Schizophrenia possible causes

If schizophrenia is caused by abnormal early brain development (cf. Figs. 10—15 and 10—16), it may be virtually impossible to reverse such abnormalities in adulthood. On the other hand, some day it may be possible to compensate for such postulated neurodevelopmental difficulties by other mechanisms or to interrupt an ongoing mechanism still present in the symptomatic patient. Therefore, it will be critical to learn what neurodevelopmental abnormalities may exist in schizophrenia in order to devise strategies for reducing their potential impact. It may even be possible to identify such abnormalities in presymptomatic individuals or to exploit the plasticity of adult neurons to compensate for neurodevelopmentally endowed dysfunction. These are bold and unsubstantiated theoretical extrapolations based on... 

Q9 Schizophrenia appears to involve both genetic and environmental factors. Possible causes of schizophrenia are ... 

I look at many possible causes of fetal damage in this book, but give particular emphasis to man-made environmental toxins, be they chemical pollutants in our air, water, and land, or substances in the consumer marketplace, legal and otherwise. The effects of these toxins are often connected to more than one type of fetal damage. Prenatal exposure to lead, for example, is connected to postnatal occurrences of lower IQ, ADHD, and schizophrenia, usually in different individuals. Prenatal exposure to tobacco smoke, as another example, is connected to a host of effects with adverse postnatal consequences as well. The effects of both sorts of toxins can also be related to other fetal impacts, which in turn are often connected to important social... 

The postulation of a possible role of trace amines in the context of schizophrenia was kindled early on by the structural similarity between PEA and amphetamine. Symptoms such as hallucinations and paranoid episodes caused by a prolonged amphetamine intoxification are reminiscent of patients suffering from acute schizophrenia. Further support for a role of trace amines in the context of schizophrenia comes from clinical studies... 

Possibly increased DA function is not the actual cause of schizophrenia and its symptoms are just mediated by normally functioning DA systems that appear overactive because of the loss of some counteracting function or other NT(s). To date there is no evidence to fully implicate any other NT but there is growing interest in 5-HT and glutamate (see below). 

Faulty Wiring and/or Developmental Delay. Remember that neurotransmission moves through brain circuits. Some mental illnesses may be caused by misconnections in the circuitry that can result in the brain s equivalent of crosstalk that occurs when telephone lines are crossed. Examples of this problem are the so-called neurodevelopmental disorders such as autism, certain forms of mental retardation, and possibly schizophrenia. 

Because of the brain s complexity, physicians and researchers have not made as much progress as they would like in efforts to understand disorders such as depression and schizophrenia. Scientists have been studying schizophrenia and related illnesses since before Bleuler s time, but as yet no one knows what causes schizophrenia. The symptoms of the disease usually make their initial appearance early in the patient s life. Since schizophrenia runs in families, there is a genetic component to the disease. It is possible that problems arise in the early stages of development, possibly due to faulty genes or perhaps in part due to exposure to environmental toxins, which fester imtil the disease arises in yoimg adulthood. 

Many researchers have come to believe that schizophrenia is a complex disease, possibly with a number of different causes or courses. PET studies of schizophrenia have found possible contributions of other receptors, including the dopamine D receptor as well as receptors for other neurotransmitters such as glutamate. Genetic researchers are searching for the genes involved in the expression and regulation of these receptors, any or all of which may be involved in some number of patients. 

Shortly after iproniazid was shown to have antidepressant properties, imipramine was introduced as the first tricyclic antidepressant. These drugs received the name tricyclic because their structure contains three molecular rings. At first, imipramine was investigated as a possible treatment for the psychotic episodes associated with schizophrenia, a severe mental disorder that causes hallucinations and delusions, because it was chemically similar to another effective anti-schizophrenia drug. Imipramine did not reduce the severity of psychotic episodes, but it did elevate the mood of the patients who took it. In the late 1950s, it was released in the United States under the name Tofranil for the treatment of depression. 

Whereas the development of classic disorders such as schizophrenia in a dying patient with no previous history is an unlikely occurrence, many symptoms, such as hallucinations, delusions, and disordered thinking, are commonly encountered. Some episodes may be reversible and, when the causative source is recognized, can be readily treated by the physician. For example, high-dose steroids are often used to manage metastatic brain lesions, but it is also well known that they can induce a psychotic state. Simply reducing the dose, when possible, may quickly abort a psychotic episode. 

FIGURE 10—34. Neurodegenerative causes of schizophrenia may lead to a final common pathway either of neuronal death or possibly of destruction of synapses and the axons and dendrites of such synapses. The causes can range from predetermined genetic programming of neuronal or synaptic destruction to fetal insults such as anoxia, infection, toxins, or maternal starvation to perhaps a destructive effect of the positive symptoms themselves on synapses and neurons via glutamate-mediated excitotoxicity. 

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