pathophysiology of schizophrenia

  1. 0
    hello to all!
    anyone here who could help me to make the pathophysiology of schizophrenia?
    tnx!!!!
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  4. 2
    Neurochemical factors likely involve dopamine, serotonin, norepinephrine, glutamate, and gamma-aminobutyric acid neurotransmission. Glutamate (glu), involved in learning and memory, may be responsible for some of the cognitive symptoms; glu is necessary for the breakdown of dopamine and other transmitters, which affects the efficiency of prefrontal information processing. Excessively high levels of norepinephrine are associated with positive symptoms, while paranoid symptoms have been related to increased dopamine aactivity. No single neurotransmitter is clearly responsible for schizophrenia.
    Schizophrenia often disrupts the filtering process, causing sensory overload; when there are too many messages arriving at the cortex at the same time, thinking becomes disorganized and fragmented.
    Hope that's a start.
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  5. 2
    Besides the neurochemical link, there is thought to be a genetic link. But it is not linked to just one gene, mutiple genes located on different chromonsomes are thought to be involved. And there is also a school of thought that pregnant women who suffer a viral infection during their pregnancy are thought to give birth to children that run a higher risk. And prenatal nutritional deficiencies are thought to increase the child's risk.

    Woody
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  6. 3
    here is the information i have on this:
    (from nurse's 5-minute clinical consult: diseases from lippincott williams & wilkins, page 714):
    • "a biochemical hypothesis holds that schizophrenia results from excessive activity at dopaminergic synapses
    • other neurotransmitter alternations may also contribute to schizophrenic symptoms
    • structural abnormalities of the intraventricular system, temporal lobe abnormalities, decreased volume of the amygdala and hippocampus of the limbic system, structural changes in prefrontal white matter, and increased volume of the basal ganglia have been found."
    (from pathophysiology: the biologic basis for disease in adults and children, third edition, by kathryn l. mccance and sue e. heuther, pages 574 - 579):
    ". . .adoption studies...indicate a genetic predisposition to acquire schizophrenia. when adopted into normal families at an early age, children whose biologic parents were schizophrenic are still more likely to acquire the disease than adopted children from normal parents...it is also clear, however, from these studies that schizophrenia is not entirely a genetic disorder. in monozygotic twins there is at least a 50% nongenetic contribution to the disease and an even higher environmental contribution among nonidentical siblings.

    the current leading hypothesis for the development of schizophrenia suggests that the illness results from neurodevelopmental defects occurring during fetal life. within this neurodevelopmental framework, several hypotheses are proposed that may link an early developmental event to the eventual occurrence of schizophrenia. these include early exposure to a viral infection, prenatal nutritional deficiencies and perinatal complications.

    viral infection
    a virus is one possible culprit that may damage the brain during a critical period of development. . .was first reported. . .based on a study of finnish women exposed to the type a2 influenza virus during the second trimester of pregnancy. . .[and] diagnosis of their offspring in adulthood indicated a disproportionate increase in schizophrenia. . .viral-induced disruption of these neurodevelopmental processes may lead to the structural brain abnormalities observed in schizophrenic individuals. subsequent studies. . .have produced a number of inconsistent results. study differences may stem from unrecognized factors, such as the condition of prenatal nutrition and availability of medication. . .

    nutritional deficiency
    prenatal nutritional deficiencies increase the risk of neurodevelopmental disorders. . .recent work suggests that early prenatal nutritional deficiency may contribute also to an increased risk for schizophrenia. . .this association between prenatal nutritional deficiency and elevated risk of developing schizophrenia was obtained from an examination of records of persons born during the dutch hunger winter of 1944/1945, near the end of world war ii [when] the nazi blockade of the western netherlands led to a severe famine. at this time the exposed population received between 500 and 1000 calories per day. the risk for schizophrenia was determined on the basis of comparing medical records of exposed and unexposed birth cohorts. the study revealed that both males and females conceived at the height of the famine had a twofold increased risk for hospitalized schizophrenia in adulthood. . .implications of these results are that proper nutrition during pregnancy would substantially reduce the likelihood of developing schizophrenia [but] further information is required to determine the nutritional factor or factors that need to be monitored. . .

