PSYCHIATRIC DISORDERS PSY 3720 PSYCHIATRIC DISORDERS THE TOLL OF PSYCHIATRIC DISORDERS IS HUGE. AMERICAN STUDIES. NIMH. PSYCHIATRIC DISORDERS EPIDEMIOLOGIC CATCHMENT AREA STUDY (NIMH). COMPREHENSIVE LOOK AT THE PSYCHIATRIC HEALTH OF THE UNITED STATES. HIGHLIGHTS (NIMH) LIFE-TIME RATES FOR PSYCHIATRIC DISORDERS RANGE FROM 28-28%. SEX DIFFERENCES. WITHIN A 6 MONTH PERIOD 20% OF ADULTS SUFFER AT LEAST ONE OF THESE DISORDERS. NATIONAL COMORBIDITY STUDY 50% OF POPULATION REPORT AT LEAST ONE LIFETIME PSYCHIATRIC DISORDER. 30% reported at least one in a 12 month period. SCHIZOPHRENIA Emil Kraeplin’s (1919) book became the cornerstone of this field of study. He searched for coherent patterns in the many symptoms of psychiatric disorders. He argued that schizophrenia fit into several distinct clinical forms. KRAEPLIN Features common to the varied forms of schizophrenia include bizarre disturbances in thought, paranoid and grand delusions, auditory hallucinations, and an odd array of emotional changes. Thought disorder begins during adolescence and moves relentlessly to a chronic state of cognitive impairment. EUGEN BLEULER Introduced the term schizophrenia. He examined more closely the underlying psychological processes of the disorder. Identified the key symptom as dissociative thinking (a major impairment in the logical structure of thought). SCHIZOPHRENIA During the 1980’s and 1990’s researcher’s continued to refine diagnostic and descriptive categories so that both convey a common understanding of the basic features and withstand the rigors of reliability assessments. SCHIZOPHRENIA DSM-IV. DIAGNOSTIC AND STATISTICAL MANUAL OF MENTAL DISORDERS. SCHIZOPHRENIA Some have argued for a major division of symptoms into two separate groups. Positive symptoms. Negative symptoms. GENETIC CONTRIBUTIONS Family studies. Twin studies. Adoption studies. GENETIC CONTRIBUTIONS STRUCTURAL CHANGES IN THE BRAIN VENTRICULAR ENLARGEMENTS. VENTRICULAR ENLARGEMENTS STRUCTURAL CHANGES IN THE BRAIN LIMBIC SYSTEM ABNORMALITIES. Pyramidal cells in hippocampus of chronic schizophrenics were reported to be disorientated. LIMBIC SYSTEM ABNORMALITIES REGIONAL AND CELLULAR ABNORMALITIES Altered gene expression relevant for inhibitory neurons. STRUCTURAL CHANGES IN THE BRAIN Hypofrontality hypothesis. HYPOFRONTALITY THE DOPAMINE HYPOTHESIS 1) Amphetamine psychosis. 2) chlorpromazine. 3) Parkinson’s. THE DOPAMINE HYPOTHESIS Criticisms of this model have emerged. ALTERNATIVE MODEL Alterations in the prenatal development of the hippocampus and/or amygdala may be a critical event in the overall etiology of schizophrenia. ALTERNATIVE MODEL Some combination of GDE factors would alter the development of hippocampus and/or amygdala and their functional relationships to the rest of the brain. RAT MODELS Several developmental rat models of schizophrenia have been developed. Idea is that hippocampus and/or the amygdala are altered early during brain development and that this event fundamentally alters the organization of the brain in adulthood. Leading to the symptoms associated with schizophrenia. RAT MODELS Changes include alterations in areas like the nucleus accumbens and prefrontal cortex. Changes in the relationship of the hippocampus and amygdala to these and other brain regions. RAT MODELS Neonatal lesions of the ventral hippocampus or amygdala. Lead to the emergence of abnormalities in various behaviours in adulthood. RAT MODELS Abnormalities include: enlarged ventricles. increased action of postsynpatic dopamine receptors. Morphological changes in prefrontal cortex. Related deficits on tasks sensitive to prefrontal cortex function. Memory Amygdala Striatum Hippocampus Systems (balanced) GDE factors Nucleus Other Prefrontal Accumbens Cortex Brainstem Neural nuclei Systems Memory Striatum Hippocampus Systems Amygdala Interaction Schizophrenia Neonatal lesion/DA changes GDE factors Prefrontal Nucleus Other Cortex Accumbens Brainstem Neural nuclei Systems SUMMARY According to this model the alterations in dopamine-related behaviour and prefrontal function are a secondary consequence of prenatal alterations in learning and memory systems.