Sleep and Violence*

1984 ◽  
Vol 29 (2) ◽  
pp. 132-134 ◽  
Author(s):  
L.B. Raschka
Keyword(s):  
Differential Diagnosis ◽  
Sleep Apnea ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Violent Behaviour ◽  
Car Accidents ◽  
Prevention And Treatment ◽  
Respiratory Pathology ◽  
The Brain

Most violence connected with sleep disorder is assumed to be related to sleep walking. It is less well known that other sleep disorders can also give rise to violence. The role of narcolepsy in car accidents is mentioned. Sleep drunkenness can lead to confusion resulting in violent behaviour especially on forced awakening. This condition is associated to sleep apnea. Primary or central sleep apnea is caused by disorders of the brain stem affecting the respiratory center. Secondary or upper airway sleep apnea can be caused by virtually any condition that results in cessation of the airflow due to occlusion of the upper airway. The author describes one patient who engaged in assaultive behaviour on forced awakening following earlier alcohol consumption. The pathomechanism of violent behaviour generated by a combination of sleep apnea and respiratory pathology is described. The differential diagnosis, prevention and treatment is outlined. The use of polysomnography in diagnosis and the potentially dangerous effects of drugs with respiratory depressing effects is highlighted.

scholarly journals A Review on Complications of Sleep Apnea

2021 ◽  
Vol 11 (6) ◽  
pp. 265-271
Author(s):  
JOHN DAVID ◽  
Cindy Jose ◽  
N Venkateswaramurthy ◽  
R Sambath Kumar
Keyword(s):  
Obstructive Sleep Apnea ◽  
Pulmonary Hypertension ◽  
Sleep Apnea ◽  
Cardiac Arrhythmia ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Review Article ◽  
Occupational Disability ◽  
Obstructive Sleep ◽  
The Brain

Sleep apnea occurs when the upper airway repeatedly becomes blocked during sleep, reducing or entirely blocking airflow. This is referred to as obstructive sleep apnea. If the brain fails to provide the necessary impulses for breathing, the disease is known as central sleep apnea. Sleep apnea and other sleep breathing problems are a leading cause of medical, social, and occupational disability. Sleep apnea is also linked to pulmonary hypertension, cardiac arrhythmia and other neurocognitive effects, majority of individuals with sleep apnea go undetected, putting them at danger during surgery. It is critical to identify these patients so that relevant steps can be implemented as soon as possible. In this review article, we will discuss about sleep apnea issues and their possible causes. Keywords: Sleep apnea, Bradycardia, Tachycardia, Breathing, Hypercapnia

827 Central Sleep Apnea in a patient with Multiple Sclerosis

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A322-A323
Author(s):  
Rahul Dasgupta ◽  
Sonja Schütz ◽  
Tiffany Braley
Keyword(s):  
Multiple Sclerosis ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Disordered Breathing ◽  
Central Sleep Apnea ◽  
Progressive Multiple Sclerosis ◽  
Obstructive Sleep ◽  
Increased Risk ◽  
Demyelinating Lesions ◽  
The Brain

