Johns Hopkins Sleep Disorders Center

Baltimore, MD, United States

Johns Hopkins Sleep Disorders Center

Baltimore, MD, United States

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Dorsey E.R.,University of Rochester | De Roulet J.,University Hospitals Case Medical Center | Reminick J.I.,University of Rochester | Thai A.,Johns Hopkins Sleep Disorders Center | And 5 more authors.
JAMA - Journal of the American Medical Association | Year: 2010

Context: With the exception of the American Recovery and Reinvestment Act, funding support for biomedical research in the United States has slowed after a decade of doubling. However, the extent and scope of slowing are largely unknown. Objective: To quantify funding of biomedical research in the United States from 2003 to 2008. Design: Publicly available data were used to quantify funding from government (federal, state, and local), private, and industry sources. Regression models were used to compare financial trends between 1994-2003 and 2003-2007. The numbers of new drug and device approvals by the US Food and Drug Administration over the same period were also evaluated. Main Outcome Measures: Funding and growth rates by source; numbers of US Food and Drug Administration approvals. Results: Biomedical research funding increased from $75.5 billion in 2003 to $101.1 billion in 2007. In 2008, funding from the National Institutes of Health and industry totaled $88.8 billion. In 2007, funding from these sources, adjusted for inflation, was $90.2 billion. Adjusted for inflation, funding from 2003 to 2007 increased by 14%, for a compound annual growth rate of 3.4%. By comparison, funding from 1994 to 2003 increased at an annual rate of 7.8% (P<.001). In 2007, industry (58%) was the largest funder, followed by the federal government (33%). Modest increase in funding was not accompanied by an increase in approvals for drugs or devices. In 2007, the United States spent an estimated 4.5% of its total health expenditures on biomedical research and 0.1% on health services research. Conclusion After a decade of doubling, the rate of increase in biomedical research funding slowed from 2003 to 2007, and after adjustment for inflation, the absolute level of funding from the National Institutes of Health and industry appears to have decreased by 2% in 2008. ©2010 American Medical Association. All rights reserved.


Kezirian E.J.,University of California at San Francisco | Boudewyns A.,University of Antwerp | Eisele D.W.,University of California at San Francisco | Schwartz A.R.,Johns Hopkins Sleep Disorders Center | And 3 more authors.
Sleep Medicine Reviews | Year: 2010

Upper airway occlusion in obstructive sleep apnea has been attributed to a decline in pharyngeal neuromuscular activity occurring in a structurally narrowed airway. Surgical treatment focuses on the correction of anatomic abnormalities, but there is a potential role for activation of the upper airway musculature, especially with stimulation of the hypoglossal nerve and genioglossus muscle. We present evidence from research on upper airway neuromuscular electrical stimulation in animals and humans. We also present results from eight obstructive sleep apnea patients with a fully implanted system for hypoglossal nerve stimulation, demonstrating an improvement in upper airway collapsibility and obstructive sleep apnea severity. Future research, including optimization of device features and stimulation parameters as well as patient selection, is necessary to make hypoglossal nerve stimulation a viable alternative to positive airway pressure therapy and upper airway surgical procedures. © 2009 Elsevier Ltd.


Schwartz A.R.,Johns Hopkins Sleep Disorders Center | Barnes M.,Austin Hospital | Hillman D.,Sir Charles Gairdner Hospital | Malhotra A.,Brigham and Women's Hospital | And 6 more authors.
American Journal of Respiratory and Critical Care Medicine | Year: 2012

Rationale: Hypoglossal nerve stimulation (HGNS) recruits lingual muscles, reduces pharyngeal collapsibility, and treats sleep apnea. Objectives: We hypothesized that graded increases in HGNS relieve pharyngeal obstruction progressively during sleep. Methods: Responses were examined in 30 patients with sleep apnea who were implanted with an HGNS system. Current (milliampere) was increased stepwise during non-REMsleep. Frequency and pulse-width were fixed. At each current level, stimulationwas applied on alternating breaths, and responses inmaximal inspiratory airflow(VImax) and inspiratory airflow limitation (IFL) were assessed. Pharyngeal responses to HGNS were characterized by the current levels at which VImax first increased and peaked (flowcapture and peak flowthresholds), and by the VImax increase fromflow capture to peak (DVImax). Measurements and Main Results: HGNS produced linear increases in VImax from unstimulated levels at flow capture to peak flow thresholds (215±21 to 509±37 ml/s; mean±SE; P<0.001) with increasing current from 1.05±0.09 to 1.4±60.11m A.V Imax increased in all patients and IFL was abolished in 57% of patients (non-IFL subgroup). In the non-IFL compared with IFL subgroup, the flow response slope was greater (1241 ± 199 vs. 674 ± 166 ml/s/mA; P < 0.05) and the stimulation amplitude at peak flow was lower (1.23 ± 0.10 vs. 1.80 ± 0.20 mA; P < 0.05) without differences in peak flow. Conclusions: HGNS produced marked dose-related increases in airflow without arousing patients from sleep. Increases in airflow were of sufficient magnitude to eliminate IFL in most patients and IFL and non-IFL subgroups achieved normal or near-normal levels of flow, suggesting potential HGNS efficacy across a broad range of sleep apnea severity. Copyright © 2012 by the American Thoracic Society.


