To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
This chapter discusses the interactions between obstructive sleep apnea syndrome (OSAS) and cardio- and cerebrovascular diseases, focusing on the mechanisms by which OSA may contribute to the onset and progression of cardiovascular diseases. The autonomic nervous system (ANS) is closely related to sleep from anatomical, physiological and neurochemical points of view, resulting in dynamic synchronous fluctuations in sleep phases and autonomic functions. Analysis of the circadian rhythm of heart rate variability shows that the mean high-frequency value from morning to noon is lower, whereas the mean low-frequency/high-frequency ratio is higher in OSAS patients than in controls. Measuring ANS function by means of spontaneous baroreflex cardiac modulation or other methods may not only help recognize the severity and prognostic relevance of the cardiovascular effect of OSA, but can shed light on the pathophysiological mechanisms that transform transient nocturnal alterations into sustained 24-hour derangements that require treatment.
Anecdotal recognition of the relationship between sleep apnea and atrial fibrillation has recently given way to more rigorous observational data. The risk of recurrence after atrial fibrillation interventions has also been studied longitudinally. There are numerous pathophysiological mechanisms that may link sleep apnea to atrial fibrillation. One of the most important mechanisms may be the significant changes, both acute and chronic, in autonomic tone that occur with obstructive apneas. Most observational data suggest that the success rates of atrial fibrillation interventions, such as cardioversions and ablation, are significantly improved for patients whose sleep apnea is treated. Epidemiological studies suggest that sleep apnea is a risk factor for new-onset atrial fibrillation, and that its presence reflects a poorer prognosis after atrial fibrillation interventions. Randomized controlled trials are necessary to clarify the effects of sleep apnea therapy on atrial fibrillation outcomes in individuals and communities.
This chapter discusses the case of a 54-year-oldwoman with disturbing respiratory noise during nocturnal sleep. It presents the clinical history, examination, follow-up, treatment, diagnosis, and the results of the procedures performed on the patient. EMG investigation of laryngeal muscle activity was subsequently performed during wakefulness and sleep, placing fine-wire electrodes in the posterior cricoarytenoid, cricothyroid and thyroarytenoid muscles. The specialist made a diagnosis of nocturnal inspiratory stridor based on the characteristics of the noise present only during sleep, particularly during NREM sleep. A diagnosis of REM-sleep behavior disorder (RBD) was also made due to the characteristic clinical history of violent motor behaviors during sleep associated with polysomnography (PSG) evidence of REM sleep without atonia. Tracheostomy and continuous positive airway pressure (CPAP) are effective treatments of stridor; however, they do not always prevent death in multiple-system atrophy.
This chapter presents the clinical history, examination, follow-up, treatment, diagnosis, and the results of the procedures performed on a 73-year-old patient who complained of two recent violent dreams that resulted in significant injury. His past medical history included an anterior wall myocardial infarction, sinusitis and a remote history of tuberculosis. The patient was treated with clonazepam 1.0 mg every evening before sleep, with complete resolution of all violent dream-related behaviors over the following year. The MRI scan revealed a right subdural hematoma without mass effect, and a few small 2-3mm foci of deep white matter changes. The polysomnography (PSG) study revealed significant periodic limb movements. A follow-up assessment by a movement disorders specialist led to the diagnosis of Parkinson's disease. The patient's history and PSG analysis are classical for, and diagnostic of, REM-sleep behavior disorder (RBD), which is defined in ICSD-2 as a parasomnia associated with REM sleep.
This chapter discusses the case of a 55-year-old woman who reported that for the previous 6 years she had been having episodes at night where she had dreams that often had a fearful content. It presents the clinical history, examination, diagnosis, and the results of the procedures performed on the patient. On examination she was anxious and cried during the interview. The differential diagnosis of paroxysmal nocturnal events includes parasomnia, seizures during sleep or a psychogenic disturbance. Parasomnia classification is usually based on the sleep phase during which the parasomnia occurs. Seizures seen in nocturnal frontal lobe epilepsy (NFLE) are sleep-related seizures that may be difficult to distinguish from other paroxysmal events at night. This is because the motor activity and vocalization may resemble other paroxysmal events with features such as cycling movements of the lower limbs and because patients may be partially responsive during the seizures.
Email your librarian or administrator to recommend adding this to your organisation's collection.