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A Summary Report of Abnormal Psychology:

Prevalence and Causes of Schizophrenia

Alyzza Jane G. Buna

PSY109 Abnormal Psychology

Professor Weigela Shaeina Besar

January 17, 2022

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Abstract

Schizophrenia is characterized by a broad spectrum of cognitive and emotional dysfunctions that

include delusions and hallucinations, disorganized speech and behavior, and inappropriate

emotions. A number of causative factors have been implicated for schizophrenia, including

genetic influences, neurotransmitter imbalances, structural damage to the brain caused by a

prenatal viral infection or birth injury, and psychological stressors. Relapse appears to be

triggered by hostile and critical family environments characterized by high expressed emotion.

Treatment typically involves antipsychotic drugs that are usually administered with a variety of

psychosocial treatments, with the goal of reducing relapse and improving skills in deficits and

compliance in taking the medications. The effectiveness of treatment is limited, because

schizophrenia is typically a chronic disorder.

Keywords: Schizophrenia, relapse, antipsychotic drugs,

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Schizophrenia

Schizophrenia is characterized by a broad spectrum of cognitive and emotional

dysfunctions that include delusions and hallucinations, disorganized speech and behavior, and

inappropriate emotions.

Prevalence And Causes of Schizophrenia

Studying schizophrenia reveals the many levels on which we must decipher what makes

us behave the way we do. To uncover the causes of this disorder, researchers look in several

areas: (1) the possible genes involved in schizophrenia, (2) the chemical action of the drugs that

help many people with this disorder, (3) abnormalities in the working of the brains of people

with schizophrenia, and (4) environmental risk factors that may precipitate the onset of the

symptoms (Harrison, 2012; Murray & Castle, 2012).

 Schizophrenia is roughly equivalent for men and women, and it is estimated to be 0.2%

to 1.5% in the general population. Schizophrenia is generally chronic, and most people with the

disorder have a difficult time functioning in society. Unlike the delusions of people with other

psychotic disorders, the delusions of people with schizophrenia are likely to be outside the realm

of possibility. Finally, even when individuals with schizophrenia improve with treatment, they

are likely to experience difficulties throughout their lives.

 Up to 85% of people who later develop schizophrenia go through a prodromal stage—a

1- to 2-year period before the serious symptoms occur but when less severe yet unusual

behaviors start to show themselves (Jablensky, 2012). Schizotypal personality disorders include

ideas of reference (thinking insignificant events relate directly to them), magical thinking

(believing they have special abilities such as being clairvoyant or telepathic), and illusions.
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Common symptoms include isolation, marked impairment in functioning, and a lack of initiative,

interests, or energy.

 Once the symptoms of schizophrenia develop, it typically takes 1–2 years before the

person is diagnosed and receives treatment (Woods et al., 2001).

 Schizophrenia is so complex, the diagnosis itself can be controversial. Some have argued

that "schizophrenia" does not really exist but is a derogatory label for people who behave in

ways outside the cultural norm. We now know that people in extremely diverse cultures have the

symptoms of schizophrenia, which supports the notion that it is a reality for many people

worldwide. Schizophrenia is thus universal, affecting all racial and cultural groups studied so far.

 Despite the possibility that schizophrenia may be several different disorders, we can

safely make one generalization: Genes are responsible for making some individuals vulnerable to

schizophrenia. We look at a range of research findings from family, twin, adoptee, offspring of

twins, and linkage and association studies. We conclude by discussing the compelling reasons

that no one gene is responsible for schizophrenia; rather, multiple gene variances combine to

produce vulnerability (Murray & Castle, 2012).

Neurobiological Influences

Dopamine. In schizophrenia, attention has focused on several dopamine sites, in

particular those referred to simply as D1 and D2.

In a story that resembles a mystery plot, several pieces of “circumstantial evidence” are

clues to the role of dopamine in schizophrenia:

1. Antipsychotic drugs (neuroleptics) often effective in treating people with schizophrenia are

dopamine antagonists, partially blocking the brain’s use of dopamine (Creese, Burt, & Snyder,

1976; Seeman, Lee, Chau Wong, & Wong, 1976).

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2. These neuroleptic drugs can produce negative side effects similar to those in Parkinson’s

disease, a disorder known to be caused by insufficient dopamine.

3. The drug L-dopa, a dopamine agonist used to treat people with Parkinson’s disease, produces

schizophrenia-like symptoms in some people (Davidson et al., 1987).

4. Amphetamines, which also activate dopamine, can make psychotic symptoms worse in some

people with schizophrenia (van Kammen, Docherty, & Bunney, 1982).

In other words, when drugs are administered that are known to increase dopamine (agonists),

there is an increase in schizophrenic behavior; when drugs that are known to decrease dopamine

activity (antagonists) are used, schizophrenic symptoms tend to diminish.

