Nocturnal Hypermotor Activity during Apnea-Related Arousals.
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ABSTRACT:
SUBMITTER: Hoque R
PROVIDER: S-EPMC4990955 | biostudies-literature | 2016 Sep
REPOSITORIES: biostudies-literature
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Nocturnal Hypermotor Activity during Apnea-Related Arousals.
Hoque Romy R DelRosso Lourdes M LM
Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine 20160915 9
<h4>Abstract</h4>We present a case of a 50-year-old patient who exhibits nocturnal hypermotor activity occurring exclusively during apnea-related arousals consisting of repetitive lower extremity hip-flapping. This movement is unusual and reflects a new form of lower extremity movement associated with apnea-related arousals. ...[more]
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Project description:PurposeArousals may contribute to the pathogenesis of sleep-disordered breathing (SDB) and central sleep apnea (CSA). We aimed to determine the effect of the nonbenzodiazepine hypnotic zolpidem on the frequency of respiratory-related arousals and central apnea in patients with moderate-to-severe SDB. We hypothesized that zolpidem decreases the severity of SDB by decreasing the frequency of respiratory-related arousals.MethodsPatients with apnea-hypopnea index ≥ 15 events/hour and central apnea-hypopnea index ≥ 5 events/hour underwent a sleep study on zolpidem 5 mg and a sleep study with no medication in a randomized order. The respiratory arousal index was compared between the two studies using a randomized crossover design. Sleep, respiratory, and physiologic parameters, including the CO2 reserve and the respiratory arousal threshold, were also compared.ResultsEleven participants completed the study. Compared to no treatment, zolpidem reduced the respiratory arousal index (39.7 ± 7.7 vs. 23.3 ± 4.4 events/h, P = 0.031). Zolpidem also lowered the total apnea-hypopnea index (55.6 ± 8.5 vs. 41.3 ± 7.5 events/hour, P = 0.033) but did not affect other clinical and physiologic parameters. Compared to control, zolpidem did not widen CO2 reserve (- 0.44 ± 1.47 vs. - 0.63 ± 0.86 mmHg, P = 0.81). The respiratory arousal threshold did not show a significant change on zolpidem compared to control (- 8.72 ± 2.1 vs. - 8.25 ± 2.81 cmH2O, P = 0.41).ConclusionNocturnal arousals and overall SDB severity were reduced with a single dose of zolpidem in patients with moderate-to-severe sleep-disordered breathing with increased susceptibility for central apnea. Zolpidem did not widen the CO2 reserve or increase the arousal threshold.Trial registrationClinicaltrials.gov. Sleep and Breathing in the General Population - Chemical Stimuli (NCT04720547).
| S-EPMC9470768 | biostudies-literature
Project description:Sleep apnea has been related to brain changes such as atrophy. However, which component of sleep apnea, the apnea-hypopnea index (AHI), nocturnal oxygen desaturation or arousals, can explain this association is unclear. In this large population-based study (n=681, mean age 62.1 years), we investigated the associations of AHI, nocturnal oxygen desaturation and arousals with global and regional gray matter and white matter volumes and with white matter lesion volumes. All participants underwent one night of polysomnography and MRI scanning of their brain. Gray matter, white matter and white matter lesion volumes adjusted for intracranial volume were studied as markers of brain atrophy. Nocturnal oxygen desaturation was related to whole brain white matter atrophy independent of covariates (multivariable adjusted B=-8.3, 95% CI=-16.7; -0.02). This association was most prominently reflected in the association between more oxygen desaturation and a smaller white matter parietal volume (B=-3.95 ml, 95% CI=-6.02; -1.88). Furthermore, oxygen desaturation was related to a smaller hippocampus (B=-0.22 ml, 95% CI=-0.42; -0.01). Although a higher AHI was related to smaller parietal gray (B=-0.05, 95% CI=-0.09; -0.004) and white matter (B=-0.06, 95% CI=-0.12; -0.10) volumes, these associations disappeared when adding oxygen desaturation to the model. We did not find a relation between arousals and gray and white matter brain atrophy and white matter lesion volumes. This suggests that oxygen desaturation mainly explains the association between sleep apnea and brain damage.
