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Aging is marked by cognitive decline, which in the case of Alzheimer’s disease is associated with tremendous global economic burden. Identifying modifiable risk factors for cognitive decline is therefore of paramount importance. In this chapter, we describe how aging compromises sleep quality and sleep architecture at a rate that parallels normal age-related cognitive decline. We argue that understanding the neurocognitive functions of sleep – frontal lobe restoration, memory consolidation, and metabolite clearance – and how such functions change in later life will be key to informing why some older individuals maintain healthy cognitive functioning and other older individuals do not. Critically, by investigating how sleep, cognition, and aging interact, researchers and clinicians can develop sleep-related treatments that target preventing, or at least ameliorating, pathologies such as Alzheimer’s disease.
This chapter shows that the study of dreams provides meaningful and valuable information about cognitive and affective processes occurring during sleep. It demonstrates that typical features in large dream samples can be identified using statistical methods and that these features are in good correspondence with known patterns of brain activity during sleep, in particular rapid eye movement (REM) sleep. These analyses are based on the frequency of occurrence and degree of uniformity of dream contents, irrespective of whether the dreams mimicked real-life experiences or were extremely bizarre. The chapter also shows that bizarre but common aspects in dreams have much in common with known neuropsychological syndromes. Integrated approach to sleep and dreaming undoubtedly contribute to redefining the links between brain processes and the varieties of dream experiences, and lead to a more comprehensive model of human brain function during sleep.
This chapter focuses on the neuroimaging of cataplexy using a case of a 68-year-old woman, who had suffered from narcolepsy since she was 15 years old, as an example. Her mean sleep latency during a multiple sleep latency test was 0.5 minutes, with three sleep onset rapid eye movement (REM) periods among the four naps. The patient underwent two 99mTc-ethylcysteinate dimer brain single-photon emission computed tomography (SPECT) studies during symptomatic and asymptomatic periods of cataplexy on two non-consecutive days. Symptomatic SPECT images were coregistered with asymptomatic images and both images were then co-registered with 3-dimensional magnetic resonance imaging (MRI). The normalized subtracted SPECT and MRI volumes were merged for visual analysis. A characteristic of human REM sleep is right-hemisphere activation, as shown by SPECT imaging and spectral electroencephalographic (EEG) analysis. The right hemisphere is also more activated during cataplexy than the left hemisphere.
This chapter examines possible neuronal networks and mechanisms responsible for the switch from waking to non-rapid eye movement (NREM) and REM sleep. The activated cortical state during waking is induced by the activity of multiple waking neurochemical systems. In contrast to the complex and extensive neurochemical network involved in waking, the neurons inducing slow-wave sleep (SWS) are localized in the lateral preoptic area and the adjacent basal forebrain. A cluster of these neurons is localized in a small nucleus called the ventrolateral preoptic nucleus (VLPO), which is situated above the optic chiasm. Neurons specifically active during paradoxical sleep (PS) were recorded in the posterior hypothalamus (PH) of cats or head-restrained rats. One-third of these GABAergic neurons were immunoreactive for the neuropeptide melanin concentrating hormone (MCH). PS onset would be due to the activation of glutamatergic PS-on neurons from the sublaterodorsal tegmental nucleus (SLD).
Extensive electroencephalographic (EEG) sleep studies have demonstrated increases in rapid eye movement (REM) sleep and changes in non-rapid eye movement (NREM) sleep in depression. Preclinical evidence shows that REM sleep is generated in the brainstem. It also shows that NREM sleep is characterized by slower frequency, higher amplitude thalamocortical electrical oscillations. The alterations in NREM sleep in depressed patients may lead to impaired restoration of prefrontal cortex function during NREM sleep. Functional neuroimaging studies of sleep extend the preclinical understanding of the mechanisms of sleep/wake regulation by providing potential links between neural systems involved in emotional behavior and those involved in sleep. The notion of hyperarousal in paralimbic structures in depressed patients has received further support from an extensive literature describing the functional neuroanatomical correlates of the antidepressant response to sleep deprivation in depressed patients. Patients with schizophrenia are known to have severely disturbed subjective sleep.
This chapter reviews the current neuroimaging literature regarding disorders of arousal and parasomnias, particularly non-rapid eye movement (NREM) parasomnias. During REM sleep the patient exhibited REM behavior disorder (RBD) with mumbling, complex hand movements, and arm/leg jerks. A repeat magnetic resonance imaging (MRI) showed persistent increased T2 weighted image (WI) hyper intense/T1 WI hypo intense lesions in the right mesencephalic/ pontine tegmentum and the right medulla. MRI of the head revealed a T2 WI hyper intense lesion at the pontomesencephalic lesion presumed to be neurosarcoidosis. Imaging modalities when used in combination with clinical electrophysiology (e.g. EEG and PSG) provide better understanding into both structure and function of electrophysiologically verified parasomnias. Future studies combining both electrophysiology and multiple neuroimaging modalities may help in both the assessment of sleep-related dissociative disorders and the development of new treatment modalities.
This chapter outlines basic aspects of magnetoencephalography (MEG) technology, and provides an example of how the method is used clinically. In the clinical arena, MEG is most commonly used for presurgical planning purposes with the goal of localizing epileptogenic regions in patients with medically refractory seizures. In many of these cases, MEG provides unique clinical information that alters clinical care in a positive manner. Resective surgery was performed in the epileptogenic zone as originally identified by MEG and the patient has been seizure free for more than 2.5 years. The chapter describes how MEG is being used in sleep research. MEG is starting to play an increased role in the understanding of how brain circuits are modulated during sleep, with the most significant insights coming in relationship to the origins of sleep spindles and the complex modulation of neural interactions during rapid eye movement (REM) sleep.
Rapid eye movement (REM) sleep behavior disorder (RBD) was first formally identified in 1986 by Schenck and Mahowald in five elderly subjects presenting similar motor behavioral patterns during REM sleep consisting of violent dream-enacting behaviors. The clinical manifestations of RBD are typically dream-related motor-behavioral manifestations that appear to be the enactment of a fight. Subclinical or preclinical RBD, status dissociatus and parasomnia overlap syndrome are the clinical-pathophysiological subtypes of RBD, according to ICSD-2. The literature contains anecdotal reports of co-existing RBD and narcolepsy in both adults and children, in some cases with the RBD episodes as the presenting symptoms. The parasomnia and non-parasomnia disorders are taken into account in the differential diagnosis of RBD. In humans, RBD has been associated with several etiologies and abnormalities. Anecdotal reports and uncontrolled, retrospective studies of small patient series suggest that levodopa and pramipexole (D3 agonist) reduce RBD manifestations.
Arousal parasomnias occur mainly during non-rapid eye movement (NREM) sleep. This group consists of confusional arousals, sleepwalking and sleep terrors. Sleepwalking and sleep terrors can be triggered by stress, sleep deprivation, alcohol ingestion, and almost all sedative medications. This group of parasomnias is composed of three disorders occurring essentially during rapid eye movement (REM) sleep. Sleep paralysis is one of the main symptoms associated with narcolepsy, but it can also occur individually. REM sleep behavior disorder is characterized by a loss of generalized skeletal muscle REM-related atonia and the presence of physical dreamenactment. Polysomnographic recordings of individuals with RBD showed a reduction of the tonic phenomena of REM sleep and the activation of the phasic phenomena. Parasomnias are frequent in the general population; more than 30% of individuals experiences at least one type of parasomnia. At the genetic level, there is growing evidence that many parasomnias have a genetic component.
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