![]() The first is static narrowing of the airways due to swelling of structures that block the airway. There are two basic mechanisms for obstructive sleep apnea. Significantly, a broad anterior midline area of cortex and subcortex (the “anterior paramedian REM sleep activation area” selectively activates during REM sleep following relative deactivation during non-REM (NREM) sleep, and this region encompasses both the fear expression and extinction memory networks. Similarly, regulation of mood and working through of emotional responses to intra- and interpersonal stressors have been linked with REM sleep and associated dreaming. The “anterior paralimbic REM activation area” overlaps with fear and extinction circuits. Fluoro-deoxyglucose PET image of areas that reactivate during REM sleep following relative quiescence during NREM sleep…Walker and colleagues suggest that REM sleep serves the dual purpose of consolidating the content of emotional memory and diminishing the memory’s emotional charge. “Fluoro-deoxyglucose PET imaging shows that fear-conditioning and extinction are located in the amygdala and dorsal anterior cingulate cortex (dACC) and other areas associated with memory for the extinction (inhibition) of this fear (an “extinction memory network”) that includes the hippocampus and ventromedial prefrontal cortex (vmPFC). reported in Sleep and REM sleep disturbance in the pathophysiology of PTSD: the role of extinction memory: This results in collapse of the airway leading to sleep apnea. In REM sleep, there are both tonic excitatory inputs and phasic inhibitory inputs in the brain respiratory centers that account for irregularities in breathing pattern, as well as the loss of excitation, which contributes to hypotonia of the muscles of the upper airway. ![]() An excitatory drive to breathe is common in REM, with increased diaphragmatic EMG activity and increased activity in many medullary respiratory neurons above those levels observed in NREM sleep or quiet wakefulness. Electrical activity from medullary inspiratory neurons, and EMG activity of diaphragm and abductor muscles of the upper airway in healthy humans show reductions in amplitude upon the transition from awake to NREM sleep, usually accompanied by a mild to moderate hypoventilation and two- to fivefold increases in upper airway resistance.Ī fast and highly variable breathing frequency is a hallmark of rapid eye movement (REM) sleep in mammals. In fact, the great majority of people with sleep apnea possess ventilatory control systems that are capable of precise regulation of their alveolar ventilation and arterial blood gases with extremely small variations from the norm. Remarkably, sleep apnea patients experience little or no problems with their breathing or airway patency while awake. OSA patients were shown to maintain their upper airway patency in wakefulness via a compensatory, augmented EMG activity of their airway dilator muscles, during wakefulness. For rating purposes, the rating table does not distinguish between obstructive, central and mixed sleep apnea. Obstructive sleep apnea has become the term of art for all sleep apnea. I have yet to encounter a single case, however, that was not diagnosed as obstructive sleep apnea. Thus, all sleep apnea cases are in fact mixed sleep apnea. The brain does not send proper signals to the muscles that control breathing during sleep. Thus, it is clear that in obstructive sleep apnea cases, the brain is also involved. Interestingly, in all these cases there is no mechanical blockage to the airway during wakefulness obstruction occurs only during sleep. large adenoids, deviated septum).Ĭentral sleep apnea (ICD –9-CM 327.27) occurs when the brain does not send proper signals to the muscles that control breathing which results in the person awakening with shortness of breath.Ĭomplex or mixed sleep apnea is a combination of both obstructive and central sleep apnea.Īs mentioned earlier, pure obstructive sleep apnea involves abnormalities of the upper airway such as enlarged tonsils, large tongue or blocked nasal passages. True obstructive sleep apnea occurs when tissues block the upper airway (e.g. The brain then senses the inability to breathe and briefly arouses the person to begin breathing again. Obstructive sleep apnea (OSA) (ICD-9-CM 327.23) is the most common form of sleep apnea and is caused by an airway blockage that occurs when the soft tissue in the back of the throat narrows or closes during sleep.
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