by Elizabeth Hall
Schizophrenia is one of the most misunderstood mental disorders that psychologist must treat in the field today. In this paper, we have extensively studied the environmental, genetic, and biological influences of the disorder. We have looked at how they affect the development of schizophrenia, and what treatments are currently available for patients suffering from this terrifying disease. While there is no cure for schizophrenia, researchers continue to study the disease because the symptoms of this mental illness require lifetime care and medicine. Through the study of Shonda, who is diagnosed with paranoid schizophrenia and suffering a psychotic episode, we explore a comprehensive view of this devastating illness.
Shonda’s Case Information
Eastern State Hospital Behavioral Health Client Case File
Client:Wilson, Shonda DOB:8/15/1979 Client CISID#ES10854
Address:3543 Sunnyvale Lane Client SSN:401-85-7530
City:Lexington State:KY Zip:40517 Health Insurance Co:Anthem
Phone(859) 849-5298 Eemail@example.com Health Plan: Access
Case Type: Patient File- Continuous Paranoid Schizophrenia
Initial Patient Screening Date: 2/12/2004
Extra Background Information:Employed at Eastern State, performs light janitorial duties. Supervisor- Zachary Brown Phone Number- (859)652-5305
Medical History: Has frequent, almost continual audible hallucinations, accompanied by delusions. Has been on antipsychotics for almost 12 years, most recently prescribed haloperidol (Haldol)
Family Background: Older brother lives in Florida, parents live in Versailles, KY. Patient has not seen any of her family members for years. Parents have always been emotionally distant, with this worsening with diagnosis of schizophrenia. Home life was volatile, with parents constantly bickering, and the father has a violent temper, often beating wife and children. Father possibly an alcoholic. One aunt on her father’s side was institutionalized for a nervous breakdown. There is no other history of mental illness in the family history.
Current Issues: This morning I received a call from Zachary Brown advising that Shonda had not shown up for work today. Upon visiting her at her residence, I found her anxious, fidgety, and very frightened of the voices she has been hearing in the past week. Client has been hearing audible hallucinations since her first diagnosis of Paranoid Schizophrenia 12 years ago, but normally can function enough to work. Client reports that voices are getting more intense, and frightening, critical, harsh, and louder. Shonda also states that she has been attempting to hide from the voices in closets and under beds but is having no success. She currently is delusional, and believes that she is under surveillance by the CIA and the FBI, and that they have planted cameras in her home and workplace. Client is visibly agitated, and confused with disjointed speech patterns and alogia.
Recommendations:I recommend immediate hospitalization, with adjustment of medicine.
Among all of the mental disorders that affect our society, schizophrenia is one of the hardest to deal with as stated by the University of Texas Harris County Psychiatric Center at Houston (1997). This is attributed to the vast array of symptoms both positive and negative, such as delusions, hallucinations, alogia, and affective flattening to name a few. This disorder according to Barlow and Durand (2007) is divided into five subtypes, paranoid, catatonic, residual, disorganized, and undifferentiated, which further complicates this disease. In this paper, we intend to shed some light on this disorder, discuss genetic, environmental and biological influences on the disorder, treatments, and relate this research and study to a specific case of paranoid schizophrenia.
What Exactly is Schizophrenia?
According to the University of Texas Harris County Psychiatric Center at Houston (1997), of all of the mental disorders it is possible to have, schizophrenia is one of the most convoluted and misconstrued of them all. The symptoms that define this disease are horrifying and frightening to the patients, their families, and even to society as a whole. Patients suffer from audible and visual hallucinations according to Barlow and Durand (2007), along with delusions, and catatonia. They also suffer from negative symptoms such as alogia, negative flattening, and avolition. These symptoms are the most prevalent in the disorder regardless of the type of schizophrenia that you have, as there are five different subtypes associated with schizophrenia, paranoid, catatonic, undifferentiated, residual, and disorganized (Johns Hopkins Medicine, n.d.).
Each of these subtypes present differently, contributing to the general public misconception of this complex disease (Barlow and Durand, 2007). While the delusions and hallucinations are the main symptoms across the subtypes, and considered positive symptoms, the complete set of symptoms, is much larger and include negative symptoms as well, such as avolition, alogia, anhedonia, and affective flattening. This disorder also manifests disorganized symptoms including disorganized speech, and catatonic immobility. While it has happened that, the disease has manifested earlier and later in life, the disease usually presents in young adults in their twenties and early thirties, according to Barlow and Durand (2007).
Cola, Findling, Lee, Meltzer, Rabinowitz, Ranjan, and Thompson (1997), note that there are several factors, which change the degree of the disorder in relation to the age of onset. They find that the earlier the onset, the greater level of dysfunction the disorder produces in the patient, along with inferior response to treatments, and the greater chance of having to be hospitalized more than once during the patient’s lifetime. Although mental disorders have been around for “thousands of years” as stated by Johns Hopkins Medicine (n.d.), Emil Kraeplin was the first person to separate mental conditions into different classifications, calling what is now known as schizophrenia, dementia praecox. In 1911 the term schizophrenia, was adopted by Eugen Bleuler, and both he and Kraeplin had subdivided the disease into the five different subtypes by this time. The current classification system for mental disorders according to Johns Hopkins Medicine (n.d.) is the Diagnostic and Statistical Manual for Mental Disorders –Fourth Edition (DSM-IV-TR).
The DSM-IV-TR classifies schizophrenia as an unrelenting, chronic disease, which affects the patient’s thinking process, emotions, and even behavior, holds BehaveNet (2011). In order for a patient to receive a classification of schizophrenia, certain diagnostic criteria must be met, from a range of criterion listed in the DSM-IV divided into six categories. These categories, described as characteristic, social/occupational dysfunction, persistent duration, the ruling out of schizoaffective and mood disorders, the exclusion of substance or medical related psychosis, and finally whether there is any presence of pervasive developmental disorder all have different durations to meet the criteria. After one year of persistent symptoms, the disorder can be further classified as episodic with interepisode residual symptoms, with or without prominent negative symptoms, episodic without interepisode residual symptoms, continuous, and other unspecified pattern symptoms as well. There is also a classification for single episodes with partial or full remission notes BehaveNet (2011).
During studies of the offspring of twins, it was discovered that it is possible to be a carrier of the disorder, and able to pass it down genetically without ever having shown signs of the disorder, notes Barlow and Durand (2007). Genetic linkage association studies have shown that the easiest way to study disorders of this type are through marker genes, and receptors. In schizophrenics, this means the study of the dopamine process in the brains of patients. Now, we should look at the research and what the DSM-IV-TR says, and compare it to our original case study about Shonda Wilson.
