On the Safety and Efficacy of Buspirone (BuSpar) in the Management of Snoring, Sleep Apnea, and Bruxism (Teeth Grinding) – Dale Mortimer, M.D.
There have been a handful of case reports published on the efficacy of buspirone (BuSpar) in the treatment of a number of sleep disorders. Here, Dr. Mortimer summarizes the studies about which he am familiar. Mendelson and colleagues (1991) found buspirone effective in decreasing the frequency of episodes of sleep apnea in adults with obstructive sleep apnea. Ellison and Stanziani (1993) reported on the efficacy of buspirone in the treatment of four patients with fluoxetine (Prozac)– and sertraline (Zoloft)– induced nocturnal bruxism. Romanelli and colleagues (1996) published a case of a woman with bruxism–onset following initiation of treatment with paroxetine (Paxil) who subsequently experienced relief of bruxism when buspirone was added. Bostwich and Jaffee (1999) reported on the successful use of buspirone as an antidote to sertraline–induced bruxism in four cases. Jaffee (2000) reported on the efficacy of buspirone as an antidote to venlafaxine (Effexor)–induced bruxism in two patients.
It is not uncommon for those with sleep disturbances to report: daytime sleepiness; impaired concentration; increased distractibility; irritability; word–retrieval difficulties; and/ or short tempers. These complaints can be mistaken for symptoms of, for example, attention–deficit/hyperactivity disorder (ADHD); oppositional defiant disorder; conduct disorder; a depressive disorder; or antisocial personality disorder – although one often finds comorbidity between these disorders and sleep disorders as illustrated below.
I wish to report here that I have witnessed often excellent results (in at least 339 out of 849 children, adolescent and adult patients in my private practice plus another 90 cases in my adult male prison population) using buspirone off–label for the treatment of snoring, obstructive sleep apnea, and/or nocturnal bruxism in children, adolescents, and adults (living both in and out of prison), with subsequent improved ability for my patients to awaken refreshed, well–rested, and clear–headed, and typically with better concentration and improved impulse control.
In a general adult psychiatric out–patient practice, I suspect that in at least some cases of patients diagnosed with major depression, they might, in fact, be experiencing manifestations of a primary sleep disorder. While not necessarily highlighted in all of the clinical vignettes below, in some children and adolescents with symptoms of what appears to be oppositional defiant disorder and/or attention–deficit/hyperactivity disorder symptoms, I suspect that their behavioral disturbances are the direct result of an unidentified primary sleep disorder. Likewise, in the adult prison (– i.e., not jail!) population, during my time as Oregon Department of Correction's principle psychiatrist (1990-1997), I identified about 90 inmates with previously unsuspected sleep disorders (– that is, not all inmates complaining of poor sleep and problems concentrating are malingering in order to obtain sedatives to sleep through their durance).
Below is a selection of clinical vignettes from both my solo, outpatient private practice and my prison psychiatric practice demonstrating the efficacy of buspirone in treating sleep–disordered patients [– the names and identifying inmate patient data have been altered to protect the guilty]. I then provide brief discussions of: snoring, sleep apnea, and bruxism; the pharmacology and adverse effects of buspirone; and finally my dosing schedule for using buspirone in the off–label treatment of snoring, sleep apnea, and/or bruxism.
Case A: This was an 11 year–old boy in my private psychiatric practice with attention-deficit/hyperactivity disorder (ADHD), multiple simple phobias, nocturnal bruxism, and frequent morning headaches. Adding Adderall (mixed amphetamine salts) Immediate Release tablets at a dose of 20 mg every morning was successful in optimally managing his ADHD symptoms (– the improvement was confirmed by patient, parents, teachers, and MedChek – that latter of which is a computerized objective measure of attention, concentration, impulse control, and reaction time). The subsequent addition of buspirone 10 mg at bedtime resulting in a prompt resolution of the boy’s night–time bruxism (– the success of which was confirmed by his parents), and resolution of the boy’s morning headaches. As anticipated, there was no change in the severity of the boy’s simple phobia (which eventually resolved with a course of hypnotherapy).
