygiene is important in treating the conditions I’ve described, and it’s also critical to understanding the ADHD-sleep conundrum. More than once, we’ve tried to help a client manage stimulants and sleep, only to learn that the client is staying up late and, in extreme cases, reversing the sleep-wake cycle. Those with ADHD hate a sleep routine because it feels like a restriction of their freedom. We suggest that they consider a good sleep-cycle more like sharpening a saw than restricting their free expression.

Wes Crenshaw, Ph.D., ABPP, is a licensed psychologist board certified in couples and family psychology by the American Board of Professional Psychology. He is the author of I Always Want to Be Where I’m Not: Successful Living with ADD and ADHD (#CommissionsEarned) and a member of the ADDitude ADHD Medical Review Panel.

How to Help Teens with ADHD Sleep Better

1. Make time for it. The worst and most common sleep mistake teens make is failing to set aside eight hours to get it done, plus about an hour of prep before going to bed. For those with ADHD, it’s easy to put off sleep or to avoid it altogether. What could possibly be more boring than sleeping, especially when the night world is so interesting? It takes discipline to go to bed and to get up, but few life changes will make a bigger difference than this one in managing ADHD.

2. Turn off screens. Everyone hates this advice, including adults, but think back to a time when gaming consoles were in the family room, not the bedroom. Bedrooms shouldn’t look like mission control, they should look like sleeping quarters, and all screen time should end about an hour before bedtime. Not only are games too stimulating for late-evening use, they generate too much light.

3. Say goodnight to the (artificial) sun. Light is crucial in regulating the sleep cycle. Get teens in the habit of minimizing or shutting down artificial light in the evening after study time is over. This signals to the body that the night cycle is coming, and that it should prepare for sleep. Artificial light does the opposite. Get shades for windows to black out exterior light.

4. Rise with the light. When fall arrives and mornings become dark, go online or to your favorite home improvement store and buy a 4 x 4 or 4 x 8 daylight LED light panel. Install an extension cord (many shop lights have them already), or have an electrician do it for about $20. The panel doesn’t weigh much, so you can easily hang it on the wall of your teen’s bedroom. Set a timer for 20 minutes before your teen is scheduled to wake. If you’re feeling inventive, hang it in the window and use an auto dimmer to have the lights become progressively brighter like a sunrise.

5. No napping. Researchers consider naps to be evidence of unhealthy sleep. The only exception is the “micro-nap,” a 10- to 15-minute siesta one grabs mid-afternoon. These may improve functioning and improve sleep. Naps are hard to resist, but the fewer naps teens take, the better they’ll sleep at night.

Wes Crenshaw, Ph.D., is a member of the ADDitude ADHD Medical Review Panel.

#CommissionsEarned As an Amazon Associate, ADDitude earns a commission from qualifying purchases made by ADDitude readers on the affiliate links we share. However, all products linked in the ADDitude Store have been independently selected by our editors and/or recommended by our readers. Prices are accurate and items in stock as of time of publication


Buspirone (BuSpar)

Learn the common signs of mental illness in adults and adolescents.

Mental health conditions

Learn more about common mental health conditions that affect millions.

Call the NAMI Helpline at

800-950-NAMI

Brand name: BuSpar®

Generic name: buspirone (byoo SPYE rone)

All FDA black box warnings are at the end of this fact sheet. Please review before taking this medication.

What Is Buspirone And What Does It Treat?

Buspirone is in a class of medications called anti-anxiety medications. Buspirone is not related to other anti-anxiety medications, such as benzodiazepines, barbiturates or other sedative/ anxiolytic drugs. It is approved for the treatment of generalized anxiety disorder (GAD).

Generalized Anxiety Disorder (GAD) occurs when a person experiences excessive anxiety or worry for at least six months. Other symptoms include:

  • Restlessness
  • Fatigue (low energy, feeling tired all the time)
  • Difficulty concentrating
  • Irritability
  • Muscle tension
  • Sleep disturbance (difficulty falling asleep or waking up in the middle of the night)

What Is The Most Important Information I Should Know About Buspirone?

Do not drive a car or operate machinery until you know how this medication affects you because you may notice that you feel tired or dizzy.

Alcohol may increase any drowsiness or dizziness when taken with buspirone. You should avoid the use of alcohol while taking buspirone.

It may take 3 to 4 weeks before you start to feel better. Initially you may begin to notice a decrease in irritability and worry. Do not stop taking this medication without talking to your healthcare provider first. With input from you, your health care provider will assess how long you will need to take the medicine.

Unlike other anti-anxiety medications, buspirone has very low abuse potential.

Are There Specific Concerns About Buspirone And Pregnancy?

If you are planning on becoming pregnant, notify your healthcare provider to best manage your medications. People living with anxiety disorders who wish to become pregnant face important decisions. It is important to discuss this with your doctor and caregivers.

Regarding breastfeeding, caution is advised since it is unknown whether buspirone passes into breast milk.

What Should I Discuss With My Healthcare Provider Before Taking Buspirone?

  • Symptoms of your condition that bother you the most
  • If you have thoughts of suicide or harming yourself
  • Medications you have taken in the past for your condition, whether they were effective or caused any adverse effects
  • If you experience side effects from your medications, discuss them with your healthcare provider. Some side effects may pass with time, but others may require changes in the medication.
  • Any other psychiatric or medical problems you have
  • All other medications you are currently taking (including over the counter products and herbal and nutritional supplements) and any medication allergies you have
  • Other non-medication treatment you are receiving such as talk therapy or substance abuse treatment. Your provider can explain how these different treatments work with the medication.
  • If you are pregnant, plan to become pregnant, or are breast-feeding
  • If you drink alcohol or use drugs

How Should I Take Buspirone?

Buspirone should be taken twice a day with or without food.

Your healthcare provider will determine the dose that is right for you based upon your response.

Use a calendar, pillbox, alarm clock, or cell phone alert to help you remember to take your medication. You may also ask a family member a friend to remind you or check in with you to be sure you are taking your medication.

What Happens If I Miss A Dose Of Buspirone?

If you miss a dose of buspirone, take it as soon as you remember, unless it is closer to the time of your next dose. Discuss this with your healthcare provider. Do not double your next dose or take more than what is prescribed.

What Should I Avoid While Taking Buspirone?

Avoid drinking alcohol and using illegal drugs while you are taking buspirone. They may decrease the benefits (e.g., worsen your condition) and increase the adverse effects (e.g., sedation) of the medication.

What Happens If I Overdose With Buspirone?

If an overdose occurs, call your doctor or 911. You may need urgent medical care. You may also contact the poison control center at 1-800-222-1222.

A specific treatment to reverse the effects of buspirone does not exist.

What Are Possible Side Effects Of Buspirone?

Common side effects

Rare/serious side effects

Changes in weight or appetite, fainting, changes in blood pressure, muscle cramps or spasms, and redness or itching of eyes may occur in some instances.

Allergic reaction (difficulty breathing hives swelling of your lips, tongue or face) chest pain or an irregular heartbeat slurred speech confusion or blurred vision numbness or tingling in your hands, feet, arms, or legs or uncontrollable movements of your arms, legs, tongue, or lips.

Are There Any Risks For Taking Buspirone For Long Periods Of Time?

To date, there are no known problems associated with the long term use of buspirone. It is a safe and effective medication when used as directed.

What Other Medications May Interact With Buspirone?

If you have taken a monoamine oxidase inhibitor (MAOI), such as phenelzine (Nardil®), isocarboxazid (Marplan®), selegiline (Eldepryl®, EMSAM®) or tranylcypromine (Parnate®), within the past 2 weeks, do not take buspirone. The use of buspirone with these agents can cause a severe increase in your blood pressure.

The following medications may increase the levels and effects of buspirone:

  • Diltiazem (Cardizem®, Dilacor®, Tiazac®)
  • Verapamil (Calan®, Covera-HS®, Isoptin®, Verelan®)
  • Erythromycin (E-Mycin®, E.E.S.®, Ery-Tab®, Eryc®, others)
  • Consuming large amounts of grapefruit juice can increase the amount of buspirone in your blood

The following medications may decrease the levels and effects of buspirone:

How Long Does It Take For Buspirone To Work?

It may take 3 to 4 weeks of taking buspirone every day before you start to feel better.

Summary of FDA Black Box Warnings

There are no FDA black box warnings for buspirone.

©2019 The College of Psychiatric and Neurologic Pharmacists (CPNP) and the National Alliance on Mental Illness (NAMI). CPNP and NAMI make this document available under the Creative Commons Attribution-No Derivatives 4.0 International License. Last Updated: January 2016.

This information is being provided as a community outreach effort of the College of Psychiatric and Neurologic Pharmacists. This information is for educational and informational purposes only and is not medical advice. This information contains a summary of important points and is not an exhaustive review of information about the medication. Always seek the advice of a physician or other qualified medical professional with any questions you may have regarding medications or medical conditions. Never delay seeking professional medical advice or disregard medical professional advice as a result of any information provided herein. The College of Psychiatric and Neurologic Pharmacists disclaims any and all liability alleged as a result of the information provided herein.


Reevaluating Antidepressant Selection in Patients With Bruxism and Temporomandibular Joint Disorder

Temporomandibular joint disorder (TMD) is a broad pain disorder that refers to several conditions affecting the temporomandibular joint of the jaw and the muscles of mastication. As with most pain disorders, a high prevalence of depression and anxiety is associated with TMD. Research has shown that selective serotonin reuptake inhibitors (SSRIs), the first-line drug therapy for major depressive disorder, may not be suitable for TMD patients because SSRIs can induce teeth-grinding, otherwise known as bruxism. This is problematic because bruxism is believed to further exacerbate TMD. Therefore, the purpose of this literature review is to better understand the mechanism of SSRI-induced bruxism, as well as discuss alternative antidepressant options for treating depression and anxiety in patients with bruxism and TMD. Alternative classes of antidepressants reviewed include serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, atypical antidepressants, and monoamine oxidase inhibitors. Findings indicate that dopamine agonists and buspirone are currently the most effective medications to treat the side effects of SSRI-induced bruxism, but results regarding the effectiveness of specific antidepressants that avoid bruxism altogether remain inconclusive.


The Human Study

So they went from the petri dish – in vitro – to animals – in vivo – but what about in humans?

The human study came next – 134 patients with moderate Major Depression volunteered to test the new combo therapy in a 6-week randomized controlled trial. Everyone either got placebo, buspirone 15mg, or the buspirone-melatonin combination – which was 15mg of buspirone and 3mg of melatonin SR.

The melatonin they used was from Mellen Medical Products (although it appears available on their website for $10, some readers have told me that you can’t actually order from them. In that case check our list of clinical and laboratory tested melatonin products).

The buspirone-melatonin combo had a significant effect on the primary outcome – the clinical global improvement scale – as well as on secondary outcomes like overall CGI severity, Hamilton anxiety, and remission rates on the QIDS depression inventory, but not on the total QIDS score itself.

So the combo did better than placebo, but did it do better than buspirone alone?

Yes, it did better than both on all those measures. Buspirone did not work on any of them alone, not even anxiety, which is not too surprising since the dose was only 15mg/day.

OK but I have a theory. What if this just proves that helping sleep with melatonin and helping anxiety with a little buspirone treats depression? I mean there are studies where eszopiclone (Lunesta) is added to an SSRI and it makes the SSRI work better – I’ve seen that in controlled trials of depression as well as generalized anxiety disorder.

