Defining Schizophrenia: A Testable Model for Schizophrenia Incorporating Homogeneous Subtypes
Matthew P. Rick Rochester Institute of Technology
This paper examines new research into the area of schizophrenia with an eye to defining it in a more concrete and easily testable way. It attempts to maintain validity by explaining the notable heterogenity of schizophrenia as a disorder, while still providing a useful definition of the condition. A new model for classifying the different subtypes of schizophrenia will be presented, as well as a proposal for testing of this model.
One of the most difficult problems presented to those attempting to define schizophrenia has traditionally been the great degree of heterogeneity with regard to the symptomatology of the disease. This has led to an almost haphazard convention in classifying the condition, with various models basing their various schemes on nearly any observable criterion which might in some way classify what appears, at first glance, to be a purely heterogeneous collection of symptoms.
Due to the heterogeneity of schizophrenia, it therefore stands to reason that any definition of the disorder should take into account this heterogeneity. More simply put, such a definition needs to be both sufficiently general in order to fully contain the symptomatology of the condition, but also specific enough to provide both for rigorous testing as well as to be of any practical use.
Most earlier models rely on classifying schizophrenia based on the symptoms of the sufferer, thus catatonic schizophrenia, paranoid schizophrenia, and a whole host of other subtypes were born over the years. The main problem with these classifications is twofold. First, the classifications are based on qualitative judgments. As such, the same patient might be classified at different times, by different clinicians, as belonging to differing subtypes of the condition. Second, it is not unknown for these symptoms to change from time to time. So that a patient diagnosed initially with type 'x' schizophrenia might later be validly diagnosed with type 'y' schizophrenia at some later time in life.
It has been shown that those closely related to individuals with schizophrenia are at greater risk of developing the disease themselves at some point in their lives. It is suspected that this increased risk is due to an inherited liability which manifests as a deficit in executive function, mental control and encoding, attention and verbal and learning memory (Byrne et al, 2003). It would therefore seem reasonable to assume that the diathesis/stress model may be useful in understanding the disorder.
A New Approach
Since this vulnerability appears to be genetic, it would stand to reason that it stems from some deviation from the norm in brain physiology. The problem in determining what physiological deviations have occurred is compounded by the fact that there are two main processes which could be failing, either of which could be expected to produce results similar to those observed in patients, namely, encoding errors and retrieval errors. Further confounding this process is the fact that patients, when tested, have been found to possess both types of errors, sometimes in combination (Turetsky et al. 2002). These findings give rise to the notion of two separate types of schizophrenia, with separate causes.
Furthermore, it has been shown that certain symptoms of schizophrenia, specifically, referential communication disturbances, are largely stable and not effected by the treatment status of the patient (Docherty et al, 2003). This seems to indicate that some aspects of schizophrenia may be present throughout the life of the patient, whether or not the patient ever expresses their symptoms.
This leads to the notion that schizophrenia is a lifetime illness, whether or not the individual ever expresses their schizophrenic symptoms. It is an illness which is based in the brain's physiology and one which is at least partially genetically heritable. Finally, we can conclude that schizophrenia is not so much a condition that is not necessarily as obvious or crippling as previous definitions would suggest, but rather a liability to the full blown, post-break symptomatology of what is currently thought of as schizophrenia.
As mentioned earlier, there are three patterns for the mental disturbances experienced by those suffering from schizophrenia. These three patterns shall be refereed to as the cortical subtype, the subcortical subtype and the composite subtype.
The cortical subtype exhibits formal thought disorder, attention disturbance and algolia, with a relative absence of delusions and less affective flattening. Clearly, this type is similar to the DSM-IV disorganized schizophrenic type. This type possesses memory effects similar to Alzheimer's disease, although to a lesser extent, including impaired immediate recall, limited retention over time, and poor recognition performance, indicative that the label cortical is accurate in that these symptoms are suggestive of a primary encoding and storage impairment (Turetsky et al, 2002).
The subcortical subtype exhibits widely diffuse positive symptoms, dementia and a broad range of "negative" symptoms. This type possesses memory effects similar to Huntington's syndrome, including such symptoms as similarly poor immediate recall, better retention over time, fewer intrusion errors and improved recognition. These symptoms are indicative of a primary retrieval deficit (Turetsky et al, 2002).
