Study Objectives: Spinal cord injury (SCI) is associated with 2-5 times greater prevalence of sleep disordered breathing (SDB) than the general population. The contribution of SCI on sleep and breathing at different levels of injury using two scoring methods has not been assessed. The objectives of this study were to characterize the sleep disturbances in the SCI population and the associated physiological abnormalities using quantitative polysomnography and to determine the contribution of SCI level on the SDB mechanism. Methods: We studied 26 consecutive patients with SCI (8 females; age 42.5 ± 15.5 years; BMI 25.9 ± 4.9 kg/m 2 ; 15 cervical and 11 thoracic levels) by spirometry, a battery of questionnaires and by attended polysomnography with fl ow and pharyngeal pressure measurements. Inclusion criteria for SCI: chronic SCI (> 6 months post injury), level T6 and above and not on mechanical ventilation. Ventilation, end-tidal CO 2 (P ET CO 2 ), variability in minute ventilation (V I -CV) and upper airway resistance (R UA ) were monitored during wakefulness and NREM sleep in all subjects. Each subject completed brief history and exam, Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Berlin questionnaire (BQ) and fatigue severity scale (FSS). Sleep studies were scored twice, fi rst using standard 2007 American Academy of Sleep Medicine (AASM) criteria and second using new 2012 recommended AASM criteria. Results: Mean PSQI was increased to 10.3 ± 3.7 in SCI patients and 92% had poor sleep quality. Mean ESS was increased 10.4 ± 4.4 in SCI patients and excessive daytime sleepiness (ESS ≥ 10) was present in 59% of the patients. Daytime fatigue (FSS > 20) was reported in 96% of SCI, while only 46% had high-risk score of SDB on BQ. Forced vital capacity (FVC) in SCI was reduced to 70.5% predicted in supine compared to 78.5% predicted in upright positions (p < 0.05). Likewise forced expiratory volume in fi rst second (FEV1) was 64.9% predicted in supine compared to 74.7% predicted in upright positions (p < 0.05). Mean AHI in SCI patients was 29.3 ± 25.0 vs. 20.0 ± 22.8 events/h using the new and conventional AASM scoring criteria, respectively (p < 0.001). SCI patients had SDB (AHI > 5 events/h) in 77% of the cases using the new AASM scoring criteria compared to 65% using standard conventional criteria (p < 0.05). In cervical SCI, V I decreased from 7.2 ± 1.6 to 5.5 ± 1.3 L/min, whereas P ET CO 2 and V I -CV, increased during sleep compared to thoracic SCI. Conclusion:The majority of SCI survivors have symptomatic SDB and poor sleep that may be missed if not carefully assessed. Decreased V I and increased P ET CO 2 during sleep in patients with cervical SCI relative to thoracic SCI suggests that sleep related hypoventilation may contribute to the pathogenesis SDB in patients with chronic cervical SCI. S C I E N T I F I C I N V E S T I G A T I O N SS pinal cord injury (SCI) affects a large number of adults worldwide, with an estimated incidence rate of 15 to 40 cases per million populations. The ...

The Syrian crisis, now in its fifth year, has created an unprecedented strain on health services and systems due to the protracted nature of the warfare, the targeting of medics and health care infrastructure, the exodus of physicians and nurses, the shortage of medical supplies and medications, and the disruption of medical education and training. Within a few short years, the life expectancy of resident Syrians has declined by 20 years. Over the first 4 years of the conflict, more than 75,000 civilians died from injuries incurred in the violence. More than twice as many civilians, including many women and children, have died prematurely of infectious and noninfectious chronic diseases for want of adequate health care. Doctors, local administrators, and nongovernmental organizations are struggling to manage the consequences of the conflict under substandard conditions, often using unorthodox methods of health care delivery in field hospitals and remotely by telehealth communication. Much-needed medical supplies are channeled through dangerous routes across the borders from Lebanon, Jordan, and Turkey. Physicians in the United States and other western nations have helped Syrian physicians make the most of the situation by providing training on introducing innovations in technology and treatment. Portable ultrasound machines have been introduced and are being used extensively in the management of trauma and shock. This report, prepared by members of the Syrian American Medical Society, documents current needs for health care relief within Syria, focusing on pulmonary, critical care, and sleep medicine, and some of the efforts currently underway to meet those needs.

