Table of Contents:

I. Introduction
II. Explanation of Current Insight Measurement Tools
III. The Psychological Defense Model of Insight
IV. The Cognitive Deficit Model of Insight
V. The Neuropsychological Model of Insight, and Evidence for a Neurological Basis

1. Frontal Lobe Deficits and Poor Insight
2. Relationship of Symptom Pathology to Poor Insight

VI. Implications of Neurological Findings on Future and Current Treatments for Insight
VII. Conclusion
VIII. References

Introduction:

Unawareness of one's own illness among people with schizophrenia has been a documented phenomenon ever since Eugene Bleuler first coined the diagnostic term. Several large field studies (Amador et al. 1994, Fennig et al. 1996) in more recent times continue to confirm the fact that 40-60% of people diagnosed with schizophrenia have partial or no insight into their illness. Such poor insight has profound consequences for treatment compliance, frequency of hospitalizations and relapse, disease prognosis, potential to commit violent acts, and general quality of life. However, the multi-faceted appearance of insight as a concept, as well as the different ways it can manifest within the schizophrenia population, has prevented the creation of a comprehensive system of management for this deeply important facet of schizophrenia. Certain biases in the research of insight (including small and heterogenous sample sizes, subjects in different phases of the illness and/or with different treatment histories, and the use of different scales of insight assessment) have contributed to inconsistent findings and conflicting results with respect to the etiology and course of insight as it relates to schizophrenia. Hlthough there is growing evidence suggesting that impaired insight is heavily related to generalized or specific pathological brain deficits (Keshavan et al. 2004, Smith et al. 2004, Flashman et al. 2001, McEvoy 1996, Young 1993) . Whatever the etiological cause, it is quite possible that any future therapy for insight deficits will end up being as complex as the condition itself.

The term "poor insight" has only recently evolved from a very broad definition to one that includes many different facets. The most widely accepted definition of insight, as documented in current studies on the subject, include three recurring aspects: a general recognition of mental illness, the capacity to correctly attribute symptoms to the pathology of said illness, and the ability to recognize the benefits of (and consequently cooperate with) treatments. (Rickelman 2004, Kemp and Lambert 1995). A dimension added by Amador and colleagues (1994) is the existence of current vs. retrospective insight; that is, whether a patient recognizes that he/she is currently ill or has ever been ill in the past.

Explanation of Measurement Tools for Insight:

The multi-faceted nature of the condition has naturally resulted in a few different measurement scales. The Scale for the Assessment of Unawareness of Mental Disorder (SUMD, developed by Amador et al. 1993) is generally accepted as the most comprehensive measure of different insight aspects. It contains six general items and four subscales which yield 10 summary scores related to different elements of insight. The Awareness of Illness scale (AI) developed by David (1990) is another common assessment scale; however, this test is much more limited, including only three questions that relate to overall awareness of insight. Moreover, one could argue that questions such as "Do you have an illness, or is something wrong with you?" followed by "Is it a psychiatric or mental illness" can be confusing for someone who has not yet familiar with medical vocabulary, and stigmatizing for anyone who objects to the mental illness label. The Insight and Treatment Attitude Questionnaire (ITAQ, developed by McEvoy et al. 1989) is a third measurement scale used in the literature. This assessment test measures several aspects of insight (notably the existence of mental problems, the understanding of need for psychiatric treatment, and the need for medication), and it also has the added strength of applying several temporal measures to the same patient (each subject is assessed at time of hospital admission, at a time defined as "the present", and at time after discharge), thereby establishing the progression of insight over time. Studies that use the ITAQ as their primary measure should be aware that this scale may be more heavily weighted towards compliance-related items in the assessment of insight (Rosch and Corrigan, 2002), and that insight cannot be absolutely correlated with treatment compliance or attitudes towards medication (Kampman et al., 2002). Therefore, use of one assessment scale or another in studies attempting to correlate insight with disease progression, neuro-cognitive function, neurological abnormalities, or pscyhological defensiveness may produce biased results. It is likewise difficult to compare the results of studies which used different systems of measurement.

