Unstable Ventilatory Control During Sleep After High Spinal Cord Injury: The Contribution Of Chemosensitivity And Hypoventilation

<p>ABSTRACT</p> <p>UNSTABLE VENTILATORY CONTROL DURING SLEEP AFTER HIGH SPINAL CORD INJURY: THE CONTRIBUTION OF CHEMOSENSITIVITY AND HYPOVENTILATION</p> <p>by</p> <p>Amy T. Bascom</p> <p>May 2015</p> <p>Advisor: Dr. Harry G. Goshgarian</p> <p>Major: Anatomy and Cell Biology</p> <p>Degree: Doctor of Philosophy</p> <p>A high prevalence of sleep-disordered breathing (SDB) after spinal cord injury (SCI) has been reported in the literature; however, the underlying mechanisms are not well understood. My studies had 2 aims: 1) to determine the effect of the withdrawal of the wakefulness drive to breathe on the degree of hypoventilation in SCI patients and able-bodied controls and 2) to determine the response of the peripheral chemoreceptors to brief hyperoxia (60 seconds of >60% FiO2) and hypercapnia (a single breath of elevated CO2). I studied subjects with chronic cervical and high thoracic SCI and matched able-bodied subjects. For the first aim subjects underwent polysomnography, which included quantitative measurement of ventilation, timing, and upper airway resistance (RUA) on a breath-by-breath basis during transitions from wake to stage N1 sleep. Compared to able-bodied controls, SCI subjects had a significantly greater reduction in tidal volume during the transition from wake to N1sleep (from 0.51±0.21 L to 0.32±0.10 L vs. 0.47±0.13 L to 0.43±0.12 L; respectively, p<0.05). Moreover, end-tidal CO2 and O2 were significantly altered from wake to sleep in SCI (38.9±2.7 vs. 40.6±3.4 mmHg; 94.1±7.1 vs. 91.2±8.3 mmHg; respectively, p˂0.05), but not in able-bodied controls (39.5±3.2 vs. 39.9±3.2 mmHg; 99.4±5.4 vs. 98.9±6.1 mmHg; respectively, p=ns). RUA was not significantly altered in either group. In aim 2 SCI subjects had a greater reduction in ventilation with hyperoxia administration (63.9±23.0 % of baseline VE) compared to able-bodied subjects (91.4±15.1 % of baseline VE, p<0.05) and a higher ventilatory response to a single breath of CO2 (SCI: 0.78±0.4 L/min/mmHg vs. able-bodied: 0.26±0.1 L/min/mmHg, p<0.05). In conclusion, individuals with SCI experience hypoventilation at sleep onset, which cannot be explained by upper airway mechanics and a high peripheral chemoreflex response to O2 and CO2. Sleep onset hypoventilation and high peripheral chemoresponsiveness may contribute to the development SDB in the SCI population.</p>

Name thesis:degree_name

Ph.D.

Level thesis:degree_level

Open Access Dissertation

Discipline thesis:degree_discipline

Anatomy and Cell Biology

Year dc:date.available

2015

Author dc:creator

• Bascom, Amy Therese

Contributors dc:contributor

• Harry G. Goshgarian

• Carotid Body
• EEG
• Respiration
• Sleep Apnea
• Spinal Cord Injury
• Ventilation
• Neurosciences
• Physiology

Repository record dc:identifier

https://digitalcommons.wayne.edu/oa_dissertations/1117

OAI identifier oai:identifier

oai:digitalcommons.wayne.edu:oa_dissertations-2116