That’s a good theory, but in this case the melatonin didn’t actually improve any sleep items on the rating scale, so the thinking is that its antidepressant effects were due to some kind of pharmacodynamic synergy with buspirone – perhaps neurogenesis – rather than direct effects on sleep. On the other hand, they did look at cognitive symptoms in a separate study, and from that analysis it looks like improvements in cognition – rather than sleep – were driving the change in depression. When they compared patients who responded to the combo vs. those who did not, it was the change in cognitive symptoms that seemed to make the difference.

That makes sense if we’re talking about a treatment that enhances growth in the hippocampus – the memory center. What specific cognitive symptoms did it help?

Word-finding difficulties, forgetfulness, mental slowness, apathy and motivation.

OK if I’m going to find a criticism of this study then it’s that it’s just one study – why hasn’t anyone tried to replicate it?

That’s a mystery. I wrote to Dr. Fava who shared that his best guess is that there is no financial incentive here. If a company went through the trouble to license a combination pill with buspirone and melatonin in it, most physicians would bypass the combo pill by prescribing the two generic ingredients on their own. Their work on neurogenesis and depression has continued to yield fruit, however. After screening some 10,000 compounds through that neurogenesis cell line, they arrived at one with promise: NSI-189. It’s currently being developed for major depression by Neuralstem. The results have been mixed, but here’s something interesting – it seems to have better effects on cognition than on depression.

OK so what’s the bottom line, should we use melatonin with buspirone?

We tend to reserve these half-tested therapies for treatment resistant cases – and I would put it there at the end of the line along with other novel therapies like celecoxib, amantadine, minocycline, and D-cycloserine. But the buspirone-melatonin combo has two advantages: it is safe, and it improved cognition, which I wish we could say for more of our therapies.


The First Line of Treatment for Insomnia That'll Surprise You

Whenever most people have serious trouble sleeping, they automatically reach for a sleeping aid, whether that&rsquos a prescription or over-the-counter medication or a natural remedy.

But these solutions, as psychologist and sleep specialist Stephanie Silberman, Ph.D, explained, are anything but.

In fact, the preferred solution &mdash the one that research also supports &mdash is a treatment that many people, even medical professionals, are unaware of.

Research has shown that cognitive-behavioral therapy (CBT) is highly effective for insomnia. (Effective results have been shown in a recent meta-analysis and article review .)

Below, Dr. Silberman, author of The Insomnia Workbook: A Comprehensive Guide to Getting the Sleep You Need, offers insight into insomnia and its treatment and shares several strategies readers can try at home.

What is Normal Sleep?

Before thinking about disturbed sleep, it&rsquos important to understand what normal sleep really is. Normal slumber involves falling asleep relatively easily once you&rsquore in bed, Silberman said. &ldquoPeople have a range of how quickly they go to sleep,&rdquo she said, but typically they can drift off to sleep anywhere from a few minutes to 15 minutes.

Normal sleepers will also go through four stages of sleep several times a night, she said. According to The Insomnia Workbook, the stages are:

  • Stage N1: the lightest stage, which usually makes up 10 percent of your total sleep time.
  • Stage N2: unlike stage N1, you lose awareness of external stimuli, and people spend most of their sleep time in this stage.
  • Stage N3: known as slow-wave sleep, and believed to be the most restorative.
  • Stage R: known as REM sleep, or rapid eye movement. It&rsquos the most active of the stages for your brain and body functions, such as breathing and heart rate. Your muscles relax, however, so you don&rsquot act out your dreams.

It&rsquos also normal for it to take about 20 to 30 minutes to feel truly awake in the morning.

What Is Insomnia?

&ldquoMost people with insomnia have difficulty either falling asleep, known as sleep onset insomnia, or staying asleep, known as sleep maintenance insomnia,&rdquo Silberman writes in her book, which provides readers with information on insomnia and strategies to treat it and sleep better.

People with insomnia also might feel moody or fatigued during the day. (Here&rsquos more on insomnia.) The most common type of insomnia is conditioned or learned insomnia. Initially, a person starts sleeping poorly because of a stressor, Silberman writes. Then the insufficient sleep almost becomes routine because you continue to ruminate about your sleeping problems, leading to increased arousal before bed. This then becomes &ldquoa conditioned physiological response that contributes to difficulties falling asleep.&rdquo

Insomnia Myths

There also are many myths that can undermine your sleep and insomnia treatment. One of the biggest, Silberman reiterated, is the idea that sleeping pills are an effective remedy that improves your sleep. In fact, research has found that CBT is more effective than pharmacological interventions.

Specifically, sleeping pills actually make you feel groggy and sleepy during the day, they cause dependency and disrupt and change sleep architecture. (Sleep architecture refers to the structure of your sleep and the &ldquocycling in and out of the different stages of sleep during the night,&rdquo Silberman writes in her book.)

For instance, benzodiazepines are commonly prescribed for sleep but they actually &ldquosuppress the slow-wave sleep,&rdquo she said. The problem? Recall that slow-wave sleep is essential to a good, restorative sleep. Plus, as she noted, we don&rsquot know the long-term consequences of disrupted slow-wave sleep.

Nonbenzodiazepines, a class of sedative-hypnotic drugs, such as Lunesta and Ambien, &ldquoaffect other areas of sleep,&rdquo such as respiration, Silberman said. They have potentially serious side effects and also can lead to psychological and physiological dependence.

Some sedative hypnotics can cause rebound insomnia after they&rsquore discontinued. Naturally, many people get discouraged, thinking they can&rsquot sleep without the sleeping aid. But, as Silberman said, &ldquothis is par for the course,&rdquo because you&rsquore taking away a medication that caused changes to your body.

Herbal and &ldquonatural&rdquo remedies, such as melatonin, valerian root and kava, are not any better. In fact, they aren&rsquot regulated by the Food and Drug Administration, so they&rsquore not tested for effectiveness or safety. In her book, Silberman discusses the disturbing results of one consumer agency study that tested valerian products. It found that some products didn&rsquot contain measurable amounts of the ingredient, others contained half of the amount stated on the bottle and one bottle even contained a poisonous metal!

Also, people erroneously believe that &ldquothere is no rhyme or reason to their sleep,&rdquo Silberman said. Similar to that, they believe they have little control over their sleep. (This might be another reason why people turn to sleeping pills.) But in reality, there are targeted and well-tested techniques you can do to have a good night&rsquos sleep. Also, once you observe your sleeping, you&rsquoll be able to pick up on patterns that affect your sleep, so it&rsquos not so random after all.

Another misconception is that spending more time in bed will increase your chances of sleeping longer. To the contrary, this can actually sabotage your sleep and create a negative association with your bed. As Silberman said, &ldquothe more time a person spends in bed, the more they reinforce the idea that the bed is not a sleep-promoting place.&rdquo

How CBT for Insomnia Works

What does CBT for insomnia look like? When a client first sees Silberman, they work on uncovering the client&rsquos current sleep pattern and the factors that are negatively affecting their sleep. They accomplish this by completing sleep logs, for instance.

They talk about a variety of potential issues, such as: &ldquoWhat&rsquos causing them to have these problems at night? Are they tossing and turning because they can&rsquot turn off their brain at night or is it some kind of pain or an environmental stimulus, such as a baby waking you up?&rdquo Is smoking one of the culprits? (Smoking is a stimulant, so smoking right before bed can make it tougher to fall asleep.) They ponder whether physiological factors are to blame. For instance, a medication you&rsquore taking might be causing poor sleep.

When treating insomnia, in addition to sleep logs, other techniques include sleep restriction (described later) and reducing any anxious or worrisome thoughts the person may be having around sleep or their life in general.

Sleeping Strategies To Try

Silberman shared the following strategies you can try on your own to improve your sleep.

1. Observe your sleep.

Gathering data is key when trying to treat insomnia or any kind of sleep trouble, Silberman said. In her book, she provides readers with several worksheets to log in your sleep. This is essential because it helps you figure out what habits are hindering your sleep (such as a stressful event, caffeine intake, daytime napping or TV watching) and how long you&rsquore actually sleeping.

In fact, Silberman said that many different things can affect your sleep. At first, sleep or lack thereof seems random. But once you commit your habits to paper, you might notice that the three glasses of wine or two cups of coffee you had led to your sleeping poorly. Maybe another day, you ate a super-spicy meal for dinner, leading to heartburn and little sleep.

When observing your sleep, it&rsquos helpful to consider: what time you went to bed, how long it took you to fall asleep, how often you woke up during the night, what time you finally got up and how many hours you slept. Recording this information each morning for a week helps you spot patterns.

2. Restrict your time in bed.

Sleep studies have shown that sleep restriction is effective for treating insomnia. This is why collecting your sleep data is so important. It gives you a good idea of how long you&rsquore actually sleeping, because you want to be in bed for that number of hours. Lying awake in bed only &ldquoincreases frustration, anxiety and annoyance with the process,&rdquo Silberman said.

&ldquoBy restricting the amount of time to bed,&rdquo she said, you &ldquowill start getting more solid sleep.&rdquo How do you calculate the time you spend in bed? Just add up the time you&rsquove actually spent sleeping each night for a week and divide by seven to get an average time.

Then about 30 minutes to an hour before bedtime, establish a routine that primes your body for relaxation. For instance, you might listen to soothing music, take a warm bath or read a book.

3. Practice good sleep hygiene and habits.

While good sleep hygiene won&rsquot dramatically change your insomnia, it does help you optimize your sleep, Silberman said. Some examples are limiting caffeine and alcohol intake, making your room cool and dark and exercising four or five hours before bedtime.

Other helpful habits include engaging in relaxation techniques and working through any worry thoughts. &ldquoIn particular it&rsquos important to practice [relaxation techniques] when you&rsquore not anxious or stressed out, so they work better when you need them.&rdquo

One way to reduce anxious thoughts is by asking yourself &ldquowhat&rsquos the evidence for and against these thoughts I&rsquom having,&rdquo Silberman said. Not surprisingly, there&rsquos usually &ldquovery little evidence for the irrational thought.&rdquo Then, you &ldquocan come up with an alternative thought or new explanation.&rdquo

Again, remember that you do have control over your sleep. Studies have repeatedly shown that CBT is a highly effective treatment for insomnia.

To learn more about sleep specialist and clinical psychologist Stephanie Silberman and her work, please visit her website.


Who is most likely to benefit from using Buspar for depression?

There’s no definitive way to know who is likely to benefit most from administration of buspirone for the treatment of depression. Since buspirone is an effective anxiolytic, it should be suspected that most benefit will be attained from individuals in which anxiety influences severity of depressive symptoms. Anyone with depression plus comorbid anxiety (i.e. “anxious depression”) should stand to benefit more from buspirone than others. There is modest evidence suggesting that individuals with the most severe symptoms of depression may benefit from adjunctive buspirone.

  • Depression with anxiety: Those with simultaneously occurring depression and anxiety often report a bidirectional relationship between depressed mood and anxious symptoms. When the anxiety flares up, they isolate themselves from others and it makes them depressed. The depression leads them to think poorly of themselves and their abilities, causing increased future anxiety – it’s a vicious circle. It is known that buspirone is effective for the treatment of anxiety and preliminary evidence suggests it could improve mood. Evidence suggests that it is an effective option among those with “anxious depression.”
  • Severe depression: Analysis of data from a standalone randomized controlled trial indicated that adjunct buspirone may help individuals with severe depression. The “severe depression” was classified as MADRS scores exceeding 30. In the event that a person exhibits severe depression to the extent that they’re scoring at least 30 (or above) on the MADRS (Montgomery-Asberg Depression Rating Scale), adjunct buspirone may be helpful.