Despite these confounds, several correlational patterns have begun to emerge within the study of insight in schizophrenia. These have solidified into three main schools of thought regarding etiology: the Psychological Defense Model, the Cognitive Deficit Model, and the Neuropsychological Deficit Model (Rickelman 2004). As these are not necessarily mutually exclusive theories, the following sections will briefly review each (with particular emphasis on evidence of neuropsychological deficits), explore the possibility of a more comprehensive model using the original three as a foundation, and discuss certain implications about the future of treatment for insight deficits in psychiatric illness.

The Psychological Defense Model:

The earliest discussions of poor insight within psychiatric disorders engendered what is now known as the Psychological Defense Model. This was practically the only existing school of thought about insight prior to 1990. The prevailing assumption was that failure to recognize or admit to a psychiatric illness was a conscious (or sub-conscious) refusal rather than an inability. It was further assumed that knowledge of the illness did exist at some cogntive level. There is modest evidence that psychological defense is one aspect of poor insight; for example, numerous studies (Smith et al. 2004, Rusch and Corrigan 2002, Weiler et al. 2000, Carroll et al. 1999) have all noted a positive correlation between increasing insight and increasing depression, as well as a significant tendency for patient populations with depressive disorders to have better insight when compared to other diagnostic groups. Smith et al. (2004) suggest that, in keeping with accepted cognitive models that relate depression to a greater accuracy in describing negative events, poor insight may be a psychodynamic coping mechanism to reduce anxiety and depression. However, there are alternate explanations for the positive correlation between depression and insight; for instance, one could surmise that those patients who show depressive tendencies receive more comprehensive psychological care, or that depression is simply the natural result of independently improving insight, and a sudden pessimistic vision of a future with a major psychiatric illness. Other research (Rickelman 2004) agrees that psychological defense is likely only a small part of impaired insight. Nevertheless, it is important for caregivers to be aware of the increasing risk of depression that seems to occur with improving insight, and include care for depressive symptoms into a comprehensive treatment program.

The Cognitive Deficit Model:

In contrast, the Cognitive Deficit Model acknowledges a slightly more organic etiology to impaired insight. Drawing on research that has linked decreasing insight to increasingly poor scores on the Wisconsin Card Sorting Test (WCST) and other measures of cognitive function (Keshavan 2004, Lele 1998, Young 1993) the Cognitive Deficit Model suggests that poor insight is a result of progressively degenerating cognitive functioning over the course of the illness. Given the high frequency of poor insight seen in first-episode schizophrenia patients (Keshavan 2004), progressive degeneration does not seem to be a likely causal factor of poor insight. However, this does not discount cognitive functions as a correlation factor. In fact, the link between poor WCST scores, a known measure of frontal lobe function, and poor insight in schizophrenia patients may be evidence for a more neurological basis of impaired insight.

The Neuropsychological Deficit Model - Relationship of Poor Insight to Anosognosia:

The Neuropsychological Deficit Model developed out of an identified similarity between the symptoms of poor insight and a neurological condition called anosognosia. Generally developing secondary to a specific lesion (such as focal traumatic brain injury) or diffuse brain damage (such as a stroke), anosognosia is an acknowledged neurological deficit. Patients afflicted with anosognosia share striking similarities with psychiatric patients who have impaired insight (Amador and Paul-Odouard, 2000, Lele et al. 1998): both have a severe lack of awareness of their deficits, which persist despite all evidence to the contrary, both have a strong desire to prove their own assertions, and as such invent confabulations to explain away pathological symptoms. Furthermore, both sets of patients often demonstrate (through functional or imaging tests) frontal lobe deficits. Lele and Joglekar (1998) have carried the analogy further, pointing out that both anosognosia and poor insight in schizophrenia can be either generalized (relating to all aspects of the disease) or domain-specific (patient is aware of certain symptoms or functional deficits, but not others). Amador et al (1994) have likewise identified what they call "spotty insight" among schizophrenia patients.

While the deficit in cases of anosognosia is related to either focal or diffuse brain damage, it has not yet been proven that impaired frontal lobe functioning is a causal explanation for poor insight. However, the evidence amassing for a prominent role of the frontal lobe (as well as other brain structures) is intriguing, and merits a more careful review.

