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      Intraoral Neuromuscular Stimulation Device and Rapid Eye Movement-Dependent Obstructive Sleep Apnea

      case-report
      1 , , 1 , 2 , 3 , 4
      ,
      Cureus
      Cureus
      muscle skeletal, rem, neuromuscular electrical stimulation, motor neurons, obstructive sleep apnea (osa)

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          Abstract

          Obstructive sleep apnea (OSA) is a sleep breathing disorder characterized by recurrent pharyngeal collapse secondary to the decreased tone of the pharyngeal dilator muscles. The genioglossus muscle is a major pharyngeal dilator responsible for maintaining the upper airway. Research has shown that patients with OSA have a stronger but less endurant genioglossus muscle. Research has also demonstrated that neuromuscular electrical stimulation of the skeletal muscles in the genioglossus was associated with improvement in muscular endurance and hence improvement in mild OSA. This has led to the development of a novel intraoral neuromuscular stimulation device for treating snoring and mild OSA. It is known that OSA is worse in rapid eye movement (REM) sleep compared to other stages of sleep due to neurologically mediated impairment of skeletal muscles. What has not been demonstrated so far is if the intraoral neuromuscular stimulation device improves the apnea-hypopnea index (AHI) in REM sleep. Our case report highlights the significant improvement of REM-dependent OSA in a middle-aged female with consistent use of an intraoral neuromuscular stimulation device marketed as eXciteOSA® (Signifier Medical Technologies, Needham, MA).

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          Most cited references6

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          REM Sleep at its Core – Circuits, Neurotransmitters, and Pathophysiology

          Rapid eye movement (REM) sleep is generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. Within these circuits lies a core region that is active during REM sleep, known as the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus. It is hypothesized that glutamatergic SubC neurons regulate REM sleep and its defining features such as muscle paralysis and cortical activation. REM sleep paralysis is initiated when glutamatergic SubC cells activate neurons in the ventral medial medulla, which causes release of GABA and glycine onto skeletal motoneurons. REM sleep timing is controlled by activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal paragigantocellular reticular nucleus as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the laterodorsal and pedunculo-pontine tegmentum in the brainstem. Determining how these circuits interact with the SubC is important because breakdown in their communication is hypothesized to underlie narcolepsy/cataplexy and REM sleep behavior disorder (RBD). This review synthesizes our current understanding of mechanisms generating healthy REM sleep and how dysfunction of these circuits contributes to common REM sleep disorders such as cataplexy/narcolepsy and RBD.
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            Sensorimotor function of the upper-airway muscles and respiratory sensory processing in untreated obstructive sleep apnea.

            Numerous studies have demonstrated upper-airway neuromuscular abnormalities during wakefulness in snorers and obstructive sleep apnea (OSA) patients. However, the functional role of sensorimotor impairment in OSA pathogenesis/disease progression and its potential effects on protective upper-airway reflexes, measures of respiratory sensory processing, and force characteristics remain unclear. This study aimed to gain physiological insight into the potential role of sensorimotor impairment in OSA pathogenesis/disease progression by comparing sensory processing properties (respiratory-related evoked potentials; RREP), functionally important protective reflexes (genioglossus and tensor palatini) across a range of negative pressures (brief pulses and entrained iron lung ventilation), and tongue force and time to task failure characteristics between 12 untreated OSA patients and 13 controls. We hypothesized that abnormalities in these measures would be present in OSA patients. Upper-airway reflexes (e.g., genioglossus onset latency, 20 ± 1 vs. 19 ± 2 ms, P = 0.82), early RREP components (e.g., P1 latency 25 ± 2 vs. 25 ± 1 ms, P = 0.78), and the slope of epiglottic pressure vs. genioglossus activity during iron lung ventilation (-0.68 ± 1.0 vs. -0.80 ± 2.0 cmH(2)O/%max, P = 0.59) were not different between patients and controls. Maximal tongue protrusion force was greater in OSA patients vs. controls (35 ± 2 vs. 27 ± 2 N, P < 0.01), but task failure occurred more rapidly (149 ± 24 vs. 254 ± 23 s, P < 0.01). Upper-airway protective reflexes across a range of negative pressures as measured by electromyography and the early P1 component of the RREP are preserved in OSA patients during wakefulness. Consistent with an adaptive training effect, tongue protrusion force is increased, not decreased, in untreated OSA patients. However, OSA patients may be vulnerable to fatigue of upper-airway dilator muscles, which could contribute to disease progression.
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              Neuromuscular electrical stimulation training induces atypical adaptations of the human skeletal muscle phenotype: a functional and proteomic analysis.

              The aim of the present study was to define the chronic effects of neuromuscular electrical stimulation (NMES) on the neuromuscular properties of human skeletal muscle. Eight young healthy male subjects were subjected to 25 sessions of isometric NMES of the quadriceps muscle over an 8-wk period. Needle biopsies were taken from the vastus lateralis muscle before and after training. The training status, myosin heavy chain (MHC) isoform distribution, and global protein pattern, as assessed by proteomic analysis, widely varied among subjects at baseline and prompted the identification of two subgroups: an "active" (ACT) group, which performed regular exercise and had a slower MHC profile, and a sedentary (SED) group, which did not perform any exercise and had a faster MHC profile. Maximum voluntary force and neural activation significantly increased after NMES in both groups (+∼30% and +∼10%, respectively). Both type 1 and 2 fibers showed significant muscle hypertrophy. After NMES, both groups showed a significant shift from MHC-2X toward MHC-2A and MHC-1, i.e., a fast-to-slow transition. Proteomic maps showing ∼500 spots were obtained before and after training in both groups. Differentially expressed proteins were identified and grouped into functional categories. The most relevant changes regarded 1) myofibrillar proteins, whose changes were consistent with a fast-to-slow phenotype shift and with a strengthening of the cytoskeleton; 2) energy production systems, whose changes indicated a glycolytic-to-oxidative shift in the metabolic profile; and 3) antioxidant defense systems, whose changes indicated an enhancement of intracellular defenses against reactive oxygen species. The adaptations in the protein pattern of the ACT and SED groups were different but were, in both groups, typical of both resistance (i.e., strength gains and hypertrophy) and endurance (i.e., a fast-to-slow shift in MHC and metabolic profile) training. These training-induced adaptations can be ascribed to the peculiar motor unit recruitment pattern associated with NMES.
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                Author and article information

                Journal
                Cureus
                Cureus
                2168-8184
                Cureus
                Cureus (Palo Alto (CA) )
                2168-8184
                28 July 2022
                July 2022
                : 14
                : 7
                : e27418
                Affiliations
                [1 ] Family and Community Medicine, Southern Illinois University School of Medicine, Springfield, USA
                [2 ] General Practice, Shadan Institute of Medical Sciences, Hyderabad, IND
                [3 ] Family Medicine, Ruth Temple Clinic, Los Angeles, USA
                [4 ] Family Medicine, Southern Illinois University Center for Family and Community Medicine, Springfield, USA
                Author notes
                Article
                10.7759/cureus.27418
                9418763
                36046328
                0fb37338-f4a6-401a-938f-271440909746
                Copyright © 2022, Wasey et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 28 July 2022
                Categories
                Family/General Practice
                Otolaryngology
                Pulmonology

                muscle skeletal,rem,neuromuscular electrical stimulation,motor neurons,obstructive sleep apnea (osa)

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