Case B: This was a 12 year–old, short–tempered boy in my private psychiatric practice with aggressive attention-deficit/hyperactivity disorder (i.e., frequent assaults on peers and siblings), and developmental reading and spelling disorders, who had chronic interrupted sleep, snoring, nocturnal bruxism, and severe irritability upon awakening. Adding methamphetamine time release tablets (i.e., Desoxyn Gradumets) at a carefully titrated dose of 60 mg every morning resulted in optimal control of his ADHD symptoms. I then added trazodone 100 mg at bedtime to improve the boy’s interrupted sleep, but the snoring, bruxism and recurring assaults continued. The subsequent addition of buspirone 10 mg at bedtime resulted in resolution of the boy’s snoring and nocturnal bruxism. The boy’s morning irritability along with the frequency and severity of his assaultive behaviors improved dramatically following the addition of buspirone.
Case C: This was a 13 year–old girl in my private psychiatric practice who was diagnosed with attention-deficit/hyperactivity disorder (ADHD), developmental arithmetic disorder, snoring, and nocturnal bruxism. Ms C’s daytime sleepiness was legendary – as documented in her pediatric medical record, during her office appointments, Ms C would routinely fall asleep in her pediatrician's exam room! With a buspirone dose of 30 mg at bedtime, the girl’s snoring and nocturnal bruxism resolved, and her daytime alertness greatly improved. Management of the girl’s comorbid ADHD symptoms improved with the subsequent addition of methamphetamine time–release (i.e., Desoxyn Gradumets) at a carefully–titrated dose of 30 mg every morning.
Case D: This was a 14 year–old girl in my private psychiatric practice with attention–deficit/hyperactivity disorder, tobacco dependence, and nocturnal bruxism. The girl’s attention-deficit/hyperactivity disorder (ADHD) symptoms, and her cigarette craving resolved with the addition of bupropion sustained–release tablets (Wellbutrin SR) 200 mg twice daily. Subsequent addition of buspirone 10 mg twice daily during the day, plus 20 mg at bedtime decreased the frequency of the girl’s comorbid nocturnal bruxism, with subsequent improvement in both her daytime alertness – and her manners.
Case E: This was a 24 year–old male inmate serving time for felony–murder whom I evaluated at Oregon State Penitentiary. Inmate E's childhood history was notable for: multiple learning disabilities, impairing social anxiety disorder, repeated physical and sexual abuse by his father as a child, chronic short temper, and polysubstance dependence (starting at 14 years of age with alcohol and cigarettes, then adding cannabis, hallucinogens and cocaine by 17 years of age). Trazodone 200 mg at bedtime was helpful in managing Inmate E's symptoms of post–traumatic stress disorder, but his morning headaches and complaints of a sore temporomandibular joint continued. Dental inspection (by me) revealed markedly ground–down teeth. The addition of buspirone 5 mg thrice daily resulted in the complete resolution of Inmate E's headaches, jaw soreness, and nocturnal bruxism. Inmate E became significantly more pleasant in the presence of both correctional staff and other inmates.
Case F: This was a 29 year–old male inmate with a sixth–grade education who was abandoned by his parents when he was 10 years old. His past criminal record included 12 Burglary convictions, and one Prison Escape. When last I saw him (– again, I left my position at principle psychiatrist for the Oregon Department of Corrections in 1997), Inmate F was serving prison time for Arson, and had most recently accrued two additional convictions of Inmate in Possession of a Weapon. Inmate F repeatedly demonstrated profound difficulty tolerating anxiety and uncertainty, and he often misinterpreted the benign intentions of correctional staff and other inmates. Inmate F had multiple somatic complaints of near–delusional intensity; he had a history of intentionally lacerated his arms (when frustrated) on over 100 documented occasions; and had a history of polysubstance dependence beginning by age 14 years old (including: alcohol and cannabis; and intravenous cocaine, amphetamines and heroin). With the initiation of venlafaxine immediate–release tablets at a dose of 75 mg thrice daily plus trazodone 400 mg at bedtime, Inmate F was able to successfully attend school (in an Oregon State Penitentiary classroom), and was a motivated and active participant in group therapy (led by OHSU Department of Psychiatry Professor Ed Scott, Ph.D.) Inmate F’s somatic complaints resolved, and episodes of frustration–related self–injurious behaviors resolved. However, Inmate F continued to complain of interrupted sleep and daytime cognitive “foggy–headedness.” Further inquiry with Inmate F’s cellmate revealed that Inmate F snored and bruxed loudly throughout the night. Visual inspection of Inmate F's teeth (by me) revealed ground–down molars. The addition of buspirone at 15 mg thrice daily resulted in resolution of Inmate F’s snoring and bruxism (– which was confirmed by his cellmate), resolution of his headaches, and improvement in his daytime wakefulness, frustration tolerance, and his manners.