Treatment of Insomnia in Anxiety Disorders

Insomnia is highly prevalent in psychiatric disorders, and it has significant implications. This review focuses on insomnia in the context of anxiety disorders. The prevalence of comorbid insomnia in anxiety disorders is addressed and the clinical implications associated with insomnia are discussed as well as when and how to treat this important comorbidity.

Just how specifically insomnia relates to and possibly affects anxiety disorders is highlighted by the fact that insomnia is one of the defining criteria in a number of the DSM-IV-TR anxiety disorders. For example, difficulty in falling or staying asleep is a criterion for PTSD, acute stress disorder, and generalized anxiety disorder (GAD).

The relationship of insomnia to anxiety disorders is also influenced by comorbid major depression. The severity of insomnia is increased when an anxiety disorder is comorbid with a major depressive disorder (MDD). 1 This is highly relevant because 58% of MDD patients have a lifetime anxiety disorder. 2

The presence of insomnia has a deleterious effect on daytime functioning and negative effects on quality of life, including social and work relationships. 3 Also, there is clear evidence that the presence of insomnia in anxiety disorders is associated with increased morbidity. For example, in patients with PTSD, insomnia is associated with an increased likelihood of suicidal behavior, depression, and substance abuse as well as nonresponsiveness to treatment. 4-6 In addition, insomnia as an early symptom in traumatized patients increases the risk of the development of PTSD 1 year later. 7

Early assessment

It is important to carefully assess for insomnia early in the evaluation of patients with anxiety disorders and to aggressively treat this complicating comorbidity. Insomnia is an underrecognized and undertreated problem. Patients rarely report their symptoms of insomnia spontaneously to their doctor. Adding to the problem of detecting insomnia is the finding that doctors rarely inquire about insomnia in their patients. 3,8,9 Thus, a carefully taken history is an important first step in the assessment of insomnia.

Self-rating sleep questionnaires and direct clinical interviews are used to obtain a history of potential sleep disorders (eg, insomnia). A number of well-validated sleep questionnaires have been widely used. The most widely used and validated questionnaire is the 19-question Pittsburg Sleep Quality Index. The questions cover sleep quality, sleep problems, sleep medications, and so on, within the past month. 10 Another widely used questionnaire is the Leeds Sleep Evaluation Questionnaire (LSEQ). The LSEQ consists of 10 self-rating questions that cover sleep and aberrant sleep behaviors. 11

Besides self-rating questionnaires that depend on memory of sleep disturbances, a sleep log or diary can confirm questionable sleep disturbances prospectively. The use of a sleep log allows for an analysis of day-to-day sleep patterns, such as the time that the patient went to bed, sleep latency, and nighttime awakenings. 8,9 The log is filled out by the patient shortly after awakening in the morning (see Morin 9(p38) for an example of a sleep log). If at all possible, monitoring for up to 2 weeks is highly recommended because it allows for sleep abnormalities that might show marked day-to-day variability and would more likely be detected by extensive monitoring. 12,13

What is already known about insomnia in patients with anxiety disorder?? Anxiety disorders frequently coexist with insomnia. The latter is believed to be part and parcel of various anxiety disorders and is one of the defining criteria of a number of them.

What new information does this article provide?? Our article clarifies new approaches to considering insomnia in anxiety disorders. The presence of insomnia should be considered a comorbid illness and treated on its own. Pharmacotherapy, cognitive-behavioral therapy, and a combination of both are discussed. Insomnia is an added pathology that brings increased morbidity to patients with anxiety disorders. Our review suggests that successful treatment of insomnia actually increases the responsiveness of anxiety disorders to many antianxiety treatments.

What are the implications for psychiatric practice?? When evaluating patients with anxiety disorders, psychiatrists should carefully evaluate for the presence of insomnia. Patients infrequently bring up this symptom on their own. If insomnia is present, aggressive treatment early in the course of therapy is highly suggested.

If the presence of insomnia is suspected, interviewing a spouse, a significant other, or a caregiver is helpful. Some patients who believe they have insomnia symptoms appear to have “sleep state misperception,” where their partners clearly state that their sleep is normal. 14 These “others” can also report problems that are likely not obvious to the patient:

• Apnea spells or excessive snoring as seen in obstructive apnea

• Excessive body movements as seen in periodic leg movement disorder and restless legs syndrome

• Various sleep-related behaviors (sometimes violent and aggressive) as seen in rapid eye movement behavior disorder (RBD)

Referral to a sleep specialist and sleep polysomnography has been recommended if pharmacological or nonpharmacological options are not working. Referral is also warranted for patients with insomnia in whom a specific sleep disorder, such as obstructive sleep apnea, periodic limb movements, narcolepsy, or RBD, is suspected. 12,15 Even when a visit to a sleep laboratory is suggested, the cost of an overnight visit is often prohibitive-more than $1000 per night usually 2 nights are required with the first being an adaptation night for the patient. Insurance frequently does not cover these costs. 16 If it is found that the patient has sleep apnea, a sleep movement disorder, RBD, or a number of other sleep disorders, specific nonhypnotic treatments may be required (eg, continuous positive airway pressure for sleep apnea is the treatment of choice).

Before beginning treatment of anxiety disorder–associated insomnia symptoms, rule out any concurrent medical illness, medication treatment, or substance use that might be inducing or worsening insomnia. Many medical illnesses, such as cardiovascular disorders (eg, congestive heart failure), pulmonary disorders (eg, emphysema), endocrinopathies (eg, thyroid disorders), GI disorders (eg, acid reflux), and neurological disorders (eg, pain syndromes), are associated with insomnia. 12

Carefully assess the use of medications for medical and psychiatric disorders that may be implicated in insomnia as well as caffeine or alcohol use. Even small amounts of the latter have been associated with increased nighttime awakenings.

One should be highly suspicious of alcohol or substance use or abuse in patients with anxiety disorders because these are frequently comorbid. 4 Various medications are associated with insomnia, including psychostimulants (eg, ephedrine found in cold medication, amphetamines used in ADHD), bronchodilators (eg, theophylline, albuterol), pain medication (eg, oxycodone), and antidepressants (eg, SSRIs). 12 The latter category is particularly important because many antidepressants are FDA-approved and are prescribed for anxiety disorders.

Before providing any significant intervention for insomnia, a careful evaluation regarding behaviors that might contribute to insomnia should be made. Daytime naps, late nighttime snacks or meals, watching television in bed, nighttime exercise, or excessive light or loudness in the bedroom should be identified and modified. Eliminating these behaviors can lead to significant sleep improvements. A 13-item self-rating questionnaire by Mastin and colleagues 17 can help elicit sleep hygiene information.

Pharmacological options

The treatment of insomnia in patients with anxiety disorders is, for the most part, the same as the treatment of insomnia per se: pharmacological, nonpharmacological, or a combination of the two.

The primary treatment of insomnia is pharmacological because of the rapid onset of action (eg, hypnotics are usually effective within days to 1 week of use). The most common nonpharmacotherapy, cognitive-behavioral therapy for insomnia (CBT-I) takes considerably longer. 3,8,12 Currently, the FDA has 11 approved drugs for the treatment of insomnia:

• Nonbenzodiazepines: eszopiclone, zolpidem, zolpidem ER, and zaleplon

• Benzodiazepines: estazolam, flurazepam, quazepam, temazepam, and triazolam

• A tricylic antidepressant: low-dose sinequan

• A melatonin agonist: ramelteon

In recent years, nonbenzodiazepines have become the most recommended of the approved hypnotics. (There has been less and less reliance on benzodiazepines.) Not only are nonbenzodiazepines effective in treating insomnia (equivalent to the benzodiazepines), but there is a notion that they are safer than benzodiazepines. 3,12

Both nonbenzodiazepines and benzodiazepines are associated with adverse effects that include fatigue, dizziness, ataxia, and the development of dependence and tolerance with long-term use. Although head-to-head studies comparing these classes of hypnotics have been minimal, a recent meta-analysis supports the finding of reduced adverse effects for the nonbenzodiazepines. 18 The nonbenzodiazepines typically have a shorter half-life and are more selective at the γ-aminobutyric acid receptor, factors that are partially responsible for less residual daytime sedation and other adverse effects.

In the treatment of anxiety disorders with comorbid insomnia, the latter should be treated concurrently with, but independently of, the anxiety disorder per se. The idea that one should wait to see whether the insomnia resolves with only the treatment of the anxiety disorder is no longer valid. Clinical experience has shown that without targeted insomnia treatment, insomnia frequently persists. 3,19

When adding a hypnotic to an antidepressant in the treatment of anxiety, the risk to benefit ratio must be considered. Pollack and colleagues 20 looked at a large group of patients with GAD comorbid with insomnia (N = 595). The patients received either 10 mg of escitalopram coadministered with 3 mg of eszopiclone or the escitalopram with placebo. Those in the active hypnotic treatment group had a significant response in their insomnia by the first week. The combination of medications was well tolerated with no significant increase in adverse effects.

Most surprisingly, the anxiety scores for those patients who received the hypnotic significantly improved starting at week 4 even after removing insomnia symptoms from the anxiety assessment. The time to onset of the anxiolytic response was also reduced. In addition, the combination treatment led to a slightly better symptom response and remission rate for the anxiety disorder.

Similar results were reported in a 12-week open-label study (N = 27) undertaken by Gross and colleagues. 21 The researchers evaluated ramelteon (8 mg/d), a melatonin agonist, in patients who had GAD comorbid with insomnia and whose condition was partially responsive to an SSRI or a serotonin norepinephrine reuptake inhibitor. The hypnotic was well tolerated, effective for insomnia, and appeared to facilitate the treatment of GAD.

A double-blind placebo-controlled study by Fava and colleagues 22 evaluated the efficacy and safety of zolpidem extended-release (12.5 mg/d) versus placebo in patients with comorbid GAD and insomnia who were being treated with escitalopram (10 mg/d). Sleep measures improved significantly by the end of week 1, and there was no added burden of adverse effects. Zolpidem did not show a beneficial anxiolytic effect.

Approximately 50% of patients with insomnia continue to have insomnia 3 years after initial diagnosis, and many patients require months to years of treatment. Nonbenzodiazepines for primary insomnia were found to have continued efficacy and to be well tolerated with no evidence of abuse or withdrawal symptoms on discontinuation of use after 12 months. 23,24 Ramelteon was also found to be efficacious with no significant issues of abuse or tolerance in a 24-week open-label study. 25 The literature for longer use of hypnotics is scarce.

Anxiety disorders are frequently comorbid with alcohol or substance use disorders. 4,26 Consider ramelteon or low-dose sinequan to avoid potential issues of abuse and addiction. Nonbenzodiazepines are preferred over benzodiazepines there is evidence that the former have decreased potential for abuse and a better adverse-effect profile.

In some patients with insomnia, benzodiazepines are clearly necessary. The other hypnotics may not be as effective for some patients, and the anxiolytic properties of benzodiazepines may be helpful.