We can see from the facts detailed in Figure 1, that Shonda has been diagnosed with continuous paranoid schizophrenia, and has had the diagnosis of schizophrenia for many years. According to BehaveNet (2011) and the DSM-IV-TR, she does seem to fit the criteria for this disorder. Shonda has had audible hallucinations and alogia throughout the entire time she has had the diagnosis. The fact that the hallucinations are constantly present is what qualifies her for the diagnosis of continuous paranoid schizophrenia.
However, even with the addition of a new antipsychotic medicine (Haldol), her condition seems to be worsening. Now, along with the hallucinations, which are getting more insistent and frightening, and the alogia, Shonda is also delusional and unable to function at work. She believes that the FBI and CIA are monitoring her and have put cameras in her house and workplace, and her hallucinations have turned harsh, critical, and insistent. When considering the research, Cola, Findling, Lee, Meltzer, Rabinowitz, Ranjan, and Thompson (1997), have stated that the earlier the onset of the disorder, the less positive results that are found by treatment, and that seems to be the case here.
Although Shonda has not had much contact with her family, and not much is known about her history, we can see that there is some mental disorder in the family, as there was emotional distance by both, mother and father, alcoholism, and violence, along with an aunt who was hospitalized. Not enough is known about this aspect of her past to make justifiable considerations to diagnosis and research in this case, however we can speculate that it is possible that the violence and abuse that the mother may have endured during the pregnancy as a suspected cause. It is important to explore the biological, genetic, and environmental aspects of this disorder anyway.
Biological andGenetic Aspects of Schizophrenia
Yale University School of Medicine, Psychiatry (2005), holds that the main neurotransmitter involved in schizophrenia is dopamine, however there are actually three neurotransmitters involved according to the National Institute of Mental Health (NIMH) (2004). The dopamine neurotransmitter was the first one related to schizophrenia, but glutamate has been related to this disorder for some time now. The glutamate receptor GR3, which regulates the amount of glutamate present in the synaptic clefts, relates to possible negative impacts on cognitive functions. Recently, NIMH (2007) has also associated GABA with schizophrenia, and it is because of the reduction of enzymes such as the gene GAD1, which aids in the production of the neurotransmitter GABA that affects schizophrenics’ development of the disorder.
Barlow and Durand (2007) tie the distinction of genetics to schizophrenia by making this statement, “we can safely make one generalization: Genes are responsible for making some individuals vulnerable to schizophrenia”. There have been numerous findings in relation to genetics and schizophrenia such as the one by Frank Kallmann. It is a quantitative trait locus, which offers us the best explanation into the variances of the disease. This includes why we have gradations of severity, and that the studies show the correlation between the number of family members with the disease and the chances of developing it increasing with the addition of each new family member diagnosed (Barlow and Durand, 2007). Along with the genetic studies, there have been proven abnormalities in the brain structure of schizophrenics.
The Journal of Psychiatry and Neuroscience (2002) maintains that schizophrenia as a disease of the brain, and that it has always been classified in this way. Now that researchers have the MRI, and Computed Topography (CT), it is much easier to see these abnormalities. What they see is that patients have lateral ventricles that appear larger than normal while cortical grey matter and hippocampal masses appear to be smaller than normal. Barlow and Durand (2007, p490 par3-4) report that the disease is at least caused in part by “excessive stimulation of striatal dopamine D2 receptors” and by the “deficiency in the stimulation of prefrontal D1, receptors”. You will find them in the basil ganglia and the prefrontal cortex. Scientists also have gone into another newer area that has been researched, which takes modifications in the prefrontal cortex action that regulates glutamate communication into consideration. This modified interaction between the dopamine receptors happens in conjunction with the N-methyl-d-aspartate (NMDA) receptors in the brain, and was discovered by studying effects of certain drugs on the brain (Barlow and Durand, 2007).
Barlow and Durand (2007) states that the frontal lobes seem to maintain less activity in people diagnosed with schizophrenia than those in other people. Particularly this hypofrontality is found in the dorsolateral prefrontal cortex in these patients, and presents earlier than other cognitive dysfunctions in relation to schizophrenia and other symptoms and signs. There is also new research as of August 2011, showing a definite link to 40 mutations in different genes in cases of sporadic (non-hereditary) schizophrenia holds Priedt (2011). This study also notes that most of these are protein altering, and that Columbia University Medical Center staff who did this research think that the finding of the “de novo mutations” has changed the face of schizophrenia study drastically (Priedt, 2011).
What the patient experiences, because of the biological abnormalities is a diminished ability to react to emotional and social situations, and have experiences in which they may see or hear things that are in reality not there (Barlow and Durand, 2007). They may also take direction from these hallucinations, and have beliefs that are unlikely, or even impossible. This applies to Shonda as well; as we remember that she believes that, the CIA and FBI are spying on her and hearing voices continually. She is also experiencing alogia. Because schizophrenia affects everyone differently, the patient could also have a combination of lack of speech, lack of emotional expression, inability to move, and or a lack of motivation, along with difficulty processing and retrieving information (Barlow and Durand, 2007).
There is no known cure for schizophrenia, however according to Barlow and Durand (2007); there are treatments to minimize the frightening symptoms of the disorder. Usually this is done by administering antipsychotic medications, and psychosocial treatments along with developing social, physical, and cognitive skills to help patients cope. This is designed to minimize relapses, reduce hospitalization, help to regulate their medicine, and help them develop skills they may be personally lacking. The antipsychotic drugs available to treat schizophrenia fall into four classes, Phenothiazines (Chloropromazine/Thorazine, or Fluphenazine/Proloxin for example), Butyrophenones (Haldol), Others (Loxapine/Loxitane for example), and Second Generation Agents (Ariprazole/Abilify, Clozapine/Clozaril, or Quetiapine/Seroquel for examples of these) (Barlow ad Durand, 2007). While these medicines work to reduce and regulate the dopamine system and our neurotransmitters, and are effective in that respect, they often produce side effects that are equally annoying such as drowsiness, rapid heartbeat, dizziness, sensitivity to the sun, and lowered libido (NIMH, 2004). The Surgeon General (1999) also states that patients with this disorder suffer severe symptoms that affect our most basic human functions such as “language, thought, perception, affect, and sense of self”.
