Sleep Apnea Secondary to Service-Connected Tinnitus

Approximately 60% of patients with tinnitus experience disturbances of the normal sleep pattern.

German scientists performed polysomnography on 26 patients with tinnitus and sleep disturbances.  In 17 of 26 patients, polysomnography revealed a pathological sleep analysis.  10 patients were diagnosed with obstructive sleep apnea syndrome, and 4 were diagnosed with insomnia and an increased index of arousals as well as a reduction of deep sleep and REM-phases.  Pathological movements of the legs were seen in 3 cases.  Six of 9 patients with normal sleep during the whole night displayed a prolonged latency period until falling asleep.

Sleep disturbance is a common and frequent complaint reported by tinnitus sufferers.  Recent studies have shown that when insomnia and depression are associated with tinnitus there is decreased tolerance and increased discomfort with the tinnitus.

The apparent cause of sleep apnea in patients suffering from tinnitus is the disruption of sleep patterns, specifically disruption of rapid eye movement (REM).

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 [and non-rapid eye movement (NREM) sleep]. Remarkably, sleep apnea patients experience little or no problems with their breathing or airway patency while awake.  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.

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.

A fast and highly variable breathing frequency is a hallmark of rapid eye movement (REM) sleep in mammals. 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. 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. This results in collapse of the airway leading to sleep apnea.

In a recent study, scientists observed:

“All tinnitus patients had a statistically significant alteration in sleep stages. Average percentage of stage 1 + stage 2 was 85.4% ± 6.3, whereas, in the control group, the average percentage of stage 1 + stage 2 was 54.9 ± 11.2 (p < 0.001). Stages 3 and 4 and rapid eye movement (REM) sleep was lacking in all tinnitus patients with an average percentage of 6.4 ± 4.9 of REM sleep, and 6.4 ± 4.9 of stages 3 + 4. The control group showed an average percentage of 21.5 ± 3.6 of REM sleep and 21.5 ± 3.6 of stages 3 + 4 (p < 0.001).”

Quantitative non-rapid eye movement sleep analysis revealed lower spectral power in the delta frequency band in the tinnitus group compared to controls, and this decrease was correlated with subjective sleep complaints (the lower the delta spectral power, the greater the complaints).


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