When hypnotics are used (particularly, benzodiazepines and nonbenzodiazepines), their use should be reassessed-every 3 to 4 weeks. 3,12 Many patients with insomnia do not experience sleep disturbances nightly. Therefore, the use of hypnotics on an as-needed basis or a few times a week helps cut down on the amount and exposure to medication. 27

Trazodone and mirtazapine are also widely used for insomnia, as are atypical antipsychotics and herbal preparations. Unfortunately, these agents have not been rigorously studied for insomnia and thus their effectiveness and safety remain unclear. 3

Nonpharmacological interventions

CBT-I is an important, widely accepted, multimodal treatment for insomnia and the best-studied of the nonpharmacological approaches for this disorder. It is a manualized treatment that focuses on various components of CBT (ie, cognitive restructuring and the use of psychological interventions, such as the practice of good sleep hygiene, stimulus control, sleep restriction, and relaxation therapy). These methods address negative and distorted cognitions and behaviors that initiate and perpetuate insomnia. 9,28 Treatment duration is relatively short. It is administered for 5 hours divided over 4 to 6 weeks and can subsequently be used as a maintenance treatment in monthly sessions. There are approximately 12 well-designed CBT-I trials that have clearly demonstrated that it is a highly effective intervention for insomnia for 1 year or longer. 29,30

Studies that compared CBT-I with pharmacotherapy found equivalent efficacy. 31 This has led the NIH Consensus and State of the Science Statement to conclude that CBT-I is “as effective as prescription medications are for short-term treatment of chronic insomnia. Moreover, there are indications that the beneficial effects of CBT, in contrast to those produced by medications, may last well beyond the termination of active treatment.” 3 In contrast to hypnotics, learned CBT-I skills may persist even when active treatment ends. 9 Furthermore, some patients may prefer CBT-I over hypnotic drugs because of their possible adverse effects or because of concerns about drug interactions or taking a drug during pregnancy. 9

In general, CBT-I is underutilized-only about 1% of patients with chronic insomnia receive this therapy. 32 To increase the availability of CBT, it can be administered via self-help strategies (eg, educational books and materials) and in group formats. In addition, the use of the Internet to provide CBT has been shown to be effective. Nonetheless, patients frequently prefer face-to-face contact. 33

Besides CBT-I, a number of other nonpharmacological therapies, such as bright light, physical exercise, acupuncture, tai chi, and yoga, have been used to treat insomnia. Unfortunately, the results have been inconsistent. 32,34

Combination therapy

Is a combination of pharmacotherapy and nonpharmacotherapy more effective than either alone in the treatment of anxiety disorders with insomnia? Combination therapy has not been addressed in studies of this particular patient population. Furthermore, the question has been minimally addressed even in the treatment of insomnia per se. Study findings suggest only modest differences in outcomes with a combination of therapies. Similar results were seen in a study that compared CBT with CBT plus zolpidem. The 6-week acute study demonstrated a 60% response rate and a 40% remission rate the group with the combination treatment did have a significant increase in sleep time of 15 minutes, but the researchers question the clinical significance of this isolated finding. 29

Anxiety disorders with comorbid insomnia are highly prevalent with potential negative consequences. Therefore, assess for insomnia with self-rating scales and careful clinical interviews. When appropriate, refer patients for polysomnography.

Insomnia should be treated aggressively with pharmacotherapy, nonpharmacotherapy (particularly CBT-I), or a combination. Some of the hypnotic treatments actually appear to facilitate successful therapy for the anxiety disorder.

Benzodiazepines and nonbenzodiazepines have a number of adverse effects and can lead to abuse and dependence. Patients with an anxiety disorder may be particularly vulnerable, especially those with a history of alcohol and drug abuse. Treatment with benzodiazepine and nonbenzodiazepine hypnotics needs to be reassessed monthly. Alternatively, ramelteon, low-dose sinequan, and CBT-I should be considered because they have minimal adverse effects and no risk of abuse.

Successful treatment of insomnia is an important goal in patients with anxiety disorders. Both pharmacological and nonpharmacological interventions have response rates of approximately 60%.

References:

van Mill JG, Hoogendijk WJ, Vogelzangs N, et al. Insomnia and sleep duration in a large cohort of patients with major depressive disorder and anxiety disorders.

Kessler RC, Berglund P, Demler O, et al. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R).

National Institutes of Health. National Institutes of Health State of the Science Conference statement on Manifestations and Management of Chronic Insomnia in Adults.

Marcks BA, Weisberg RB. Co-occurrence of insomnia and anxiety disorders: a review of the literature.

Maher MJ, Rego SA, Asnis GM. Sleep disturbances in patients with post-traumatic stress disorder: epidemiology, impact and approaches to management.

Harvey AG, Jones C, Schmidt DA. Sleep and posttraumatic stress disorder: a review.

Koren D, Arnon I, Lavie P, Klein E. Sleep complaints as early predictors of posttraumatic stress disorder: a 1-year prospective study of injured survivors of motor vehicle accidents.

Sateia MJ, Doghramji K, Hauri PJ, Morin CM. Evaluation of chronic insomnia. An American Academy of Sleep Medicine review

Morin CM. Cognitive-behavioral approaches to the treatment of insomnia.

Buysse DJ, Reynolds CF 3rd, Monk TH, et al. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research.

Parrott AC, Hindmarch I. Factor analysis of a sleep evaluation questionnaire.

Schutte-Rodin S, Broch L, Buysse D, et al. Clinical guideline for the evaluation and management of chronic insomnia in adults.

Bastien CH. Insomnia: neurophysiological and neuropsychological approaches.

Edinger JD, Fins AI. The distribution and clinical significance of sleep time misperceptions among insomniacs.

Kushida CA, Littner MR, Morgenthaler T, et al. Practice parameters for the indications for polysomnography and related procedures: an update for 2005.

Boeve BF, Molano JR, Ferman TJ, et al. Validation of the Mayo Sleep Questionnaire to screen for REM sleep behavior disorder in an aging and dementia cohort.

Mastin DF, Bryson J, Corwyn R. Assessment of sleep hygiene using the Sleep Hygiene Index.

Buscemi N, Vandermeer B, Friesen C, et al. The efficacy and safety of drug treatments for chronic insomnia in adults: a meta-analysis of RCTs.

Neubauer DN. Current and new thinking in the management of comorbid insomnia.

Pollack M, Kinrys G, Krystal A, et al. Eszopiclone coadministered with escitalopram in patients with insomnia and comorbid generalized anxiety disorder.

Gross PK, Nourse R, Wasser TE. Ramelteon for insomnia symptoms in a community sample of adults with generalized anxiety disorder: an open label study.

Fava M, Asnis GM, Shrivastava R, et al. Zolpidem extended-release improves sleep and next-day symptoms in comorbid insomnia and generalized anxiety disorder.

Roth T, Walsh JK, Krystal A, et al. An evaluation of the efficacy and safety of eszopiclone over 12 months in patients with chronic primary insomnia.

Roehrs TA, Randall S, Harris E, et al. Twelve months of nightly zolpidem does not lead to dose escalation: a prospective placebo-controlled study.

Uchiyama M, Hamamura M, Kuwano T, et al. Long-term safety and efficacy of ramelteon in Japanese patients with chronic insomnia.

Longo LP, Johnson B. Addiction: Part I. Benzodiazepines-side effects, abuse risk and alternatives.

Perlis ML, McCall WV, Krystal AD, Walsh JK. Long-term, non-nightly administration of zolpidem in the treatment of patients with primary insomnia.

Insomnia: A Clinical Guide to Assessment and Treatment.

Morin CM, Vallières A, Guay B, et al. Cognitive behavioral therapy, singly and combined with medication, for persistent insomnia: a randomized controlled trial.

Wilson SJ, Nutt DJ, Alford C, et al. British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders.

Riemann D, Perlis ML. The treatments of chronic insomnia: a review of benzodiazepine receptor agonists and psychological and behavioral therapies.

Riemann D, Spiegelhalder K, Espie C, et al. Chronic insomnia: clinical and research challenges-an agenda.

Anderson G. The promise and pitfalls of the Internet for cognitive behavioral therapy.

Haynes PL, Bootzin RR. Insomnia treatments: moving from efficacy to effectiveness.


What Is Trazodone, Anyway?

Trazodone was first approved as an antidepressant by the Food and Drug Administration in 1981. Although doctors can legally prescribe trazodone (and all drugs, for that matter) for any reason, even if it’s not FDA-approved for that use, the drug has never been approved to treat insomnia.

A handful of studies have shown that trazodone may improve sleep during the first two weeks of treatment. But the drug hasn’t been well-studied for longer than six weeks for people whose primary problem is insomnia. As a result, little is known about how well it works or how safe it is past that point for the treatment of chronic insomnia. Also, an effective dose range has never been established for the drug when it’s being used to treat insomnia, although lower doses are typically given.

Updated treatment guidelines from the American Academy of Sleep Medicine published in 2021 recommend that doctors turn first to cognitive behavioral therapy (CBT) before drugs for most people suffering from insomnia. The AASM 2017 guidelines for doctors using medication to treat chronic insomnia do not recommend trazodone because there’s so little data to support its use. The American College of Physicians also does not recommend trazodone in its 2021 insomnia treatment guidelines. And a May 2018 Cochrane review found that there’s no good evidence to support the use of any antidepressant to treat insomnia, including trazodone.

Still, prescribing data suggests that some doctors remain convinced that trazodone is an appropriate sleep medication for many people, even those without depression. And it might be helpful for some people: A small “open label” study (participants are aware they are taking a specific drug) published in December 2020 in the Journal of Clinical Sleep Medicine involving people whose insomnia causes them to sleep less than 6 hours (as measured by a sleep test) once they do fall asleep, found that trazodone was helpful in keeping this small group of people asleep longer compared with people who received CBT.


The Problem With Relying on Medicine

Medications should always be your last resort when it comes to treating your anxiety. The reason is not just because anxiety medications (known as anxiolytics) have side effects - although that is a problem with every mental health medication - but because medications prevent you from learning to cope without them.

That's the greatest issue with medication. All anxiety medications dull anxiety without teaching you how to control it. Anxiety isn't like getting an infection. You cannot simply take an antibiotic and have your anxiety go away. Those who rely too much on medication often find that they don't use or learn the skills necessary to cope with anxiety.

As soon as your stop taking any medicine your anxiety will most likely come back. And if you haven't learned any new coping skills, it may even be worse than before.


Treatment of Insomnia in Anxiety Disorders

Insomnia is highly prevalent in psychiatric disorders, and it has significant implications. This review focuses on insomnia in the context of anxiety disorders. The prevalence of comorbid insomnia in anxiety disorders is addressed and the clinical implications associated with insomnia are discussed as well as when and how to treat this important comorbidity.

Just how specifically insomnia relates to and possibly affects anxiety disorders is highlighted by the fact that insomnia is one of the defining criteria in a number of the DSM-IV-TR anxiety disorders. For example, difficulty in falling or staying asleep is a criterion for PTSD, acute stress disorder, and generalized anxiety disorder (GAD).

The relationship of insomnia to anxiety disorders is also influenced by comorbid major depression. The severity of insomnia is increased when an anxiety disorder is comorbid with a major depressive disorder (MDD). 1 This is highly relevant because 58% of MDD patients have a lifetime anxiety disorder. 2

The presence of insomnia has a deleterious effect on daytime functioning and negative effects on quality of life, including social and work relationships. 3 Also, there is clear evidence that the presence of insomnia in anxiety disorders is associated with increased morbidity. For example, in patients with PTSD, insomnia is associated with an increased likelihood of suicidal behavior, depression, and substance abuse as well as nonresponsiveness to treatment. 4-6 In addition, insomnia as an early symptom in traumatized patients increases the risk of the development of PTSD 1 year later. 7

Early assessment

It is important to carefully assess for insomnia early in the evaluation of patients with anxiety disorders and to aggressively treat this complicating comorbidity. Insomnia is an underrecognized and undertreated problem. Patients rarely report their symptoms of insomnia spontaneously to their doctor. Adding to the problem of detecting insomnia is the finding that doctors rarely inquire about insomnia in their patients. 3,8,9 Thus, a carefully taken history is an important first step in the assessment of insomnia.