Psychosocial therapy models include several treatments designed to improve the quality of life that the patients have notes Barlow and Durand (2007). The behavior therapy model is used to teach family members of schizophrenics’ tools to deal with the family member that has the disorder. Patients go through a model called the token economy model that teaches appropriate actions and behavior by rewarding them when they act appropriately through a token system. Another example of psychosocial therapy models is the independent living program that helps patients recapture some independence by helping them gain skills they are lacking to function in society and gain a higher quality of life (Barlow and Durand, 2007)
Environmental Aspects Influencing Schizophrenia
Although there are biological and genetic factors, there are also some environmental factors, which associate with triggers beginning the onset of this disorder according to Leask (2004). He goes on to say, that there have been various studies, which explore the environmental influences on the development of schizophrenia, also taking the particular subtypes associated with the disease into consideration. They study such environmental factors like the season a person is born, the geographical location they live in, immigration status, and even substance abuse along with their actual birthplace, which is often referred to as urbanisation. The studies refer to these as external environmental influences.
Another type of study that has been researched is the environment that the patient experienced while in the womb, because we are in the early stages of neural and physical development during this time (Leask, 2004). He also discusses that the nuclear environment is a cyclic factor because environment influences genetic reactions and then genetic reactions influence behavior, which in turn affects environmental reactions.
According to Leask (2004), studies have shown that people born in the winter and spring in the north hemisphere, and those born in the spring in the south hemisphere of the earth are at risk, an extra 5% - 8% for presenting with schizophrenia later in life. Geographically, it is proven that developing countries have a higher presence of schizophrenia by a considerable amount. This, he goes on to say is based on the first-rank symptoms as defined by the IC-9, and the Present State Examination (PSE). The World Health Organization (WHO), conducted this study involving ten countries, “Colombia, Czechoslovakia, Denmark, England, India, Ireland, Japan, Nigeria, the USA and the (then) USSR” reports Leask (2004), involving both rural and urban areas coming up with this conclusion.
Ten different studies involving urbanisation resulted in the conclusion that at least one third of all cases of schizophrenia is attributed to this factor, notes Krabbendam and van Os (2005). If you look at the science, it can be said that he reason for this is the overcrowded, poor conditions that people live in urbanized areas, has undesirable consequences on developing neurological functions of young minds. The statistics prove that this disorder develops in urban conditions in excess of two to one over rural area development of schizophrenia. Krabbendam and van Os (2005) also pointed out that the ten studies prove that there is a direct correlation between having genetic predisposition to schizophrenia and urbanisation.
Leask (2004) discusses immigrant status as an environmental influence, particularly Norwegian, Danish and African Caribbean immigrants are effected, but states that because of the immigrant status it is hard to conduct and maintain studies and data because they can be undocumented or migrant in nature. He also mentions that due to differences in cultural norms, this disorder may not be diagnosed as often. Another environmental factor that should be noted is substance abuse, however inconclusive the results are, because patients diagnosed with schizophrenia have considerably higher rates of abuse than other people do. Leask (2004) brings up at least one more environmental factor, prenatal influences.
The prenatal theory about schizophrenia is founded on the reflection that patients with this disorder are different from other people in the way they process thoughts, behaviors, brains structure, and their pathological histories holds Leask (2004). A few of the influences that affect the neurological development of children are prenatal stress, prenatal famine, prenatal influenza, and obstetric complications while the child is in utero. Other influences of this nature notes Leask (2004), include low birth weight, pre-eclampsia, and Rhesus incompatibility. This makes sense, when one considers the importance of our earliest neurological development. A final environmental factor that can influence this disease is viral infection, which can alter brain performance (Barlow and Durand, 2007).
There are also psychosocial factors that are considered environmental, for example, stress, high expressed emotion, and reactions within families that contain schizophrenia according to Barlow and Durand (2007). When people genetically predisposed to schizophrenia experience a major loss such as death, loss of a job, or combat situations, this can act as a trigger, beginning the onset of the disorder. It is often also found that families of schizophrenia patients will criticize them, treat them with hostility, or even over involve themselves with the person. When this happens, researchers call it high expressed emotion and it can often cause or contribute to the patient’s relapse. Even though there are many studies and conclusions, there is one environmental cause, which does seem to overshadow the rest as concluded by Leask (2004).
This is the urbanization theory, which as stated earlier accounts for a least one third of all schizophrenia patients as stated by Leask (2004). This is the theory that holds that it is your geographic location and or birthplace that affects your chances of developing schizophrenia. While prenatal influences and stress/loss do have plenty of merit, the statistics do not lie. We do have to consider however, that all of the research really points to the fact that the nuclear environment, involving gene-environment reactions really is at the heart of this research.
What this research concludes is that the environment influences genetic factors, as much as the environment is influenced by choices derived from genetic factors. In schizophrenia, it seems that genetic predispositions can trigger environmental reactions. The studies also conclude that one’s genetic propensities also can affect their behavior, which then has a direct effect on the environment that a person chooses (Leask, 2004). This environmental effect has direct influence and interacts with the patient’s biological systems (Barlow and Durand, 2007).
Barlow and Durand (2007), conclude that there are only three neurotransmitter abnormalities in patients with schizophrenia, however NIMH (2007) states that there are four at work in schizophrenics’ brains. The first three identified by Barlow and Durand (2007), are that the striatal dopamine D2 receptors, which are part of the basil ganglia, disrupt the functional movements such as walking, balance, and movement. This is also responsible for deficiencies in the prefrontal D1 receptors. Along with the dopamine receptors in the prefrontal cortex, there has been research into the modification of the receptors that regulate glutamate communication.
This communication deals directly with N-methyl-d-aspartate (NMDA) (Barlow and Durand, 2007). The fourth neurotransmitter involved, GABA, is affected by the reduction of enzymes such as the gene GAD1 that aid in the production of GABA (NIHM, 2007). It is these interactions which cause the biggest changes in neurotransmitters and changes in the frontal lobes have also been noted which function to maintain less activity in people diagnosed with schizophrenia. According to Barlow and Durand (2007), these cognitive dysfunctions begin to appear in patients before other symptoms and signs of the disease.
Again, we go back to our original case study, Shonda Wilson. When considering the environmental influences on this case. What we see is that she is a classic candidate for prenatal environmental influence on the disorder due to the abuse that her mother probably suffered during her pregnancy with Shonda. At her age of onset, which was a mere 20 years of age, she can also be classified as an early age onset schizophrenic, since the disease does not usually affect women until their late twenties or early thirties. Environmentally speaking, Shonda’s case really does fit into the nuclear environment theory. We can see the probability that she was originally affected by abuse and stress emitted by her mother during the prenatal stages. However, because of the situation with her parents being emotionally distant, and her father being an abusive alcoholic, we must also conclude that her environment also affects her throughout her entire life until the diagnosis and her moving away.