Abstract Introduction Sleep-disordered breathing is common in persons with multiple sclerosis (PwMS), and may contribute to debilitating fatigue and other chronic MS symptoms. The majority of research to date on SDB in MS has focused on the prevalence and consequences of obstructive sleep apnea; however, PwMS may also be at increased risk for central sleep apnea (CSA), and the utility of methods to assess CSA in PwMS warrant further exploration. We present a patient with secondary progressive multiple sclerosis who was found to have severe central sleep apnea on WatchPAT testing. Report of case(s) A 61 year-old female with a past medical history of secondary progressive multiple sclerosis presented with complaints of fragmented sleep. MRI of the brain, cervical spine, and thoracic spine showed numerous demyelinating lesions in the brain, brainstem, cervical, and thoracic spinal cord. Upon presentation, the patient noted snoring, witnessed apneas, and daytime sleepiness. WatchPAT demonstrated severe sleep apnea, with a pAHI of 63.3, and a minimum oxygen saturation of 90%. The majority of the scored events were non-obstructive in nature (73.1% of all scored events), and occurred intermittently in a periodic fashion. Conclusion The differential diagnosis of fatigue in PwMS should include sleep-disordered breathing, including both obstructive and central forms of sleep apnea. Demyelinating lesions in the brainstem (which may contribute to impairment of motor and sensory networks that control airway patency and respiratory drive), and progressive forms of MS, have been linked to both OSA and CSA. The present data illustrate this relationship in a person with progressive MS, and offer support for the WatchPAT as a cost-effective means to evaluate for both OSA and CSA in PwMS, while reducing patient burden. PwMS may be at increased risk for CSA. Careful clinical consideration should be given to ordering appropriate sleep testing to differentiate central from obstructive sleep apnea in PwMS, particularly for patients with demyelinating lesions in the brainstem. Support (if any) 1. Braley TJ, Segal BM, Chervin RD. Obstructive sleep apnea and fatigue in patients with multiple sclerosis. J Clin Sleep Med. 2014 Feb 15;10(2):155–62. doi: 10.5664/jcsm.3442. PMID: 24532998; PMCID: PMC3899317.

scholarly journals Computed tomographic evaluation of the role of craniofacial and upper airway morphology in obstructive sleep apnea in Chinese

2004 ◽  
Vol 98 (4) ◽  
pp. 301-307 ◽  
Author(s):  
Bing Lam ◽  
Clara G.C Ooi ◽  
Wilfred C.G Peh ◽  
I Lauder ◽  
Kenneth W.T Tsang ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Computed Tomographic ◽  
Obstructive Sleep ◽  
Airway Morphology

scholarly journals 1244 A Curious Case of ASV Failure

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A474-A474
Author(s):  
Nishant Chaudhary ◽  
Mirna Ayache ◽  
John Carter
Keyword(s):  
Sleep Apnea ◽  
Airway Obstruction ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Upper Airway Obstruction ◽  
Neck Extension ◽  
Sleep Study ◽  
Obstructive Sleep

Abstract Introduction Positive airway pressure-induced upper airway obstruction has been reported with the treatment of obstructive sleep apnea (OSA) using continuous positive airway pressure (CPAP) along with an oronasal interface. Here we describe a case of persistent treatment emergent central sleep apnea (TECSA) inadequately treated with adaptive servo ventilation (ASV), with an airflow pattern suggestive of ASV-induced upper airway obstruction. Report of Case A 32-year-old male, with severe OSA (apnea hypopnea index: 52.4) and no other significant past medical history, was treated with CPAP and required higher pressures during titration sleep studies to alleviate obstructive events, despite a Mallampati Class II airway and a normal body mass index. Drug-Induced Sleep Endoscopy (DISE) showed a complete velopharynx and oropharynx anterior posterior (AP) collapse, long soft palate, which improved with neck extension. CPAP therapy, however, did not result in any symptomatic benefit and compliance reports revealed high residual AHI and persistent TECSA. He underwent an ASV titration sleep study up to a final setting of expiratory positive airway pressure 9 cm H2O, pressure support 6-15 cm H2O (auto-rate), with a full-face mask due to high oral leak associated with the nasal interface. The ASV device detected central apneas and provided mandatory breaths, but did not capture the thorax or abdomen, despite normal mask pressure tracings. Several such apneas occurred, with significant oxyhemoglobin desaturation. Conclusion We postulate that the ASV failure to correct central sleep apnea as evidenced by the absence of thoracoabdominal inspiratory effort, occurred due to ASV-induced upper airway obstruction. Further treatment options for this ASV phenomenon are to pursue an ASV-assisted DISE and determine the effectiveness of adjunctive therapy including neck extension, nasal mask with a mouth closing device and a mandibular assist device.