Self-rating sleep questionnaires and direct clinical interviews are used to obtain a history of potential sleep disorders (eg, insomnia). A number of well-validated sleep questionnaires have been widely used. The most widely used and validated questionnaire is the 19-question Pittsburg Sleep Quality Index. The questions cover sleep quality, sleep problems, sleep medications, and so on, within the past month. 10 Another widely used questionnaire is the Leeds Sleep Evaluation Questionnaire (LSEQ). The LSEQ consists of 10 self-rating questions that cover sleep and aberrant sleep behaviors. 11

Besides self-rating questionnaires that depend on memory of sleep disturbances, a sleep log or diary can confirm questionable sleep disturbances prospectively. The use of a sleep log allows for an analysis of day-to-day sleep patterns, such as the time that the patient went to bed, sleep latency, and nighttime awakenings. 8,9 The log is filled out by the patient shortly after awakening in the morning (see Morin 9(p38) for an example of a sleep log). If at all possible, monitoring for up to 2 weeks is highly recommended because it allows for sleep abnormalities that might show marked day-to-day variability and would more likely be detected by extensive monitoring. 12,13

What is already known about insomnia in patients with anxiety disorder?? Anxiety disorders frequently coexist with insomnia. The latter is believed to be part and parcel of various anxiety disorders and is one of the defining criteria of a number of them.

What new information does this article provide?? Our article clarifies new approaches to considering insomnia in anxiety disorders. The presence of insomnia should be considered a comorbid illness and treated on its own. Pharmacotherapy, cognitive-behavioral therapy, and a combination of both are discussed. Insomnia is an added pathology that brings increased morbidity to patients with anxiety disorders. Our review suggests that successful treatment of insomnia actually increases the responsiveness of anxiety disorders to many antianxiety treatments.

What are the implications for psychiatric practice?? When evaluating patients with anxiety disorders, psychiatrists should carefully evaluate for the presence of insomnia. Patients infrequently bring up this symptom on their own. If insomnia is present, aggressive treatment early in the course of therapy is highly suggested.

If the presence of insomnia is suspected, interviewing a spouse, a significant other, or a caregiver is helpful. Some patients who believe they have insomnia symptoms appear to have “sleep state misperception,” where their partners clearly state that their sleep is normal. 14 These “others” can also report problems that are likely not obvious to the patient:

• Apnea spells or excessive snoring as seen in obstructive apnea

• Excessive body movements as seen in periodic leg movement disorder and restless legs syndrome

• Various sleep-related behaviors (sometimes violent and aggressive) as seen in rapid eye movement behavior disorder (RBD)

Referral to a sleep specialist and sleep polysomnography has been recommended if pharmacological or nonpharmacological options are not working. Referral is also warranted for patients with insomnia in whom a specific sleep disorder, such as obstructive sleep apnea, periodic limb movements, narcolepsy, or RBD, is suspected. 12,15 Even when a visit to a sleep laboratory is suggested, the cost of an overnight visit is often prohibitive-more than $1000 per night usually 2 nights are required with the first being an adaptation night for the patient. Insurance frequently does not cover these costs. 16 If it is found that the patient has sleep apnea, a sleep movement disorder, RBD, or a number of other sleep disorders, specific nonhypnotic treatments may be required (eg, continuous positive airway pressure for sleep apnea is the treatment of choice).

Before beginning treatment of anxiety disorder–associated insomnia symptoms, rule out any concurrent medical illness, medication treatment, or substance use that might be inducing or worsening insomnia. Many medical illnesses, such as cardiovascular disorders (eg, congestive heart failure), pulmonary disorders (eg, emphysema), endocrinopathies (eg, thyroid disorders), GI disorders (eg, acid reflux), and neurological disorders (eg, pain syndromes), are associated with insomnia. 12

Carefully assess the use of medications for medical and psychiatric disorders that may be implicated in insomnia as well as caffeine or alcohol use. Even small amounts of the latter have been associated with increased nighttime awakenings.

One should be highly suspicious of alcohol or substance use or abuse in patients with anxiety disorders because these are frequently comorbid. 4 Various medications are associated with insomnia, including psychostimulants (eg, ephedrine found in cold medication, amphetamines used in ADHD), bronchodilators (eg, theophylline, albuterol), pain medication (eg, oxycodone), and antidepressants (eg, SSRIs). 12 The latter category is particularly important because many antidepressants are FDA-approved and are prescribed for anxiety disorders.

Before providing any significant intervention for insomnia, a careful evaluation regarding behaviors that might contribute to insomnia should be made. Daytime naps, late nighttime snacks or meals, watching television in bed, nighttime exercise, or excessive light or loudness in the bedroom should be identified and modified. Eliminating these behaviors can lead to significant sleep improvements. A 13-item self-rating questionnaire by Mastin and colleagues 17 can help elicit sleep hygiene information.

Pharmacological options

The treatment of insomnia in patients with anxiety disorders is, for the most part, the same as the treatment of insomnia per se: pharmacological, nonpharmacological, or a combination of the two.

The primary treatment of insomnia is pharmacological because of the rapid onset of action (eg, hypnotics are usually effective within days to 1 week of use). The most common nonpharmacotherapy, cognitive-behavioral therapy for insomnia (CBT-I) takes considerably longer. 3,8,12 Currently, the FDA has 11 approved drugs for the treatment of insomnia:

• Nonbenzodiazepines: eszopiclone, zolpidem, zolpidem ER, and zaleplon

• Benzodiazepines: estazolam, flurazepam, quazepam, temazepam, and triazolam

• A tricylic antidepressant: low-dose sinequan

• A melatonin agonist: ramelteon

In recent years, nonbenzodiazepines have become the most recommended of the approved hypnotics. (There has been less and less reliance on benzodiazepines.) Not only are nonbenzodiazepines effective in treating insomnia (equivalent to the benzodiazepines), but there is a notion that they are safer than benzodiazepines. 3,12

Both nonbenzodiazepines and benzodiazepines are associated with adverse effects that include fatigue, dizziness, ataxia, and the development of dependence and tolerance with long-term use. Although head-to-head studies comparing these classes of hypnotics have been minimal, a recent meta-analysis supports the finding of reduced adverse effects for the nonbenzodiazepines. 18 The nonbenzodiazepines typically have a shorter half-life and are more selective at the γ-aminobutyric acid receptor, factors that are partially responsible for less residual daytime sedation and other adverse effects.

In the treatment of anxiety disorders with comorbid insomnia, the latter should be treated concurrently with, but independently of, the anxiety disorder per se. The idea that one should wait to see whether the insomnia resolves with only the treatment of the anxiety disorder is no longer valid. Clinical experience has shown that without targeted insomnia treatment, insomnia frequently persists. 3,19

When adding a hypnotic to an antidepressant in the treatment of anxiety, the risk to benefit ratio must be considered. Pollack and colleagues 20 looked at a large group of patients with GAD comorbid with insomnia (N = 595). The patients received either 10 mg of escitalopram coadministered with 3 mg of eszopiclone or the escitalopram with placebo. Those in the active hypnotic treatment group had a significant response in their insomnia by the first week. The combination of medications was well tolerated with no significant increase in adverse effects.

Most surprisingly, the anxiety scores for those patients who received the hypnotic significantly improved starting at week 4 even after removing insomnia symptoms from the anxiety assessment. The time to onset of the anxiolytic response was also reduced. In addition, the combination treatment led to a slightly better symptom response and remission rate for the anxiety disorder.

Similar results were reported in a 12-week open-label study (N = 27) undertaken by Gross and colleagues. 21 The researchers evaluated ramelteon (8 mg/d), a melatonin agonist, in patients who had GAD comorbid with insomnia and whose condition was partially responsive to an SSRI or a serotonin norepinephrine reuptake inhibitor. The hypnotic was well tolerated, effective for insomnia, and appeared to facilitate the treatment of GAD.

A double-blind placebo-controlled study by Fava and colleagues 22 evaluated the efficacy and safety of zolpidem extended-release (12.5 mg/d) versus placebo in patients with comorbid GAD and insomnia who were being treated with escitalopram (10 mg/d). Sleep measures improved significantly by the end of week 1, and there was no added burden of adverse effects. Zolpidem did not show a beneficial anxiolytic effect.

Approximately 50% of patients with insomnia continue to have insomnia 3 years after initial diagnosis, and many patients require months to years of treatment. Nonbenzodiazepines for primary insomnia were found to have continued efficacy and to be well tolerated with no evidence of abuse or withdrawal symptoms on discontinuation of use after 12 months. 23,24 Ramelteon was also found to be efficacious with no significant issues of abuse or tolerance in a 24-week open-label study. 25 The literature for longer use of hypnotics is scarce.

Anxiety disorders are frequently comorbid with alcohol or substance use disorders. 4,26 Consider ramelteon or low-dose sinequan to avoid potential issues of abuse and addiction. Nonbenzodiazepines are preferred over benzodiazepines there is evidence that the former have decreased potential for abuse and a better adverse-effect profile.

In some patients with insomnia, benzodiazepines are clearly necessary. The other hypnotics may not be as effective for some patients, and the anxiolytic properties of benzodiazepines may be helpful.

When hypnotics are used (particularly, benzodiazepines and nonbenzodiazepines), their use should be reassessed-every 3 to 4 weeks. 3,12 Many patients with insomnia do not experience sleep disturbances nightly. Therefore, the use of hypnotics on an as-needed basis or a few times a week helps cut down on the amount and exposure to medication. 27

Trazodone and mirtazapine are also widely used for insomnia, as are atypical antipsychotics and herbal preparations. Unfortunately, these agents have not been rigorously studied for insomnia and thus their effectiveness and safety remain unclear. 3

Nonpharmacological interventions

CBT-I is an important, widely accepted, multimodal treatment for insomnia and the best-studied of the nonpharmacological approaches for this disorder. It is a manualized treatment that focuses on various components of CBT (ie, cognitive restructuring and the use of psychological interventions, such as the practice of good sleep hygiene, stimulus control, sleep restriction, and relaxation therapy). These methods address negative and distorted cognitions and behaviors that initiate and perpetuate insomnia. 9,28 Treatment duration is relatively short. It is administered for 5 hours divided over 4 to 6 weeks and can subsequently be used as a maintenance treatment in monthly sessions. There are approximately 12 well-designed CBT-I trials that have clearly demonstrated that it is a highly effective intervention for insomnia for 1 year or longer. 29,30

Studies that compared CBT-I with pharmacotherapy found equivalent efficacy. 31 This has led the NIH Consensus and State of the Science Statement to conclude that CBT-I is “as effective as prescription medications are for short-term treatment of chronic insomnia. Moreover, there are indications that the beneficial effects of CBT, in contrast to those produced by medications, may last well beyond the termination of active treatment.” 3 In contrast to hypnotics, learned CBT-I skills may persist even when active treatment ends. 9 Furthermore, some patients may prefer CBT-I over hypnotic drugs because of their possible adverse effects or because of concerns about drug interactions or taking a drug during pregnancy. 9

In general, CBT-I is underutilized-only about 1% of patients with chronic insomnia receive this therapy. 32 To increase the availability of CBT, it can be administered via self-help strategies (eg, educational books and materials) and in group formats. In addition, the use of the Internet to provide CBT has been shown to be effective. Nonetheless, patients frequently prefer face-to-face contact. 33

Besides CBT-I, a number of other nonpharmacological therapies, such as bright light, physical exercise, acupuncture, tai chi, and yoga, have been used to treat insomnia. Unfortunately, the results have been inconsistent. 32,34

Combination therapy

Is a combination of pharmacotherapy and nonpharmacotherapy more effective than either alone in the treatment of anxiety disorders with insomnia? Combination therapy has not been addressed in studies of this particular patient population. Furthermore, the question has been minimally addressed even in the treatment of insomnia per se. Study findings suggest only modest differences in outcomes with a combination of therapies. Similar results were seen in a study that compared CBT with CBT plus zolpidem. The 6-week acute study demonstrated a 60% response rate and a 40% remission rate the group with the combination treatment did have a significant increase in sleep time of 15 minutes, but the researchers question the clinical significance of this isolated finding. 29

Anxiety disorders with comorbid insomnia are highly prevalent with potential negative consequences. Therefore, assess for insomnia with self-rating scales and careful clinical interviews. When appropriate, refer patients for polysomnography.

