Sleep Bruxism—What To Consider

Each month I see a consistent number of patients with Sleep Bruxism who self-report, have a provider diagnosis, or both.

What’s fascinating is that they report a variable list and severity of morning symptoms due to the same thing: grinding or clenching their teeth during the sleeping hours. What’s even more fascinating is there are countless people out there who also grind and clench, but have virtually no symptoms and never seek care.

For those seeking care, symptoms include jaw muscle soreness or pain, limited or stiff jaw motion, temporal headaches, sensitive teeth, earaches, a bite that feels off-balance, TM joint noises of all types, jaw locking requiring self manipulation to disengage, neck pain, brain fog, jaw muscle fatigue, and a few others I am probably forgetting.

Some patients exhibit only one specific symptom and others report a collection of concerns. For many, the symptoms have been present for an extended period without escalation. For others, symptoms are progressing and cause great concern. However, they all ask the same two questions:

“Why am I doing this?” and “How can I stop?”

The answers to both are elusive.

For many years the typical thinking has been this: the fuel that prompts Sleep Bruxism is centered on life’s stresses. Some studies, in fact, have revealed elevated A.M. catecholamines in the bloodstream of patients who have the signs and symptoms of Sleep Bruxism and describe themselves as “stressed”.

Other studies, however, identify patients who live with persistent ongoing stress and have morning catecholamine elevation, but no Sleep Bruxism. In addition, large groups of patients who have been diagnosed with primary anxiety disorders seem to not have a higher prevalence of Sleep Bruxism than does the general population.

Clearly, a consensus has not been reached. It may boil down to whether, when stressed, a person’s coping skills are sufficient to keep physiologic manifestations from occurring. I suspect this debate will continue.

The ADHD Medication – Sleep Bruxism Connection

From a different perspective, the last few years have brought a host of patients to the office as a result of Sleep Bruxism, which was induced by the use of certain medications or substances. A common theme appears to be the use of medications, which are typically prescribed for attention deficit disorder and hyperactivity. These medications activate the sympathetic nervous system and turn on the body’s fight or flight system. Strattera, Vyvanse, and Adderall lead the list. When used by high school and college students, Sleep Bruxism symptoms often become a concern.

Mature adults are not spared, either. Recently two longstanding patients with controlled Sleep Bruxism experienced increased acute morning pain symptoms when they started a trial of medication to address daily focus issues. Interestingly enough, equal numbers of men and women are seen when this risk factor has been identified, which is a departure from the usual 70/30 split, favoring women.

The Nicotine – Sleep Bruxism Connection

Patients using nicotine vapes during the day are driving a new trend, too. Flavored vape pens have become ubiquitous on NYC streets and based upon the quantity of nicotine being absorbed, I’m not surprised that this stimulant may be encroaching upon sleep physiology and the emergence or intensity of Sleep Bruxism. It is something to be watched.

The SSRI – Sleep Bruxism Connection

Not to be forgotten are SSRIs and their established ability to initiate Sleep Bruxism activity in some patients, Effexor and Paxil being the most commonly identified. The prevalence of SSRI-induced bruxism is cited as 12-14%, and a neurochemical mechanism involving serotonin and dopamine has been researched. This possibility must also be considered when screening patients.

The Airway Insufficiency – Sleep Bruxism Connection

Lastly, much has been written about airway insufficiency and its potential to initiate Sleep Bruxism. Some researchers have postulated that bruxism activity represents a CNS-driven reflex to move the jaw forward to facilitate airflow. This theory remains unproven.

However, it’s clear that a percentage of patients with obstructive sleep apnea and/or upper airway resistance also exhibit Sleep Bruxism. The best thinking at the moment is that airflow restriction leads to oxygen deprivation, brain arousal (so breathing resumes), activation of the sympathetic nervous system, and the occurrence of Sleep Bruxism. Although this sequence is plausible, many patients with moderate and/or severe sleep apnea do not exhibit Sleep Bruxism. Unquestionably, however, if airway problems are suspected the patient who exhibits Sleep Bruxism must be questioned, screened, examined, and sometimes tested with overnight studies.

So there you have it. There are many avenues to explore when evaluating Sleep Bruxism. Next month I will revisit treatment strategies.

I welcome your questions and comments.