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Psycology » Psychiatry and psychotherapy » Schizophrenia » Schizophrenia: etiology and pathogenesis

  1. Schizophrenia: Introduction
  2. Schizophrenia: signs and symptoms
  3. Schizophrenia: course and form of the disease
  4. Schizophrenia: etiology and pathogenesis
  5. Schizophrenia: differential diagnosis
  6. Schizophrenia: the treatment of disease

During the study of schizophrenia were different assumptions about the nature of the disease and its causes. E. Bleuler, who put forward the concept of schizophrenia as a group of diseases that are comparable with the group of organic psychoses, believed that the main etiological factor is auto-intoxication, leading to disruption of the brain. Since the time of Kraepelin and SS Korsakov was known that hereditary factors, special predisposition to the disease are fairly obvious fact. Used the expression "a schizophrenic mother", "father of the schizophrenic" to emphasize frequently observed features relatives of the patient. In the U.S., used to explain the theory of schizophrenia psychogenesis expressed belief about the role of "mother schizophrenogenic" overwhelming other family members, including the future of the schizophrenic patient (son or daughter) who "shizoidirovalsya" under the influence of such "giperprotektivnoy" mother (A. Mayer). In our country, MA Morozov and VM Morozov speculated on the role of viral factors in the origin of some types of schizophrenia. In the future, these views developed in the UK (T. Crow, etc.).

Both biological and genetic concepts proved vulnerable in terms of their apparent evidence theory of etiology and pathogenesis, they complemented each other, indicating that the benefit polietiologichesky endogenous nature of the disease process. Among the biological factors of schizophrenia emphasizes the role of dopamine, the relationships between features sharing dopamine in the brain structures and behavior disorders with specific endogenous process manifestations. In accordance with the dopamine theory suggests that schizophrenia increases the activity of the dopamine system in the brain to increase dopamine release, increased dopamine neurotransmission, dopamine receptor hypersensitivity, whereby dopamine neurons are hyperactive state. Negative symptoms are associated with a decrease in the activity of the dopaminergic mesocortical system, and the positive - with hyperactivity of subcortical dopaminergic structures.

Antipsychotic effect of neuroleptics associated with schizophrenia in accordance with this theory, the ability of drugs to bind at least 70% of the dopamine D-2 receptors. The latest generation of atypical antipsychotics (risperidone, olanzapine, clozapine, aripiprazole, etc.) not only inhibit dopamine receptors D-2, D-3, D-4, but serotonergic, histaminergic, adrenergic, cholinergic receptor brain structures. Thus, the concept of dopamine etiopathogenesis of schizophrenia is closely intertwined with neyroretseptornogo-neurochemical theory, which includes serotonin and noradrenergic hypothesis hypothesis.

Hereditary origin hypothesis of schizophrenia considers the development of the disease as a result of hereditary predisposition and the risk of developing schizophrenia in the immediate family of the patient, and also involves the study of the genetic profile of patients with schizophrenia in families, the creation of collections of DNA in patients with schizophrenia (Erlemeyer-Kimling, VI Trubnikov TP Panteleeva etc.). If both parents are sick, you will suffer from schizophrenia 14.3% of children. When the disease schizophrenia one of monozygotic twins its development in other twin noted in 86.2% of cases. Concordance for schizophrenia in dizygotic twins is 16.4%. In general, schizophrenia can not be considered a genetic disease with complete penetrance, indicating that the well-known contribution to its development of exogenous factors.

In this sense, the most universal hypothesis seems developmental disorders of the brain in schizophrenia (dizontogeneticheskie theory). She adequately correlated with those observed in the clinic schizophrenia dizontogeneza phenomena. AN Bernstein (1914) suggested that the disease may begin in utero, and the baby is born already schizophrenia. TE Sukharev (1965) showed the presence of schizophrenia dizontogeneza retardirovannogo and distorted types. Currently supporters dizontogeneticheskie hypothesis considering the formation of the disease at the cellular and subcellular levels (G. Roberts, 1986; K. Berman and D. Weinberger, 1989). According to them, the brain damage (toxic, infectious, etc.) may occur in utero, during pregnancy, when there is a formation of the limbic system, which creates a known weakness of the brain structures.

R. Murray and S. Levy (1987), suggesting that brain maturation is characterized by not only the proliferation and migration of cellular structures, but also mortality and elimination believe that schizophrenia may be excessive destruction of nerve cells that makes the immaturity of cellular structures. However, such changes being compensated due to the high plasticity of the developing brain, may precede the disease not progressing. Dizontogeneza phenomena manifested in the fact that the brain pathology is not expressed in gross morphological defects, but only as an immature cell structures or distortion of their development as the consequences of proliferation and migration of cells, changing their orientation, communication failure between individual cell populations, particularly at the level of synaptic formations and receptors, cell-cell contacts.

Just deviations in the development of brain structures, in accordance with this theory is determined at the subcellular level, underlie the risk for schizophrenia, and the development of clinical manifestations of disease symptoms, ie its manifestation is influenced by stress factors causing decompensation respective imperfect structures.

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