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Running head: JIM KEEFAUVER CHAPTER 16 SUMMARY 1

Summary of Chapter 16 Schizophrenia and the Affective Disorders

Jim Keefauver

Western Illinois University

Author Note

This summary was written to fulfill a course requirement for Psy 343 Behavioral

Neuroscience, taught by Dr. S. L. McFadden, Fall 2018. The paper was submitted on April 19th,

2019.
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Schizophrenia and the Affective Disorders

Schizophrenia is a neurological disorder that has fascinated me for quite some time.

Being one of the major neurological disorders, it has been stigmatized by pop culture, film, and

media. Movies have had a long history of portraying schizophrenic as being axe wielding

murderers or incomprehensible hermits living on the fringe of society. Throughout my university

studies, I’ve come across this topic many times. I’ve had the privilege of learning about the

disorder on a general level, as well as a clinical level. While the clinical level did summarize the

neurological aspect of schizophrenia, I feel it would be of particular benefit to understand it on a

deeper level in that context. Understanding the mechanisms behind a disorder should prepare me

to offer formulated and well thought out explanations for the disease to those who may only

know it by the over-exaggerated portrayals in the media. On a more particular level, my

understanding of this disease will increase success in my pursuit to become a clinical

psychologist. I will only be focusing on schizophrenic sections of the chapter.

The term schizophrenia was created and defined by Eugen Bleuler in 1908. The word

means “split mind” and is indicative of the break in a person’s ability to distinguish between

reality and intrusive, irrational, disorganized and often hallucinatory thoughts. Often times this

word has been mistaken for and used in place of split personality disorders. The symptomology

of schizophrenia includes positive, negative, and cognitive symptoms. Most researchers agree

that negative and cognitive symptoms are so alike, that they do not discern between the two.

Firstly, positive symptoms are those that are forward in their existence and include

thought disorder, delusions, and hallucinations. The most important of these is thought disorder,

which is the inability for a schizophrenic to organize their thoughts logically and rationally.

Often this results in the adoption of absurd beliefs as they are unable to conclude what is

plausible and what is not about their thinking. Delusions also include three types and are
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persecution, or, the thought that someone is conspiring against the individual; grandeur, the

thought that the person is capable of action or knowledge well beyond the scope of a normal

person; and control delusions, the irrational thought that the thoughts and behavior of the

individual are being controlled by outside influencers. The last of the positive symptoms is

hallucinations. The most common type of hallucination is of the auditory type. While not limited

to this aspect, it is the most prominent and most associated positive symptom stigmatized with

regards to schizophrenia. The individual may hear sounds or voices that appear to be real.

Negative and cognitive symptoms are closely related in that they represent the depression

of normal or expected behavior. These include learning, memory, emotion, psychomotor, and

problem-solving skills. Negative symptoms will often appear first and are followed by cognitive

and positive symptoms, respectfully. The development of schizophrenia in an individual could

take many years as the brain loses tissue slowly, which is why this disease is onset in young

adulthood, generally.

Researchers have been able to conclude that schizophrenia is an inheritable disease but

are unable, as of yet, to pinpoint where exactly the abnormality begins. Much research has gone

on in order to examine the many aspects that may lead to schizophrenia – including those of the

developing brain, genetic deformities, and environmental factors. Though, many researchers

agree that it is highly likely to be a combination of many of these variables that produce the

symptoms of schizophrenia. Research has explored the option that a single gene may be

responsible for the disorder, however if that were the case it would be more prevalent than it

currently is. Another study suggested that there may be multiple genes involved in the

development of schizophrenia, and a person may carry these genes but are not guaranteed to

express the disorder. Rather, it would make them more susceptible to developing it. They believe
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that adverse environmental conditions could trigger the development of the disorder.

Epidemiological studies on schizophrenia have been able to identify many environmental factors

that may play a role in the development of the disorder. These include population density, season

of birth, epidemics, maternal stress, and prenatal malnutrion. Environment seems to play the

most important role as even children whose relatives do not have a history of schizophrenia are

still able to develop the disorder, generally earlier in life, as a result of complications prenatally

due to factors that contribute to abnormal fetal development. Another variable discussed was the

mutation of genes carried by sperm cells of the father. The older a male gets, the more times his

spermatocytes divide, which presents more opportunities for genetic mutations to occur.

