Table of Contents:
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
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
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
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.
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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