As might be expected, the composite subtype demonstrates both sets of symptoms, although to a lesser degree. It should be noted that in most cases, the performance on tests of ability of the composite subgroup is very close to that of controls. For this reason it has been refereed to as the "unimpaired" subgroup, although it should be clear that this is a misnomer.
Various studies have presented some evidence to the effect that schizophrenia seems to often be comorbid with other mental conditions. Three notable studies are those of Barrowclough et al 2003 and Resnick et al 2003. These articles will be reviewed with an eye to determining the relationship between schizophrenia and its comorbid conditions.
Barrowclough, in her 2003 article, states the rate of depression amongst those suffering from schizophrenia to be between 22% and 75% depending on the measures used, which is in general higher than the averages for the entire population. However, when she attempts to determine some kind of relationship between poor self evaluations and symptomatology in schizophrenia she fails to find anything but a few weak correlations. Could this be because the poor self evaluations and mood of people with schizophrenia are unrelated to the schizophrenia but merely comorbidity between schizophrenia and depression? If so, how can we explain the fact that poor self evaluations, a common symptom of depression seem to somehow factor into overall patient outcome?
In his 2003 article, "Trauma and Posttraumatic Stress Disorder in People With Schizophrenia", Resnick summarizes saying, "[this] provides preliminary support for the hypothesis that trauma and PTSD are related to higher levels of symptoms in people with schizophrenia." Furthermore, according to his research he was able to state that in studies specifically examining individuals with schizophrenia the measured rates of PTSD were 28% and 29%, which is much higher than the stated lifetime occurrence in non-schizophrenics, which is 8% to 9% (Resnick, 2003).
One possible explanation of these facts is to define schizophrenia as a vulnerability not just to the schizophrenic break with reality, but also as a vulnerability to other mental conditions. It can be surmised that due to the lower level of reality testing that schizophrenics are able to take part in, their condition helps to both increase the probability of other conditions but also to exacerbate those condition's symptoms once they are present.
If this were the case, then the problem of heterogeneity would be easily solved. For instance, it would be clear that a paranoid schizophrenic, for instance, is an individual suffering from a schizophrenic break with reality while simultaneously suffering from the effects of paranoia, which has been exacerbated by the schizophrenia. Similar explanations of other subtypes should present themselves intuitively.
There have been several attempts to indicate that individuals somehow learn schizophrenia or get it as a result of some experience that they may have. These are founded on the concept that schizophrenia is a condition not of the brain itself, but rather of the mind. While this paper will make no effort to dispute their claims, it will focus on their most important arguments and attempt to demonstrate how this definition can be used to understand the data that is presented by their studies with an eye to proving that what had been thought of as problems with the old definition are actually conveniently explained by this definition.
Although largely in line with the posited theory, Barton Palmer's 1997 article "Is it possible to be schizophrenic . . ." provides some interesting controversy in that it concludes that about 30% of surveyed patients seemed to have little to no neuropsychological impairments. However, in summation he points out that despite the fact that 23% of patients that fell into "normal" subgroup showed learning deficits, of which only 30% of them were taking drugs that would interfere with such tests.
One article selected for its ability to illustrate how this theory can be constructively applied was John Reed's 1997 article "Child Abuse and Psychosis . . ." (Read 1997). In it Read attempts to suggest a causal relationship between childhood sexual abuse and schizophrenia. Although his paper fails to provide any solid proof of the point, instead finding a fair amount of correlation, it illustrates the idea that trauma could potentially be much more devastating to those with a predisposition to schizophrenia than non-schizophrenics.
Obviously, this is far from proved and much closer to being mere conjecture, but there are a great many things that could be done to help validate this definition. Possibly the most important finding which would lend support to this definition would be an analysis of relative commorbidities of various disorders with schizophrenia. Armed with this information it would be fairly easy to determine whether or not these numbers support the theory that schizophrenia represents, at least in part, an enhanced vulnerability to other disorders, although in no way proving that assertion.
What Needs to Be Done
Further tests of high risk individuals is needed in order to determine whether or not the composite subgroup really consists of a combination of both types of biological impairment. Even if the rest of this theory proves incorrect, this information would be invaluable in furthering the study of schizophrenia. Additionally, more research needs to be done along the life span of high risk individuals. Tracking the conditions of these individuals seems to be of tantamount importance, as they can help us to gain a better understanding of what causes schizophrenia to affect some of those susceptible individuals but not others.