Case G: This was a 35 year–old man in my private psychiatric practice with snoring, nocturnal bruxism, profoundly impairing dyslexia, and attention-deficit/hyperactivity disorder (ADHD). Bupropion (Wellbutrin) immediate release tablets at 150 mg thrice daily successfully managed his ADHD symptoms. Subsequent addition of buspirone 15 mg at bedtime resulted in complete resolution of this man’s snoring and bruxism (– the absence of both were confirmed by his wife).
Case H: This was a 36 year–old woman in my private psychiatric practice who had chronic headaches and temporomandibular pain. I was unable to elicit any history of bruxism, nor was there obvious dental evidence for a bruxism clinical hypothesis. Nevertheless, the addition of 10 mg of buspirone at bedtime resulted in prompt resolution of her daily morning jaw pain and morning headaches.
Case I: This was a 37 years old woman in my private psychiatric practice with post–traumatic stress disorder (PTSD), bulimia nervosa, attention-deficit/hyperactivity disorder (ADHD), major depression with a seasonal component (“winter depression”), tobacco dependence, nocturnal bruxism and snoring. Her mood, eating disorder, and PTSD symptoms improved following the addition of fluoxetine (Prozac) 20 mg in the morning. Her job efficiency and comorbid ADHD symptoms subsequently improved with the addition of 30 mg of methamphetamine time–release tablets (Desoxyn Gradumets) every morning. The subsequent addition of buspirone 30 mg at bedtime resulted in significant improvement in snoring and grinding (confirmed by her husband). Ms I also commented that the buspirone decreased her tobacco craving. The tobacco craving resolved completely with an increase of the buspirone dose to 10 mg thrice daily (in addition to buspirone 30 mg at bedtime).
Case J: This was a 38 year old woman in my private psychiatric practice with obsessive compulsive disorder (OCD), attention-deficit/hyperactivity disorder (ADHD), snoring, and “difficulty getting up and getting started” every morning. Fluoxetine (Prozac) 20 mg and mixed amphetamine salts (Adderall immediate release tablets) 30 mg every morning were used successfully to treat her OCD and ADHD symptoms respectively. Adding buspirone 15 mg at bedtime further improved OCD symptoms, as well as resolved the snoring and dysania.
Case K: this was a 38 year–old woman in my private psychiatric practice with attention-deficit/hyperactivity disorder (ADHD), winter depression, bulimia nervosa, tobacco dependence, generalized anxiety disorder, severe nocturnal bruxism, snoring and daily morning headaches. Fluoxetine (Prozac) successfully managed Ms K’s depression and eating disorder. Methamphetamine time–release (Desoxyn Gradumets) effectively managed her ADHD symptoms. Adding buspirone 10 mg twice daily plus an additional 30 mg at bedtime subsequently improved her perceived quality of sleep. The buspirone also dramatically decreased both her tobacco craving and general anxiety symptoms.
Case L: This was a 42 year–old man in my private psychiatric practice with a short, thick neck (22 inch neck collar size), obesity, hypertension, snoring, bruxism both day and night, chronic headaches, and daytime somnolence. Mr. L said that he frequently would awaken at night “spitting tooth chips out of my mouth.” Adding buspirone 5 mg thrice daily plus 20 mg at bedtime resulted in prompt resolution of his snoring, bruxism, and chronic headaches.
