Access Type

Open Access Dissertation

Date of Award

January 2015

Degree Type

Dissertation

Degree Name

Ph.D.

Department

Anatomy and Cell Biology

First Advisor

Harry G. Goshgarian

Abstract

ABSTRACT

UNSTABLE VENTILATORY CONTROL DURING SLEEP AFTER HIGH SPINAL CORD INJURY: THE CONTRIBUTION OF CHEMOSENSITIVITY AND HYPOVENTILATION

by

Amy T. Bascom

May 2015

Advisor: Dr. Harry G. Goshgarian

Major: Anatomy and Cell Biology

Degree: Doctor of Philosophy

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.

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