Insomnia should be treated aggressively with pharmacotherapy, nonpharmacotherapy (particularly CBT-I), or a combination. Some of the hypnotic treatments actually appear to facilitate successful therapy for the anxiety disorder.

Benzodiazepines and nonbenzodiazepines have a number of adverse effects and can lead to abuse and dependence. Patients with an anxiety disorder may be particularly vulnerable, especially those with a history of alcohol and drug abuse. Treatment with benzodiazepine and nonbenzodiazepine hypnotics needs to be reassessed monthly. Alternatively, ramelteon, low-dose sinequan, and CBT-I should be considered because they have minimal adverse effects and no risk of abuse.

Successful treatment of insomnia is an important goal in patients with anxiety disorders. Both pharmacological and nonpharmacological interventions have response rates of approximately 60%.

References:

van Mill JG, Hoogendijk WJ, Vogelzangs N, et al. Insomnia and sleep duration in a large cohort of patients with major depressive disorder and anxiety disorders.

Kessler RC, Berglund P, Demler O, et al. The epidemiology of major depressive disorder: results from the National Comorbidity Survey Replication (NCS-R).

National Institutes of Health. National Institutes of Health State of the Science Conference statement on Manifestations and Management of Chronic Insomnia in Adults.

Marcks BA, Weisberg RB. Co-occurrence of insomnia and anxiety disorders: a review of the literature.

Maher MJ, Rego SA, Asnis GM. Sleep disturbances in patients with post-traumatic stress disorder: epidemiology, impact and approaches to management.

Harvey AG, Jones C, Schmidt DA. Sleep and posttraumatic stress disorder: a review.

Koren D, Arnon I, Lavie P, Klein E. Sleep complaints as early predictors of posttraumatic stress disorder: a 1-year prospective study of injured survivors of motor vehicle accidents.

Sateia MJ, Doghramji K, Hauri PJ, Morin CM. Evaluation of chronic insomnia. An American Academy of Sleep Medicine review

Morin CM. Cognitive-behavioral approaches to the treatment of insomnia.

Buysse DJ, Reynolds CF 3rd, Monk TH, et al. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research.

Parrott AC, Hindmarch I. Factor analysis of a sleep evaluation questionnaire.

Schutte-Rodin S, Broch L, Buysse D, et al. Clinical guideline for the evaluation and management of chronic insomnia in adults.

Bastien CH. Insomnia: neurophysiological and neuropsychological approaches.

Edinger JD, Fins AI. The distribution and clinical significance of sleep time misperceptions among insomniacs.

Kushida CA, Littner MR, Morgenthaler T, et al. Practice parameters for the indications for polysomnography and related procedures: an update for 2005.

Boeve BF, Molano JR, Ferman TJ, et al. Validation of the Mayo Sleep Questionnaire to screen for REM sleep behavior disorder in an aging and dementia cohort.

Mastin DF, Bryson J, Corwyn R. Assessment of sleep hygiene using the Sleep Hygiene Index.

Buscemi N, Vandermeer B, Friesen C, et al. The efficacy and safety of drug treatments for chronic insomnia in adults: a meta-analysis of RCTs.

Neubauer DN. Current and new thinking in the management of comorbid insomnia.

Pollack M, Kinrys G, Krystal A, et al. Eszopiclone coadministered with escitalopram in patients with insomnia and comorbid generalized anxiety disorder.

Gross PK, Nourse R, Wasser TE. Ramelteon for insomnia symptoms in a community sample of adults with generalized anxiety disorder: an open label study.

Fava M, Asnis GM, Shrivastava R, et al. Zolpidem extended-release improves sleep and next-day symptoms in comorbid insomnia and generalized anxiety disorder.

Roth T, Walsh JK, Krystal A, et al. An evaluation of the efficacy and safety of eszopiclone over 12 months in patients with chronic primary insomnia.

Roehrs TA, Randall S, Harris E, et al. Twelve months of nightly zolpidem does not lead to dose escalation: a prospective placebo-controlled study.

Uchiyama M, Hamamura M, Kuwano T, et al. Long-term safety and efficacy of ramelteon in Japanese patients with chronic insomnia.

Longo LP, Johnson B. Addiction: Part I. Benzodiazepines-side effects, abuse risk and alternatives.

Perlis ML, McCall WV, Krystal AD, Walsh JK. Long-term, non-nightly administration of zolpidem in the treatment of patients with primary insomnia.

Insomnia: A Clinical Guide to Assessment and Treatment.

Morin CM, Vallières A, Guay B, et al. Cognitive behavioral therapy, singly and combined with medication, for persistent insomnia: a randomized controlled trial.

Wilson SJ, Nutt DJ, Alford C, et al. British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders.

Riemann D, Perlis ML. The treatments of chronic insomnia: a review of benzodiazepine receptor agonists and psychological and behavioral therapies.

Riemann D, Spiegelhalder K, Espie C, et al. Chronic insomnia: clinical and research challenges-an agenda.

Anderson G. The promise and pitfalls of the Internet for cognitive behavioral therapy.

Haynes PL, Bootzin RR. Insomnia treatments: moving from efficacy to effectiveness.


The First Line of Treatment for Insomnia That'll Surprise You

Whenever most people have serious trouble sleeping, they automatically reach for a sleeping aid, whether that&rsquos a prescription or over-the-counter medication or a natural remedy.

But these solutions, as psychologist and sleep specialist Stephanie Silberman, Ph.D, explained, are anything but.

In fact, the preferred solution &mdash the one that research also supports &mdash is a treatment that many people, even medical professionals, are unaware of.

Research has shown that cognitive-behavioral therapy (CBT) is highly effective for insomnia. (Effective results have been shown in a recent meta-analysis and article review .)

Below, Dr. Silberman, author of The Insomnia Workbook: A Comprehensive Guide to Getting the Sleep You Need, offers insight into insomnia and its treatment and shares several strategies readers can try at home.

What is Normal Sleep?

Before thinking about disturbed sleep, it&rsquos important to understand what normal sleep really is. Normal slumber involves falling asleep relatively easily once you&rsquore in bed, Silberman said. &ldquoPeople have a range of how quickly they go to sleep,&rdquo she said, but typically they can drift off to sleep anywhere from a few minutes to 15 minutes.

Normal sleepers will also go through four stages of sleep several times a night, she said. According to The Insomnia Workbook, the stages are:

  • Stage N1: the lightest stage, which usually makes up 10 percent of your total sleep time.
  • Stage N2: unlike stage N1, you lose awareness of external stimuli, and people spend most of their sleep time in this stage.
  • Stage N3: known as slow-wave sleep, and believed to be the most restorative.
  • Stage R: known as REM sleep, or rapid eye movement. It&rsquos the most active of the stages for your brain and body functions, such as breathing and heart rate. Your muscles relax, however, so you don&rsquot act out your dreams.

It&rsquos also normal for it to take about 20 to 30 minutes to feel truly awake in the morning.

What Is Insomnia?

&ldquoMost people with insomnia have difficulty either falling asleep, known as sleep onset insomnia, or staying asleep, known as sleep maintenance insomnia,&rdquo Silberman writes in her book, which provides readers with information on insomnia and strategies to treat it and sleep better.

People with insomnia also might feel moody or fatigued during the day. (Here&rsquos more on insomnia.) The most common type of insomnia is conditioned or learned insomnia. Initially, a person starts sleeping poorly because of a stressor, Silberman writes. Then the insufficient sleep almost becomes routine because you continue to ruminate about your sleeping problems, leading to increased arousal before bed. This then becomes &ldquoa conditioned physiological response that contributes to difficulties falling asleep.&rdquo

Insomnia Myths

There also are many myths that can undermine your sleep and insomnia treatment. One of the biggest, Silberman reiterated, is the idea that sleeping pills are an effective remedy that improves your sleep. In fact, research has found that CBT is more effective than pharmacological interventions.

Specifically, sleeping pills actually make you feel groggy and sleepy during the day, they cause dependency and disrupt and change sleep architecture. (Sleep architecture refers to the structure of your sleep and the &ldquocycling in and out of the different stages of sleep during the night,&rdquo Silberman writes in her book.)

For instance, benzodiazepines are commonly prescribed for sleep but they actually &ldquosuppress the slow-wave sleep,&rdquo she said. The problem? Recall that slow-wave sleep is essential to a good, restorative sleep. Plus, as she noted, we don&rsquot know the long-term consequences of disrupted slow-wave sleep.

Nonbenzodiazepines, a class of sedative-hypnotic drugs, such as Lunesta and Ambien, &ldquoaffect other areas of sleep,&rdquo such as respiration, Silberman said. They have potentially serious side effects and also can lead to psychological and physiological dependence.

Some sedative hypnotics can cause rebound insomnia after they&rsquore discontinued. Naturally, many people get discouraged, thinking they can&rsquot sleep without the sleeping aid. But, as Silberman said, &ldquothis is par for the course,&rdquo because you&rsquore taking away a medication that caused changes to your body.

Herbal and &ldquonatural&rdquo remedies, such as melatonin, valerian root and kava, are not any better. In fact, they aren&rsquot regulated by the Food and Drug Administration, so they&rsquore not tested for effectiveness or safety. In her book, Silberman discusses the disturbing results of one consumer agency study that tested valerian products. It found that some products didn&rsquot contain measurable amounts of the ingredient, others contained half of the amount stated on the bottle and one bottle even contained a poisonous metal!

Also, people erroneously believe that &ldquothere is no rhyme or reason to their sleep,&rdquo Silberman said. Similar to that, they believe they have little control over their sleep. (This might be another reason why people turn to sleeping pills.) But in reality, there are targeted and well-tested techniques you can do to have a good night&rsquos sleep. Also, once you observe your sleeping, you&rsquoll be able to pick up on patterns that affect your sleep, so it&rsquos not so random after all.

Another misconception is that spending more time in bed will increase your chances of sleeping longer. To the contrary, this can actually sabotage your sleep and create a negative association with your bed. As Silberman said, &ldquothe more time a person spends in bed, the more they reinforce the idea that the bed is not a sleep-promoting place.&rdquo

How CBT for Insomnia Works

What does CBT for insomnia look like? When a client first sees Silberman, they work on uncovering the client&rsquos current sleep pattern and the factors that are negatively affecting their sleep. They accomplish this by completing sleep logs, for instance.