Case M: During my first meeting with the parents of a young boy (– i.e., the boy was the identified patient), I learned that the boy’s 45 year–old mother was taking atenolol for the management of her hypertension, and the boy’s 54 year–old father snored loudly throughout the night. The father’s snoring repeatedly interrupted the mother’s sleep. I suggested to the father that he talk with his primary care physician about a trial of buspirone at bedtime to see if this would control the father’s snoring. I subsequently learned that the father followed my suggestion, and his primary care physician did indeed prescribe buspirone at bedtime – with prompt resolution of this man’s snoring. The mother (his wife) subsequently slept soundly throughout the night. Several months later, she mentioned that she was able to stop her atenolol without a return of her hypertension. This report “fits” with what I have heard from surgeons: successful surgical treatment of sleep apnea typically results in the additional benefit of the resolution of hypertension.
Case N: This was a 45 year–old married man in my private psychiatric practice with attention-deficit/hyperactivity disorder (ADHD), tobacco dependence, flat ground–down teeth, loud night–time snoring, daytime drowsiness and irritability. Bupropion (Wellbutrin) immediate–release 75 mg tablets twice daily was effective in controlling ADHD symptoms, and the medication also eradicated his nicotine craving. The addition of buspirone 10 mg at bedtime resulted in improved, restful sleep and daytime clear–headedness. Mr. N’s wife was very pleased to report to me that with the addition of buspirone, her husband’s snoring had completely resolved.
Case O: This was a 46 year–old man in my private psychiatric practice with attention-deficit/hyperactivity disorder (ADHD), short temper, and snoring. Adding methylphenidate (30 mg immediate–release tablets plus 20 mg of the sustained–release tablet) and lithium 450 mg at bedtime effectively managed the ADHD and short temper. The subsequent addition of buspirone 30 mg at bedtime dramatically decreased the frequency and intensity of this man’s snoring. His chronic daytime irritability completely resolved with the addition of buspirone.
Case P: This was a 50 year–old, remarried man with attention-deficit/hyperactivity disorder (ADHD) who didn’t realize that he snored nightly until her heard his ex–wife say to me (in his presence) that his terribly loud snoring and daytime sleepiness “were seventy–five per cent of the reason we got divorced. He would fall asleep everywhere and anytime – except in his own bed!” Adding buspirone 20 mg at bedtime resulted in resolution of his snoring and improved daytime wakefulness. The subsequent addition of methamphetamine immediate release (Desoxyn tablets) successfully managed Mr. P’s comorbid ADHD symptoms. The post–divorce relationship between Mr. P and his ex–wife became more amicable, but as of the last time I saw them, they had not remarried.
Case Q: This was a 52 year–old man with attention-deficit/hyperactivity disorder (ADHD), snoring, and – according to his wife – apneic episodes. I could not elicit evidence of nocturnal bruxism. Adding bupropion immediate–release 150 mg tablets twice daily was helpful for ADHD symptom management. Subsequent addition of buspirone 10-20 mg at bedtime resulted in improved sleep, decreased snoring, and improved daytime wakefulness. A follow–up phone call with Mr. Q and his wife two years later revealed that Mr. Q’s primary care physician had assumed responsibility for prescribing and monitoring the buspirone. Mr. Q continued to take buspirone at bedtime, and continued to sleep soundly throughout the night without any observed apneic episodes.
Case R: This was a 56 year–old man with a 17–inch neck collar size, obesity, snoring, apneic episodes, flat ground–down lower central incisors, and attention-deficit/hyperactivity disorder (ADHD). Adding methamphetamine time–release (Desoxyn Gradumets) 15 mg in the morning managed his ADHD symptoms. Subsequent addition of buspirone improved his snoring and resolved his apneic episodes (which was confirmed by Mr. R’s wife).
Case S: This was a 60 year–old man who had been recently diagnosed with moderate obstructive sleep apnea, and mild periodic limb movements associated with sleep (PLMS). CPAP was prescribed, but not tolerated by Mr. S because of the noisiness of the CPAP apparatus. Adding buspirone 10-20 mg at bedtime resulted in prompt resolution of snoring (– which was confirmed by his wife), and improved daytime wakefulness.