Brain Structure. Ventricle enlargement is not seen in everyone who has schizophrenia.

Studies show that some individuals with schizophrenia show hyper frontality (that is, too much

activity), indicating that the dysfunction is reliable, but hyper frontality displays itself differently

in different people (Callicott et al., 2003; Garrity et al., 2007). It appears that several brain sites

are implicated in the cognitive dysfunction observed among people with schizophrenia,

especially the prefrontal cortex, various related cortical regions, and subcortical circuits,

including the thalamus and the stratum (Shenton & Kubicki, 2009).

Prenatal and Perinatal Influences. Fetal exposure to viral infection, pregnancy

complications, and delivery complications are among the environmental influences that seem to

affect whether or not someone develops schizophrenia. Several studies have shown that

schizophrenia may be associated with prenatal exposure to influenza.

The indications that virus like diseases may cause damage to the fetal brain, which later

may cause the symptoms of schizophrenia, are suggestive and may help explain why some

people with schizophrenia behave the way they do (Murray & Castle, 2012).
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Psychological and Social Influences

Stress. It is important to learn how much and what kind of stress makes a person with a

predisposition for schizophrenia develop the disorder. Researchers have studied the effects of a

variety of stressors on schizophrenia. Living in a large city, for example, is associated with an

increased risk of developing schizophrenia—suggesting the stress of urban living may precipitate

its onset (Boydell & Allardyce, 2012).

Families and Relapse. A great deal of research has studied how interactions within the

family affect people who have schizophrenia. Double bind communication was used to portray a

communication style that produced conflicting messages, which, in turn, caused schizophrenia to

develop (Bateson, 1959). Additional research results indicated that if the levels of criticism

(disapproval), hostility (animosity), and emotional overinvolvement (intrusiveness) expressed by

the families were high, patients tended to relapse (Brown, Monck, Carstairs, & Wing, 1962).

Cultural variations in how families react to someone with schizophrenia and their reactions do

not cause the disorder (Singh, Harley, & Suhail, 2013).

Treatment of Schizophrenia

Biological Interventions. Insulin coma therapy was thought for a time to be helpful, but

closer examination showed it carried great risk of serious illness and death. During this time,

psychosurgery, including prefrontal lobotomies, was introduced, and in the late 1930s,

electroconvulsive therapy (ECT) was advanced as a treatment for schizophrenia. As with earlier

drastic treatments, initial enthusiasm for ECT faded because it was found not to be beneficial for

most people with schizophrenia.

Antipsychotic Medications. Neuroleptics provided the first real hope that help was

available for people with schizophrenia. When they are effective, neuroleptics help people think
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more clearly and reduce hallucinations and delusions. They work by affecting the positive

symptoms (delusions, hallucinations, and agitation) and to a lesser extent the negative and

disorganized ones, such as social deficits.

The earliest neuroleptic drugs, called conventional or first-generation antipsychotics (such as

Haldol and Thorazine), are effective for approximately 60%-270% of people who try them

(Cunningham Owens & Johnstone, 2012). Many people are not helped by antipsychotics,

however, or they experience unpleasant side effects.

Psychosocial Interventions. Research suggests that individual social skills training,

family intervention, and vocational rehabilitation may be helpful additions to biological (drug)

treatment for schizophrenia. Significant relapses may be avoided or delayed by such

psychosocial interventions. Some research indicates that participation may help reduce relapses,

but as it is also possible that those who participate may be a special group of individuals, it is

difficult to interpret improvements (Goering et al., 2006). Because schizophrenia is a complex

disorder that affects multiple areas of functioning, effective treatment is carried out at several

levels.

Treatment across Cultures. Treatment for the symptoms of schizophrenia vary widely by

culture— from humane approaches using empirically validated interventions to simply removing

the person from society.

Prevention

One strategy for preventing a disorder such as schizophrenia— which typically first

shows itself in early adulthood—is to identify and treat children who may be at risk for getting

the disorder later in life.

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One approach to prevention of schizophrenia receiving increased attention is the

treatment of persons in the prodromal stages of the disorder. Here the individual is beginning to

show early mild signs of schizophrenia (e.g., hallucinations, delusions) but is aware of these

changes. Efforts to intervene with these individuals are being investigated as a means of either

stopping to progression of the disorder or preventing relapses (Cunningham Owens & Johnstone,

2012).

References:

Barlow, D. H., & Durand, M. V. (2014). Abnormal Psychology: An Integrative Approach, 7th

Edition (7th ed.). Cengage Learning.

Bateson, G. (1959). Cultural problems posed by a study of schizophrenic process. In A.