They talk about a variety of potential issues, such as: &ldquoWhat&rsquos causing them to have these problems at night? Are they tossing and turning because they can&rsquot turn off their brain at night or is it some kind of pain or an environmental stimulus, such as a baby waking you up?&rdquo Is smoking one of the culprits? (Smoking is a stimulant, so smoking right before bed can make it tougher to fall asleep.) They ponder whether physiological factors are to blame. For instance, a medication you&rsquore taking might be causing poor sleep.

When treating insomnia, in addition to sleep logs, other techniques include sleep restriction (described later) and reducing any anxious or worrisome thoughts the person may be having around sleep or their life in general.

Sleeping Strategies To Try

Silberman shared the following strategies you can try on your own to improve your sleep.

1. Observe your sleep.

Gathering data is key when trying to treat insomnia or any kind of sleep trouble, Silberman said. In her book, she provides readers with several worksheets to log in your sleep. This is essential because it helps you figure out what habits are hindering your sleep (such as a stressful event, caffeine intake, daytime napping or TV watching) and how long you&rsquore actually sleeping.

In fact, Silberman said that many different things can affect your sleep. At first, sleep or lack thereof seems random. But once you commit your habits to paper, you might notice that the three glasses of wine or two cups of coffee you had led to your sleeping poorly. Maybe another day, you ate a super-spicy meal for dinner, leading to heartburn and little sleep.

When observing your sleep, it&rsquos helpful to consider: what time you went to bed, how long it took you to fall asleep, how often you woke up during the night, what time you finally got up and how many hours you slept. Recording this information each morning for a week helps you spot patterns.

2. Restrict your time in bed.

Sleep studies have shown that sleep restriction is effective for treating insomnia. This is why collecting your sleep data is so important. It gives you a good idea of how long you&rsquore actually sleeping, because you want to be in bed for that number of hours. Lying awake in bed only &ldquoincreases frustration, anxiety and annoyance with the process,&rdquo Silberman said.

&ldquoBy restricting the amount of time to bed,&rdquo she said, you &ldquowill start getting more solid sleep.&rdquo How do you calculate the time you spend in bed? Just add up the time you&rsquove actually spent sleeping each night for a week and divide by seven to get an average time.

Then about 30 minutes to an hour before bedtime, establish a routine that primes your body for relaxation. For instance, you might listen to soothing music, take a warm bath or read a book.

3. Practice good sleep hygiene and habits.

While good sleep hygiene won&rsquot dramatically change your insomnia, it does help you optimize your sleep, Silberman said. Some examples are limiting caffeine and alcohol intake, making your room cool and dark and exercising four or five hours before bedtime.

Other helpful habits include engaging in relaxation techniques and working through any worry thoughts. &ldquoIn particular it&rsquos important to practice [relaxation techniques] when you&rsquore not anxious or stressed out, so they work better when you need them.&rdquo

One way to reduce anxious thoughts is by asking yourself &ldquowhat&rsquos the evidence for and against these thoughts I&rsquom having,&rdquo Silberman said. Not surprisingly, there&rsquos usually &ldquovery little evidence for the irrational thought.&rdquo Then, you &ldquocan come up with an alternative thought or new explanation.&rdquo

Again, remember that you do have control over your sleep. Studies have repeatedly shown that CBT is a highly effective treatment for insomnia.

To learn more about sleep specialist and clinical psychologist Stephanie Silberman and her work, please visit her website.


Reevaluating Antidepressant Selection in Patients With Bruxism and Temporomandibular Joint Disorder

Temporomandibular joint disorder (TMD) is a broad pain disorder that refers to several conditions affecting the temporomandibular joint of the jaw and the muscles of mastication. As with most pain disorders, a high prevalence of depression and anxiety is associated with TMD. Research has shown that selective serotonin reuptake inhibitors (SSRIs), the first-line drug therapy for major depressive disorder, may not be suitable for TMD patients because SSRIs can induce teeth-grinding, otherwise known as bruxism. This is problematic because bruxism is believed to further exacerbate TMD. Therefore, the purpose of this literature review is to better understand the mechanism of SSRI-induced bruxism, as well as discuss alternative antidepressant options for treating depression and anxiety in patients with bruxism and TMD. Alternative classes of antidepressants reviewed include serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, atypical antidepressants, and monoamine oxidase inhibitors. Findings indicate that dopamine agonists and buspirone are currently the most effective medications to treat the side effects of SSRI-induced bruxism, but results regarding the effectiveness of specific antidepressants that avoid bruxism altogether remain inconclusive.


Substance/Medication-Induced Sleep Disorder

Armeen Poor, MD, is a board-certified pulmonologist and intensivist. He specializes in pulmonary health, critical care, and sleep medicine.

Substance or medication-induced sleep disorder is the official diagnostic name for insomnia and other sleep problems which are caused by the use of alcohol, drugs, or taking certain medications. Roughly translated, that means that one of the effects of drinking alcohol, using a drug, or taking a medication, is having a problem with getting to sleep at the time you want to sleep, staying asleep at the time you want to sleep, excessive sleepiness during the day, or unusual behaviors when you do sleep.

Substance or medication-induced sleep disorder is different from the occasional difficulty with getting to sleep or staying asleep that is actually quite normal.

Substance or medication-induced sleep disorder is also different from the temporary insomnia or exhaustion that often affects people straight after alcohol or drug use, which is a normal response to the substance, or the activities of people who use alcohol or drugs, such as staying up later than your usual bedtime or participating in tiring activities during the time that alcohol or drugs are used (such as dancing). In contrast to these normal responses to alcohol or drugs, substance/medication-induced sleep disorder interferes with sleep more significantly, and the negative effects last for much longer.


Buspirone (BuSpar)

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Learn more about common mental health conditions that affect millions.

Call the NAMI Helpline at

800-950-NAMI

Brand name: BuSpar®

Generic name: buspirone (byoo SPYE rone)

All FDA black box warnings are at the end of this fact sheet. Please review before taking this medication.

What Is Buspirone And What Does It Treat?

Buspirone is in a class of medications called anti-anxiety medications. Buspirone is not related to other anti-anxiety medications, such as benzodiazepines, barbiturates or other sedative/ anxiolytic drugs. It is approved for the treatment of generalized anxiety disorder (GAD).

Generalized Anxiety Disorder (GAD) occurs when a person experiences excessive anxiety or worry for at least six months. Other symptoms include:

  • Restlessness
  • Fatigue (low energy, feeling tired all the time)
  • Difficulty concentrating
  • Irritability
  • Muscle tension
  • Sleep disturbance (difficulty falling asleep or waking up in the middle of the night)

What Is The Most Important Information I Should Know About Buspirone?

Do not drive a car or operate machinery until you know how this medication affects you because you may notice that you feel tired or dizzy.

Alcohol may increase any drowsiness or dizziness when taken with buspirone. You should avoid the use of alcohol while taking buspirone.

It may take 3 to 4 weeks before you start to feel better. Initially you may begin to notice a decrease in irritability and worry. Do not stop taking this medication without talking to your healthcare provider first. With input from you, your health care provider will assess how long you will need to take the medicine.

Unlike other anti-anxiety medications, buspirone has very low abuse potential.

Are There Specific Concerns About Buspirone And Pregnancy?

If you are planning on becoming pregnant, notify your healthcare provider to best manage your medications. People living with anxiety disorders who wish to become pregnant face important decisions. It is important to discuss this with your doctor and caregivers.

Regarding breastfeeding, caution is advised since it is unknown whether buspirone passes into breast milk.

What Should I Discuss With My Healthcare Provider Before Taking Buspirone?

  • Symptoms of your condition that bother you the most
  • If you have thoughts of suicide or harming yourself
  • Medications you have taken in the past for your condition, whether they were effective or caused any adverse effects
  • If you experience side effects from your medications, discuss them with your healthcare provider. Some side effects may pass with time, but others may require changes in the medication.
  • Any other psychiatric or medical problems you have
  • All other medications you are currently taking (including over the counter products and herbal and nutritional supplements) and any medication allergies you have
  • Other non-medication treatment you are receiving such as talk therapy or substance abuse treatment. Your provider can explain how these different treatments work with the medication.
  • If you are pregnant, plan to become pregnant, or are breast-feeding
  • If you drink alcohol or use drugs

How Should I Take Buspirone?

Buspirone should be taken twice a day with or without food.

Your healthcare provider will determine the dose that is right for you based upon your response.

Use a calendar, pillbox, alarm clock, or cell phone alert to help you remember to take your medication. You may also ask a family member a friend to remind you or check in with you to be sure you are taking your medication.

What Happens If I Miss A Dose Of Buspirone?

If you miss a dose of buspirone, take it as soon as you remember, unless it is closer to the time of your next dose. Discuss this with your healthcare provider. Do not double your next dose or take more than what is prescribed.

What Should I Avoid While Taking Buspirone?

Avoid drinking alcohol and using illegal drugs while you are taking buspirone. They may decrease the benefits (e.g., worsen your condition) and increase the adverse effects (e.g., sedation) of the medication.

What Happens If I Overdose With Buspirone?

If an overdose occurs, call your doctor or 911. You may need urgent medical care. You may also contact the poison control center at 1-800-222-1222.

A specific treatment to reverse the effects of buspirone does not exist.

What Are Possible Side Effects Of Buspirone?

Common side effects

Rare/serious side effects

Changes in weight or appetite, fainting, changes in blood pressure, muscle cramps or spasms, and redness or itching of eyes may occur in some instances.

Allergic reaction (difficulty breathing hives swelling of your lips, tongue or face) chest pain or an irregular heartbeat slurred speech confusion or blurred vision numbness or tingling in your hands, feet, arms, or legs or uncontrollable movements of your arms, legs, tongue, or lips.

Are There Any Risks For Taking Buspirone For Long Periods Of Time?

To date, there are no known problems associated with the long term use of buspirone. It is a safe and effective medication when used as directed.

What Other Medications May Interact With Buspirone?

If you have taken a monoamine oxidase inhibitor (MAOI), such as phenelzine (Nardil®), isocarboxazid (Marplan®), selegiline (Eldepryl®, EMSAM®) or tranylcypromine (Parnate®), within the past 2 weeks, do not take buspirone. The use of buspirone with these agents can cause a severe increase in your blood pressure.

The following medications may increase the levels and effects of buspirone:

  • Diltiazem (Cardizem®, Dilacor®, Tiazac®)
  • Verapamil (Calan®, Covera-HS®, Isoptin®, Verelan®)
  • Erythromycin (E-Mycin®, E.E.S.®, Ery-Tab®, Eryc®, others)
  • Consuming large amounts of grapefruit juice can increase the amount of buspirone in your blood

The following medications may decrease the levels and effects of buspirone:

How Long Does It Take For Buspirone To Work?

It may take 3 to 4 weeks of taking buspirone every day before you start to feel better.

Summary of FDA Black Box Warnings

There are no FDA black box warnings for buspirone.

©2019 The College of Psychiatric and Neurologic Pharmacists (CPNP) and the National Alliance on Mental Illness (NAMI). CPNP and NAMI make this document available under the Creative Commons Attribution-No Derivatives 4.0 International License. Last Updated: January 2016.

