Schizophrenia
Schizophrenia is the most serious and disabling of all mental disorders, affecting just under 1 % of the population. While its etiological bases remain obscure and consequently its nosological boundaries are uncertain, the condition classically has its on
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Introduction to Schizophrenia Schizophrenia is the most serious and disabling of all mental disorders, affecting just under 1 % of the population. While its etiological bases remain obscure and consequently its nosological boundaries are uncertain, the condition classically has its onset in childhood or early adolescence [1]. It is characterized by (1) “positive” psychotic symptoms like delusions (fixed false ideas that are held with unshakable conviction), hallucinations (perceptions without a stimulus), and thought disorder (difficulty in assembling a coherent stream of speech); (2) socalled negative symptoms like lack of motivation and pleasure, inability of expressing the full range of emotions, neglect of personal appearance, and disinterest in life events; and (3) cognitive impairment (memory and attention difficulties) [2]. All of these attributes, persistent over time, culminate in a decline in social and occupational performance. These features – coupled with the consequences of sustained impairment – result in comorbid depression (see chapter “Major depressive disorder”) among people with schizophrenia. Approximately 50 % of patients attempt and about 4 % of patients commit suicide. Schizophrenia is poorly understood by the public, and it is often highly stigmatizing [3].
P.F. Buckley, MD (*) • A. Foster, MD Department of Psychiatry and Health Behavior, Medical College of Georgia, Georgia Regents University, 1120 15th St., AA 1002, Augusta, GA 30912, USA e-mail: [email protected]; [email protected]
Pathophysiology of Schizophrenia and Metabolic Alterations The causes of schizophrenia are largely unknown [4, 5]. However, an ever-increasing portfolio of extensive, multinational genetic studies point to subtle yet reproducible genetic findings [6, 7]. Replicated genes like COMT (catechol-Omethyltransferase), implicated in dopamine and norepinephrine degradation, neuregulin-1 implicated in expression and activation of neurotransmitter receptors, including glutamate, dysbindin gene, DISC (disrupted in schizophrenia), DRD2 (dopamine receptor D2), and DAT (dopamine active transporter), likely represent only a minor part of genetic makeover of schizophrenia, while genome-wide studies reveal DNA variants (single nucleotide polymorphisms), which are common to schizophrenia and bipolar disorder, and structural genomic variants (copy number variants) shared by schizophrenia and neurodevelopmental disorders like autism [6]. Nongenetic influences include obstetric events like hypoxia and maternal malnutrition, birth during late winter and spring, advanced paternal age, urbanality, prenatal infections (such as rubella and maternal influenza), changes in inflammatory markers like cytokines, head injury, and use of cannabis [8]. The exact mixture and confluence of etiological factors that result in schizophrenia most likely differs from one patient to another [5]. On postmortem brain, patients with schizophrenia reveal a series of macroscopic and histological
E. Lammert, M. Zeeb (eds.), Metabolism of Human Diseases, DOI 1
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