Case T: This was a 64 year–old inmate who was convicted of Sodomy of several young boys. The inmate’s medical problems included: hypertension, angina, and non–insulin–dependent diabetes mellitus. The inmate’s snoring was so loud in what is called “mainline population” of Oregon’s maximum security prison where he was housed that neighboring inmates respectfully informed security staff: “Either you take care of the problem, or we will.” As a safety precaution, Inmate T was emergently administratively transferred to Oregon State Penitentiary’s Special Management Unit (– where I spent the majority of my “prison time” two days weekly from 1990 to 1997). My psychiatric exam of this inmate revealed a 17–inch neck collar size, and flat, ground–down teeth. A telephone conversation with Inmate T’s wife revealed a history consistent with sleep apneic episodes. Adding buspirone 10 mg thrice daily resulted in complete resolution of bruxism and snoring (confirmed by SMU graveyard shift correctional staff and Inmate T’s neighboring SMU inmates), resolution of morning headaches, and improved daytime wakefulness. Inmate T was then safely returned to the prison’s general population but as a safety precaution, SMU’s Lieutenant Don Mills requested that the Watch Commander house Inmate T in another cell block. The change of housing was graciously granted by the Watch Commander, and Inmate T was continued on buspirone while living in mainline population. During a follow–up appointment with Inmate T in mainline population a month later, I met with an alert and confident man who simply said to me – with a genuine smile: “I’m doing great!”
SO, WHAT EXACTLY IS BUSPIRONE? Buspirone is a novel, non–addictive, psychotropic medication which was first approved by the Food and Drug Administration in 1985 for use in the treatment of generalized anxiety disorder. Subsequently published case reports have suggested that buspirone is occasionally effectively (– although frequently in combination with other psychoactive medications) in the treatment of: refractory depression (e.g., combining buspirone with an SSRI such as fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, etc.), obsessive compulsive disorder, social anxiety disorder, post–traumatic stress disorder, migraine headaches, transvestic fetishism, autistic spectrum disorder, nicotine craving, alcohol craving, and aggressive behavior in those with what was once categorized as organic brain disorders. Buspirone is a partial agonist of 5-hydroxytryptamine 1A (5–HT1A) serotonin receptors in the brain. In addition to buspirone’s effects on serotonin receptors, buspirone’s major metabolite stimulates noradrenergic receptors and blocks presynaptic dopamine (D2) receptors.
Buspirone’s mode of action in the treatment of neuropsychiatric disorders, obstructive sleep apnea, and bruxism remains largely a mystery. Why exactly would buspirone be effective in snoring and sleep apnea? Buspirone’s benefit in the management of snoring and sleep apnea is thought (– that is, by me at least) to be via increasing soft palate muscle tone, thus “splinting” open the soft palate to prevent collapse of the airway during inspiration.
BRUXISM. Bruxism, characterized by clenching and/or teeth grinding, is a common condition affecting somewhere between 8% and 21% of the general population. Bruxism is a nonspecific term for numerous entities with multiple potential etiologies, most of which have a dopamine unbalance in common (this is known as “central bruxism”). The bruxism may also be the result of dental malocclusion (known as “peripheral bruxism”). The benefit of buspirone in at least some cases of bruxism is not simply due to its anti–anxiety effect, since other anxiolytics are typically ineffective for this problem, and since buspirone’s benefit in the management of bruxism is prompt while its benefit in the treatment of generalized anxiety disorder might not be evident for a month or longer after initiating buspirone therapy.