In Rick's article, he discussed the disorder known as schizophrenia. He first pointed out the shortcomings in the methods of classification and in the symptomatology of schizophrenia. Rick postulated that, because schizophrenia is hereditary, it is biological--a disorder of the brain rather than of the mind. He suggested that the numerous subtypes of schizophrenia such as paranoid schizophrenia or catatonic schizophrenia spring from three different types of malfunctions with the brain: a problem with encoding data (the cortical subtype), a problem with retrieving data (the subcortical subtype), or a combination of the two (the composite subtype). It was then suggested that schizophrenia was a disorder that made a person susceptible to other mental disorders. Rick rounded it all off by pointing out that his theory is a theory and nothing more. Far more research needs to be conducted on his theory for it to be corroborated.
Attempting to Classify Schizophrenia: Just Plain "Crazy"
Jonathan S. Byrd
Rochester Institute of Technology
Rick postulated a highly interesting point that the subclasses of schizophrenia were based primarily on the notion that people with schizophrenia were more susceptible to other mental disorders--that a person who is classified with paranoid schizophrenia may in fact be a person with schizophrenia while at the same time affected by paranoia. He also claimed that the other mental disorders such as paranoia, when combined with schizophrenia, were intensified to the point that it seemed like a subtype or symptom of schizophrenia, whereas it is not a subtype at all. This is quite a novel idea in the area of classifying schizophrenia and its subtypes, one that should probably be the point of further study.
Rick made a number of interesting points and suggested many new ideas with regards to the classification of schizophrenia. One of the biggest problems inherent with classifying schizophrenia, however, was not discussed--namely, the fact that for a long time schizophrenia has been used as a blanket diagnosis for people who are "crazy." Anyone who obviously had a mental disorder and did not fit into any other category got lumped into the realm of schizophrenia. If need be, new symptoms or even new subclasses were added to make this new case “fit.”
The paper touched upon the fact that the requirements for being classified as schizophrenic are vague at best. It also mentioned the fact that the differences among the subtypes are so minor that one psychologist could classify a person into a certain subclass, whereas another could classify the same person into a different subclass.
In my opinion, the mental disorder known as schizophrenia should not be reworked, nor should it be fixed. Instead it should be completely erased of all notions affiliated with schizophrenia, and researchers should start over from scratch. We need to come up with a better way of diagnosing people with this disorder. The old "wastebasket" diagnosis of schizophrenia is so fundamentally flawed that attempting to repair it or theorize upon it is a lesson in futility.
In "Defining Schizophrenia: A Testable Model for Schizophrenia Incorporating Homogeneous Subtypes," Matthew P. Rick critiqued the currently accepted model for classification of schizophrenia. He explored the traditional problems and difficulties encountered in this categorical approach and suggested another possible model that could be used to classify the different subtypes of this disorder.
Examination of an Alternative Model for the Classification of Schizophrenia Subtypes
Erica L. Greppo
Rochester Institute of Technology
The traditional classification of schizophrenia is a categorical model that splits the disorder into a variety of subtypes. The basis for a categorical model is a set of discrete categories in which all patients can fit into one and only one category. Rick stated what is, in my opinion, the largest flaw in a categorical model of classification. This is that when one is dealing with a disorder such as schizophrenia, one will always be able to find cases that do not clearly fit into any of the defined categories. Rick also stated that although at one point in time a patient may fit into one category, the patient can later be diagnosed to fit into a different category. It seems to me that this is an example of researchers forcing a disorder to fit within a given model, when in fact the model should evolve to fit the disorder.
The concept of one patient fitting into more than one of the established subtypes during different points in time also lent support to Rick's next conclusions. Rick looked at schizophrenia as a lifetime illness and considered more than just the symptoms that are visible during a schizophrenic episode. This is important because it forces attention onto the constant elements of the disorder rather than the shifting visible symptoms. Focusing on these more stable disorder elements will bring researchers closer to a true understanding of the disorder, and it is only through a true understanding of the disorder that a valid model can be created.