Evidence for A Neurological Basis for Poor Insight:

Neuroanatomic abnormalities are now a well-documented reality of schizophrenia. Findings have consistently included smaller brain volumes, smaller hippocampal volume, enlarged ventricles, a reduction in dorsolateral pre-frontal cortex neuropil (i.e. synaptic tissue between axons), and an overall reduction and disorganization of synapses (Flashman et al., 2004). Some of these abnormalities may be a unique function of schizophrenia rather than a simple reflection of symptoms; Gogtay et al. (2004) documented significantly greater frontal, temporal, and parietal gray cortical matter reduction in subjects with childhood-onset schizophrenia, as compared to subjects with transient psychosis and behavioral problems, and healthy control subjects. Cuesta et al. (1996) demonstrated that 97% of 66 tested schizophrenia subjects showed at least one frontal neurological sign (out of seven), and that these frontal signs were correlated with poor cognitive performance, increased negative symptom pathology, and treatment naivety. Ho et al. (2003) also showed rapid progressive atrophy of frontal lobe gray and white matter volume in schizophrenia patients over a three-year period, correlated with decreased executive functioning and increasing negative symptom severity. Uranova et al. (2004) showed a decrease in oligodendroglial size and density in the prefrontal cortex of schizophrenia patients, suggesting that reduced frontal lobe volume and tissue atrophy observed in other studies may be in part due to a specific deficit in glial cells that act as neuronal satellites and myelinating agents for other brain cells.

Frontal Lobe Deficits and Poor Insight:

Several authors have made specific connections between frontal lobe deficits and impaired insight. The most precise correlation to date was demonstrated by Flashman et al. (2001), who tested insight in schizophrenia patients as a function of neuroanatomic abnormalities in 15 subregions of the frontal lobe. Their results showed an inverse correlation between unawareness and bilateral mid-frontal gyrus volume, right gyrus rectus volume, left anterior cingulated gyrus volume, and bilateral superior frontal gyrus volume. Moreover, the authors correlated specific aspects of insight with each anatomic subregion; overall unawareness of psychiatric illness was associated with smaller mid-frontal gyrus, right gyrus rectus, and left anterior cingulated gyrus, while misattribution of specific symptoms was associated with reduced superior frontal gyrus volume. The various studies that have demonstrated the poor performance of insight-impaired schizophrenia patients on tasks that require frontal lobe activation (Keshavan 2004, Lele 1998, Young 1993) add evidence to the hypothesis that frontal lobe deficits are an important part of declining insight. The work of Uranova et al. (2004) suggests a possible mechanism for this frontal atrophy. They found a decrease of oligodendroglial size and density in the prefrontal cortex region of subjects with schizophrenia. These glial cells act as neuronal satellites (i.e. synaptic anchor points) in frontal gray matter, and form myelin sheaths for neuronal axons in frontal white matter. Uranova et al. found fewer oligodendrocytes (as compared to control subjects) specifically in the gray matter portions of layer V1 of the prefrontal cortex, suggesting that a lack of neuronal support in this area may contribute to brain tissue atrophy and a decrease of metabolic function. Since cortical oligodendrocytes mature mostly during adolescence and early adulthood, early interventions in high-risk populations (such as the children of parents with schizophrenia, infants exposed to hypoxic insult or prenatal infections, substance abusers, etc) targeted specifically towards the preservation of supporting glial cells may be key in preventing a subsequent atrophy of frontal brain regions.

Relationships Between Symptom Pathology and Poor Insight:

Evidence for the involvement of the frontal lobe regions can also be derived from certain correlations observed between aspects of schizophrenia pathology and poor insight. Although these findings have been somewhat contradictory, it is possible to interpret this as a reflection of the multi-faceted nature of insight. One possible association is found between increased negative symptom pathology, frontal lobe deficits, and a general unawareness of mental illness. Cuesta et al (1998) found that poorer insight was associated with more negative symptoms; Kemp and Lambert (1995) likewise showed that improving negative symptom pathology has a significant correlation with improving insight. Several authors (Flashman et al. 2004, Cuesta et al. 1995) have linked negative symptom pathology to decreasing performance on cognitive tests, particularly those that demonstrate frontal lobe function. A hypothesis that links poor insight to cognitive dysfunctions in the frontal lobe area appears to fit well with the specific frontal neuroanatomical abnormalities identified by Flashman et al. (2001).