What is the Best Treatment Approach for Schizophrenia and Shonda?
When considering how to treat this disorder, all options have been considered by researchers. The conclusion has been reached, based on the research conducted on treatment options, that ECT, electroconvulsive therapy will help to end episodes of severe psychosis and mania, according to the Mayo Clinic (2010), but it has been redacted to limited use because of social factors and the lack of evidence that prolonged effects result from treatment. It is obvious that the most effective means of treating schizophrenics has to be combined treatments. This includes several elements of psychosocial models, behavior and cognitive models, all with included pharmacological options. The complexity of this disease combined with the fact that there is no cure, only symptom treatments, denotes that there is no single treatment option that is effective alone. The particular course of treatment needs to be tailored to the patient and their specific symptoms in order to reach the most effective method for treatment, which is based on the degree and frequency of the symptoms.
In the case study of Shonda Wilson, a paranoid schizophrenic should be receiving case management, cognitive therapies, and family treatments, however, in her specific case, she has no family so that may be excluded. These therapies should be in conjunction with pharmacological treatments. Since Shonda has been on antipsychotic medicines for the better part of twelve years already, and has recently been prescribed haloperidol (Haldol), she should have her medicine adjusted, since she had shown some improvements previously with Haldol it is recommended to stay with this medicinal approach. For the immediate future, Shonda should be immediately hospitalized for stabilization. While she remains hospitalized, careful adjustments of her medicine should be explored, as she will be monitored in this setting. She already has a case management program, however while she is hospitalized she needs to be introduced to cognitive therapies, to aid in the reduction of the hallucinations and delusions, along with an independent treatment to serve in the place of the family therapy. When she is stabilized, and released, this course of treatment should continue for a minimum of one year and longer if needed.
When considering the best model for understanding and treating schizophrenia, we will look at the psychodynamic model, the behavioral model, the humanistic model, and the cognitive model. In relation to the psychodynamic model, Cooper, Michaels, and Perry (2006) convey that this will help the practitioner understand the nature of the delusions, meaning that it manifests because of fears they may be having about control, losing control, and being dependant and vulnerable. This is important because an in depth understanding of the nature of the patient’s specific problems can help the therapist tailor the treatment to best suit client fears, problems, and needs. The cognitive model looks at this differently according to McFarr (2010), with his model following the premise that they way a person views themselves, the world around them, and what they believe the future holds will influence their behavior.
This model, holds McFarr (2010), has been shown to be effective with helping patients remember to take their medicines which has long been a struggle. Research also seems to point in the direction that this model has also been effective in other problems as well, including symptom management. It has been definitively shown that patients who receive cognitive therapy have less frequent and extreme delusions and hallucinations. With the cognitive model, the therapist can assist the patient in identifying faulty thinking patterns and interpretations, helping them to see reality (McFarr, 2010).
It seems that the behavior model is also helpful in treating schizophrenia, but only when paired with cognitive therapy as well according to Bradshaw (2000). If you are trying to understand or explain this disorder, however, this model suggests that every behavioral abnormality is to be explained by the social learning or learned behavior theory, holds Barlow and Durand (2007). This cannot apply to schizophrenia because there are too many genetic and biological abnormalities in schizophrenics to attribute it to a real explanation. We however, cannot discount, that there are many behavioral model therapies, which does help in the treatment of this disease. Operant conditioning used in the form of the token economy for example would be one of them (Barlow and Durand, 2007).
The humanistic model suggests that self-actualization is the answer, and that we should realize the individuality of everyone, suggests Barlow and Durand (2007). This model is actually more effective on people who do not have mental illness. This does apply loosely to schizophrenia in the fact that the disorder presents, and changes in everyone individually regardless of their genetic and environmental history, which inherently affects both genetic and environmental factors. In deciding, what the bet model is for explaining and treating schizophrenia this author would have to go with the cognitive model if forced to choose just one.
This is because according to Barlow and Durand (2007), the cognitive model seems to help on many levels with this complicated disease. The first way that this model is more effective is in aiding the patient to remember to take their medicines, as this was noted to be a problem for them. The second way that this model is useful in understanding and treating these patients is the effectiveness that it helps to reduce the symptoms which is a huge problem in the way of patients leading productive lives. The final way that this model is effective with the treatment and understanding the disease is because it can aid the therapist in retraining the patient to identify their faulty thinking patterns and correct them (McFarr, 2010). It does need to be noted that all research indicates that this disorder is best treated using multiple treatment approaches including cognitive, behavioral and pharmacological treatments in conjunction with each other.
There have been new treatments explored recently involving possible pharmacological changes in the way therapists treat this disorder. In a study conducted by NIH, scientists have found a rare gene mutation in roughly one third of schizophrenic patients. They found that these patients “multiple copies of a gene on Chromosome 7, according to Asher (2011), specifically in the gene receptor VIPR2, which is the vasoactive intestinal peptide (VIP). Other new treatments involve new medicines.
PsychCentral (2009) discusses a new drug that was approved by the Food and Drug Administration (FDA), called Saphris (asenapine), which is a new atypical antipsychotic associated with schizophrenia treatment. It has proven to be effective when tested against a placebo, and has been on the market since 2009. The adverse reactions to this pill, in schizophrenics, are that it makes them restless and unable to sit still. Another treatment option according to Science Daily (2010), is working with serotonin, as it has a different signal pathway than traditional hallucinogens.
This neurotransmitter affects our “perception, cognition, sleep, appetite, pain, and mood” notes Science Daily (2010). The hypothesis is that the hallucinations in schizophrenia may actually arise due to elevated levels of serotonin. Further study is needed in this matter; however, what is needed is a way to conserve the effects of the serotonin while at the same time, avoiding the harmful effects that come with excessive metabolites (Science Daily, 2010). While there seem to be new treatments and research on this disorder, we must remember that there is no cure for this disease, and currently the only help manage the symptoms.
Unfortunately, for our case study subject Shonda Wilson, her future only seems to hold better symptom management and functionality in her life, as there is no current cure for this disorder according to our research. In the immediate future, based on this research and study, Shonda should be immediately hospitalized for stabilization. During this stabilization process, she should be monitored closely, while the doctors adjust her dosage of Haldol. She should continue her case management program; however, she needs to be introduced to cognitive therapies, to aid in the reduction of the hallucinations and delusions, along with an independent treatment to serve in the place of the family therapy. When she is stabilized, and released, this course of treatment should continue for a minimum of one year and longer if needed. The real prognosis of this disorder is that Shonda will have to be on medicines for the rest of her life, along with psychosocial treatment, but with the introduction of these new treatments, it is possible for her to have more stability and symptom management.
