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A previous review of the neuroimaging studies in obstructive sleep apnea (OSA) called for specific attention to longitudinal studies of the treatment effects of OSA on neuroimaging. This chapter focuses on those studies where treatment effects were considered. The structural studies suggest that there are some notable changes in the structure of the human brain when continuous positive airway pressure (CPAP) is used to correct OSA. Some of these changes are even associated with cognitive changes in the expected cognitive domains and are seen with as little as only three months of treatment. The functional imaging studies together suggest that changes in brain function associated with working memory are evident when comparing treatment with no-treatment conditions in patients with OSA. Specifically, treatment often results in the recruitment of fewer cognitive resources to perform at the same level or better.
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.
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.
The major confirmation of the relationship between sleep and autonomic nervous system (ANS) is the presence of dynamic synchronous fluctuations in sleep phases and autonomic functions. Nocturnal monitoring of breathing, pulse rate, systemic arterial pressure, and peripheral vasomotor activation discloses autonomic deactivation that, appearing at sleep onset, continues into deep sleep. The increased prevalence of sleep disorders with aging may be influenced by medical co-morbidities and medications that alter sleep architecture. Age-related changes in ANS function are linked to changes in body composition, neuronal loss, neurotransmitter underproduction or reduced receptor function, tissue damage, and hormonal changes. Autonomic function testing may be very helpful to evaluate the extent of autonomic involvement and to monitor the course of the disorder and the response to therapy. The effect of age on sudomotor pathway and control of core temperature is complex and involves different levels of ANS.