However, some of the same authors (Cuesta et al. 1998, Kemp and Lambert 1995, Amador et al. 1994) have also found links between increasing positive symptoms and poorer insight. It is now important to point out the specific measure of insight that is showing correlation. Cuesta et al (1998) and Kemp and Lambert (1995) specifically note that increased psychosis and grandiosity (both positive symptoms of schizophrenia) are associated with increased misattribution of psychiatric symptoms. This is a specific aspect of insight (as identified by Amador and colleagues with the SUMD insight scale) that may have a different etiology than general unawareness; as has been previously demonstrated, schizophrenia patients may have selective awareness of some attributes of their illness, but not others (Smith et al. 2004, Lele and Joglekar 1998, Amador et al. 1994), Breibon et al. (2002) have demonstrated that schizophrenia patients with increased positive symptoms (hallucinations, delusions) show a source monitoring deficiency (i.e., a tendency to misattribute one's own productions to another, outside source) opposite of the source monitoring pattern observed in patients with more negative pathology. This implies that positive and negative symptom clusters may be the result of distinctive pathological abnormalities (a suggestion corroborated by evidence from Smith et al. 2004), and thus could logically correlate with equally distinct aspects of insight.

The degree of differential correlations described in the findings above strongly support a multi-faceted model of insight, in which different insight aspects might correlate with different pathological, cognitive, or social deficits. The evidence for cognitive dysfunction (measured largely by poor WCST scores) and many of the physiological brain abnormalities identified in the frontal lobes (see Flashman et al. 2004) complement each other particularly well, indicating that the frontal area of the brain (a known seat of self-monitoring and executive functioning powers) may be a key area in this deficit. However, the variable correlations between different symptom clusters (positive vs. negative) and improving or declining insight suggests that the different elements of insight identified by Amador et al. (1994) and others may be associated with the pathology of these different symptom clusters or sub-disorders of schizophrenia. Looking at the brains of schizophrenia patients using microstate analysis (a technique that can separate out the activity of different populations of neurons and associate these circuits with specific cognitive functions) indicates that information processing circuitry in the temporal lobe region may terminate prematurely (Strelets et al., 2003), resulting in the perception and monitoring deficits that may lead to the positive symptoms like hallucinations and delusions. Other research (Keshavan 2004, Carter 2001, Shenton 1992) has associated specific temporal lobe deficits with increased positive symptomology, self-monitoring deficits, and thought disorder in subjects with schizophrenia. Thus, two possible associative groups begin to emerge with respect to the etiology of insight: one involving negative symptom clusters, physiological and cognitive abnormalities centered in the frontal lobe regions, and general unawareness of a psychiatric disorder, and another relating positive symptomology to source-monitoring and perceptual processing deficits, physiological temporal lobe abnormalities, and misattribution of psychiatric symptoms.

These associations have important implications for future treatments; they suggest that approaches to improving insight should focus on the possible etiology of the insight problem, and tailor the treatment accordingly. For example, if (as evidence from Breibon et al. 2002 suggests) poor source-monitoring ability is correlated more with misattribution than with overall unawareness, then a patient showing specific misattribution problems might have treatment targeted towards temporal lobe structures that control source-monitoring, a different approach than might be taken if the patient did not realize any aspect of their illness at all.


Implications of Neurological Findings on Current and Future Treatments of Poor Insight:

Research has reported the variable success of several different methods of treatment for improving insight. Given that many of these studies fail to specify the aspect and/or degree of insight being measured, and also fail to control for any other ongoing pharmacological or psychosocial treatment of the subjects, it is difficult to compare the overall efficacy of these treatment methods. However, each is worth considering as an important element to a future management model of insight.

From a pharmacological standpoint, clozapine is the only medication reported in literature to have a substantial effect on patient insight (Pallanti et al, 1999). The study was relatively small (including only 53 subjects initially, and 22 for a follow-up evaluation), consisting of chronic paranoid schizophrenia patients being treated with clozapine following a relapse episode. Results showed a modest improvement in positive symptoms, and a greater improvement in negative symptoms, after a six-month treatment period. The authors also noted a specific improvement in patient insight. They suggest that clozapine might improve frontal lobe processing through early gene expression, which correlates with previous research findings indicating that clozapine improves WCST scores in schizophrenia patients (Schall et al, 1995), and that poor WCST scores are an indicator of impaired insight (Keshavan et al. 2004, Lele and Joglekar 1998, Young et al. 1993). However, Pallanti et al. also point out that clozapine may indirectly improve insight by improving negative symptom pathology, which in turn might make patients more amenable to psychosocial intervention programs. This suggested mechanism correlates with other findings (Weiler et al. 2000, Kemp and Lambert 1995), indicating that improving insight is closely correlated with an improvement in negative symptom pathology over time.