Asher, J., (2011). NIH News: Rare Gene Glitch May Hold Clues for Schizophrenia: -NIH Funded Study. Retrieved From: http://www.nih.gov/news/health/feb2011/nimh-23.htm
Barlow, Durand, (2007). Essentials of Abnormal Psychology. Mason, Ohio. Cengage Learning
BehaveNet (2011). BehaveNet Clinical Capsule: DSM-IV & DAM-IV-TR: Schizophrenia. Retrieved From: http://www.behavenet.com/capsules/disorders/schiz.htm
Bradshaw, W. (2000). Integrating cognitive-behavioral psychotherapy for persons with schizophrenia into a psychiatric rehabilitation program: results of a three-year trial. Abstract. Retrieved From: http://www.ncbi.nlm.nih.gov/pubmed/10994682
Cola, P.A., M.A., Findling, R.L., M.D., Lee, M.A., M.D., Meltzer, H.Y., M.D., Rabinowitz, J., M.S.W., Ranjan, R., M.D., and Thompson, P.A., Ph.D. (1997). Age at Onset and Gender of Schizophrenic Patients in Relation to Neuroleptic Resistance. American Journal of Psychiatry 154:4, April 1997.
Cooper, A.M., M.D., Michels, R., M.D., and Perry, S., M.D., (2006). The Psychodynamic Formulation: Its Purpose, Structure, and Clinical Application. American Psychiatric Publishing, Inc. Retrieved From:
Abnormal Psychology: Case Study
Shonda has a 12 year history diagnosis of continuous schizophrenia paranoid type. Shonda is constantly preoccupied with delusions and frequent auditory hallucinations. Shonda is under the occasional supervision of a caseworker from a local community health center. Shonda lives alone and rarely sees family members. While growing up Shonda heard that an aunt suffered a nervous breakdown but other than that her immediate family shows no sign of mental illness. Shonda’s medication and treatment has been reassessed multiple times due to the frequency of hospitalization and number of different complaints which include auditory hallucinations and many other delusions.
Shonda’s suffers from a pattern of confused speech often lacking orderly continuity. After interviewing Shonda for a period of more than an hour, her caseworker reports Shonda’s paranoia has her convinced that she is under the surveillance of the FBI and CIA. This topic of conversation encourages further agitation by Shonda. Shonda has attempted to hide from audio hallucinations as well without success.
Shonda has been hospitalized for many years and due to her recent escalation of symptoms she will be recommended for reassessment and an increase in antipsychotic medication.
Durand (2007, p. 471) defines Schizophrenia as, “Devastating psychotic disorder that may involve characteristic disturbances in thinking (delusions), perception (hallucinations), speech, emotions and behavior.” Well, it is certain that schizophrenia is a curious disorder marred with a mixture of signs and symptoms. Schizophrenia is complex and fastidious to diagnose due to the different types, symptoms, cognitive and emotional dysfunctions, and the etiology (how the disorder originates.) The complexity of the disorder combined with the mixture of signs and symptoms, which may or may not be present, makes schizophrenia difficult to understand. At some point of the disorder there is a psychotic phase. The psychotic phase must persist for at least one month. The disorder is presented by delusions, hallucinations, disorganized speech and behavior during the psychotic phase. Schizophrenia is usually found to present itself in early adulthood, with some exceptions of adolescence. (Schizophrenia Symptoms, 2009)
The complexity of schizophrenia is further exacerbated by the complications exhibited by individuals suffering from the disorder. The mood abnormalities such as significant loss of impetus to continue with pleasurable activities, depression, anxiety, and anger, all contribute to the patience’s lack of awareness or concern they are suffering from a psychotic illness. Without an understanding or a belief of illness, the patient is much more likely to avoid therapy. (Symptoms and Treatment, 2009).
Withstanding over 100 years of classifying psychotic disorders into specific forms, and the fact that psychotic disorders have been recognized throughout history, it is quite an accomplishment that a definition by a German psychiatrist, Emil Kraepelin, who originally termed schizophrenia as “dementia praecox” due to its chronic, rapid cognitive disintegration, still stands. The name, “schizophrenia” was later defined by Kraepelin and a team of psychiatrists. It was Eugen Bleuler who suggested renaming it to “schizophrenia” due to the “fragmented mind” characteristic of the disorder. Kraepelin attempted to identify the multiplicity of symptoms (catatonia, hebephrenia, and paranoia) and further suggested that the term “dementia praecox” should be superseded and that schizophrenia should be recognized as a “group” of disorders for which a fragmentation of associations were the foundation of the symptoms. Kurt Schneider followed Bleuler’s interest in identifying and classifying the fundamental feature of the disorder. And so, he developed “The Schneiderian System” of finding the correlations, or commonalities of patients’ symptoms. Schneider developed a set of “First Rank Symptoms” specific to diagnosis of schizophrenia’s psychotic phase. Again, the complexity of the disorder to this day and in the future will continue to divide clinicians’ diagnosis until specificities of schizophrenia’s pathophysiology and etiology are clearly uncovered and defined. (How was schizophrenia discovered?, 2005)
The Diagnostic and Statistical Manual of Mental Disorders (DSM) is the standard used by mental health professionals in the United States to classify mental disorders. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), was published in 2004 and was the last major revision of the DSM. According to the DSM-IV, schizophrenia is classified as a mental disorder. There are several subtypes of schizophrenia, but because of the usefulness to the DSM-IV, schizophrenia remains divided into three (aforementioned) major subtypes: paranoid (delusions of grandeur or persecution), disorganized (or hebephrenic; silly and immature emotionality), and catatonic (alternate immobility and exited agitation). There are two additional schizophrenia subtypes; undifferential and residual types. These two subtypes are the catch-all for which essentially all of the other disorders which symptoms are present but do not fully met the criteria of the three major subtypes. (Durand, 2007)
There are many studies and infinite archives on the topic of schizophrenia. It is yet a great conundrum to the brightest scientists, sociologist, pathopsychologists, and psychiatrists. Many studies link marijuana and other drugs to schizophrenia. Other studies link a genetic mutation (22q11) which hinders communication between the hippocampus and the prefrontal cortex to schizophrenia. Similar genetic studies reveal “undetectable genetic variations” lead to schizophrenia. The National Institute of Mental Health conducts a wide range of studies, one of which examined the effects of D-cycloserine augmentation on cognitive remediation for patients diagnosed with schizophrenia. Many institutes have focused on two studies on schizophrenia and motion perception and the propensity to develop schizophrenia in individuals who have difficulties tracking moving objects. The Genome News Network (2001) suggested that certain individuals with two copies of the dopamine D3 receptor gene (DRD3) scored significantly low on visual exams. Many epidemiological studies have observed an association between obstetric complications during intrauterine life and schizophrenia. Quite often the studies that include medication produce as many or more questions than the number of answers. There continues to be countless “new studies” suggesting new theories and hypothesis on the topic of schizophrenia. (Clinical Trials, Schizophrenia, Featured Studies, 2010)
Case Study, presented Shonda, a patient diagnosed with continuous paranoid schizophrenia. The case study provided an intimate and detailed perspective into the life of someone with mental illness and the people with whom they might associate. Shonda’s description which included her family history and current familial relationships provided a typical expectation for someone diagnosed with schizophrenia based what I have learned about the background, DSM-IV criteria, and the research that has been conducted on schizophrenia. After all of my research and reading, I feel that this could be a hypothetical case study while it could very well be quite legitimately a real-life case study.