The model that Rick proposed is very interesting. It divided the disorder into three subtypes, but the subtypes were not based on symptoms. Instead they were based on brain anomalies and malfunctions that are the sources of the symptoms. I believe that this model got closer to what was really behind schizophrenia than simply categorizing the symptoms, with no real thought as to what caused people to display the symptoms.
The theory presented in this paper shed light on the weaknesses of the current model of classification. The alternative model suggested has great possibilities and should definitely be further explored. As a whole, I think that the model suggested could very possibly replace the model used today and eventually could lead to a much clearer understanding of schizophrenia as disorder, its causes and symptoms.
In "Defining Schizophrenia: A Testable Model for Schizophrenia Incorporating Homogeneous Subtypes," Rick postulated a new look at the causes of schizophrenia and some possible identification techniques that could be used to aide in diagnosis. Many people would agree that the DSM-IV-TR does a less-than-perfect job in helping diagnose schizophrenia as well as many other disorders. I found that Rick's approach of using the physiological defects found in schizophrenic persons as a means of categorizing them very compelling. It seems as though using this method of categorization, which relies on purely physical evidence, would reduce the risk of misdiagnosis based on a clinician's qualitative judgments. This would in turn aide in research, because misdiagnoses would be less frequent, so there would not be as much false patient data in the literature.
Taking the Next Step
Shane K. Porzio
Rochester Institute of Technology
On the whole I felt that Rick did a very good job of summarizing the problem he was addressing and that he developed a fairly accurate and understandable theory for identifying and diagnosing schizophrenia. The description gave good background, outlining the problems with the existing methods as well as providing good corroborating evidence for his theory by describing the different types and subtypes that can be used to identify different manifestations of the disorder. Lastly, the final section in which Rick detailed further studies and tests that need to be performed also rounded out his presentation of the possible implications and further gains to which this theory could give rise.
I felt that there was one other major implication from Rick's theory, which was sparked by his statement "...schizophrenia is a lifetime illness, whether or not the individual ever expresses schizophrenic symptoms.” Assuming this can be held as a truth, it could be assumed that a test could be developed to detect the physical brain defect and at the very least let the person would know he or she is at risk for developing the disorder; a treatment for the disorder could even potentially be developed that would not rely on a lifelong drug regimen. Of course, this would really only be of benefit if the physical defect was easily identifiable as well as treatable.
By tying the physiological explanation to psychological factors, including comorbidity with other disorders, Rick gave a viable path to incorporate possible correlations with other non-physiologically based theories. I felt that this was a very smart move, because it can be used as a way to explain away a lot of possible problems with his theory. Unfortunately, it also came with the negative implication that it could be used merely to explain away these criticisms without a valid reason.
I wholeheartedly support Rick's postulation as far as this theory is concerned, and I would very much like to see what further research based on this theory would uncover. I believe it has a very good base and could ultimately be a huge step towards developing a reliable testable model for schizophrenia. Consequently, I feel that care for the mentally ill inflicted with this disorder could greatly improve and that some so afflicted could be removed from permanent care facilities so they could, it is hoped, lead a full life.
Rick's paper shows some promise, proposing a very interesting redefinition of traditional theories on schizophrenia. The lack of a coherent model for schizophrenia has troubled psychologists for many years, and if his theory is correct, then diagnosing and treating schizophrenia may one day mean treating the individual disorders that comprise a particular case, rather than ineffectively attempting to treat the condition as if it were but one disorder.
Promising Beginning, But Lacking Focus
Joshua M. Rosenberg
Rochester Institute of Technology
My only problem with the paper is that it seemed to trail off near the end. Although Rick made several introductory statements that illustrated the aim of the paper and provided some evidence for specific points in the theory, it never felt like they were adequately tied together. Even though field research was probably not in question for a simple theory paper, it would help if Rick would provide a more coherent closing, stating how each of the sources he introduced tied together. Providing more specific information on his theory at the end, defining schizophrenia as it fits within his theory, and providing several examples of how specific cases might be defined under his diagnostic system would all improve this paper markedly.