Sleep-disordered breathing (SDB) is highly prevalent in patients with spinal cord injury (SCI); the exact mechanism(s) or the predictors of disease are unknown. We hypothesized that patients with cervical SCI (C-SCI) are more susceptible to central apnea than patients with thoracic SCI (T-SCI) or able-bodied controls. Sixteen patients with chronic SCI, level T6 or above (8 C-SCI, 8 T-SCI; age 42.5 ± 15.5 years; body mass index 25.9 ± 4.9 kg/m(2)) and 16 matched controls were studied. The hypocapnic apneic threshold and CO2 reserve were determined using noninvasive ventilation. For participants with spontaneous central apnea, CO2 was administered until central apnea was abolished, and CO2 reserve was measured as the difference in end-tidal CO2 (PetCO2) before and after. Steady-state plant gain (PG) was calculated from PetCO2 and VE ratio during stable sleep. Controller gain (CG) was defined as the ratio of change in VE between control and hypopnea or apnea to the ΔPetCO2. Central SDB was more common in C-SCI than T-SCI (63% vs. 13%, respectively; P < 0.05). Mean CO2 reserve for all participants was narrower in C-SCI than in T-SCI or control group (-0.4 ± 2.9 vs.-2.9 ± 3.3 vs. -3.0 ± 1.2 l·min(-1)·mmHg(-1), respectively; P < 0.05). PG was higher in C-SCI than in T-SCI or control groups (10.5 ± 2.4 vs. 5.9 ± 2.4 vs. 6.3 ± 1.6 mmHg·l(-1)·min(-1), respectively; P < 0.05) and CG was not significantly different. The CO2 reserve was an independent predictor of apnea-hypopnea index. In conclusion, C-SCI had higher rates of central SDB, indicating that tetraplegia is a risk factor for central sleep apnea. Sleep-related hypoventilation may play a significant role in the mechanism of SDB in higher SCI levels.

Cardiorespiratory plasticity induced by acute intermittent hypoxia (AIH) may contribute to recovery following spinal cord injury (SCI). We hypothesized that patients with cervical SCI would demonstrate higher minute ventilation (V̇e) following AIH compared with subjects with thoracic SCI and able-bodied subjects who served as controls. Twenty-four volunteers (8 with cervical SCI, 8 with thoracic SCI, and 8 able-bodied) underwent an AIH protocol during wakefulness. Each subject experienced 15 episodes of isocapnic hypoxia using mixed gases of 100% nitrogen (N2), 8% O2, and 40% CO2 to achieve oxygen saturation ≤90% followed by room air (RA). Measurements were obtained before, during, and 40 min after AIH to obtain ventilation and heart rate variability data [R-R interval (RRI) and low-frequency/high-frequency power (LF/HF)]. AIH results were compared with those of sham studies conducted in RA during the same time period. Individuals with cervical SCI had higher V̇e after AIH compared with able-bodied controls (117.9 ± 23.2% vs. 97.9 ± 11.2%, P < 0.05). RRI decreased during hypoxia in all individuals (those with cervical SCI, from 1,009.3 ± 65.0 ms to 750.2 ± 65.0 ms; those with thoracic SCI, from 945.2 ± 65.0 ms to 674.9 ± 65.0 ms; and those who were able-bodied, from 949 ± 75.0 to 682.2 ± 69.5 ms; P < 0.05). LH/HF increased during recovery in individuals with thoracic SCI and those who were able-bodied (0.54 ± 0.22 vs. 1.34 ± 0.22 and 0.67 ± 0.23 vs. 1.82 ± 0.23, respectively; P < 0.05) but remained unchanged in the group with cervical SCI. Our conclusion is that patients with cervical SCI demonstrate ventilatory long-term facilitation following AIH compared with able-bodied controls. Heart rate responses to hypoxia are acutely present in patients with cervical SCI but are absent during posthypoxic recovery.