This information is being provided as a community outreach effort of the College of Psychiatric and Neurologic Pharmacists. This information is for educational and informational purposes only and is not medical advice. This information contains a summary of important points and is not an exhaustive review of information about the medication. Always seek the advice of a physician or other qualified medical professional with any questions you may have regarding medications or medical conditions. Never delay seeking professional medical advice or disregard medical professional advice as a result of any information provided herein. The College of Psychiatric and Neurologic Pharmacists disclaims any and all liability alleged as a result of the information provided herein.


Who is most likely to benefit from using Buspar for depression?

There’s no definitive way to know who is likely to benefit most from administration of buspirone for the treatment of depression. Since buspirone is an effective anxiolytic, it should be suspected that most benefit will be attained from individuals in which anxiety influences severity of depressive symptoms. Anyone with depression plus comorbid anxiety (i.e. “anxious depression”) should stand to benefit more from buspirone than others. There is modest evidence suggesting that individuals with the most severe symptoms of depression may benefit from adjunctive buspirone.

  • Depression with anxiety: Those with simultaneously occurring depression and anxiety often report a bidirectional relationship between depressed mood and anxious symptoms. When the anxiety flares up, they isolate themselves from others and it makes them depressed. The depression leads them to think poorly of themselves and their abilities, causing increased future anxiety – it’s a vicious circle. It is known that buspirone is effective for the treatment of anxiety and preliminary evidence suggests it could improve mood. Evidence suggests that it is an effective option among those with “anxious depression.”
  • Severe depression: Analysis of data from a standalone randomized controlled trial indicated that adjunct buspirone may help individuals with severe depression. The “severe depression” was classified as MADRS scores exceeding 30. In the event that a person exhibits severe depression to the extent that they’re scoring at least 30 (or above) on the MADRS (Montgomery-Asberg Depression Rating Scale), adjunct buspirone may be helpful.

How Does Sleep Impact ADHD — and Vice Versa?

Few things impact mental health more than sleep. Poor or insufficient sleep makes almost every psychological problem worse. In extreme cases, it can be the cause of the problem. With attention deficit disorder (ADHD or ADD), that link is obvious and complicated, because there are several ways sleep and ADHD affect each other.

Poor sleep can lead to ADHD-like symptoms and complicate a diagnosis. A few years ago, some researchers joined the “ADHD Is a Myth” crowd and declared all people with ADHD to be victims of chronic insomnia. That’s an overreach, but their findings did support the idea that quality of sleep must be considered in making an ADHD diagnosis. This is why you should start your teen’s diagnostic journey at the door of a qualified professional, and why you should study your child’s sleep patterns to answer the provider’s questions.

Are Sleep Problems Misdiagnosed as ADHD?

In my experience, insomnia-induced ADHD isn’t common, but I have referred two dozen teens and young adults for sleep studies to avoid misdiagnosing them. Some were found to have sleep apnea, narcolepsy, or primary insomnia, and treatment improved sleep and reduced symptoms. But those teens also wound up being treated at our clinic for ADHD. Nevertheless, I believe that severe sleep deprivation can present with ADHD-like symptoms, but most of such cases should be screened out from an ADHD diagnosis with an evaluation.

Poor sleep can result from ADHD, complicating diagnosis. This condition is common but under-recognized. Both of my children have what I call “ADHD-related insomnia.” I made up this name for it because I saw it so often among my clients, whose active minds didn’t shut down just because it was 10:30 p.m. It’s hard to know if this condition describes your child because you can’t easily separate this kind of insomnia from the one previously described. Which comes first: the chicken or the egg? The best solution the prescriber at our clinic has found is to begin treatment with stimulant medication, and follow the case closely for a month. Some teens will sleep better after beginning stimulants. A few will have daytime sleepiness despite taking them. That generally proves the diagnosis, but it also suggests it’s time to try a different stimulant or to pursue a sleep study.

How Can You Treat ADHD-Related Sleep Problems?

Sleep problems sometimes improve by treating the ADHD. More often, the insomnia remains but doesn’t worsen on stimulants, just as it has for my kids. In such cases, the prescriber may consider sleep medication as an adjunct. This is a complex decision, but our experience has been that, even when ADHD symptoms are improved by stimulants, ADHD-related insomnia will limit the effectiveness of treatment unless it too is addressed.

How Does ADHD Medication Impact Sleep?

Poor sleep can result from taking ADHD medication, complicating treatment. The point of stimulant medication is to stimulate the part of the brain that focuses attention. That’s the opposite of what we need when it’s time to hit the hay. However, for some people with ADHD, stimulants help sleep. For many others, insomnia predates stimulant use, which is another reason to assess sleep problems before any medication is prescribed. Figuring this out is subject to the “Hawthorne Effect.” If one is warned that sleep may be impaired by a stimulant, one gets worried about sleep, and may notice it isn’t very good. That makes it easy to blame the stimulant, rather than a chronic sleep impairment. Many teens compensate for poor sleep by taking naps. After starting a stimulant, one may not be able to nap as easily or as deeply.

On the other hand, if the teen hasn’t had sleep problems before, hasn’t over-used napping, begins to lose sleep after starting on medication, and doesn’t revert to better sleep in two or three weeks, a decision must be made. A common strategy is to discontinue stimulants and/or switch to a non-stimulant for ADHD. If the stimulants are working, we prefer to tinker with their timing and release to improve sleep. We find the Daytrana patch helpful for those with stimulant-induced insomnia, because it’s the only medication that can be shut off early (by removing the patch). In other cases, we find that treating the sleep problem directly is a better long-term solution than eliminating the stimulant.

Poor sleep reflects an unregulated life. Poor sleep may be the result of a dysregulated sleep-wake cycle and poor sleep hygiene. The worst thing about bad sleep is that it is self-perpetuating. The worse a teen sleeps, the more out of rhythm he will become. When he tries to compensate, the sleep gets worse. Good sleep hygiene is important in treating the conditions I’ve described, and it’s also critical to understanding the ADHD-sleep conundrum. More than once, we’ve tried to help a client manage stimulants and sleep, only to learn that the client is staying up late and, in extreme cases, reversing the sleep-wake cycle. Those with ADHD hate a sleep routine because it feels like a restriction of their freedom. We suggest that they consider a good sleep-cycle more like sharpening a saw than restricting their free expression.

Wes Crenshaw, Ph.D., ABPP, is a licensed psychologist board certified in couples and family psychology by the American Board of Professional Psychology. He is the author of I Always Want to Be Where I’m Not: Successful Living with ADD and ADHD (#CommissionsEarned) and a member of the ADDitude ADHD Medical Review Panel.

How to Help Teens with ADHD Sleep Better

1. Make time for it. The worst and most common sleep mistake teens make is failing to set aside eight hours to get it done, plus about an hour of prep before going to bed. For those with ADHD, it’s easy to put off sleep or to avoid it altogether. What could possibly be more boring than sleeping, especially when the night world is so interesting? It takes discipline to go to bed and to get up, but few life changes will make a bigger difference than this one in managing ADHD.

2. Turn off screens. Everyone hates this advice, including adults, but think back to a time when gaming consoles were in the family room, not the bedroom. Bedrooms shouldn’t look like mission control, they should look like sleeping quarters, and all screen time should end about an hour before bedtime. Not only are games too stimulating for late-evening use, they generate too much light.

3. Say goodnight to the (artificial) sun. Light is crucial in regulating the sleep cycle. Get teens in the habit of minimizing or shutting down artificial light in the evening after study time is over. This signals to the body that the night cycle is coming, and that it should prepare for sleep. Artificial light does the opposite. Get shades for windows to black out exterior light.

4. Rise with the light. When fall arrives and mornings become dark, go online or to your favorite home improvement store and buy a 4 x 4 or 4 x 8 daylight LED light panel. Install an extension cord (many shop lights have them already), or have an electrician do it for about $20. The panel doesn’t weigh much, so you can easily hang it on the wall of your teen’s bedroom. Set a timer for 20 minutes before your teen is scheduled to wake. If you’re feeling inventive, hang it in the window and use an auto dimmer to have the lights become progressively brighter like a sunrise.

5. No napping. Researchers consider naps to be evidence of unhealthy sleep. The only exception is the “micro-nap,” a 10- to 15-minute siesta one grabs mid-afternoon. These may improve functioning and improve sleep. Naps are hard to resist, but the fewer naps teens take, the better they’ll sleep at night.

Wes Crenshaw, Ph.D., is a member of the ADDitude ADHD Medical Review Panel.

#CommissionsEarned As an Amazon Associate, ADDitude earns a commission from qualifying purchases made by ADDitude readers on the affiliate links we share. However, all products linked in the ADDitude Store have been independently selected by our editors and/or recommended by our readers. Prices are accurate and items in stock as of time of publication


The Human Study

So they went from the petri dish – in vitro – to animals – in vivo – but what about in humans?

The human study came next – 134 patients with moderate Major Depression volunteered to test the new combo therapy in a 6-week randomized controlled trial. Everyone either got placebo, buspirone 15mg, or the buspirone-melatonin combination – which was 15mg of buspirone and 3mg of melatonin SR.

The melatonin they used was from Mellen Medical Products (although it appears available on their website for $10, some readers have told me that you can’t actually order from them. In that case check our list of clinical and laboratory tested melatonin products).

The buspirone-melatonin combo had a significant effect on the primary outcome – the clinical global improvement scale – as well as on secondary outcomes like overall CGI severity, Hamilton anxiety, and remission rates on the QIDS depression inventory, but not on the total QIDS score itself.

So the combo did better than placebo, but did it do better than buspirone alone?

Yes, it did better than both on all those measures. Buspirone did not work on any of them alone, not even anxiety, which is not too surprising since the dose was only 15mg/day.

OK but I have a theory. What if this just proves that helping sleep with melatonin and helping anxiety with a little buspirone treats depression? I mean there are studies where eszopiclone (Lunesta) is added to an SSRI and it makes the SSRI work better – I’ve seen that in controlled trials of depression as well as generalized anxiety disorder.

That’s a good theory, but in this case the melatonin didn’t actually improve any sleep items on the rating scale, so the thinking is that its antidepressant effects were due to some kind of pharmacodynamic synergy with buspirone – perhaps neurogenesis – rather than direct effects on sleep. On the other hand, they did look at cognitive symptoms in a separate study, and from that analysis it looks like improvements in cognition – rather than sleep – were driving the change in depression. When they compared patients who responded to the combo vs. those who did not, it was the change in cognitive symptoms that seemed to make the difference.

That makes sense if we’re talking about a treatment that enhances growth in the hippocampus – the memory center. What specific cognitive symptoms did it help?

Word-finding difficulties, forgetfulness, mental slowness, apathy and motivation.

OK if I’m going to find a criticism of this study then it’s that it’s just one study – why hasn’t anyone tried to replicate it?

That’s a mystery. I wrote to Dr. Fava who shared that his best guess is that there is no financial incentive here. If a company went through the trouble to license a combination pill with buspirone and melatonin in it, most physicians would bypass the combo pill by prescribing the two generic ingredients on their own. Their work on neurogenesis and depression has continued to yield fruit, however. After screening some 10,000 compounds through that neurogenesis cell line, they arrived at one with promise: NSI-189. It’s currently being developed for major depression by Neuralstem. The results have been mixed, but here’s something interesting – it seems to have better effects on cognition than on depression.

OK so what’s the bottom line, should we use melatonin with buspirone?

We tend to reserve these half-tested therapies for treatment resistant cases – and I would put it there at the end of the line along with other novel therapies like celecoxib, amantadine, minocycline, and D-cycloserine. But the buspirone-melatonin combo has two advantages: it is safe, and it improved cognition, which I wish we could say for more of our therapies.