| S-EPMC6580891 | biostudies-literature
Project description:Background Sleep fragmentation induced by repetitive arousals is a hallmark of obstructive sleep apnea (OSA). Sleep fragmentation has been linked to hypertension in community-based studies, but it is unclear if this association is manifest in OSA. We aimed to explore whether frequent arousals from sleep modify the relationship between OSA and prevalent hypertension. Methods and Results A total of 10 102 patients with OSA and 1614 primary snorers were included in the study. Hypertension was defined on either direct blood pressure measures or diagnosis by a physician. Spontaneous, respiratory, and movement arousals were derived by polysomnography. Logistic regression models were used to estimate the associations between arousals and prevalent hypertension in patients with OSA and primary snorers. For every 10-unit increase of total arousal index, odds of hypertension significantly increased in both the total sample (odds ratio [OR], 1.08; 95% CI, 1.03-1.14; P=0.002) and patients with OSA (OR, 1.10; 95% CI, 1.04-1.16; P<0.001), but not in the primary snoring group. Total arousal index was significantly associated with systolic blood pressure and diastolic blood pressure in the total sample (β=0.05 and β=0.06; P<0.001) and in patients with (β=0.05 and β=0.06; P<0.01), but not in primary snorers. In addition, a greater influence of respiratory events with arousals than respiratory events without arousals on blood pressure in OSA was also noted. Results were independent of confounders, including apnea-hypopnea index and nocturnal hypoxemia. Conclusions We conclude that repetitive arousals from sleep are independently associated with prevalent hypertension in patients with OSA.
| S-EPMC9075207 | biostudies-literature
Project description:(1) Aim: We aim to evaluate the association between arousals during sleep and subclinical coronary atherosclerosis detected by coronary computed tomography angiography (CTA) in patients with obstructive sleep apnea (OSA). (2) Methods: This was a cross-sectional study. Consecutive newly diagnosed OSA patients, who underwent coronary CTA examinations within 3 months of the sleep study, were eligible. We used the arousal index (ArI) derived from polysomnography to assess arousals during sleep and a semi-automated plaque quantification software to characterize and quantify the subclinical coronary atherosclerosis. Multiple regression models were used to evaluate the associations of the ArI with the coronary atherosclerotic plaque presence, volume, and composition. (3) Results: A total of 99 patients with OSA were included in the study. In the multivariable models, patients with a high ArI (ArI > 32.2 events/h) were more likely to have coronary plaques compared to those with a low ArI (ArI ≤ 32.2 events/h) (OR: 3.29 [95% CI: 1.284 to 8.427], p = 0.013). Furthermore, the ArI exhibited significant associations with total (β = 0.015), noncalcified (β = 0.015), and low-attenuation (β = 0.012) coronary plaque volume after accounting for established risk factors (p = 0.008, 0.004, and 0.002, respectively). However, no association between the ArI and calcified plaque volume was found. (4) Conclusion: Repetitive arousals during sleep are associated with an increased coronary plaque burden in patients with OSA, which remained robust after adjusting for multiple established cardiovascular risk factors.
| S-EPMC9599630 | biostudies-literature
Project description:ObjectiveWe assessed the mutation frequency in nicotinic acetylcholine receptor (nAChR) subunits CHRNA4, CHRNB2, and CHRNA2 in a cohort including autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) and sporadic nocturnal frontal lobe epilepsy (NFLE). Upon finding a novel mutation in CHRNA2 in a large family, we tested in vitro its functional effects.MethodsWe sequenced all the coding exons and their flanking intronic regions in 150 probands (73 NFLE, 77 ADNFLE), in most of whom diagnosis had been validated by EEG recording of seizures. Upon finding a missense mutation in CHRNA2, we measured whole-cell currents in human embryonic kidney cells in both wild-type and mutant α2β4 and α2β2 nAChR subtypes stimulated with nicotine.ResultsWe found a c.889A>T (p.Ile297Phe) mutation in the proband (≈0.6% of the whole cohort) of a large ADNFLE family (1.2% of familial cases) and confirmed its segregation in all 6 living affected individuals. Video-EEG studies demonstrated sleep-related paroxysmal epileptic arousals in all mutation carriers. Oxcarbazepine treatment was effective in all. Whole-cell current density was reduced to about 40% in heterozygosity and to 0% in homozygosity, with minor effects on channel permeability and sensitivity to nicotine.ConclusionADNFLE had previously been associated with CHRNA2 dysfunction in one family, in which a gain of function mutation was demonstrated. We confirm the causative role of CHRNA2 mutations in ADNFLE and demonstrate that also loss of function of α2 nAChRs may have pathogenic effects. CHRNA2 mutations are a rare cause of ADNFLE but this gene should be included in mutation screening.
