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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 summarizes findings from structural and functional neuroimaging studies in individuals with idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD). In humans, functional brain imaging has been used to evaluate the neural mechanisms and structures that regulate REM sleep. Dysfunction of the REM sleep atonia network forms the neuropathological basis for RBD. In humans, iRBD is diagnosed when a patient with videopolysomnographic confirmation of REM sleep without atonia has no evidence of a neurological disease or other possible causes. The chapter summarizes the neuroimaging abnormalities that have been identified in Parkinson disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Several neuroimaging studies have evaluated the morphological and functional state of the substantia nigra in iRBD. These studies have evaluated the echogenicity of the substantia nigra with transcranial sonography (TCS) and the nigrostriatal dopaminergic system with functional imaging.
In human language the mapping between symbol and meaning is arbitrary, and any symbol or set of letters may represent any object, action, or descriptor. As such, both the lexical meaning and the emotional meaning of words and sentences are entirely acquired through learning. This chapter reviews current empirical evidence on the processing of emotional content in human language. Regarding emotional semantics, the question of whether the right hemisphere plays a special role is of considerable theoretical interest because of its implications for the organization of the semantic system in general. The temporal dynamics of emotional language processing is also discussed here. Unlike lesion studies, functional neuroimaging studies generally do not indicate a pronounced role of the right hemisphere in the processing of emotional semantics. The chapter outlines how the processing of emotional language content differs from the processing of semantically neutral language.
The normal and abnormal variations in conscious state operate through three fairly well-understood physiological processes: activation (A), input-output gating (I), and modulation (M). This chapter provides an account of the phenomenology of the variations in conscious state, and shows how three mediating brain processes, activation, input-output gating, and modulation, interact over time so as to account for those variations in a unified way. It focuses on variations in consciousness during the sleep-wake cycle across species and draws on evidence from lesion, electrophysiological, and functional neuroimaging studies. By studying the way that consciousness is normally altered when we fall asleep and when we dream, it is possible to obtain insights about how the brain mediates consciousness. Armed with the AIM model, it is possible to obtain a unified view of the genesis of a wide variety of normal and abnormal changes in conscious experience.
Disgust has a characteristic facial expression which is recognised across all cultures. Functional neuroimaging studies have provided an evidence for the role of the insula and the basal ganglia in the identification of facial expressions of disgust. This chapter discusses the involvement of the insula in the perception of disgust and in the processing of smells. It explores the insula, its connections, and its functions in more detail. Insula activation has been demonstrated in human neuroimaging studies in response to both odours and tastes. The insula is ideally located to integrate information from different sensory modalities and from the autonomic system, and could therefore be involved in both the perception of disgust from various sensory modalities and the subjective experience of disgust. The chapter focuses on two psychiatric disorders which have been linked to both abnormal processing of disgust and to olfactory deficits: obsessive-compulsive disorder (OCD) and schizophrenia.
This chapter deals with the developmental theories of schizophrenia to provide a foundation for a discussion of functional brain imaging studies of childhood-onset schizophrenia. Neurochemical brain imaging methodologies have permitted testing of the dopamine hypothesis of schizophrenia. Clinical studies have demonstrated prominent premorbid developmental delays in childhood-onset schizophrenia, especially in the areas of speech and language. Neurobiologic studies of the NIMH childhood-onset schizophrenia sample have generally supported neurobiologic continuity between childhood- and adult-onset schizophrenia. Very few functional brain imaging studies have been conducted in patients with childhood-onset schizophrenia. The only study of cerebral glucose metabolism in childhood-onset schizophrenia has been conducted with a subset of the National Institute of Mental Health (NIMH) childhood-onset schizophrenia sample. The finding of cerebellar hypermetabolism in childhood-onset schizophrenia, seen with both data analytic approaches, is notable in light of recent evidence implicating the cerebellum in higher cortical processes.
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