[For those of you who don’t routinely discuss neurotransmitter systems over breakfast: feel free to skip this paragraph – I don’t make any claims to originality for the content in this paragraph – which some might dismiss as “psychopharmacological psycho–babble.” Here we go.] Central bruxism can occur in various conditions of increased dopamine activity in the brain such as those conditions induced by such chemicals/medications as the amphetamines and by levo–dopa. These medications elevate dopamine concentrations in the brain’s striatum [the striatum is composed of the caudate and putamen which together are adjacent to one another in the center of the brain. The striatum is part of what is considered the brain’s basal ganglia. The striatum takes in messages from parts of the brain involved in the control of body movement, sensation, and the thinking and planning that involve those movements and feelings. The caudate and putamen function in unison like an automatic transmission, assuring the smooth transition from one behavior to another], and can occasionally induce exaggeration of normal dopaminergic functioning – which in the masseter muscles is manifested as teeth–grinding. Relative increased dopamine “tone” is also seen in the presence of cholinergic hypofunction. Lastly, the dopamine receptor hypersensitivity which is thought to be the result of long–term exposure to neuroleptics (e.g., anti–psychotic medications such as Thorazine and Haldol) can also cause masticatory muscle hyperactivity, characteristically manifested as the bruxism seen in the various facial dyskinesias. For those experiencing bruxism from various causes, dopamine agonists (e.g., the amphetamines and levo–dopa) and cholinergic antagonists aggravate jaw clenching, while dopamine–depleting agents improve symptoms. The clenching movements of dystonias, on the other hand, are thought to result for hypodopaminergic states encountered in extrapyramidal system dysfunction. Also of interest: serotonin is thought to exert a modulatory influence on dopamine tone – and dopamine is the primary neurotransmitter involved in motor activity. Movement disorders very likely result when strong serotonin reuptake inhibitors (SSRI)–type medications (e.g., Prozac, Zoloft, Paxil, Luvox, Celexa, Lexapro, and Effexor) enhance serotonin levels and reduce dopaminergic activity in either the mesocortical or nigrostriatal tracts in the brain. There is convincing clinical evidence that suggests a prominent role for serotonergic modulation of the dopaminergic neurons that directly control masticatory muscle motor activity. For example, Bostwick and Jaffee (1999) have suggested that SSRI–induced bruxism is a variant of akathisia, with the SSRIs altering dopamine levels in multiple central nervous system tracts, the most sensitive and the first affected being the mesocortical dopamine tract, with the absence of dopaminergic autoreceptors possibly explaining its heightened sensitivity to serotonin’s presynaptic anti–dopaminergic modulation. The resulting mesocortical disinhibition takes the form of akathisia in general, with SSRI–induced bruxism thought to be a specific form of akathisia. Got it now?}
Why does non–SSRI–associated bruxism improve with the addition of buspirone as illustrated in some of the case vignettes above? I don’t know, and I suspect that no–one else knows either.
BUSPIRONE SAFETY. There are no absolute contraindications to buspirone except a history of buspirone–hypersensitivity. Buspirone is a benign, generally well–tolerated medication, and carries a low risk of adverse effects. Commercially available buspirone tablets contain lactose, so in those who are lactose–intolerant, I recommend that your prescribing physician consult with his or her favorite compounding pharmacist to decide on a buspirone option without lactose. Unlike benzodiazepines, buspirone does not impair psychomotor performance (– e.g., using buspirone doesn’t interfere with safely using a chain saw or driving a motor vehicle) or memory; it does not cause sedation, muscle relaxation, reinforcing effects, or withdrawal symptoms; it does not add to the depressant effects of alcohol or other drugs on the central nervous system; it is not an anticonvulsant, it is ineffective in blocking benzodiazepine withdrawal, buspirone lacks anti–panic activity; and, finally, it is not an FDA–scheduled medication (i.e., buspirone does not have any risk of chemical dependence). It is not contraindicated in patients with seizure and/or eating disorders. Unlike many other first–line medications for the management of anxiety (e.g., the SSRIs), buspirone has an FDA Category B classification, meaning animal studies have shown no adverse events during pregnancy. No adverse events have been reported from abrupt discontinuation of buspirone. There is no lethal dose of buspirone. Thus, the most likely manner in which one might die from buspirone would be the result of a large, buspirone tablet–containing crate falling on one’s head!
