Sleep Apnea is a prevalent and potentially life-threatening disorder in which a person experiences intermittent cyclical cessations, or reductions, of airflow during sleep. As of 2016, 42 million Americans suffer from sleep-disordered breathing (ResMed, 2016). There are three main forms of the disorder. Obstructive sleep apnea, the most common form, occurs when throat muscles relax, causing throat tissue to collapse and consequently obstructing the flow of air to the lungs. Central sleep apnea is caused by abnormal signaling from the brain to the muscles that control breathing. Complex sleep apnea, also known as treatment-emergent central sleep apnea, is characterized by the presence of both Obstructive and Central Sleep Apnea (Mayo Clinic Staff, 2015). The prevalence of Sleep Apnea varies based on a multitude of risk factors such as excess weight, gender, hypertension, genetics, and chronic nasal congestion. Both Obstructive and Central sleep apnea can cause complications to arise such as daytime fatigue and sleepiness, however, Obstructive apnea can cause cardiovascular problems like arrhythmia, eye problems such as glaucoma, and sleep-deprived partners (Mayo Clinic Staff, 2016).
There are several treatment methods for ameliorating the symptoms of Sleep Apnea such as Continuous positive airway pressure (CPAP), in which the patient wears a mask to receive a continuous flow of compressed air, and oral appliances such as Jaw Advancing Devices (JAD) to bring the lower jaw forward to open the airway (Afzal, 2015). In some cases, Sleep Apnea can be cured by weight loss and surgery, however these are situational. Despite the various ways in which the symptoms of Sleep Apnea can be treated, they are not universally effective therefore more research is exhorted.
Observations of periodic breathing during sleep were first reported in the mid 1850s, and in the 1870s British Physicians described obstructive apneas as “fruitless contractions of the inspiratory and expiratory muscles against glottic obstruction with accompanying cyanosis during sleep” (Lavie, 2003). There were some reports in the 1950s of obese patients who experienced daytime sleepiness, but were labeled under “Pickwickian Syndrome”--a condition of hypoventilation caused by excessive weight (Bickelmann et al., 1956). It was not until the mid 1950s that a link between obesity and disordered breathing was fully acknowledged as the Pickwickian Syndrome was rediscovered. Surprisingly, no link to sleep disorders were considered. Indeed, physiologists studying the control of breathing never considered the extrathoracic upper airway as an integral factor in this control system, and at that time, we knew little about its neuromuscular regulation. Furthermore, descriptions of the connection between sleep and ventilation were not reported until the comprehensive studies of Bulow in the 1960s (Bulow, 1963). Eventually, by the mid 1960s, Gastaut et al. recognized obstructive sleep apnea in obese patients as cyclical airway obstruction with frequent arousals, thereby providing the first comprehensive links between excessive weight, sleep-induced airway obstruction, sleep fragmentation, and daytime sleepiness (Dempsey et al., 2010). One early form of treatment for obstructive sleep apnea, following this key discovery, was chronic tracheostomy in the early 1970s (Lugaresi et al., 1971). Since then, research has progressed with case reports about patients with sleep-disordered breathing.
The most noticeable sign of Sleep Apnea is chronic snoring, which can be observed by a partner or family member. There are many shared symptoms between Obstructive and Central Sleep Apnea patients such as excessive daytime sleepiness (hypersomnia), difficulty concentrating during the day, and mood changes like depression and irritability. Because of these similarities, advanced tests such as esophageal pressure (Pes) and diaphragm electromyogram (EMGdi) are required to distinguish the two forms. Pes monitoring can be performed during polysomnography with a thin, water filled catheter connected to a transducer to determine what fraction of airway pressure is applied to overcome lung and chest wall elastance (Akoumianaki et al., 2014). EMGdi recorded from an electrode which can be used to assess neural respiratory drive, a physiological biomarker indicating exacerbated breathlessness, and diaphragm function (Luo et al., 2008). Despite the close similarities, the two forms of the disorder are fundamentally different. Uniquely, patients with Obstructive Sleep Apnea experience awakening to a sore/dry throat, high blood pressure, nighttime sweating, and decreased libido (Mayo Clinic Staff, 2016). Those with Central Sleep Apnea experience insomnia, chest pain, and shortness of breath during the night (Mayo Clinic Staff 2016).
The clearest distinction between both forms of Sleep Apnea is their causes. Obstructive Sleep Apnea occurs when muscles in the throat over relax, disrupting normal breathing. These muscles bolster structures like the soft palate, the uvula, the tonsils, and the tongue. When the airway becomes obstructed by the relaxed muscles, breathing is stopped for a short amount of time (usually 10-20 seconds) which may lower the amount of oxygen in the blood and increase the amount of carbon dioxide. The brain senses the impaired breathing and briefly awakens the person to open the airways (the awakening is too short to be remembered). The continuous disruption of breathing during the night impair the person’s ability to reach the desired sleep, completion of sleep stages, and will leave the person sleepy during the day. Typically, those who suffer from Obstructive Sleep Apnea fail to notice their interrupted sleep, which leads them to believe they slept well (Mayo Clinic Staff, 2016).
As briefly mentioned above, Central Sleep Apnea is a result of the brain’s failure to communicate with the motor neurons that control breathing by interacting with muscle tissue in the throat. This failure is caused by various factors that affect the brainstem--which links the CNS and controls involuntary actions such as heart rate and breathing--to control breathing. Central Sleep Apnea has a multitude of forms caused by specific factors. One notable example of a variation of Central Sleep Apnea is Cheyne-Strokes, this form is associated with congestive heart failure or stroke. This condition is characterized by an insidious progression and regression in breathing and airflow. During the weakest breathing effort, a complete lack of airflow (Central Sleep Apnea) can occur (Mayo Clinic Staff, 2016).
There are various methods of treating and curing sleep-disordered breathing, however these solutions are, for the most part, unique to the individual. A constellation of factors contribute to the onset and the progression of Sleep Apnea, which is why there is not a universal remedy.
My name is Brendan Mitchell, I recently graduated from the University of California, Riverside with a B.S. in Neuroscience. Since my first year at UCR, I worked in Dr. Xiaoping Hu's Bioengineering Lab. Since then, I’ve been privileged to receive research grants, publish my research as a primary author in a peer-reviewed journal, and present my work at UCR-hosted research symposiums. I recently submitted my Honors Capstone Thesis titled "Multimodal MRI Study using Convolutional Neural Networks for Schizophrenia Classification" for publication. And starting this fall, I will be working at the NIH via the IRTA Postbac Fellowship.