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Chapter: Psychiatric Mental Health Nursing : Schizophrenia

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Etiology - Schizophrenia

When question for researchers and clinicians for as long as they have studied the illness.

ETIOLOGY

When question for researchers and clinicians for as long as they have studied the illness. In the first half of the 20th cen-tury, studies focused on trying to find a particular patho-logic structure associated with the disease, largely through autopsy. Such a site was not discovered. In the 1950s and 1960s, the emphasis shifted to examination of psychologi-cal and social causes. Interpersonal theorists suggested that schizophrenia resulted from dysfunctional relation-ships in early life and adolescence. None of the interpersonal theories has been proved, and newer scientific studies are finding more evidence to support neurologic/neurochemi-cal causes. However, some therapists still believe that schizophrenia results from dysfunctional parenting or family dynamics. For parents or family members of per-sons diagnosed with schizophrenia, such beliefs cause agony over what they did “wrong” or what they could have done to help prevent it.

 

Newer scientific studies began to demonstrate that schizophrenia results from a type of brain dysfunction. In the 1970s, studies began to focus on possible neurochemi-cal causes, which remain the primary focus of research and theory today. These neurochemical/neurologic theories are supported by the effects of antipsychotic medications, which help to control psychotic symptoms, and neuroimag-ing tools such as computed tomography, which have shown that the brain of people with schizophrenia differs in struc-ture and function from the brain of control subjects.Whether schizophrenia is an organic disease with under-lying physical brain pathology has been an important question for researchers and clinicians for as long as they have studied the illness. In the first half of the 20th cen-tury, studies focused on trying to find a particular patho-logic structure associated with the disease, largely through autopsy. Such a site was not discovered. In the 1950s and 1960s, the emphasis shifted to examination of psychologi-cal and social causes. Interpersonal theorists suggested that schizophrenia resulted from dysfunctional relation-ships in early life and adolescence. None of the interpersonal theories has been proved, and newer scientific studies are finding more evidence to support neurologic/neurochemi-cal causes. However, some therapists still believe that schizophrenia results from dysfunctional parenting or family dynamics. For parents or family members of per-sons diagnosed with schizophrenia, such beliefs cause agony over what they did “wrong” or what they could have done to help prevent it.

 

Newer scientific studies began to demonstrate that schizophrenia results from a type of brain dysfunction. In the 1970s, studies began to focus on possible neurochemi-cal causes, which remain the primary focus of research and theory today. These neurochemical/neurologic theories are supported by the effects of antipsychotic medications, which help to control psychotic symptoms, and neuroimag-ing tools such as computed tomography, which have shown that the brain of people with schizophrenia differs in struc-ture and function from the brain of control subjects.


Biologic Theories

 

The biologic theories of schizophrenia focus on genetic factors, neuroanatomic and neurochemical factors (struc-ture and function of the brain), and immunovirology (the body’s response to exposure to a virus).

 

Genetic Factors

 

Most genetic studies have focused on immediate families (i.e., parents, siblings, and offspring) to examine whether schizophrenia is genetically transmitted or inherited. Few have focused on more distant relatives. The most important studies have centered on twins; these findings have demon-strated that identical twins have a 50% risk for schizophre-nia; that is, if one twin has schizophrenia, the other has a 50% chance of developing it as well. Fraternal twins have only a 15% risk (Kirkpatrick & Tek, 2005). This finding indicates that schizophrenia is at least partially inherited.

 

Other important studies have shown that children with one biologic parent with schizophrenia have a 15% risk; the risk rises to 35% if both biologic parents have schizophre-nia. Children adopted at birth into a family with no history of schizophrenia but whose biologic parents have a history of schizophrenia still reflect the genetic risk of their biologic parents. All these studies have indicated a genetic risk or tendency for schizophrenia, but genetics cannot be the only factor: identical twins have only a 50% risk even though their genes are 100% identical (Riley & Kendler, 2005).