| S-EPMC4408286 | biostudies-literature
Project description:To determine whether there is a consistent epiglottic pressure value that predicts respiratory arousal from sleep. Thirty-one patients with obstructive sleep apnea underwent overnight polysomnography while instrumented with an epiglottic catheter to measure airway pressures. Nadir epiglottic pressures during respiration events (obstructive apneas/hypopneas) terminated with or without arousals were compared. The events were selected by two methods, (1) 20 events with/without arousals were randomly selected, and (2) Events were sampled in pairs (one terminated with arousal and one without arousal) to minimize the effect of sleep duration/stage on the measurement. A total of 1,317 respiratory events were analyzed. There was substantial variability in nadir epiglottic pressure within an individual and among different individuals. The average pressure of 20 randomly selected events with arousals was (-21.2 ± 11.2, ranged -6.68 to -63.34 cm H2O). The nadir epiglottic pressure during respiratory events in NREM stage 2 sleep terminated with arousals was more negative compared with those terminated without arousals using both sampling methods (-23.5 vs. -18.5 cm H2O, p = 0.007 and -20.3 vs. -16.3 cm H2O, p < 0.001). There were very different levels of epiglottic pressures that preceded arousals within and among individuals. However, cortical arousals are associated with a level of more negative epiglottic pressure compared to events terminated without arousal, findings which support the concept of a respiratory arousal threshold. The study used existing data to study methodology (from clinical trial "The Impact of Arousal Threshold in Obstructive Sleep Apnea" https://clinicaltrials.gov/show/NCT02264353) and it is not a clinical trial.
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Project description:ObjectivesTo evaluate functional connectivity (FC) in patients with sleep-related hypermotor epilepsy (SHE) compared to healthy controls.MethodsResting state fMRI was performed in 13 patients with a clinical diagnosis of SHE (age = 38.3 ± 11.8 years, 6 M) and 13 matched healthy controls (age = 38.5 ± 10.8 years, 6 M).Data were first analysed using probabilistic independent component analysis (ICA), then a graph theoretical approach was applied to assess topological and organizational properties at the whole brain level. We evaluated node degree (ND), betweenness centrality (BC), clustering coefficient (CC), local efficiency (LE) and global efficiency (GE). The differences between the two groups were evaluated non-parametrically.ResultsAt the group level, we distinguished 16 RSNs (Resting State Networks). Patients showed a significantly higher FC in sensorimotor and thalamic regions (p < 0.05 corrected). Compared to controls, SHE patients showed no significant differences in network global efficiency, while ND and BC were higher in regions of the limbic system and lower in the occipital cortex, while CC and LE were higher in regions of basal ganglia and lower in limbic areas (p < 0.05 uncorrected).Discussion and conclusionsThe higher FC of the sensorimotor cortex and thalamus might be in agreement with the hypothesis of a peculiar excitability of the motor cortex during thalamic K-complexes. This sensorimotor-thalamic hyperconnection might be regarded as a consequence of an alteration of the arousal regulatory system in SHE. An altered topology has been found in structures like basal ganglia and limbic system, hypothesized to be involved in the pathophysiology of the disease as suggested by the dystonic-dyskinetic features and primitive behaviours observed during the seizures.