Chin C.-H.,Johns Hopkins Sleep Disorders Center | Chin C.-H.,Chang Gung University | Kirkness J.P.,Johns Hopkins Sleep Disorders Center | Patil S.P.,Johns Hopkins Sleep Disorders Center | And 4 more authors.
Journal of Applied Physiology | Year: 2012

Defective structural and neural upper airway properties both play a pivotal role in the pathogenesis of obstructive sleep apnea. A more favorable structural upper airway property [pharyngeal critical pressure under hypotonic conditions (passive Pcrit)] has been documented for women. However, the role of sex-related modulation in compensatory responses to upper airway obstruction (UAO), independent of the passive Pcrit, remains unclear. Obese apneic men and women underwent a standard polysomnography and physiological sleep studies to determine sleep apnea severity, passive Pcrit, and compensatory airflow and respiratory timing responses to prolonged periods of UAO. Sixty-two apneic men and women, pairwise matched by passive Pcrit, exhibited similar sleep apnea disease severity during rapid eye movement (REM) sleep, but women had markedly less severe disease during non-REM (NREM) sleep. By further matching men and women by body mass index and age (n = 24), we found that the lower NREM disease susceptibility in women was associated with an approximately twofold increase in peak inspiratory airflow (P = 0.003) and inspiratory duty cycle (P = 0.017) in response to prolonged periods of UAO and an ∼20% lower minute ventilation during baseline unobstructed breathing (ventilatory demand) (P = 0.027). Thus, during UAO, women compared with men had greater upper airway and respiratory timing responses and a lower ventilatory demand that may account for sex differences in sleep-disordered breathing severity during NREM sleep, independent of upper airway structural properties and sleep apnea severity during REM sleep. Copyright © 2012 the American Physiological Society.


Kirkness J.P.,Johns Hopkins Sleep Disorders Center | Peterson L.A.,Johns Hopkins Sleep Disorders Center | Squier S.B.,Johns Hopkins Sleep Disorders Center | McGinley B.M.,Johns Hopkins Sleep Disorders Center | And 5 more authors.
Sleep | Year: 2011

Objective: The critical pressure (PCRIT), a measurement of upper airway collapsibility, is a determinant of the severity of upper airway obstruction during sleep. We examined the performance characteristics of the passive and active PCRIT by examining both within-night and between-night variability in the measurements. Methods: We studied 54 sleep apnea patients (39 men, 15 women) and 34 normal subjects (20 men, 14 women) on either 1 or 2 nights during sleep. The PCRIT was measured during relative hypotonia ("passive" state) or during periods of sustained upper airway obstruction used to recruit upper airway neuromuscular responses ("active" state) within- and between-nights. In a subgroup of 10 normal subjects, we performed repeated measurements during hypnotic-induced sleep. Bland-Altman analyses were used to determine the within-night and between-night reliability of the PCRIT measurements. Results: There were no significant within-night or between-night differences for the mean passive PCRIT. The active PCRIT was ∼1 cm H 2O more collapsible on the second night than on the first night. The limits of agreement, which bound the passive and active PCRIT, was ∼ ± 3 cm H2O and was reduced to ∼ ± 1 cm H 2O for the passive PCRIT with hypnotic-induced sleep. Conclusion: Passive and active PCRIT measurements are reasonably reliable within and between nights. An approximately 3 cm H2O change in passive or active PCRIT appears to represent the minimally significant change in PCRIT necessary to assess the effect of an intervention (e.g., positional therapy, surgical interventions, oral appliance effects, and pharmacotherapy) on upper airway mechanical loads or neuromuscular responses.


Krishnan V.,Case Western Reserve University | Patil S.P.,Johns Hopkins Sleep Disorders Center
Sleep Medicine Clinics | Year: 2013

Obstructive sleep apnea (OSA) is associated with an increased risk of accidents related to driving or mass transportation. In this article, the mechanisms for neurocognitive deficits and common subjective and objective testing for determining alertness-related impairments are reviewed. The basis of legal culpability for sleep-related accidents and the role of the clinician or sleep physician are discussed. Education of the patient and public on the risk of OSA on driving ability is a critical role of the clinician. General laws and regulations regarding OSA and driving are reviewed. Physicians are responsible for familiarizing themselves with policies that govern their jurisdiction.© 2013 Published by Elsevier Inc. All rights reserved.


Patil S.P.,Johns Hopkins Sleep Disorders Center
Sleep Medicine Clinics | Year: 2013

Obstructive sleep apnea (OSA), a highly prevalent condition affecting 24% of men and 9% of women, is associated with many comorbidities. Patients with OSA are at increased risk for postoperative respiratory and cardiovascular complications, resulting in the need for increased levels of monitoring and longer hospitalizations. Most patients at risk for OSA, however, remain undiagnosed or untreated, placing the surgical patient with OSA at risk for postoperative complications. Diagnostic testing for OSA can be performed using in-laboratory polysomnography (PSG) or limited-channel portable monitoring (PM). This article addresses the use of PM and in-laboratory PSG in the assessment of OSA. © 2013 Elsevier Inc.