Auerback (Ed.), Schizophrenia: An integrated approach (pp. 125–148). New York, NY: Ronald

Boydell, J., & Allardyce, J. (2011). Does urban density matter? In A. S. David, S. Kapur, P.

McGuffin, & R. M. Murray (Eds.), Schizophrenia: The final frontier—A festschrift for Robin M.

Murray (pp. 273–280). New York, NY: Routledge

Brown, G. W., Monck, E. M., Carstairs, G. M., & Wing, J. K. (1962). Influence of family life on

the course of schizophrenic illness. British Journal of Preventive and Social Medicine, 16, 55–

68.

Callicott, J. H., Mattay, V. S., Verchinski, B. A., Marenco, S., Egan, M. F., & Weinberger, D. R.

(2003). Complexity of prefrontal cortical dysfunction in schizophrenia: More than up or down.

American Journal of Psychiatry, 160, 2209–2215.

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Creese, I., Burt, D. R., & Snyder, S. H. (1976). Dopamine receptor binding predicts clinical and

pharmacological potencies of antischizophrenic drugs. Science, 192, 481–483.

Cunningham Owens, D. G., & Johnstone, E. C. (2012). Treatment and management of

schizophrenia. In M. G. Gelder, N. C. Andreasen, J. J. López-Ibor, Jr., & J. R. Geddes (Eds.),

New Oxford textbook of psychiatry (2nd. ed., Vol. 1, pp. 578-595). New York, NY: Oxford

University Press.

Davidson, M., Keefe, R. S. E., Mohs, R. C., Siever, L. J., Losonczy, M. F., Horvath, T. B., &

Davis, K. L. (1987). L-Dopa challenge and relapse in schizophrenia. American Journal of

Psychiatry, 144, 934–938.

Goering, P., Durbin, J., Sheldon, C. T., Ochocka, J., Nelson, G., & Krupa, T. (2006). Who uses

consumer-run self-help organizations? American Journal of Orthopsychiatry, 76, 367–373.

Harrison, P. J. (2012). The neurobiology of schizophrenia. In M. G. Gelder, N. C. Andreasen, J.

J. Lopez-Ibor, Jr., & J. R. Geddes (Eds.), New Oxford Textbook of Psychiatry (2nd. ed., Vol. 1,

pp. 561–568). New York, NY: Oxford University Press

Jablensky, A. (2012). Epidemiology of schizophrenia. In M. G. Gelder, N. C. Andreasen, J. J.

Lopez-Ibor, Jr., & J. R. Geddes (Eds.), New Oxford Textbook of Psychiatry (2nd. ed., Vol. 1, pp.

540–553). New York, NY: Oxford University Press.

Javitt, D. C., & Laruelle, M. (2006). Neurochemical theories. In J. A. Lieberman, T. S. Stroup, &

D. O. Perkins (Eds.), The American Psychiatric Publishing textbook of schizophrenia (pp. 85–

116). Washington, DC: American Psychiatric Publishing.

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Kane, J. M., Stroup, S., & Marder, S. R. (2009). Schizophrenia: Pharmacological treatment. In

B. J. Sadock, V. A. Sadock, & P. Ruiz (Eds.), Kaplan & Sadock’s comprehensive textbook of

psychiatry (9th ed., Vol. I, pp. 1547–1556). Philadelphia, PA: Lippincott Williams & Wilkins.

Murray, R. M., & Castle, D. J. (2012). Genetic and environmental risk factors for schizophrenia.

In M. G. Gelder, N. C. Andreasen, J. J. Lopez-Ibor, Jr., & J. R. Geddes (Eds.), New Oxford

textbook of psychiatry (2nd. ed., Vol. 1, pp. 553–561). New York, NY: Oxford University Press

van Kammen, D. P., Docherty, J. P., & Bunney, W. E. (1982). Prediction of early relapse after

pimozide discontinuation by response to d-amphetamine during pimozide treatment. Biological

Psychiatry, 17, 223–242.

Shenton, M. E., & Kubicki, M. (2009). Structural brain imaging in schizophrenia. In B. J.

Sadock, V. A. Sadock, & P. Ruiz (Eds.), Kaplan & Sadock’s comprehensive textbook of

psychiatry (9th ed., Vol. I, pp. 1494–1507). Philadelphia, PA: Lippincott Williams & Wilkins.

Singh, S. P., Harley, K., & Suhail, K. (2013). Cultural specificity of emotional overinvolvement:

A systematic review. Schizophrenia Bulletin, 39(2), 449-463. doi: 10.1093/schbul/sbr170.

Woods, S. W., Miller, T. J., Davidson, L., Hawkins, K. A., Sernyak, M. J., & McGlashan, T. H.

(2001). Estimated yield of early detection of prodromal or first episode patients by screening

first-degree relatives of schizophrenic patients. Schizophrenia Research, 52, 21–27