Risk of Schizophrenia

Custom Student Mr. Teacher ENG 1001-04 23 March 2016

Risk of Schizophrenia

Over the last few decades Schizophrenia has become embedded in mainstream vernacular as any behavior or emotional response that is out of touch with reality. However even with its popularity heightened through movies and headline news stories, schizophrenia is still one of the most enigmatic and least understood disorders of the brain. With current research focused on the role of neurobiology and functioning on a cellular level, investigative analysis has merited new innovations towards its source, however a single organic cause for the disorder still eludes scientists. Although the foundation of the affliction is still unknown, its effects are well documented and over the next few pages will show the changes in the brain as the disease develops, and how those alterations impact the rest of the body and alter various other functions throughout the viscera.

The term Schizophrenia was first coined in 1911 by Swiss psychiatrist Dr. Eugen Bleuler and translates from the original Greek as schizo (split) and phrene (mind), making a literal translation of split-mind, in reference to the disjointed thinking of those with the disease (Johnstone, 1994). Although the term was first used in the early twentieth century, according to scholars a ‘madness’ was described in The Ebers Papyrus, a collection of ancient Egyptian medical papers dating back to 1550 BC, which accurately depicts some of schizophrenia’s symptoms (Johnstone, 1994). With its possible documentation over three millennia ago and its symptoms documented in a myriad of medical journals throughout history, the disorder itself is very rare. Those who are at the highest risk of manifestation are offspring whose parents are both schizophrenic, although even at this rate the risk of manifestation is about forty-six percent.

Globally however its prevalence is about 0.9 percent or fifty-eight million people worldwide (Hollandsworth, 1990). According to James G. Hollandworth of the University of Southern Mississippi, schizophrenia is primarily characterized by a disintegration of reality perception, consciousness, and thought process which results in a debilitated proficiency in social and professional faculties (Hollandworth, 1990). While schizophrenia can most arguably be classified as a predominantly genetic affliction, there are others factors which can contribute to its development even without a genetic predisposition. These elements include birth defects such as hypoxia and low birth rate, neuroanatomical anomalies, viral infections, along with low IQ and cerebral atrophy (Hollandsworth, 1990). While these components in themselves are not sufficient enough to cause the disorder, they result in an increased risk for developing the disease.

One theory for the cause of schizophrenia that has been studied with great validity is the dopamine hypothesis. This theory postulates that schizophrenia is caused by an overabundance of the dopamine-dependent areas of the brain causing an imbalance that affects the entire system (Hollandsworth, 1990). For this reason many of today’s schizophrenia treatment drugs inhibit dopamine receptor activity in an attempt to return it to its natural equilibrium. Although even with advances in modern science and new drugs being developed every day, the illness is still only treatable and its symptoms still emerge even with proper medication. Even with its origin unknown, scientists have discovered several chromosomes which when damaged or mutated, greatly increase the risk of developing schizophrenia. The chromosomes in particular that act as catalysts are chromosome numbers twenty-two, six, and eleven (Klar, 2004).

Chromosome six contains several genes that are linked with immune response which has given rise to the belief that schizophrenia has some association with weakened disease fighting agents. While damage to this chromosome may be linked to the source of the ailment, it may only be the jump starter that kicks off the path to developing the illness. For as scientists know, a lacking immune response caused by chromosome damage can theoretically leave the body vulnerable to infection, which are facilitators that can bring about the emergence of the disorder (Hollandsworth, 1990). Chromosome twenty-two on the other hand is linked with the dopamine hypothesis as this area houses enzymes that aid in transporting neurotransmitters. These neurotransmitters, mainly catechol-O-methyltransferase (COMT) and proline dehydrogenase (PRODH) are essential for the breakdown of dopamine. Any disruptions in this particular area can trigger an overabundance or shortage of dopamine, potentially resulting in developing positive or negative schizophrenia symptoms (Chakravarti, 2002).

Lastly, chromosome eleven has been associated with schizophrenia on the grounds of genetic translocation, or a chromosome abnormality caused by faulty rearrangements of various strands of DNA. These faults can occur in any number of genes, however during this process it occurs at times pivotal to cell division, making it easy for genes to be incorrectly rearranged (Klar, 2004). When this happens it can potentially inhibit the development of lateralization of brain function and act as a precursor not only schizophrenia, but other forms of mental illness as well as cognitive impairments (Klar, 2004). Once the subject has developed schizophrenia it affects the brain in very specific ways. When the disorder itself first begins to emerge its early symptoms manifest themselves in a period called The Prodormal Phase (Neale &ump; Oltmanns, 1980). During this phase, which occurs anywhere from six to thirty months before the disease truly emerges, the person may experience social withdrawal, dysphoria, and irritability. As the disorder progresses the symptoms may become more intense, and newer or ‘positive’ symptoms may begin to surface.

