Is Schizophrenia a Neurocognitive Disorder? A Look at Conflicting Evidence

In recent years, there is been increasing attention among schizophrenia researchers on developing and refining tools for measuring basic neurocognitive functions, such as attention, memory, and executive function. Measurement of the functions is based on stimuli generated by the computer. Given that there is a significant correlation between performance on these computer generated tasks and negative symptoms (but not positive symptoms), there has been much speculation to the effect that, schizophrenia is basically a neurocognitive disorder. In keeping with this proposition, a variety of training tasks, labeled cognitive remediation, have been presented to the patients with the aim of improving their cognitive functions and consequently, their negative symptoms. For example, one remediation consisted of learning the numbers on license plates (UCLA study). To my knowledge, neurocognitive remediation may improve these basic neurocognitive functions, but do not have a clinically significant impact on the negative symptoms. A different line of inquiry has focused on the trajectory of negative symptoms, during an initial episode of schizophrenia. In a recent study (Gee et al., 2016), it was found that there is a tremendous increase in the frequency and intensity of negative symptoms with the onset of psychotic symptoms, but a rapid decline of negative symptoms in most patients. It is difficult to attribute this fluctuation to deficits in neurocognition, which are comparatively stable. An even more pertinent set of observations can be drawn from the responses of individuals with predominantly negative symptoms to a stimulating, normal environment. Prior to this kind of intervention, these individuals are totally withdrawn, socially inactive, and relatively unresponsive to professional and nonprofessional personnel; however, when they become engaged in a highly stimulating situation, such as having a birthday party in their honor, we observe that they become animated, and participate in group singing and dancing. Their negative symptoms, such as amotivation, antisociality, and the blankness of their faces become greatly reduced and in some cases return to normal. In our previous work on the relationships of neurocognition and negative symptoms, we’ve provided a path analysis, starting with neurocognition. We assumed that neurocognitive deficits greatly reduced social interaction and other activities; however, we assume that this role had to be indirect, which was hard to see any direct connection between deficits in attention, memory, etc., and the individual’s lack of participation in any of the aspects of normal living. We assumed that there was probably a pathway from the neurocognitive deficits, leading to poor performance in school and social interactions, leading to a negative self-concept (as a failure, social reject), and defeatist and asocial beliefs. We further assumed that these defeatist and asocial beliefs led to inactivity and social withdrawal. A series of studies supported this pathway. We found, in a randomized controlled clinical trial, that focused on neutralizing the individual’s beliefs by engaging them in rewarding and meaningful activities, had a significant impact on the negative symptoms and to some extent, the positive symptoms (Grant, Huh, Perivoliotis, Stolar, & Beck, 2011).

These findings have led us to question what role, if any, is played by supposed neurocognitive deficits. We speculated that perhaps the poor scores on these neurocognitive tests might be accelerated, due to alack of effort/motivation on the part of the individuals, in responding to the neurocognitive test. We had observed, for example, that a number of our patients were able to drive, a task which involves sharp attention, recall, and flexibility, despite poor performance on the neurocognitive test. We, therefore, thought that the low scores might have to do with the patients’ lack of motivation to make the effort to perform well on essentially meaningless tasks. We, therefore, decided to test out a different pathway, which assumed that low neurocognitive functioning was due to diminished motivation to perform on the test. We also assumed that this lack of motivation was the end result of a path consisting of negative attitudehopelessnessnegative motivationpoor performance on tests. When we tested out this sequence, we got the following statistical values.It is probable that the path is bidirectional, that is as we had assumed in our earlier work, a cycle could start with neurocognitive problems, leading to traumatic experiences involving inadequate performance in social situations, leading to negative attitudes, and consequently, a fear of failure, manifested by avoidance of performance or social challenges. Even if the initial insult starts with neurocognitive deficits, we propose that the bulk of the individual’s problems are what comes afterwards, and that the very low scores on neurocognitive tests, when the individual develops schizophrenia, are greatly exaggerated. In any event, as we pointed outpreviously, the key to helping these patients lie in enabling them to compensate for their negative problems through motivation enhancing activities.This hypothesis also has some support from a study involving the positive impact of three different, relativity discrete training sessions, with brain damaged individuals, compared to a more holistic approach, involving the entire personality (cognition, affect, emotion, etc.) (Wilson, 1997). The holistic approach had a far more beneficial effect on these individuals’ behavior.

Conclusion

We believe that some problems early in life, in neurocognition, have an initial impact on the trajectory, leading to the negative symptoms of schizophrenia, but once they have set the cycle in motion, their influence is minimal. First, neurocognition plays a role in impairing the individual’s function at the time of onset. The later low-functioning cannot be attributed to the neurocognitive impairment, but rather, to dysfunctional beliefs. As these dysfunctional beliefs are improved, the individual’s overall functioning improves, although the neurocognitive impairments may be unimproved, or even improve, as illustrated in a number of cases. Specifically, and in accord with our early formulations, neurocognitive dysfunction, during childhood and adolescence, leads to failures, disappointment’s, rejections, etc. In response to these devaluing experiences, the individuals build up clusters of defeatist and asocial beliefs. In addition, the individuals’ concepts of themselves and their concepts of how others regard them become more or less fixed in a negative mode. The negative attitudes have a direct impact on motivation and behavior, leading to avoidance and withdrawal. These tendencies towards the retreat into social isolation and inactivity become greatly magnified at the onset of psychosis. A proportion of these individuals, do not recover and go into a chronic state of negative, as well as positive symptoms.

The neurocognitive impairments, which we assume initiated this entire trajectory, no longer play an essential role in the symptomatology. Although they still are manifest in response to discrete tasks, they no longer seem to have much influence, if any, on the individuals’ latent capacities to perform highly sophisticated tasks, such as driving or to engage in meaningful activities. The continued presence of deficits in the neurocognitive tests may be mostly a residue from the past, or may be due to the individuals’ reluctance to engage in non-meaningful tests, or may be due to a regression to more limited functioning when subjected to testing. In any event, we have found that a holistic approach, engaging the patients in meaningful, rewarding activities, appears to increase their participation in social and other meaningful activities, to an extent far beyond what might be expected from the neurocognitive testing.


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