BUSPIRONE DOSING. Buspirone is currently available in 5 mg, 7.5 mg, 10 mg, 15 mg and 30 mg tablets. While buspirone has a relatively short half–life (2 to 3 hours), and while too many physicians thus prescribe buspirone 2 to 3 times a day, this prescribing practice just makes me shake my head. The reality is that the benefits of buspirone endure for many hours after the majority of buspirone has been metabolized (– just as the effects if the bombing of New York’s World Trade Center have continued long after the two planes and two buildings were destroyed). Most of my patients report a benefit from buspirone from night–time only dosing.
The optimal dose and dosing frequency of buspirone for the treatment of bruxism, snoring or obstructive sleep apnea is unknown, but I often have found that doses as low as 2.5 mg at bedtime have resulted in resolution of bruxism and/or snoring within 1-2 days of treatment initiation. I will often use buspirone as a “probe” to improve the sensitivity of identifying obstructive sleep apnea – or some milder disordered breathing variant. If there is a prompt and robust improvement in daytime alertness after starting buspirone at bedtime, then I will recommend that my patient consult with a sleep disorders physician or otolaryngologist to discuss more definitive assessments of suspected obstructive sleep apnea. Buspirone dose adjustments are not necessary for age and sex, which allows for highly consistent dosing. Lastly, do be aware that, based on my 30 years of clinical experience with using buspirone off–label for the treatment of bruxism, snoring, sleep apnea, and oppositional–defiant disorder, I have concluded buspirone is rendered ineffective in the presence of regular (i.e., weekly or more frequently) alcohol use. Thus, for those with snoring, apnea and/or bruxism who are unwilling to make a commitment to abstinence from all alcohol: your are wasting your time in pursuing a trial of buspirone for the treatment of anything. BUSPIRONE WON’T WORK IF YOU DRINK ANY ALCOHOL! With this caveat, below is my current dosing “recipe.”
- ☞Start with one–half of a 5–mg tablet (2.5 mg) of buspirone at bedtime nightly for at least three nights. If snoring, apnea or bruxism continues unchanged, then:
- ☞Increase buspirone to a whole tablet (5 mg) at bedtime nightly for at least three nights. If snoring, apnea or bruxism continues, then:
- ☞Increase buspirone to 10 mg at bedtime. If snoring, apnea or bruxism continues, then:
- ☞Increase buspirone to 15 mg at bedtime. If snoring, apnea or bruxism continues, then:
- ☞Increase buspirone to 20 mg at bedtime. If snoring, apnea or bruxism continues, then:
- ☞Increase buspirone to 30 mg at bedtime. If snoring, apnea or bruxism continues, then:
- ☞If there is not a prompt improvement in bruxism, snoring or sleep apnea after an additional week at 30 mg nightly, try 45 mg at bedtime.
- ☞If there is not a prompt improvement in bruxism, snoring or sleep apnea after an additional week at 45 mg nightly, I usually conclude that the buspirone trial is “a bust.” Might doses higher than 45 mg at bedtime be effective? Well….yes, I suppose it is possible: there are published case reports of efficacy of buspirone for the treatment of major depression in doses of 100 mg daily. And, buspirone is a benign medication. So, once in a while I will recommend that the patient increase the buspirone dose to 60 mg at bedtime – with occasional good results (i.e., resolution of snoring and/or bruxism).
BUSPIRONE ADVERSE EFFECTS. Since commercially available buspirone contains lactose, then one can expect to see or hear the usual symptoms a lactose–intolerant patient experiences when taking buspirone. Listed adverse effects of buspirone (which, if they occur, are generally mild and transitory) are, basically, two:
- dizziness and light–headedness which occurs about 30 minutes after ingestion and this side effect lasts about 20 minutes. This dizziness/light–headedness occurs in 5–10% of my patients who start buspirone. Rather than the common experience of fleeting “dizziness/light–headedness” one experiences when standing up quickly, I believe a more accurate description of this buspirone side effect is analogous to the subtly vibrating, neon, purple–electric sensation one typically experiences when, asleep in bed, one is slowly levitated up off his or her bed, floated through an adjacent open window, and then transported up into the portal of an extra–terrestrial space craft. This sensation is not dangerous, but it can be very weird. For those patients who take buspirone at bedtime and who then report this odd light–headedness, they typically then just fall asleep. For those who take buspirone during the day, this fleetingly odd side effect has been shown not to impair the safe operation of motor vehicles, chain saws, or the use of heavy machinery. But, again, when it happens, this side effect is a uniquely odd, transient sensation.