Others have suggested the importance of psychosocial interventions for improving insight. Rickelman (2004) states that good insight in schizophrenia patients is related to a strong social support network. Other interventions such as vocational rehabilitation (Lysaker and Bell, 1995), and a specifically modified form of motivational interviewing (Rusch and Corrigan, 2002) have shown some success. However, it should be noted that past studies of motivational interviewing depended on patient treatment compliance as the primary measure of insight, which (as discussed earlier in this paper) may not be a valid indicator. As cited in Keshavan et al. (2004), Thompson et al. (2001) noted that "improving insight" may be due to the socialization and education of a person as a schizophrenia patient (i.e. their exposure to hospital programs and diagnostic labels), or to their improving ability to communicate about their illness. Both researchers and caregivers must be careful with their definitions of insight, and be aware that their own selective biases and medical vocabulary can limit what they see as good or poor awareness. As Rusch and Corrigan (2002) point out, what is considered good insight in a clinical or research setting may simply be the patient agreeing with the health professional's opinions.

Cognitive-Behavioral Therapy (CBT) is one specific form of psychosocial treatment that has recently shown some promising results. Goldapple et al. (2004) showed that CBT can alter metabolic brain functions in subjects with major depression; moreover, they pointed out that although CBT appears to work through different mechanisms than a classic pharmacological treatment for clinical depression (fluoxetine), given that subjects treated with the medication showed different metabolic brain maps than those given CBT, the clinical improvement in both patient populations was comparable. The findings of Goldapple et al. indicate not only that CBT has specific functional effects on the brain, but also that a clinically successful outcome may be achieved through several distinct methods. This is promising for the treatment of insight in schizophrenia patients, not only because insight is a multi-faceted deficit, but also because individuals with unique case histories, lifestyles, and socio-economic standings may require different treatment interventions for a positive outcome. Moreover, given that inequitable distribution is still a black mark on healthcare in this country (due to, among other things, economic factors, isolated geography, and lack of adequate facilities and practitioners), cheaper and/or more accessible options like psychosocial interventions may be able to reach a greater number of people in need.

CBT has also shown potential in treating specific aspects of schizophrenia. Several authors (Rickelman 2004, Lele and Joglekar 1998) have shown that CBT improves WCST scores in schizophrenia patients. The WCST, as previously stated, is an accepted measure of frontal lobe cognitive functioning. Thus, if hypotheses linking certain aspects of insight to frontal lobe regions are correct, an improvement in WCST scores might well correlate with an improvement of insight. More research is needed to determine the specific correlation between CBT, WCST, and insight in schizophrenia.

Conclusion:

Despite some conflicting data, the bulk of literature on the basis of poor insight in schizophrenia serves to highlight a few key points. All researchers (not to mention clinical caregivers and concerned family members) agree that poor insight is a problem that afflicts a large portion of people with schizophrenia, and that the negative consequences of such unawareness are many and costly. And although there are still various schools of thought on what the etiological basis of poor insight might be, these conflicts are not necessarily contentious. On the contrary, not a small number of researchers (Weiler et al. 2001, Rusch and Corrigan 2002, Smith et al. 2004) have concluded that insight is likely a function of several cognitive, social, and biological factors, many of which may work in tandem to produce various types of insight impairments. Smith et al. 2004 have proposed one possible mechanism that integrates current models of awareness, involving frontal-cortical-striatal circuitry abnormalities; another possible integrated model might place insight in the region of the frontal lobes, as suggested earlier in this paper. The variable success of current and past treatment efforts in different patient populations also highlights the multi-faceted nature of schizophrenia as a disorder, and insight as a major part of that disorder. Hopefully, further coordination between researchers and clinicians will lead to a more integrated model of poor insight, as well as a comprehensive collection of strategies to prevent and manage all the various manifestations of this devastating aspect of schizophrenia.

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