Comparison of Schizophrenia with Parkinson’s Disorder: The Vulnerability-Stress Model of Schizophrenia

Let us consider two disorders that have been considered neurodegenerative. Kreaplinapplied the term dementia praecox because he thought these individuals had a progressive structural defect. Jung challenged this and pointed out that not only were these disorders not progressive, but a number of patients made a complete recovery. He particularly emphasizes the importance of activity and noted that once he had introduced this regimen, the number of catatonic presentations grossly diminished. The other condition, which is labeled neurodegenerative, is Parkinson disorder, attributed to degeneration of the substantia nigra, with some relief that is helpful but not permanent, coming from the administration of a dopamine compound.

Think of a person in the early stages of schizophrenia; he is 22 years old, has had one psychotic episode, is able to attend classes at college part-time, but spends the rest of his time at home, rarely speaks to his family, and has few family or friends. Now compare this when an individual who has had the disorder for 30 years, had been hospitalized many times, has plenty of delusions and believes his mind is being read by others. On the hospital unit, he pays little attention to personal hygiene, needs help in getting dressed, and would not eat, take showers, or go to the bathroom unless pressed to do so. It is clear that in both, there is a progression of the disorders and their appearance, after the same duration, which implies deterioration and irreversible are similar. But are they actually similar, except for superficially? Advanced Parkinson’s disorder is caused by a definite lesion in the brain, but where is the lesion in schizophrenia? Many investigators, relying on atrophy of certain areas of the brain revealed, by PET scans and alike, attribute the disorder to structural change. Yet, we find that in the case of the young man and the old man that their problems lay in their belief systems. In addition, those very contextual problems that depress the scores on neurocognitive tests also account for the progression of the disorder. These conditions, which depress scores on neurocognitive batteries, also combine to contribute to the individuals social withdraw, inactivity: loss of motivation and effort, low mood, stress reactivity, avoidance of unpleasant stimuli (such as tests, the formal medical setting, medical and illicit drugs, and the prevailing culture of the unit). All these conditions contribute to chronic schizophrenia because, in some way, they have an impact on the individual’s dysfunctional belief system. The individuals’ self-image of being incompetent, undesirable, worthless, and vulnerable lead to their social isolation, their hyper-reactivity to being controlled and diminished leads to the expectancies of being dominated, dejected, and experiencing social failure. The point is, that unlike progressive neurodegenerative disorders, such as Parkinson’s, schizophrenia is to varying degrees, reversible. For example, some individuals who have been sick for 5-10 years can be restored to normal functioning; those, who have been hospitalized for up to 40 years, can improve to the point of independent living but still may remain socially withdrawn and not engaged in productive activity. The take-home message is: change all of the contextual variables that interfere with the individual’s functioning (in other words, change the dysfunctional belief system), and you can facilitate real progress towards recovery.

Which models fits each of these disorders best?

It is clear that the neurodegenerative model fits Parkinson’s: a) there is clear evidence of the loss of vital brain tissue, and b) the clinical course consists of symptoms attributable to the brain lesion. The symptoms are progressive, which is consistent with a progressive brain legion.

The vulnerability-stress model fits schizophrenia better than does the neurodegenerative model. The clinical course of schizophrenia is reversible, whereas the neurodegenerative disorder is not reversible. The vulnerability to schizophrenia is indicated by the familial incidence of this disorder (even though precise genes have yet to be identified). The family members who are not afflicted in schizophrenia still show indications of the vulnerability: stress reactions to being tested. This vulnerability appears early in life, as these individuals often show attenuation of scores on intelligence tests. They also show symptoms in childhood and adolescence, therefore, showing on neurocognitive tests, during the prodromal period may be another sign of their potential reactivity. Also, on a single study of the prodromal period, in which dysfunctional attitudes were studied, it was found that the dysfunctional attitudes (which are related to vulnerability to stress, such as failure or rejection) are present and facilitate a transition into psychosis.

It is important to examine the significance of brain scans to determine how informative they are in the case of schizophrenia. From its origins in neuropsychology testing of brain damaged individuals, various functions of the brain, such as attention and short-term memory were assigned to specific regions of the brain. The same radiographic strategies and interpretations have been applied to individuals with schizophrenia. Given the findings of deactivation of certain regions of the brain, atrophy of certain areas, and shrinkage over time, a case could be made out for neurodeterioration; however, to my knowledge, no attempt has been made to correlate abnormal findings with abnormally low motivation, negative attitudes, avoidant beliefs, etc. It is also possible that the gradual shrinkage of the brain over many years could be attributed to “disuse atrophy.” It would be very interesting to conduct pre and post brain scans on individuals recovering from schizophrenia.