Individuals living with spinal cord injury or disease (SCI/D) are at increased risk for sleep-disordered breathing (SDB), with a prevalence that is three-to fourfold higher than the general population. The main features of SDB, including intermittent hypoxemia and sleep fragmentation, have been linked to adverse cardiovascular outcomes including nocturnal hypertension in patients with SCI/D. The relationship between SDB and SCI/D may be multifactorial in nature given that level and completeness of injury can affect central control of respiration and upper airway collapsibility differently, promoting central and/or obstructive types of SDB. Despite the strong association between SDB and SCI/D, access to diagnosis and management remains limited. This review explores the role of SCI/D in the pathogenesis of SDB, poor sleep quality, the barriers in diagnosing and managing SDB in SCI/D, and the alternative approaches and future directions in the treatment of SDB, such as novel pharmacologic and nonpharmacologic treatments.

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. We sought 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. We studied 18 subjects with chronic cervical and thoracic SCI (10 cervical, 8 thoracic SCI; 11 males; age 42.4 ± 17.1 years; body mass index 26.3 ± 4.8 kg/m2) and 17 matched able-bodied subjects. 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 N1 sleep (from 0.51 ± 0.21 to 0.32 ± 0.10 L vs. 0.47 ± 0.13 to 0.43 ± 0.12 L; respectively, P < 0.05). Moreover, end-tidal CO2 and end-tidal O2 were significantly altered from wake to sleep in SCI (38.9 ± 2.7 mmHg vs. 40.6 ± 3.4 mmHg; 94.1 ± 7.1 mmHg vs. 91.2 ± 8.3 mmHg; respectively, P < 0.05), but not in able-bodied controls (39.5 ± 3.2 mmHg vs. 39.9 ± 3.2 mmHg; 99.4 ± 5.4 mmHg vs. 98.9 ± 6.1 mmHg; respectively, P = ns). RUA was not significantly altered in either group. In conclusion, individuals with SCI experience hypoventilation at sleep onset, which cannot be explained by upper airway mechanics. Sleep onset hypoventilation may contribute to the development SDB in the SCI population.

SDB is common and severe among SCI/D patients. Screening questionnaires do not appear to differentiate between those with and without SDB. Even when SDB was recognized, many patients remained untreated. The increased prevalence of cardiovascular disease in SCI/D patients could represent a consequence of untreated SDB, and improving diagnosis and management of SDB has the potential to improve outcomes for these patients.

Sleep-disordered breathing has been shown to be more prevalent in patients with spinal cord injury (SCI) than the general population. The pathogenesis of increased sleep-disordered breathing in individuals with chronic SCI is unknown. The purpose of this study is to determine whether SCI level affects upper airway (UA) collapsibility and neuromuscular compensatory responses to obstruction. Twenty-four participants (8 cervical SCI, 8 thoracic SCI, and 8 controls) were studied. The ventilation, timing, UA resistance, and pharyngeal collapsibility, defined by critical closing pressure, were determined during non-rapid eye movement sleep. Inspiratory duty cycle and minute ventilation were observed in response to increasing severity of UA obstruction. Compared with controls, both cervical and thoracic SCI participants demonstrated elevated passive critical closing pressure (0.5 ± 2.2 and 0.9 ± 2.7 vs. -2.5 ± 1.0 cmH2O, respectively; P = 0.01). No difference in UA resistance was observed between groups. Cervical and thoracic SCI individuals exhibited a similar degree of hypoventilation and dose-dependent increase in inspiratory duty cycle in response to UA obstruction. Passive UA collapsibility is increased in both cervical and thoracic SCI compared with control. The neuromuscular compensatory responses to UA obstruction during sleep are preserved in chronic SCI and are independent of the level of injury.