These positive symptoms can include visual and auditory hallucinations, delusions, and disorganized thought processes. In severe cases of thought process deterioration or cognitive slippage, a person can develop schizophasia or ‘word salad’ where a person’s speech is completely incoherent with no understandable thought or message. Following the positive symptoms of the illness, ‘negative’ symptoms can appear as well. These symptoms are aspects of the person’s personality that have been negated by the disease. They are most commonly expressed by the person’s flat or expressionless demeanor, apathy, very little displayed emotion, and continued peculiar behavior (Hollandsworth, 1990). After schizophrenia has completely manifested itself, the patient is usually classified into one of four types. These types are paranoid, disorganized, catatonic, and undifferentiated. Those in the paranoid group display an obsession over their delusions or have hallucinations specifically related to a certain subject or idea, and are usually the most functional of all schizophrenics (Johnstone, 1994).

Disorganized types are typically ones who display little emotion and act in a disjointed and inarticulate manner, while catatonic schizophrenics are merely ones who appear in torpor and display lethargic indolence. The undifferentiated type however is hybrid of the three previous types and is a miscellaneous combination of all their symptoms combined (Johnstone, 1994). While the outward symptoms may be relatively easy to recognize, inside the brain is a totally different matter. Schizophrenia can cause structural changes in the brain even though a specific cause for these changes is still unknown. These changes in brain structure are illustrated by larger ventricles, a thicker corpus collosum, a decrease in dendrite spines in the frontal lobe, disordered hippocampal pyramidal cells, and a shrinkage of the cerebellar vermis, which is mainly responsible for perception.

In some studies malformed neuronal migration has been observed which can lead to disjointed thoughts as well as an overall shrinkage of the hippocampus and amygdala (Johnstone, 1994). Due to these changes, a person suffering from the disorder can have reduced functioning in the frontal lobe which can affect their logic and critical thinking skills as well as their ability to successfully plan ahead. This reduced functioning is displayed in the Wisconsin card sorting test, which is administered to measure possible brain damage and assess the functioning of the frontal lobe. Schizophrenics who participate in the test show an inability to successfully transfer their attention to the rules of the exam once they begin. Functional imaging has also shown a lack of activity in the right hemisphere of the frontal lobe during their partaking, which does not increase as the task is administered. It is also shown that in a study by a Dr. Nagy in 1963, that of 260 cases of schizophrenia, roughly fifty-eight percent of the group had some form of cerebral atrophy (Johnstone, 1994).

On a cellular level schizophrenia symptoms are thought to be caused by an overabundance of neurotransmitters released between neurons. These neurotransmitters, mainly dopamine and serotonin, in excess can cause hallucinations and delusions which are referred to as ‘positive’ symptoms. Too little of these neurotransmitters however can result in lack of emotion and motivation which mirror the ‘negative’ symptoms of the disorder. Another type of cell affected by schizophrenia is the pyramidal cell in the prefrontal cortex, or the forehead area of the brain. These cells, which are a type of neuron that serve primarily as excitation units in the prefrontal cortex, are shown to have a decrease in basilar dendrite numbers. These basilar dendrites arise from the base of the pyramidal cell’s soma, and with a decrease in their numbers it can indicate a shortened synaptic surface area resulting in possible fallacious thought processing (Broadbelt, Byne, &ump; Jones, 2002).

Pyramidal cells in the hippocampus are also known to be affected by the disorder can and cause many of the cells in that area to be thrown into disarray, causing cognitive malfunctions. The treatment of this disorder can vary greatly depending on the person; however dopamine inhibiting antipsychotics are a very popular remedy. Although prevalent, these medications are not perfect and many scientists claim there is still no concrete connection that schizophrenia is exclusively a result of faulty dopaminergic transmissions (Neale &ump; Oltmanns, 1980). It has also been noted that many of the dopamine inhibiting drugs serve only to combat the positive symptoms and leave many of the negative symptoms such as emotional absence unaffected. Another treatment that is still widely used, but much less common is electroconvulsive therapy or shock therapy.

This treatment is still very controversial but there has been success in treating schizophrenia symptoms completely, although many patients relapse within six months. Studies have also indicated that although this treatment can be effective there are risks of permanent brain damage. According to Dr. Peter Breggin (2008), a psychiatrist at the State University of New York, shock therapy in animal testing showed statistically significant brain structural abnormalities when compared to animals without it. His study showed the electrical shocks caused changes in the nerve cell walls causing gliosis, or a profound increase in the number of astrocytes in impaired areas of the central nervous system (Breggin, 2008). In conclusion, schizophrenia is unique disorder that affects the brain in many ways, yet manifests itself differently from person to person.

As there is no tangible rubric for how the disorder will impact the person, it can be a difficult illness to treat. Its effects on the brain, from enlarged ventricles to a decline in dendrite spines, shows the major impact the illness can have on living a normal life. Although the disorder afflicts just over fifty-eight million people worldwide it is still devastating to those who are affected and while the medical community makes leaps and bounds in understanding the disease, a cure is still far from the horizon. With psychology grant money from universities being invested predominantly in neuropsychology, perhaps sometime in the near future scientists will be able to fully understand this illness and find a successful and permanent cure for it.


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  • University/College: University of Chicago

  • Type of paper: Thesis/Dissertation Chapter

  • Date: 23 March 2016

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