- The second most common adverse effect from buspirone taken at bedtime is middle–of–the–night awakening. If this does occur at all, the awakening typically happens around 2–3AM. If interrupted sleep does occur after starting buspirone, then this activating side effect of buspirone can usually be circumvented by either lowering the buspirone dose taken at bedtime, or switching the dosing time of the buspirone to the morning.
Other reported possible adverse effects of buspirone include: nausea, headache, nervousness, and excitement. (– however, in my clinical population, the incidence of these side effects in my patients have been rare to non–existent).■
Successfully publicly defending his Senior Essay (– a commentary on Darwin’s Origin of Species), Dr. Mortimer received his undergraduate degree (Bachelor of Arts) in Liberal Arts from St. John’s College in Annapolis, Maryland. Subsequently earning his medical degree from Oregon Health Sciences University in 1985, Dr. Mortimer continued at OHSU to complete general adult psychiatry training, and then a two–year child & adolescent psychiatry fellowship training program. Dr. Mortimer is, thus, not only a fully trained general adult psychiatrist, but Dr. Mortimer is also a fully–trained child & adolescent psychiatrist. The value of having such broad, developmental psychiatric training first became readily apparent when Dr. Mortimer served as the principle psychiatrist for the Oregon Department of Corrections from 1990 to 1997. During this time, Dr. Mortimer evaluated 1,304 adult male and female inmates (ages 16 to 80 years old). Using his extensive medical and psychiatric training to make clinical sense of these inmates’ developmental trajectories “from play pen to state pen,” Dr. Mortimer was then able to provide – sadly, often for the first time in their lives – safe and effective psychiatric treatment for many psychiatric and some medical conditions the symptoms of which had been present (but too–often ignored or dismissed by teachers, pediatricians, parents and others) since their early years in elementary or middle school.
Among Dr. Mortimer’s professional medical accomplishments, Dr. Mortimer is a diplomate of (– that is, he has a diploma in general adult psychiatry from) the American Board of Psychiatry and Neurology (i.e., Dr. Mortimer is “Board Certified in Psychiatry”). Dr. Mortimer has also been on the clinical teaching faculty for Oregon Health Science University’s Department of Psychiatry, and for the Family Practice Training Program at Eastmoreland Osteopathic Hospital in Milwaukie, Oregon. Dr. Mortimer has served as both a principle investigator and as a clinical investigator for phase III clinical drug trials, several of which investigated stimulants in the treatment of ADHD; in other clinical drug trials, other medications were investigated for their efficacy in such psychiatric disorders as social anxiety disorder, and in post–traumatic stress disorder. Over the past 31+ years, Dr. Mortimer has enjoyed seeing some of his many clinical writings published in peer–reviewed international medical journals.
Saying a fond farewell to the State of Oregon, Dr. Mortimer is currently licensed to practice medicine only in the State of Washington, maintaining a full–time, solo private practice in child, adolescent, and general adult psychiatry in the non–incorporated Hazel Dell neighborhood of Vancouver, Washington. Also of perhaps some interest: Dr. Mortimer currently enjoys the distinction of having the longest–surviving, private practice in child & adolescent psychiatry in the county.
- American Psychiatric Association. Practice guideline for the treatment of patients with major depressive disorder. 3rd edition. https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/mdd.pdf. Published May 2010. Accessed November 2019.
- Appelberg BG, Syvälahti EK, Koskinen TE, et al. Patients with severe depression may benefit from buspirone augmentation of selective serotonin reuptake inhibitors: results from a placebo-controlled, randomized, double-blind, placebo wash-in study. J Clin Psychiatry. 2001; 62(6):448-452.
- Bostwick JM and Jaffee MS, “Buspirone as an antidote to SSRI–induced bruxism in four cases.” Journal of Clinical Psychiatry. 1999;60:857-860
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