There are neurotransmitters linked to schizophrenia. Both norepinephrine and dopamine appear to be involved with schizophrenia. Dopamine receptors are thought to mediate both the transient neurotransmitter functions as well as the neuromodulatory effects that alter cell metabolism. It is suggested that dopamine controls the metabolism of the cell, or in other words, dopamine affects the rate of synthesis of the neurotransmitter. Endorphins serve as neurotransmitters which modulate the release of dopamine by acting as presynaptic receptors. The best results in treating schizophrenia come from drugs that primarily block dopamine receptors. This further suggests that schizophrenics have “too many” receptors. As it has often been said about the human body preferring a state of homeostasis, so too do receptors and transmitters. When the sequence of release and reception amongst transmitters and receivers is upset, a disease state such as schizophrenia may occur. Human behavior is greatly influenced and the outcome is altered thought patterns, hallucinations, agitation, delusions, and social withdrawal.
The medical approaches to schizophrenia usually include hospitalization, psychotherapy, counseling, and drug treatment. I suspected that psychotherapy may have been the most common treatment for schizophrenics. From my research it seems that chemotherapy has also been used quite a bit to treat schizophrenics. Individual and family therapy seems to prove helpful in reducing relapse. Family therapy is also suggested to be helpful in order to assist the relatives with coping as well as educate. Becoming involved in community programs provides beneficial support, encourages proper social skills and vocational rehabilitation. Hospitalization is often preferred to ensure that the affected individual will receive the bare necessities; food, a place to sleep, and hygiene. Drug treatment usually prescribes the antipsychotic drugs risperidone, olanzapine, and closapine. There are many other psychopharmacological antipsychotic drugs that may be prescribed; for example, chlorpromazine and the antipsychotic drugs, phenothiazines, which are all powerful antagonists.
The impact of the antipsychotic medications on the treatment of schizophrenia has greatly assisted the efforts to reduce agitation, hallucinations, delusions, and indeed most of the other major symptoms of schizophrenia. The drugs also seem to greatly assist the prevention of relapse. At the same time, of course, the use of antipsychotic drugs can be argued strongly against prescription. There are debilitating side effects. Despite the side affects the strongest argument may be the fact that antipsychotic drugs do not cure schizophrenia. In spite of the arguments, continued use of drugs for treatment will continue. If the cause of schizophrenia is unknown, surely the cure is likely to remain a mystery as well. Using antipsychotic drugs will continue to relieve symptoms while researchers continue to search for the cause and the cure.
The major argument for the aforementioned dopamine hypothesis, which postulates that schizophrenia is likely associated with the areas of the brain that use dopamine as a neurotransmitter. This theory is heavily supported from the research on antipsychotic drugs. These drugs are effective on symptoms of thought disorder, withdrawal and moderately effective on hallucinations. The antipsychotic drugs effectively block the dopamine receptor sites. This means that the affected areas have reduced activity of neural impulses. Slowing the dopamine activity supports the hypothesis.
As previously mentioned it is thought that schizophrenia may be caused by an excess of dopamine receptors. In contrast, Parkinsonism is a movement disorder which may be caused by a deficiency of dopamine receptors. Two known facts worthy of further research are; Parkinson disease sufferers rarely develop schizophrenia and drug treatments of schizophrenia oftentimes produce irreversible Parkinson-like symptoms.
Psychological disorders are influenced in important ways genetically. In work with humans, twin, family and adoption studies indicate that certain people may be genetically vulnerable, or predisposed to psychological disorders. Among men, not as conclusive with women, alcoholism research seems to suggest that genetics play a significant role. (Durand, Barlow, 2007).
It also seems likely that schizophrenia is genetically predisposed. A belief that is well-established, or at least play a factor in schizophrenia, but as to the degree that genetics factor in varies amongst researchers. Schizophrenia is likely due to a combination of genetic factors in addition to social and environmental influences.
Many studies have been performed and much research conducted on family, twin, adoptee, offspring and close relations like aunts, uncles and cousins. These studies show a strong indication that schizophrenia is biological in nature. A person is more likely to develop schizophrenia when this person shares more genes with a person already diagnosed with schizophrenia. Studies have shown adopted children raised in an environment away from their birth parents, who have the disorder, have a much higher chance of developing the disorder themselves.
Since the 18th century there has been a belief in the theory that schizophrenia is likely passed from parent to child. Until about 30 years ago, when higher technical research started becoming possible scientists were not able to design studies that were sophisticated enough, similar to the current genetic studies conducted on family, twin, and adoptive studies.
One key-note to make regarding family studies is that the family members all share a very similar environment. This is support for the argument that environment plays a part in a person developing the disorder. Twin studies are subject to a similar objection that they not only share more similar genotype but also a more similar environment. The genotype similarity is obvious, especially for monozygotic twins, for they developed from the same sperm and ovum, resulting in 100% genetic similarity. Monozygotic twins are always the same-sex, so they tend to be dressed alike during their younger years and may choose to continue this routine on into adulthood. The study of monozygotic twins or identical twins is necessary, even to only establish a baseline, for the argument of environment. They grow up in virtually the exact same environment. However, the study may not be beneficial to the argument of genetics.