    other developmental factors
    perinatal complications such as. . .hypoxia, may be associated with increased risk of schizophrenia. in the case of hypoxia, some studies point to its effects on altering brain dopamine function. perinatal complications are associated also with an increased incidence of schizophrenia among individuals born during the winter months. . .one cause of hypoxia is rh incompatibility resulting in hemolytic disease of the fetus and newborn. . .[where] the fetus and newborn may be exposed to severe anemia and hypoxia, resulting in permanent neurologic damage. a recent study demonstrated that rh-incompatible pregnancies produced up to a twofold increased risk of schizophrenia among male offspring.

    several structural and functional abnormalities are found in the brain of individuals with schizophrenia. among the most prominent structural brain abnormalities in some affected individuals is the enlargement of the lateral and third ventricles and widening of fissures and sulci in the frontal cortex. in addition, individuals with schizophrenia may exhibit decreased cerebral blood flow to the frontal cortex and reduction in size of the temporal lobe.

    increased ventricular volume is associated with a reduction in cortical matter, such as the frontal lobes. . .no relationship has been found between ventricular size and duration of schizophrenia. hence, the neuropathologic condition is not progressive in adulthood and occurs well before the onset of schizophrenic symptoms. . .some studies suggest a relationship between poor social adjustment in childhood and the subsequent development of schizophrenia. the child may become withdrawn and fearful and report events that do not make sense. children who eventually develop schizophrenia are also likely to manifest negative symptoms and exhibit ventricular enlargement.

    postmortem brain examination of schizophrenic individuals provides a wealth of evidence consistent with an early neurodevelopmental defect. histologic analyses of the hippocampal formation, which is in the temporal lobe, indicate a marked reduction in dentate granule cell density and a disarray of pyramidal cells in the horn of ammon. in addition, a significant reduction is found in cell density and volume of the entorhinal cortex, a major subfield of the hippocampal formation receiving diverse cortical information. the reduction in cell size and number probably contributes to the overall decrease in temporal lobe volume. these structural and cellular abnormalities are believed to originate prenatally, most likely during a period of hippocampal cell proliferation and migration. . .an interaction of genetic and environmental factors (famine, hypoxia) during pregnancy may be responsible for producing these hippocampal alterations. . .

    investigators are examining closely. . .the dysfunction and pathologic findings occurring in the dorsolateral prefrontal cortex (dlpfc). this prefrontal region, which corresponds to brodmann area 9, appears to play an important role in both the origin and course of [schizophrenia]. . .data suggests that negative symptoms of schizophrenia, including the loss of affect and cognitive functions, are a result of dlpfc dysfunction.

    one of the prominent theories of the pathophysiology underlying schizophrenia initially was based on pharmacologic actions of antipsychotic medications. the dopamine hypothesis of schizophrenia suggests that an abnormal elevation in dopaminergic transmission contributes to the onset of schizophrenia. this hypothesis was formulated on the basis of studies indicating that antipsychotic drugs are potent blockers of brain dopamine receptors. a strong positive correlation is found between the clinical potencies of antipsychotic drugs and their affinity for the dopamine d2 receptor. in addition, drugs that increased dopaminergic transmission, such as levodopa (l-dopa), cocaine, and amphetamine, produced schizophrenic-like psychosis and these drug-induced psychotic states are reversed by dopamine blockers.

    additional evidence revealed that brain concentrations of dopamine or its metabolite, homovanillic acid, were increased in individuals with schizophrenia post mortem studies further indicate an increased density of d2 receptors in brain regions, including the caudate nucleus and nucleus accumbens. some neuroimaging studies have confirmed the increase in d2 receptors in schizophrenia, especially in individuals manifesting prominent positive symptoms.

    additional investigations suggested that different dopaminergic systems contribute in different ways to the pathophysiology of schizophrenia. for example, the mesocortical dopamine system plays an essential role in dlpfc functions. depletion of dopamine in the prefrontal cortex of monkeys produces deficits in cognition and affect. some investigators believe that negative symptoms of schizophrenia may result from decreased dopaminergic transmission in the frontal cortex. . .although evidence supporting the dopamine hypothesis of schizophrenia is strong, data indicate that dysregulation of d2 receptors cannot account for all aspects of schizophrenia. whereas the pharmacologic blockade of d2 receptors occurs rapidly, clinical effects do not appear until after 1 to 2 weeks of treatment. hence, the antipsychotic effects are not related directly to d2 blockade or acute suppression of dopamine hypersecretion."
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  7. 0
    hello everyone..anyone who could help me about the pathophysiology of residual type of schizophrenia?
  8. 0
    are the brains of people with schizohrenia looks different?what are the diffrences of the brain with schizophrenia to normal brain?thanks


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