A randomised controlled trial of nasal decongestant to treat obstructive sleep apnoea in people with cervical spinal cord injury.

STUDY DESIGN: Prospective, double-blind, randomised, placebo-controlled, cross-over trial of nasal decongestion in tetraplegia. OBJECTIVES: Tetraplegia is complicated by severe, predominantly obstructive, sleep apnoea. First-line therapy for obstructive sleep apnoea is nasal continuous positive airway pressure, but this is poorly tolerated. High nasal resistance associated with unopposed parasympathetic activation of the upper airway contributes to poor adherence. This preliminary study tested whether reducing nasal decongestion improved sleep. SETTING: Participants' homes in Melbourne and Sydney, Australia. METHODS: Two sleep studies were performed in participants' homes separated by 1 week. Participants were given a nasal spray (0.5 mL of 5% phenylephrine or placebo) in random order and posterior nasal resistance measured immediately. Outcomes included sleep apnoea severity, perceived nasal congestion, sleep quality and oxygenation during sleep. RESULTS: Twelve middle-aged (average (SD) 52 (12) years) overweight (body mass index 25.3 (6.7) kg/m2) men (C4-6, AIS A and B) participated. Nasal resistance was reduced following administration of phenylephrine (p = 0.02; mean between treatment group difference -5.20: 95% confidence interval -9.09, -1.32 cmH2O/L/s). No differences were observed in the apnoea hypopnoea index (p = 0.15; -6.37: -33.3, 20.6 events/h), total sleep time (p = 0.49; -1.33: -51.8, 49.1 min), REM sleep% (p = 0.50; 2.37: -5.6, 10.3), arousal index (p = 0.76; 1.15: -17.45, 19.75), 4% oxygen desaturation index (p = 0.88; 0.63: -23.5, 24.7 events/h), or the percentage of mouth breathing events (p = 0.4; -8.07: -29.2, 13.0) between treatments. The apnoea hypopnoea index did differ between groups, however, all except one participant had proportionally more hypopnoeas than apnoeas during sleep after decongestion. CONCLUSIONS: These preliminary data found that phenylephrine acutely reduced nasal resistance but did not significantly change sleep-disordered breathing severity.

Genioglossus reflex responses to negative upper airway pressure are altered in people with tetraplegia and obstructive sleep apnoea.

KEY POINTS: Protective reflexes in the throat area (upper airway) are crucial for breathing. Impairment of these reflexes can cause breathing problems during sleep such as obstructive sleep apnoea (OSA). OSA is very common in people with spinal cord injury for unknown reasons. This study shows major changes in protective reflexes that serve to keep the upper airway open in response to suction pressures in people with tetraplegia and OSA. These results help us understand why OSA is so common in people with tetraplegia and provide new insight into how protective upper airway reflexes work more broadly. ABSTRACT: More than 60% of people with tetraplegia have obstructive sleep apnoea (OSA). However, the specific causes are unknown. Genioglossus, the largest upper-airway dilator muscle, is important in maintaining upper-airway patency. Impaired genioglossus muscle function following spinal cord injury may contribute to OSA. This study aimed to determine if genioglossus reflex responses to negative upper-airway pressure are altered in people with OSA and tetraplegia compared to non-neurologically impaired able-bodied individuals with OSA. Genioglossus reflex responses measured via intramuscular electrodes to ∼60 brief (250 ms) pulses of negative upper-airway pressure (∼-15 cmH2 O at the mask) were compared between 13 participants (2 females) with tetraplegia plus OSA and 9 able-bodied controls (2 females) matched for age and OSA severity. The initial short-latency excitatory reflex response was absent in 6/13 people with tetraplegia and 1/9 controls. Genioglossus reflex inhibition in the absence of excitation was observed in three people with tetraplegia and none of the controls. When the excitatory response was present, it was significantly delayed in the tetraplegia group compared to able-bodied controls: excitation onset latency (mean ± SD) was 32 ± 16 vs. 18 ± 9 ms, P = 0.045; peak excitation latency was 48 ± 17 vs. 33 ± 8 ms, P = 0.038. However, when present, amplitude of the excitation response was not different between groups, 195 ± 26 vs. 219 ± 98% at baseline, P = 0.55. There are major differences in genioglossus reflex morphology and timing in response to rapid changes in airway pressure in people with tetraplegia and OSA. Altered genioglossus function may contribute to the increased risk of OSA in people with tetraplegia. The precise mechanisms mediating these differences are unknown.

High nasal resistance is stable over time but poorly perceived in people with tetraplegia and obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) is highly prevalent in people with tetraplegia. Nasal congestion, a risk factor for OSA, is common in people with tetraplegia. The purpose of this study was to quantify objective and perceived nasal resistance and its stability over four separate days in people with tetraplegia and OSA (n=8) compared to able-bodied controls (n=6). Awake nasal resistance was quantified using gold standard choanal pressure recordings (days 1 and 4) and anterior rhinomanometry (all visits). Nasal resistance (choanal pressure) was higher in people with tetraplegia versus controls (5.3[6.5] vs. 2.1[2.4] cmH2O/L/s, p=0.02) yet perceived nasal congestion (modified Borg score) was similar (0.5[1.8] vs. 0.5[2.0], p=0.8). Nasal resistance was stable over time in both groups (CV=0.23±0.09 vs. 0.16±0.08, p=0.2). These findings are consistent with autonomic dysfunction in tetraplegia and adaptation of perception to high nasal resistance. Nasal resistance may be an important therapeutic target for OSA in this population but self-assessment cannot reliably identify those most at risk.