A role of heart rate variability to diagnose central sleep apnea in patients with chronic heart failure

2004 ◽  
Vol 10 (5) ◽  
pp. S174
Author(s):  
Koji Fukuda ◽  
Shinozaki Tsuyoshi ◽  
Ogawa Hiromasa ◽  
Sugimura Koichiro ◽  
Kagaya Yutaka ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Sleep Apnea ◽  
Chronic Heart Failure ◽  
Central Sleep Apnea

Role of Chemical Drive in Recruiting Upper Airway and Inspiratory Intercostal Muscles in Patients with Obstructive Sleep Apnea

1993 ◽  
Vol 147 (1) ◽  
pp. 190-195 ◽  
Author(s):  
Shinichi Okabe ◽  
Tatsuya Chonan ◽  
Wataru Hida ◽  
Makoto Satoh ◽  
Yoshihiro Kikuchi ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Intercostal Muscles ◽  
Obstructive Sleep

Positive airway pressure therapy

2017 ◽  
Author(s):  
Dirk Pevernagie
Keyword(s):  
Sleep Apnea ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Therapeutic Success ◽  
Pressure Therapy ◽  
Cardiovascular Comorbidity ◽  
Adaptive Servo Ventilation ◽  
Obstructive Sleep

This chapter describes positive airway pressure (PAP) therapy for sleep disordered breathing. Continuous PAP (CPAP) acts as a mechanical splint on the upper airway and is the treatment of choice for moderate to severe obstructive sleep apnea (OSA). Autotitrating CPAP may be used when the pressure demand for stabilizing the upper airway is quite variable. In other cases, fixed CPAP is sufficient. There is robust evidence that CPAP reduces the symptomatic burden and risk of cardiovascular comorbidity in patients with moderate to severe OSA. Bilevel PAP is indicated for treatment of respiratory diseases characterized by chronic alveolar hypoventilation, which typically deteriorates during sleep. Adaptive servo-ventilation is a mode of bilevel PAP used to treat Cheyne–Stokes respiration with central sleep apnea . It is crucial that caregivers help patients get used to and be compliant with PAP therapy. Education, support, and resolution of adverse effects are mandatory for therapeutic success.

Abstract 17375: The Potential Role of Stress-Associated Neurobiological Metabolism in the Cardiovascular Sequelae of Sleep Apnea

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Ahmed Ghoneem ◽  
Michael Osborne ◽  
Shady Abohashem ◽  
Hadil Zureigat ◽  
Tawseef Dar ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Central Sleep Apnea ◽  
Sleep Fragmentation ◽  
Novel Treatments ◽  
Positron Emission ◽  
Classification Of Diseases ◽  
Icd 10 ◽  
International Statistical Classification

Introduction: Obstructive and central sleep apnea (SA) induce sleep fragmentation and associates with HTN and cardiovascular diseases (CVDs). Sleep fragmentation is known to increase stress. Further, heightened stress-associated neurobiological metabolism (particularly amygdalar activity - AmygA), potentiates atherosclerosis. However, it is unknown: 1) whether SA increases AmygA in humans, or 2) whether AmygA mediates the link between SA and its CV consequences (HTN and CVD). Hypothesis: SA associates with higher AmygA which in turn associates with hypertension (HTN) and myocardial infarction (MI). Methods: We studied a cohort of 36424 participants within the Partners Biobank. Diagnoses of MI and sleep apnea and relevant clinical data were obtained from International Statistical Classification of Diseases and Related Health Problems (ICD-10) codes. A subset of 1520 patients provided clinically indicated 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging. AmygA was measured using validated measures. Results: Of 36424 participants, 6596 (18.1%) had SA, 20881(57.3%) had HTN and 4033 (11.1%) had MI. OSA significantly associated with HTN (OR [95%CI]: 3.2 [2.95, 4.48], p<0.0001) and MI (1.30 [1.21, 1.41], p<0.001) in multivariable models. SA associated with AmygA (β [95%CI]: 0.183 [0.058, 0.337], p=0.006). AmygA associated with HTN (1.18 [1.02, 1.38], p= 0.028). Further, AmygA associated with MI (1.28 [1.11, 1.46], p=0.0005). Moreover, AmygA mediated the association between SA and HTN and between SA and MI (p<0.05 for both, figs 1a and 1b). Conclusion: Our findings suggest that SA increases the risk of HTN & MI via a mechanism that involves heightened amygdalar activity. This potential mechanism may inform novel treatments.

Sign in / Sign up

Export Citation Format

Share Document