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

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Highlights

  • Nasal resistance is often high in people with tetraplegia and sleep apnoea.

  • The ability of people with tetraplegia and sleep apnoea to sense high nasal resistance is poor.

  • Nasal resistance measured over several days is stable in both people with tetraplegia and sleep apnoea and healthy, able-bodied controls.

  • Elevated nasal resistance in people with tetraplegia is a potential therapeutic target to reduce the risk of sleep-disordered breathing.

Abstract

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.

Introduction

Obstructive sleep apnea (OSA) is highly prevalent (>60%) in people with tetraplegia (Berlowitz et al., 2005, Burns et al., 2000, Chiodo et al., 2016, Giannoccaro et al., 2013, Tran et al., 2010). The pathophysiological factors responsible for the high risk of OSA in people with tetraplegia are poorly understood. Increased nasal congestion, a risk factor for sleep-disordered breathing, is common in people with tetraplegia. Injury to the cervical spinal cord disrupts the supraspinal inputs to spinal sympathetic neurons below the level of injury (Weaver et al., 2006), while the parasympathetic drive remains largely unopposed. The result is diminished sympathetic activity overall. This increases vasodilation and mucosal thickening in the nose which may reduce nasal patency and increase nasal resistance (Baraniuk, 2008).

Nasal resistance is estimated to account for 30–50% of total upper airway resistance in non-neurologically impaired, able-bodied populations (Verin et al., 2002). Increased nasal resistance increases upper airway collapsibility (Dawson et al., 1997, Schwartz et al., 1989) and reduces compliance to therapies such as continuous positive airway pressure (CPAP) therapy in able-bodied people with OSA (Sugiura et al., 2007, Zeng et al., 2008) and in people with tetraplegia and OSA (Berlowitz et al., 2005, Burns et al., 2000). While increased nasal congestion is widely recognized clinically following tetraplegia, quantitative assessment of nasal resistance in people with tetraplegia and its potential role in pathogenesis of OSA had not been investigated until recently. The present study aimed to quantify nasal resistance in people with tetraplegia to establish whether strategies to reduce nasal congestion might be warranted as a therapeutic target to reduce OSA in this population. As such, it is important to know if nasal resistance is stable over time and how it compares to able-bodied controls.

Furthermore, there are inconsistencies between current measures of nasal congestion. Both objective and subjective measures have been used. However, it remains unclear whether the different approaches yield similar information (André et al., 2009, Clement et al., 2014, Schumacher, 2002). Therefore, the present study used three common measures of nasal congestion: (i) airway resistance measured via a choanal pressure transducer – laboratory gold standard technique to objectively quantify nasal resistance, (ii) anterior rhinomanometry – a routinely used tool to measure nasal obstruction in clinical practice and (iii) self-report nasal congestion to also determine how well the objective and subjective measures of nasal congestion correlate with one another.

Section snippets

Participants

Participants with tetraplegia were recruited from the Prince of Wales Hospital Spinal Cord Unit and the community. Able-bodied participants were recruited from the local community alone via advertisement. Participants were recruited for the tetraplegia group if they: (i) had an injury to the cervical spinal cord, (ii) had a level of injury completeness according to the ASIA (American Spinal Injury Association) impairment scale (AIS) of either AIS A or AIS B, (Kirshblum et al., 2011), and (iii)

Participant characteristics

Eight people with tetraplegia (1 female) (see Table 1 for participant characteristics) and 6 able-bodied controls (1 female) completed the study. Tetraplegia and control groups were well-matched for age (50 ± 9 vs. 48 ± 10, p = 0.8) and body mass indices (26 ± 8 vs. 26 ± 4 kg/m2, p = 0.9). The tetraplegia group had moderate to severe OSA with a mean apnea/hypopnea index of 36 ± 14 events/h sleep. One of the tetraplegia participants was on continuous positive airway pressure (CPAP) therapy at the time of the

Discussion

The main findings of this study are that objectively measured nasal resistance via the gold standard choanal pressure technique is higher in people with tetraplegia compared to non-neurologically impaired controls yet perceived nasal blockage is similar between groups. These findings indicate poor perception of elevated nasal resistance in the tetraplegia population. High nasal resistance is consistent with autonomic dysfunction associated with high spinal cord injury. Poor perception of high

Disclosures

The authors do not have any conflicts of interest to disclose.

Acknowledgments

This work was supported by the National Health and Medical Research Council (NHMRC) of Australia (1065913). DJE is supported by a NHMRC RD Wright Fellowship (1049814). ASJ is supported by an ARC Future Fellowship (FT100100203). JEB is supported by NHMRC Fellowship (1042646). The authors would like to thank the participants of the study for their contribution and the Department of Respiratory Medicine, Prince of Wales hospital, Sydney for loaning their anterior rhinomanometer for the study.

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