Sleep Bruxism—What To Consider

Each month we see a consistent number of patients who have sleep bruxism. Some self-report, while others arrive with a diagnosis from another provider. Typically, they report one or more of the following symptoms:

• Jaw locking that requires self-manipulation to disengage
• Jaw muscle soreness or pain
• Limited or stiff jaw motion
• Temporal headaches
• Sensitive teeth
• A bite that feels off-balance
• TM joint noises of all types
• Earaches
• Neck pain
• Brain fog
• Jaw muscle fatigue

(And a few others I’m probably forgetting…)

Often their symptoms have been present for an extended period of time without escalating. But for others, their symptoms are progressing, which causes them great concern.

Regardless of the number of symptoms or length of time they’ve been suffering, all of these patients ask us these two questions:

1. Why am I doing this?

2. How can I stop?

The answers can be elusive. For years, the thinking was sleep bruxism is fueled by life’s stresses. But when I look at the research and add in my personal experiences in the office, it gets complicated:

Some studies have revealed that patients who have the signs and symptoms of sleep bruxism and describe themselves as “stressed” have elevated A.M. catecholamines in their bloodstream. But, other studies identify patients who, despite living with persistent, ongoing stress and elevated A.M. catecholamine levels, do not brux.

Then, there is the large group of patients with primary anxiety disorder who exhibit no more of a prevalence of sleep bruxism than in the general population.

Clearly, a consensus has not been reached. Perhaps it boils down to whether an individual’s coping skills are sufficient enough 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.

I welcome your questions and comments.