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.
","abstract_html":"<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>","abstract_has_math":false,"creators":["Bascom, Amy Therese"],"institution":null,"degree_name":"Ph.D.","degree_level":"Open Access Dissertation","degree_discipline":"Anatomy and Cell Biology","degree_department":null,"school":null,"contributors":["Harry G. Goshgarian"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-01-01T08:00:00Z","date_published":"2015-01-01T08:00:00Z","updated_at":"2026-07-24T06:00:03Z","subjects":["Carotid Body","EEG","Respiration","Sleep Apnea","Spinal Cord Injury","Ventilation","Neurosciences","Physiology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://digitalcommons.wayne.edu/oa_dissertations/1117","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Harry G. Goshgarian"]},{"key":"dc:creator","label":"Author","values":["Bascom, Amy Therese"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2015-01-01T08:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Anatomy and Cell Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Open Access Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Carotid Body","EEG","Respiration","Sleep Apnea","Spinal Cord Injury","Ventilation","Neurosciences","Physiology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://digitalcommons.wayne.edu/oa_dissertations/1117"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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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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.
"],"dc:identifier":["https://digitalcommons.wayne.edu/oa_dissertations/1117"],"dc:subject":["Carotid Body","EEG","Respiration","Sleep Apnea","Spinal Cord Injury","Ventilation","Neurosciences","Physiology"],"dc:title":["Unstable Ventilatory Control During Sleep After High Spinal Cord Injury: The Contribution Of Chemosensitivity And Hypoventilation"],"thesis:degree_discipline":["Anatomy and Cell Biology"],"thesis:degree_level":["Open Access Dissertation"],"thesis:degree_name":["Ph.D."]},"updated_at":"2026-07-24T06:00:03Z"}