Another aspect of thought that most researchers are congruent is the genetic component involved in developing schizophrenia. If there is a genetic component, few major genes are responsible for transmitting the risk of developing schizophrenia. Many researchers believe that schizophrenia is not caused by one gene alone, but a variety of genetic subtypes that produce a range of similar disorders. Those disorders are grouped into a single category called schizophrenia.
There have been brain abnormalities indicated in schizophrenia, mainly in chronic patients. It has been noted, mostly in males but not all who suffer from the disorder a noticeable enlargement of the ventricles of the brain. Chronic patients are the ones who tend to show large ventricles which may indicate the cumulative effects of anti-psychotic drugs. However, all patients show abnormalities in the basal ganglia. This could explain why so many patients have both positive and negative symptoms.
Within the Shonda Case Study, her family history mentioned there is no indication of mental illness occurring amongst her immediate family. However, a paternal aunt was noted as being “locked away” in a hospital after experiencing a “nervous breakdown.” Shonda reports that her father never spoke about his sister and Shonda has never met her. Also mentioned within Shonda’s childhood background was a stressful environment. Shonda was exposed to constant bickering between her mother and father. Shonda and her older brother were subjected to her father’s potent temper which took the form of his “beating his two children and his wife.” Another variable which may have added to Shonda’s stressful environment is that her father would often arrive home late, after stopping at the bar.
There is a strong and some believe undeniable genetic correlation to the development of schizophrenia, but what is also being studied is the environmental element associated with schizophrenia. In identical twin studies, studies of persons who share 100% of their genes, there is only a 48% chance of developing schizophrenia. (Gottesman, 1991) This should suggest that genetics alone may not predetermine whether a person develops schizophrenia, but rather environment may also provide predetermining factors and influences. “Environmental – in this definition – includes everything from the nutritional environment or viruses that a baby is subjected in the womb, to social environment growing up, to teen drug use or stress.” (schizophrenia.com, 1996-2004)
“Schizophrenic individuals inherit genes that cause structural brain deviations which may be compounded by early environmental insults. As a result some pre-schizophrenic children exhibit subtle developmental delays, cognitive problems, or poor interpersonal relationships. ” (International Journal of Neuropsychopharmacology, March Issue, 2004) There seems to be strong empirical evidence of environmental influences determining whether a person may develop schizophrenia. It is believed that certain individuals may be predisposed to the disorder and environmental insults. Subtle changes in environmental stressors, which may occur at various stages of a person’s life, may activate or trigger the psychotic manifestations of schizophrenia’s signs and symptoms; hallucinations, delusions, disorganized speech and thought patterns, as well as profound disruption in cognition and emotion. (schizoprhenia.com)
Stressors can precipitate development of schizophrenia. A stressful environment or prolonged exposure to a stressful environment may lead to dysregulation (weak immune response) of dopamine. This susceptibility may occur through early environmental damage or due to genetic reasons. Drug abuse, social adversity, or prolonged stress may be the triggers necessary to move a pre-schizophrenic condition into a full-blown schizophrenic disorder. (International Journal of Neuropsychopharmacology, March Issue, 2004)
Schizophrenia occurs consistently amongst all groups of people worldwide. Differing perspectives and opinions arise from varying scientific opinions; however, there is agreement on the fact that schizophrenia does not arise from one specific cause. Much of the research performed studying how a person might develop schizophrenia suggests a biological predisposition. There are a lot of hypotheses about the nature and causes of schizophrenia in general. Environmental influences continue to be investigated and challenged in an effort to determine if a person’s biological predisposition to the disorder is triggered by environmental influences.
Many studies have been conducted on the environmental and biological interactions which may influence the development of schizophrenia. The following are amongst those researched; cultural factors, genetic influences, twin studies, adoption studies, offspring of twins, genetic linkage studies, evidence of multiple genes, neurobiological influences, brain structure, viral infections, psychological and social interactions, and the influence of stressors.
Pregnancy is a volatile period for mother and child. The mother’s well being and health directly affect the child’s overall development from conception, cell differentiation, and birth. This is an environmental influence that some research suggests may increase the chance of schizotypal personality disorder; a phenotype of schizophrenia genotype. The suggestion is primarily based on potential damage to the left hemisphere of the brain of the fetus. The left hemisphere is thought to be primarily responsible for the semantic and computational aspects of language. This is a possible cause of Shonda’s disconnected fragments of thought, and disjointed speech patterns. When damaged, the interactive ability between the right and left hemispheres of the brain is compromised (Scheibel, Arnold, 1997). This leads to decrements in their ability to perform on memory and learning tests. Concerning the developing fetus’ environment, the mother’s exposure to influenza, or other viruses, and a variety of influences, biological or environmental, the severity of the development of schizotypal characteristics, like paranoia or illusions, will vary from mild to moderate. (Durand & Barlow, 2007, ch 11)
Biological interventions are the oldest acceptable method of treatment. Even as late as 1930 insulin dosing was used to induce comas at the risk of serious illness or death. At the same time, psychosurgery (lobotomies), and electroconvulsive therapy (ECT) gained popularity. It was found that all three were not beneficial for most people with schizophrenia. Soon after followed antipsychotic medications. The 1950s brought with it a plethora of several neuroleptics. These medications were found to be effective at reducing or eliminating hallucinations and delusions as well as social deficits. However, clinicians and patients must be willing to run through the gamut of available medications available, because as with most schizophrenic treatment attempts, it works to varying degrees and not at all with others. (Durand & Barlow, 2007, p. 494-500)
The common treatment of schizophrenia and treatment delivery varies quite considerably across different cultures. For example, Hispanic families are most likely to take in a relative instead of sending a loved one to long-term care. Chinese medicine is relied upon among the Chinese. It could be a choice for the Chinese to use holistic remedies, herbs, acupuncture and acupressure for tradition or for the reason of expense. Sufferers are not so lucky in Africa. Most countries in Africa choose to send their schizophrenia sufferers to jails due to lack of appropriate facilities. (Durand & Barlow, 2007, p. 500)
There has been much research and work conducted in an attempt to determine which type of psychosocial treatment is most effective in treating schizophrenia. The recent work in the area of psychosocial intervention has suggested that there is high value of an approach consisting of both drug treatment and psychological methods (Tarrier et al., 1999).