Squier S.B.,Johns Hopkins Sleep Disorders Center | Patil S.P.,Johns Hopkins Sleep Disorders Center | Schneider H.,Johns Hopkins Sleep Disorders Center | Kirkness J.P.,Johns Hopkins Sleep Disorders Center | And 2 more authors.
Journal of Applied Physiology | Year: 2010

The relationship between changes in absolute end-expiratory lung volume (EELV) and collapsibility has not been rigorously quantified. We hypothesized that pharyngeal collapsibility varies inversely with absolute lung volume in sleeping humans during 1) conventional and 2) isovolume measurementsof passive critical pressure (Pcrit). Eighteen healthy subjects (11 male, 7female) slept in a negative pressure ventilator for measurements of pharyngeal collapsibility (Pcrit) during non-rapid eye movement sleep. EELV was 1)allowed to vary with changes in nasal pressure for conventional Pcrit measurements and 2) controlled by maintaining a fixed pressure difference acrossthe respiratory system (PRS) from the nose to the body surface for isovolume Pcrit measurements at elevated EELV (PRS = +10 cmH2O), reducedEELV (PRS = -5 cmH2O), and functional residual capacity (FRC; PRS = 0 cmH2O). In each condition, the absolute EELV was determined and the corresponding Pcrit was derived from upper airway pressure-flow relationships. In the entire group, Pcrit varied inversely with EELV (P <0.001). Pcrit decreased as EELV increased from the conventional to the FRC isovolume condition by -3.5 ± 1.0 cmH 2O/l (P < 0.003).Subjects with a conventional Pcrit below -2 cmH2O exhibited greater reductions in EELV and correspondingly greater decreases in the FRC isovolume compared with the conventional Pcrit (P < 0.001). The overall response, ΔPcrit/ΔEELV, was -2.0 ± 0.2 cmH2O/l (P < 0.001) and did not differ between men and women (P = 0.16). Nevertheless, men and women differed significantly in FRC (2.63 ±0.16 vs. 1.88 ± 0.13 liters, P <0.05) and FRC isovolume Pcrit (-2.3 ±0.8 vs. -7.2 ± 1.2 cmH2, P < 0.05), implying that the men had larger lungs and more collapsible airways than the women. The ΔPcrit/ΔEELV response was independent of sex, conventional Pcrit, body mass index, and neck, waist, and hip circumferences. We conclude that Pcrit varies inversely with absolute EELV, which may lead to 1) an underestimation of the magnitude of quantitative differences in Pcrit across the spectrum from health (negative Pcrit) to disease (positive Pcrit) and 2) increases in sleep apnea susceptibility in obesity. © 2010 the American Physiological Society.


Gamaldo C.E.,Johns Hopkins Sleep Disorders Center | Shaikh A.K.,Emory University | McArthur J.C.,Johns Hopkins Hospital
Neurologic Clinics | Year: 2012

Research models show a strong interrelationship between sleep quality and immune function. The proinflammatory cytokines, interleukin-1, interleukin-6, and tumor necrosis factor α are classified as official sleep-regulatory substances. However, sleep-promoting properties are also possessed by several other immune and proinflammatory cellular classes. This article reviews the current physiologic evidence for the prominent somnogenic and sleep-regulatory properties inherent to these immune substances. Clinical examples of this relationship are discussed from the perspective of infectious and primarily immune-related conditions associated with significant sleep disruption and from the perspective of immune dysregulation associated with several primary sleep disorders. © 2012 Elsevier Inc.


Schwartz A.R.,Johns Hopkins Sleep Disorders Center | Smith P.L.,Johns Hopkins Sleep Disorders Center | Oliven A.,Technion - Israel Institute of Technology
Journal of Applied Physiology | Year: 2014

Obstructive sleep apnea is characterized by recurrent episodes of pharyngeal collapse, which result from a decrease in pharyngeal dilator muscle tone. The genioglossus is a major pharyngeal dilator that maintains airway patency during sleep. Early studies in animal and humans have demonstrated that electrical stimulation of this muscle reduces pharyngeal collapsibility, increases airflow, and mitigates obstructive sleep apnea. These findings impelled the development of fully implantable hypoglossal nerve stimulating systems (HGNS), for which feasibility trial results are now available. These pilot studies have confirmed that hypoglossal nerve stimulation can prevent pharyngeal collapse without arousing patients from sleep. Potentially, a substantial segment of the patient population with obstructive sleep apnea can be treated with this novel approach. Furthermore, the feasibility trial findings suggest that the therapeutic potential of HGNS can be optimized by selecting patients judiciously, titrating the stimulus intensity optimally, and characterizing the underlying function and anatomy of the pharynx. These strategies are currently being examined in ongoing pivotal trials of HGNS. Copyright © 2014 the American Physiological Society.

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