| S-EPMC5842749 | biostudies-literature
Project description:Nocturnal frontal lobe epilepsy (NFLE) is a syndrome characterized by the occurrence of sleep related seizures of variable complexity and duration. Hypermotor seizures (HMS) represent a classic manifestation of this syndrome, associated with a perturbation of the ventromesial frontal cortex and anterior cingulate gyrus regions. Nevertheless, in recent years, reports have showed that the seizure onset zone (SOZ) need not be of frontal origin to generate HMS. Here we report an unusual case of a patient presenting with a seven-year history of drug-resistant sleep related HMS arising from the mesial parietal region. The presence of an infrequent feeling of levitation before the HMS was key to suspecting a subtle focal cortical dysplasia in the right precuneus region. A stereo-EEG investigation confirmed the extra-frontal seizure onset of the HMS and highlighted the interrelationship between unstable sleep and seizure precipitation.
| S-EPMC4513272 | biostudies-literature
Project description:The syndrome known as nocturnal frontal lobe epilepsy is recognized worldwide and has been studied in a wide range of clinical and scientific settings (epilepsy, sleep medicine, neurosurgery, pediatric neurology, epidemiology, genetics). Though uncommon, it is of considerable interest to practicing neurologists because of complexity in differential diagnosis from more common, benign sleep disorders such as parasomnias, or other disorders like psychogenic nonepileptic seizures. Moreover, misdiagnosis can have substantial adverse consequences on patients' lives. At present, there is no consensus definition of this disorder and disagreement persists about its core electroclinical features and the spectrum of etiologies involved. To improve the definition of the disorder and establish diagnostic criteria with levels of certainty, a consensus conference using formal recommended methodology was held in Bologna in September 2014. It was recommended that the name be changed to sleep-related hypermotor epilepsy (SHE), reflecting evidence that the attacks are associated with sleep rather than time of day, the seizures may arise from extrafrontal sites, and the motor aspects of the seizures are characteristic. The etiology may be genetic or due to structural pathology, but in most cases remains unknown. Diagnostic criteria were developed with 3 levels of certainty: witnessed (possible) SHE, video-documented (clinical) SHE, and video-EEG-documented (confirmed) SHE. The main research gaps involve epidemiology, pathophysiology, treatment, and prognosis.
| S-EPMC4862248 | biostudies-literature
Project description:ContextObstructive sleep apnea (OSA) is associated with diabetes and cardiovascular disease. This association may be related to metabolic changes that transpire during sleep in OSA.ObjectiveTo examine the impact of OSA, elicited by cessation of continuous positive airway pressure (CPAP), on frequently sampled nocturnal metabolic markers including plasma free fatty acids (FFAs), glucose, insulin, triglycerides (TGs), cortisol, and lactate, as well as glucose production, oral glucose tolerance, blood pressure (BP), endothelial function, cholesterol, and high-sensitivity C-reactive protein (hsCRP).Design and settingRandomized crossover trial of CPAP vs CPAP withdrawal.PatientsThirty-one patients with moderate to severe OSA acclimated to CPAP.InterventionPatients underwent attended polysomnography while sleeping with therapeutic CPAP, or after CPAP withdrawal, in random order. Venous blood was sampled at ∼20-minute intervals on both nights. In 11 patients, we assessed glucose kinetics with an infusion of 6,6-[2H2]glucose.ResultsCPAP withdrawal caused recurrence of OSA associated with hypoxemia, sleep disruption, and heart rate (HR) elevation. CPAP withdrawal dynamically increased nocturnal FFA (P = 0.007), glucose (P = 0.028), and cortisol (P = 0.037), in proportion to respiratory event frequency, HR elevation, or sleep fragmentation. Diabetes predisposed to glucose elevation. CPAP withdrawal also increased systolic BP (P = 0.017) and augmentation index (P = 0.008), but did not affect insulin, TGs, glucose production, oral glucose tolerance, cholesterol, or hsCRP.ConclusionOSA recurrence during CPAP withdrawal increases FFA and glucose during sleep, associated with sympathetic and adrenocortical activation. Recurring exposure to these metabolic changes may foster diabetes and cardiovascular disease.
| S-EPMC5587067 | biostudies-literature