![]() ![]() 9 If both parents have schizophrenia, the risk that they will produce a child with schizophrenia is approximately 40%. 9 In the case of monozygotic twins, the risk of one twin having schizophrenia is 48% if the other has the disorder, whereas the risk is 12% to 14% in dizygotic twins. Scientific evidence supports the idea that genetic factors play an important role in the causation of schizophrenia 2 studies have shown that the risk of illness is approximately 10% for a first-degree relative and 3% for a second-degree relative. 3 Infections and excess stress levels during this period have been linked to a doubling of the risk of offspring developing schizophrenia. 2 Fetal disturbances during the second trimester-a key stage in fetal neurodevelopment-have been of particular interest to researchers. 6 Obstetric complications, including bleeding during pregnancy, gestational diabetes, emergency cesarean section, asphyxia, and low birth weight, have been associated with schizophrenia later in life. One explanation for the development of schizophrenia is that the disorder begins in utero. It is widely accepted, however, that the various phenotypes of the illness arise from multiple factors, including genetic susceptibility and environmental influences. 2ĭespite more than a century of research, the precise cause of schizophrenia continues to elude investigators. For example, in addition to an increase in the size of the third and lateral ventricles, individuals at high risk of a schizophrenic episode have a smaller medial temporal lobe. The brain tissue itself appears to undergo detectable physical changes in patients with schizophrenia. 6 This, in turn, suggested that NMDA receptors are inactive in the normal regulation of mesocortical dopamine neurons, and pointed to a possible explanation for why patients with schizophrenia exhibit negative, affective, and cognitive symptoms. This theory arose in response to the finding that phenylciclidine and ketamine, two noncompetitive NMDA/glutamate antagonists, induce schizophrenia-like symptoms. 1Īnother theory for the symptoms of schizophrenia involves the activity of glutamate, the major excitatory neurotransmitter in the brain. ![]() The newer compounds were found to be effective in alleviating both the positive and negative symptoms of schizophrenia. 1 Subsequent research led to the development of drug compounds that blocked both dopamine and serotonin receptors, in contrast to older medications, which affected only dopamine receptors. The serotonin hypothesis for the development of schizophrenia emerged as a result of the discovery that lysergic acid diethylamide (LSD) enhanced the effects of serotonin in the brain. A decrease or blockade of tuberoinfundibular dopamine results in elevated prolactin levels and, as a result, galactorrhea, ammenorrhea, and reduced libido. The tuberoinfundibular pathway projects from the hypothalamus to the pituitary gland. Negative symptoms and cognitive deficits in schizophrenia are thought to be caused by low mesocortical dopamine levels. 1 The mesocortical pathway extends from the VTA to the cortex. 1 The mesolimbic pathway, extending from the ventral tegmental area (VTA) to limbic areas, may play a role in the positive symptoms of schizophrenia in the presence of excess dopamine. Low dopamine levels within this pathway are thought to affect the extrapyramidal system, leading to motor symptoms. 4, 5 The nigrostriatal pathway originates in the substantia nigra and ends in the caudate nucleus. Four dopaminergic pathways have been implicated ( Figure 1). 1Ībnormal activity at dopamine receptor sites (specifically D 2) is thought to be associated with many of the symptoms of schizophrenia. Other theories implicate aspartate, glycine, and gamma-aminobutyric acid (GABA) as part of the neurochemical imbalance of schizophrenia. Most of these theories center on either an excess or a deficiency of neurotransmitters, including dopamine, serotonin, and glutamate. ![]() Abnormalities in neurotransmission have provided the basis for theories on the pathophysiology of schizophrenia. ![]()
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