There are also a few points earlier in the paper that could use some clarification or support. Rick claimed that schizophrenia diagnoses were based on the judgment of a clinician, which makes them inherently fallible. As I understand it, schizophrenia diagnoses are based on the DSM-IV, which is one of the systems least likely to allow for clinician bias. Illustrating the cases in which overlap occurs might be more effective than simply claiming bias. Without sufficient evidence for the fallibility of the old system, it is harder to accept the need for a new system.
Evidence for the theory could definitely use some shoring up. Aside from some interesting information from the Turetsky et al. (2002) study, there was little in the way of direct support for the theory. Again, this is partially explained by the fact that this is a theory Rick came up with himself, but it might be helpful to have more evidence supporting the compartmentalization of schizophrenia and the disorders he believes are comorbid with it that confound clinicians.
Were Rick to provide more extensive support and a clearer summation of his theory, this paper would be excellent. Though its present incarnation could use some work, the paper is very compelling.
Defining anything in psychology is not an easy task; it seems that there is always another possible and reasonable viewpoint on any subject matter. Rick started out by advising readers of the difficulties of defining schizophrenia, precisely the problems arising from its heterogeneous nature. I agree with Rick on this--schizophrenia is not easy to define by any means. For him to say that the current definition is wrong or insufficient, however, would be mistaken.
Defining Schizophrenia: Is it Possible?
Jason J. Zodda
Rochester Institute of Technology
A major problem with Rick's paper lay where he described the methodology of defining the disorder. Rick stated, "...the classifications are based on qualitative judgments." This is not true. Professionals, using rigid guidelines set forth by the Diagnostic and Statistical Manual of Mental Disorders (DSM), assess schizophrenia; it is not up to the practitioners' judgments. A major reason why the DSM was created was to solve this problem of bias on behalf of the practitioner.
A second concern for me was with the three different types of schizophrenia noted: cortical, subcortical, and composite subtypes. Limiting oneself to the cerebral and sub-cerebral cortex of the brain seems to me to be making the task of defining schizophrenia more challenging.
I understand the author's point of trying to focus more on the biological aspects in defining schizophrenia. When defining a disease such as A.I.D.S., in which biology is the only determining factor, this approach works. I personally do not think, however, that any distinguished professional working in the field of mental disorders would say that schizophrenia was purely biological.
Finally, Rick told readers that other mental disorders are comorbid with schizophrenia; I could not agree with him more. He went off track, however, in stating that, because of a study that found a correlation between post traumatic stress disorder (PTSD) and schizophrenia (Resnick, Bond, & Mueser, 2003), schizophrenia causes PTSD. I highly doubt that the authors of the study meant their audience to perceive this correlation as causation.
In summation, Rick made a weak argument that this new model should replace the DSM. I am intrigued with and appreciate the notion of having better diagnostic criteria for defining schizophrenia. This new model, however, is far too biological in nature for me to accept.
There were many among my peer commentators who state that the theory presented in my paper lacked proof. To them, my answer is two-fold. First, I would like to state that, although not proof per se, there is a fairly large amount of information corroborating this theory, as a cursory glance over the paper itself will reveal. Second, I would like to agree with them in stating that this "proof" is certainly not sufficiently substantive to replace the DSM.
Every Step Forward Is Over a Broken Assumption
Matthew P. Rick
Rochester Institute of Technology
I would like to point out, however, that certain parts of this theory are generally supported by the psychological community or are major focuses of research. Discordant twin studies, as well as high risk studies, have shown that there is in all probability a biological component to schizophrenia (Byrne et al., 2003). MRI scanning and psychological tests can be used to demonstrate the three brain-structure related subtypes (Lenzenweger, Jensen, & Rubin, 2003). There is also evidence that many mental diseases increase in both frequency and intensity in the presence of schizophrenia (Barrowclough et al., 2003; Resnick, Bond, & Mueser, 2003).
The main purpose of this author response, however, is not only to suggest that I believe this theory to be sound--otherwise I would never have written the paper in the first place--but rather to appeal to those who would detract from its merit. I have one request of them: that they prove me wrong. Really, all I ask of them is that they run experiments. Attempt to determine the relation between those thought disturbances of high risk individuals and of schizophrenic individuals. Determine why there is a notable increase in frequency and severity of PTSD among schizophrenic persons (especially considering it is almost three times as high in frequency). All these things and more must be done before we finally put an end to this debilitating disorder.
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