Negative symptoms are not exclusive to schizophrenia as they are symptoms of many

other disorders and signs of damage. Research and scans of the brain have shown a loss of brain

tissue in patients with schizophrenia by measuring the size of the ventricles. Larger ventricle

sizes as compared to normal sizes were indicative of tissue loss. Although they have ruled out

the possibility that it is a degenerative disease there is an abrupt loss cortical gray matter in many

areas of the brain which occurs, generally, in early adulthood and is not marked by a progressive

(degenerative) loss of tissue after the initial loss.

Positive symptoms, on the other hand, are unique to schizophrenia. The dopamine

hypothesis explains the overactivity of the dopaminergic system, specifically, the mesolimbic

pathway which extends from the ventral tegmental area to the nucleus accumbens and amygdala.

As dopamine is involved in reinforcement, they have found plausibility in the thought that

delusions are the result of reinforced thoughts due to the hyperactivity of dopamine.

It has been found that when drugs such as cocaine and amphetamine are taken in high

doses work as agonists by blocking the reuptake of dopamine and produce positive symptoms of
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schizophrenia. Another contributor is the precursor for dopamine, L-DOPA. Counter to those

effects, chlorpromazine and similar drugs were invented that act to block the D2 and D3

dopamine receptors.

The invention of antischizophrenic drugs were beneficial and were able to at least reduce

the occurrence of positive symptoms. Negative symptoms continued to exist in the individual

and were unable to be addressed. Another pitfall of the classical antipsychotics is that after

prolonged use, one-third of patients developed a neurological disorder called tardive dyskinesia.

The symptoms expressed by this disorder are nearly opposite to those of Parkinson’s disease, and

individuals are unable to stop moving. In an effort to eliminate the occurrence of this disorder,

Clozapine and other similar drugs of the atypical antipsychotic medications classification that

were able to reduce both negative and positive symptoms and decreased the risk of tardive

dyskinesia.

Although the positive and negative symptoms are understood to be caused by entirely

different functions of the brain, evidence has found that they share similar abnormalities in the

brain. Hypofrontality is a term used to explain the decreased activity of the dorsolateral

prefrontal cortex. Studies have shown that schizophrenics show hypofrontality as a result of

lowered release of dopamine in the prefrontal cortex, resulting in the display of negative

symptoms. Concurrently, hypofrontality causes an increase of dopaminergic activity in the

mesolimbic system which is believed to cause positive symptoms of schizophrenia. Atypical

antipsychotic medication has been developed that can increase dopamine in areas where there is

less and reduce the amount of dopamine in areas that are more concentrated, acting as a “partial

agonist”. Thus, they are able to successfully reduce the presence of both positive and negative

symptoms in the individual. This is the explanation provided for why classical antipsychotic
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drugs were only able to relieve the positive symptoms and not the negative ones as they would

block most DA receptors, making it worse for negative symptoms due to hypofrontality.

Summary of Personal Thoughts

Schizophrenia is a terrible disorder. The summary at the beginning of the chapter seemed

to instill a sense of hopelessness. The fact that Larry had devolved into psychosis, was whisked

away to a state hospital, was given medication to help him recover, yet it only created another

condition for which they could only medicate him further to reduce those symptoms. It seems

like a vicious cycle. However, the chapter did well to shed light on current and past research on

schizophrenia and the development of atypical antipsychotic medication that not only reduces the

risk of developing further disabilities – but also takes care of both the negative and positive

symptoms of the disease.

The dopaminergic theory and the hypofrontal theories made much more sense after

reaching out to external web resources to help better understand it. Further research has gone in

to exploring what I thought were only illegal street drugs, PCP and ketamine. These drugs were

able to cause all symptoms of schizophrenia, while other stimulants such as cocaine were only

able to cause positive symptoms. Understanding the underlying mechanisms behind these drugs

assisted with creating atypical antipsychotics, which are better at controlling all symptoms of the

disorder.

The psychological aspect of schizophrenia took a back seat and the biological model took

front stage. Looking at it from a neurological perspective was beneficial, as I got a look at the

disorder through a different lens, the view a mechanic might see when he’s taken an engine

apart. Incredibly helpful information to know about how the different regions of the brain
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interact in seemingly opposing and cooperative ways (as with hypofrontality) where the brain is

doing two different things with the same exact neurochemical.

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