 

Neuroanatomic and Neurochemical Factors

 

With the development of noninvasive imaging techniques such as computed tomography, magnetic resonance imag-ing, and positron emission tomography in the past 25 years, scientists have been able to study the brain structure (neu-roanatomy) and activity (neurochemistry) of people with schizophrenia. Findings have demonstrated that people with schizophrenia have relatively less brain tissue and cerebrospinal fluid than those who do not have schizophre-nia (Schneider-Axmann et al., 2006); this could represent a failure in the development or a subsequent loss of tissue. Computed tomography scans have shown enlarged ventri-cles in the brain and cortical atrophy. Positron emission tomography studies suggest that glucose metabolism and oxygen are diminished in the frontal cortical structures of the brain. The research consistently shows decreased brain volume and abnormal brain function in the frontal and temporal areas of persons with schizophrenia. This pathol-ogy correlates with the positive signs of schizophrenia (temporal lobe), such as psychosis, and the negative signs of schizophrenia (frontal lobe), such as lack of volition or motivation and anhedonia. It is unknown whether these changes in the frontal and temporal lobes are the result of a failure of these areas to develop properly or if a virus, trauma, or immune response has damaged them. Intrauter-ine influences such as poor nutrition, tobacco, alcohol, and other drugs, and stress also are being studied as possiblecauses of the brain pathology found in people with schizo-phrenia (Buchanan & Carpenter, 2005).

 

Neurochemical studies have consistently demonstrated alterations in the neurotransmitter systems of the brain in people with schizophrenia. The neuronal networks that transmit information by electrical signals from a nerve cell through its axon and across synapses to postsynaptic recep-tors on other nerve cells seem to malfunction. The trans-mission of the signal across the synapse requires a complex series of biochemical events. Studies have implicated the actions of dopamine, serotonin, norepinephrine, acetyl-choline, glutamate, and several neuromodulary peptides.

 

Currently, the most prominent neurochemical theories involve dopamine and serotonin. One prominent theory suggests excess dopamine as a cause. This theory was devel-oped based on two observations: First, drugs that increase activity in the dopaminergic system, such as amphetamine and levodopa, sometimes induce a paranoid psychotic reac-tion similar to schizophrenia. Second, drugs blocking post-synaptic dopamine receptors reduce psychotic symptoms; in fact, the greater the ability of the drug to block dopamine receptors, the more effective it is in decreasing symptoms of schizophrenia (Buchanan & Carpenter, 2005).

 

More recently, serotonin has been included among the leading neurochemical factors affecting schizophrenia. The theory regarding serotonin suggests that serotonin modu-lates and helps to control excess dopamine. Some believe that excess serotonin itself contributes to the development of schizophrenia. Newer atypical antipsychotics, such as clozapine (Clozaril), are both dopamine and serotonin antagonists. Drug studies have shown that clozapine can dramatically reduce psychotic symptoms and ameliorate the negative signs of schizophrenia (Kane & Marder, 2005).

 

Researchers also are exploring the possibility that schizophrenia may have three separate symptom com-plexes or syndromes: hallucinations/delusions, disorgani-zation of thought and behavior, and negative symptoms (Buchanan & Carpenter, 2005). Investigations show that the three syndromes relate to neurobiologic differences in the brain. It is postulated that schizophrenia has (these three) subgroups, which may be homogeneous relative to course, pathophysiology, and, therefore, treatment.

 

Immunovirologic Factors

 

Popular theories have emerged stating that exposure to a virus or the body’s immune response to a virus could alter the brain physiology of people with schizophrenia. Although scientists continue to study these possibilities, few findings have validated them.

 

Cytokines are chemical messengers between immune cells, mediating inflammatory and immune responses. Specific cytokines also play a role in signaling the brain to produce behavioral and neurochemical changes needed in the face of physical or psychological stress to maintain homeostasis. It is believed that cytokines may have a role in the development of major psychiatric dis-orders such as schizophrenia (Brown, Bresnahan, & Susser, 2005).

 

Recently, researchers have been focusing on infections in pregnant women as a possible origin for schizophrenia. Waves of schizophrenia in England, Wales, Denmark, Finland, and other countries have occurred a generation after influenza epidemics. Also, there are higher rates of schizophrenia among children born in crowded areas in cold weather, conditions that are hospitable to respiratory ailments (Brown, Bresnahan, & Susser, 2005).

 

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