Schizophrenia: Description, Etiology, and Treatment About 1%

Schizophrenia: Description, Etiology, And Treatment

About 1% to 2% of the U.S. population may suffer from schizophrenic disorders (Weiten, 2007; Rosenzweig, Breedlove, & Leiman, 2002). Usually emerging during adolescence or early adulthood and only infrequently after age 45, victims of schizophrenia usually evidence a history of peculiar behavior and of cognitive and social deficits. The onset of schizophrenia itself may be gradual or sudden, and once it emerges results of treatment vary. Some patients - approximately 15%-20% - have complete recovery; these likely have had milder symptoms (Weiten, 2007). Others experience a partial recovery intermittently receiving hospital care for the remainder of their lives. Whilst the third group of schizophrenic patients endures chronic illness that occasionally results in permanent hospitalization.

First publicized by Emil Kraeplin in his book Daementia praecox and aparaphrenia (1919), Kraeplin entitled schizophrenia dementia praecox, since he considered it a disorder that originated in adolescence and was genetic in origin. Its current appellation, schizophrenia, was invented by Eugene Bleuler in his monograph Dementia praecox: or, the group of Schizophrenias (1952). Schizophrenia itself means 'Split mind' or dissasociative thinking represented by Bleuler according to the four As: loosening of associations, autism (i.e. contrary to reality), affective disturbance, and ambivalence. These characteristics can be seen in the following quote extracted from a case history (adapted from Sheehan, 1982)

"Mick Jagger wants to marry me,… Mick Jagger is St. Nicholas and the Maharishi is Santa Claus. I want to form a gospel rock group called the Thorn Oil.. Teddy Kennedy cured me of my ugliness. I'm pregnant with the Son of God. Divorce isn't a piece of paper, it's a feeling, Forget about Zip Codes. I need shock treatments. The body is run by electricity. My wiring is all faulty (Sheehan 1982, pp, 104-105).

What you have here is an instance of dissociated thinking, shot through by delusions. Thinking is chaotic rather than logical and linear, and the person -- typical of schizophrenic individual -- shifts topics in disjointed ways.

Other symptoms include noticeable deteriorating of adaptive behavior in work, social relations, and personal care; hallucinations (most commonly, auditory; these voices may be insulting, argumentative or imperative); and disturbed emotion where victims become emotionally volatile or show little emotional responsiveness, although internally they are as emotional as ever.

These and other distinct schizophrenic syndromes, have been delineated and categorized by the 1994 Diagnostic and Statistical Manual of Mental Disorders: DSM-IV of the American Psychiatric Association in order for clinicians to arrive at clear diagnosis.

Four subtypes of schizophrenia are recognized including an undifferentiated type for individuals who do not belong to the previous three categories. The three types are as follows (Weiten, 2007:

1. Paranoid schizophrenia where people have delusions of persecution along with delusions of grandeur. John Nash in the Beautiful Mind is a famous example of this type of schizophrenia.

2. Catatonic schizophrenia indicating extreme motor disturbances, ranging from muscular rigidity to random motor activity. Some go into a catatonic stupor (an extreme form of withdrawal), whilst others become hyperactive and incoherent (called catatonic excitement).

3. Disorganized schizophrenia has symptoms that include emotional indifference, frequent incoherence, and virtually complete social withdrawal, delusions often center on bodily functions.

Some researchers have proposed two groups of schizophrenia: positive and negative. Positive symptoms refer to abnormal states such as hallucinations, delusions, and catotonic excitement, whereas negative symptoms include slow and impoverished thought and speech, emotional and social withdrawal, blunted affect. However, most researchers continue to question whether schizophrenia can be neatly packaged into these two categories. After all, most patients exhibit both types of symptoms and vary only in the degree to which positive or negative type dominates. Nevertheless, one thing is clear: Schizophrenia is a universal disorder.

Etiology of Schizophrenia

1. Genetic:

Hereditary, certainly, seems to indicate a role in the development of schizophrenia. Concordance rates average 48% for identical twins in comparison to 17% for fraternal twins, whilst a child born to two schizophrenic parents has as much as a 46% chance of acquiring schizophrenia (Pinel, 2006). Many questions, however, still remain unanswered, not least being: How is the disorder transmitted? And what is being inherited? No single gene causes schizophrenia, so which genes are related to this disorder?

2. Structural abnormalities in brain

Postmortem studies corroborated by CT scans and MRI images show structural changes in the brains of individuals with schizophrenia. The cerebral ventricles, particularly the lateral ventricles, demonstrate an enlargement, although this is not clear whether this is a result of the disease or origin of the disease. There is also limbic system abnormality. More than 75% of discordant twins for instance show a marked difference in the size of the amygdale and the hippocampus, with the limbic system in the twin with schizophrenia smaller in size, likely due to attrition (Rosenzweig, Breedlove, & Leiman, 2002). Some of these changes, it is posited, might arise early in development, even in the prenatal period. There are also possible frontal cortical abnormalities, as well as cellular differences, and reduced metabolic activity in areas of the prefrontal cortex (Pinel, 2006).

3. Neurodevelopmental hypothesis

Evidence seems to indicate that schizophrenia might be caused by insults to brain before or during the birth process, which makes individuals vulnerable to schizophrenia later on. Studies of pre-or postnatal viral infections, malnutrition, or obstetrical complications support this hypothesis.

4. Neurochemical factors

The dopamine hypothesis asserts that excessive dopamine activity or excessive postsynaptic sensitivity to dopamine (especially by D2 receptors rather than at dopamine receptors in general) may be the neurochemical basis for schizophrenia. Indeed drugs that lower dopamine level, seem to positively affect schizophrenia (although that is not so clear: studies in the 1980s revealed that some patients with schizophrenia show no changes when treated with such drugs (Rosenzweig, Breedlove, & Leiman, 2002) but the evidence linking schizophrenia to high dopamine levels is contradictory and inconclusive. Clozapine, the antipsychotic drug, for instance, increases dopamine release, whilst many patients with schizophrenia have normal levels of dopamine in cerebrospinal fluid, and some postmortem and PET observations reveal an increase in dopamine receptors in patients who have been off neuroleptic drugs for some time. Currently, it is believed that excessive activity at D2 receptors is involved in the disorder but that there are other, as yet unidentified, causal factors. Serontonin, GABA, and glutamate are three of several other neurotransmitter systems that may be contributory too. Another factors contributory to relapse seems to be high stress that not only causes vulnerability to disease but also impels relapse (Pinel, 2006; Weiten, 2007). (In fact, people raised in the city are more likely to develop schizophrenia than rural dwellers. (Rosenzweig, Breedlove, & Leiman, 2002).

Treatment