It seems no matter the treatment chosen to address schizophrenia; it is a rarity that the treatment is successful enough to claim full recovery. However, the easement of the disorder may be achieved through a combination of efforts and treatments. The quality of life for schizophrenic patients can be meaningfully affected by combining antipsychotic medications with psychosocial approaches, employment support, and community-based and family interventions. (Durand & Barlow, 2007, p 500)
The effectiveness of any chosen treatment for schizophrenia is quite limited. Until recently methods of psychotherapy did not seem to be helpful. But specific types of psychotherapy, sometimes combined with drug therapy, have been starting to show signs of alleviating the personality disorder. It’s just a plain hard fact that schizophrenia is chronic and by nature it is always quite a chore to experience any relief, let alone successful recovery for any chronic disorder. Drug treatment is currently designed to temporarily affect the patient’s behavior. Psychotherapy makes attempts to help people recognize their problem and change their social behavior.
Although typical treatment may involve antipsychotic drugs and psychosocial treatments, I think I would plan a heavy psycho-social treatment with medical interventions at different or alternating intervals. This might be radical but I think that the irregularity of the medications would inhibit the body’s ability to adjust to the medications while the regularity of the psychosocial treatments builds a solid dependable foundation for the mind.
I also believe through regular conditioning or reconditioning of the social and moral aspects of human relationships, I think any person can benefit and learn from social learning. The essence of normality in our lives is self-care, calm and safe social interactions, and of course most everyone learns a vocational skill or two. Experiencing noticeable results would take more or less effort depending on the patient and more or less time as well. As with all healthy regimes, maintenance is required. I would suggest that a major stipulation of this plan would be regular practice of skills learned. This would help maintain the effects for a longer period of time, perhaps if followed diligently, without degradation in displayed skills.
Like schizophrenia itself, any psychological model applied to understanding and treating schizophrenia will be complex due to the multiple factors incorporated. The cognitive model introduced by David Hemsley suggests the summary of the formation of a persecutory delusion. In short, the precipitant is affected by the emotion or beliefs a person has about oneself, others and the world and anomalous experiences and finally cognitive biases. The search for meaning ensues and the selection of an explanation develops based on one’s belief about illness, social factors, and belief flexibility. Ultimately all of these factors conspire to create “The Threat Belief.” The model indicates exploration into newer directions. The empirical determination of internal and external events still remains. The flexible nature of the model allows for events which may be positive, negative or neutral. (Hemsley, D., 2005)
The future of schizophrenia is bleak for the mind is a vast and curious entity and will likely always remain so. Shonda will likely live her life in the mental institution heavily drugged with that same bleak prognosis. Perhaps studies will advance, or researchers will finally win a break-through and schizophrenia will finally become less convoluted to follow intelligently. Our world is changing and many developments occur daily which perpetuate the existence of our species. A strength of a world producing such research and studies is that it facilitates investigation as to the interaction of psychotic processes, non-psychotic processes, the environment, genetic predisposition, and how each affects the other.
Durand, V.M., and Barlow, D.H. (2007). Essentials of Abnormal Psychology (5th ed.). Belmont, CA: Thomson Wadsworth.
PsychNet-UK, (Date Unknown). Disorder Information Sheet. Retrieved from http://www.psychnet-uk.com/dsm_iv/schizophrenia_disorder.htm
Hogarty, 1995 Personal Therapy: A Disorder-Relevant Psychotherapy for Schizophrenia http://schizophreniabulletin.oxfordjournals.org/cgi/reprint/21/3/379.pdf
Alloy, Acocella & Bootzin, . (1996). Abonormal psychology, current perspectives, 7th edition. International Version: 1996.
Tarrier, N., Wittkowski, A., Kinney, C. McCarthy, E., Morris, J., & Humphreys, L., (1999). Durability of the effects of cognitive-behavioral therapy in the treatment of chronic schizophrenia:12 month follow-up. British Journal of Psychiatry, 174, 500-504.
Scheibel, Arnold, (1997) Embryological Development of the Human Brain, New Horizons, Retrieved from http://www.newhorizons.org/neuro/scheibel.htm
The International Journal of Neuropsychopharmacology, Volume 7, Issue 01, (March 2004, pp 1-8) doi:10.1017/S1461145703003900, Published Online by Cambridge University Press Feb 2004 05
Pathways to schizophrenia: the impact of environmental factors. (March 07, 2004) Retrieved Apr 4, 2010, from http://www.ncbi.nlm.nih.gov/pubmed/14972079?dopt
Schizophrenia.com (1996-2004) Preventing Schizophrenia: Recent Research. Retrieved April, 04, 2010, from http://www.schizophrenia.com/
Gottesman, Psychologist World, Behavioral Approach, (1991) Retrieved Apr 4, 2010 from http://www.psychologistworld.com/issues/behavioralapproach.php
Schizophrenia Symptoms. (2009). Retrieved April 6, 2010 from http://www.schizophrenia.com/diag.php
Symptoms and Treatment. (2009). Retrieved April 6, 2010 from http://www.mentalhealth.com/dis/p20-ps01.html
How was schizophrenia discovered? (2005). Retrieved April 6, 2010 from http://www.psychiatry.uiowa.edu/mhcrc/MH-CRCpages/How%20Was%20Schizophrenia%20Discovered.htm
Clinical Trials, Schizophrenia, Featured Studies. (2010). Retrieved April 6, 2010 from http://www.nimh.nih.gov/trials/schizophrenia.shtml
National Institute of Mental Health web-site. www.nimh.nih.gov
Verdoux H, Geddes JR, Takei N, Lawrie SM, McCreadie RG, McNeil TF, O’Callaghan E, Stober G, Willinger U, Wright P, Murray RM. Obstetric complications and age at onset in schizophrenia: An international collaborative meta-analysis of individual patient data. American Journal of Psychiatry 1997 Sept; 154 (9): 1220-1227.
Wang, Q. , Vassos, E. , Deng, W. , Ma, X. , Hu, X. , et al. (2010). Factor structures of the neurocognitive assessments and familial analysis in first-episode schizophrenia patients, their relatives and controls. Australian & New Zealand Journal of Psychiatry, 44(2), 109-119.
Harland, R. , Antonova, E. , Owen, G. , Broome, M. , Landau, S. , et al. (2009). A study of psychiatrists’ concepts of mental illness. Psychological Medicine, 39(6), 967-976.
David R. Hemsley, A simple (or simplistic?) cognitive model for schizophrenia, Behaviour Research and Therapy, Volume 31, Issue 7, September 1993, Pages 633-645, ISSN 0005-7967, DOI: 10.1016/0005-7967(93)90116-C.
Hemsley, D. (1996). Schizophrenia: A cognitive model and its implications for psychological intervention. Behavior Modification, 20(2), 139-169.
Hemsley, D. (2005). The development of a cognitive model of schizophrenia: Placing it in context. Neuroscience & Biobehavioral Reviews, 29(6), 977-988.