Management of insomnia in sleep disordered breathing

Abstract

Both obstructive sleep apnoea (OSA) and chronic insomnia disorder are highly prevalent in the general population. Whilst both disorders may occur together by mere coincidence, it appears that they share clinical features and that they may aggravate each other as a result of reciprocally adverse pathogenetic mechanisms. Comorbidity between chronic insomnia disorder and OSA is a clinically relevant condition that may confront practitioners with serious diagnostic and therapeutic challenges. Current data, while still scarce, advocate an integrated and multidisciplinary approach that seems superior over the isolated treatment of each sleep disorder alone.

FIGURE 1

Temporary insomnia-induced increases of apnoea–hypopnea index (AHI) under continuous positive airway pressure (CPAP) therapy. In a 75-year-old male patient diagnosed with obstructive sleep apnoea (AHI 65 events·h⁻¹), CPAP administered at a level of 8 cmH₂O was effective at controlling the AHI. He experienced two episodes of insomnia as a result of temporary marital disharmony. During these incidents AHI increased dramatically, although CPAP settings and use of drugs or alcohol remained unchanged. When normal sleep resumed the AHI fell back to baseline levels.

FIGURE 2

Potential pathophysiological feedback mechanism of COMISA. This scheme represents the potential positive feedback loop between sleep disordered breathing (obstructive sleep apnoea) and sleep disruption (insomnia), explaining why the resultant clinical picture may be worse than what can be expected from the contribution of either component alone. Moreover, as a result of this vicious circle, interventions geared to treat either insomnia or obstructive sleep apnoea may have adverse effects to the comorbid component (e.g. sleep restriction therapy may aggravate somnolence in obstructive sleep apnoea and continuous positive airway pressure therapy may worsen insomnia).