Poor insight in schizophrenia: neurocognitive basis.MV Lele, AS Joglekar
Department of Psychiatry, Seth G.S. Medical College, Mumbai.
Poor insight in schizophrenia has been recently thought to be a reflection of prominent and enduring neurocognitive impairments. Reports supporting this theory have implicated prefrontal and parietal lobe functions, among other parameters. The results of other studies have negated the role of neuropsychological abnormalities in poor insight. The analogy between poor insight in schizophrenia and anosognosia in neurological illness as proposed by one set of workers has been elucidated in this review and it appears quite promising. However, the drawing of definite conclusions from all this work has been deferred by us, because of the need for more uniform and standardized methodologies for research on the subject. Nevertheless, attempts to improve the cognitive processes, which affect insight in schizophrenia, may be done to gain better treatment outcome in this disorder.
Keywords: Awareness, Cognition, Cognitive Therapy, Denial (Psychology), Human, Schizophrenia, therapy,Schizophrenic Psychology,
Insight is defined as the patient’s self-awareness that there is a problem or an illness and the non-delusional understanding of its cause or meaning. For many years, psychological theories like denial and a wilful preference for psychosis have been propounded to explain the phenomenon of poor insight in schizophrenia. But recently, a hypothesis suggesting that poor insight in schizophrenia is a reflection of prominent and enduring neuro-cognitive impairments, has been put forward. Support for this hypothesis comes from several sources, which is elucidated in this article.
Galin, in as early as 1974, had proposed that there are differences between the two hemispheres in the affective reactions and coping strategies that appear following cerebral injuries or in the course of the intracarotid amobarbital test. He said that denial of illness or euphoria was most often seen following right lesions, while depressive reactions were most often seen following left lesions. He stated that at the time (1974), the evidences for these differences pertained only to reactions to injury and it needed to be found out whether or to what extent the two hemispheres in the intact brain may each subserve characteristic defensive styles.
After this proposal by Galin, there have been a number of controlled studies to assess the neuro-psychological basis for poor insight in psychosis, but reports are mixed. Studies have been done using various measures for assessing the neuro-psychological aspects, such as use of the Wisconsin Card Sorting test to assess frontal lobe functions,, Mini-Mental State examination to assess global cerebral function, other measures of various cognitive functions such as visual and verbal tasks, as also use of brain imaging to establish structural deficits such as cerebral ventricular enlargement. Handedness was also studied in association with poor insight. The following are some of these studies, with their findings:
David et al (1995) studied 150 psychotics with respect to insight at index and follow-up assessment and its correlation with neuro-psychological structural and functional findings. They used the Iager scale which includes a brief cognitive screen with items on orientation, serial sevens and memory; the Trail-Making test (versions A and B), a timed test of motor sequencing and set maintenance/shifting, sensitive to frontal lobe dysfunction; a test for agraphaesthesia, which depends on contralateral parietal lobe function. Verbal IQ was assessed on the National Adult Reading test (NART) and in some cases, on the Vocabulary subtest of the Weschler’s Adult Intelligence Scale (WAIS). They also used CT scanning for lateral ventricular volume and the Annett scale for handedness. They found that orientation and recall, frontal lobe dysfunction and ventricular enlargement on CT scan were not found to be related with poor insight. A relationship between verbal IQ and insight was seen i.e. those with full insight had the highest IQ, while those with lesser degrees or no insight at all had average IQs, with the absence of a linear trend. This was true on within-episode assessments, while at follow-up, insight did not correlate with IQ significantly. Among the neuro-psychological variables, insight at index assessment and follow-up was correlated with neither agraphaesthesia on the right or left sides (suggestive of parietal lobe function) nor performance on either of the Trail-Making tests (suggestive of frontal lobe function). However, a relationship with handedness was discovered on both index and follow-up assessments, with left-handers displaying considerably better insight than right-handers. The authors say that this effect cannot be explained on the basis of cognitive impairment, which was controlled for in their study. Also they state that it is unlikely that so-called “pathological left-handedness” i.e. early left hemisphere damage and subsequent shift of cerebral laterality accounts for the insight differences, since neither obstetric complications nor ventricular enlargement on CT scan was related to insight in their study. Furthermore they have quoted Mcglynn and Schachter (1989) whose article pointed towards right hemisphere damage as being especially liable to lead to lack of awareness of illness. They speculate that in the left-handed patients, the reduction in cerebral asymmetry and hence lack of regional specialisation confers some protection from the effects of focal brain disease, since specialised functions are more diffusely spread throughout the cortex. Hence, damage to the functioning of either hemisphere (or both), including the deleterious effects of right hemisphere dysfunction on insight, becomes less apparent in left-handed patients. In this manner they attempt to explain the relatively better insight found in left-handed psychotic patients. It should be noted that only 46% of the sample in this study had a DSM-IIIR diagnosis of schizophrenia, while the rest had other psychotic conditions. Hence the results of this study should be interpreted with caution with respect to schizophrenia.
In another study, Young et al (1993), in a study of 31 chronic schizophrenic patients, found that two variables on the Wisconsin Card Sorting test viz. the number of categories completed and percent perseverative responses were able to significantly discriminate between subjects of high versus low awareness. Hence they concluded that at least in some of its manifestations, lack of awareness among chronic schizophrenics has an organic aetiology probably mediated by the frontal lobes.
Lysaker and Bell (1994) administered the Wisconsin Card Sorting test repeatedly over a period of one year to 29 patients of schizophrenia with impaired insight as compared to 63 patients of schizophrenia with unimpaired insight. Results indicated that subjects with impaired insight demonstrated consistently poorer performance than subjects with unimpaired insight. Subjects with impaired insight made significantly more perservative errors and achieved fewer categories correct, a pattern of performance deficits identified with neuro-psychological dysfunction in schizophrenia.
In the light of their own results and those of Young et al, therefore, Lysaker and Bell linked poor insight in schizophrenia with cognitive impairment and deficits in the ability to process information. Hence they stated that many patients with poor insight deny illness secondary to fundamental difficulties in processing life-experiences, perhaps in a manner similar to that of neurologically impaired patients suffering from anosognosia. But they agree that since their study focussed on performance on only one neuro-psychological test, no definitive statement about the overall character of cognitive deficits associated with poor insight can be made. In a contemporary study, Lysaker, Bell et al (1994) said that poor insight was associated with cognitive disorganization and a lower intelligence quotient.
McEvoy et al (1996) employed a battery of neuro-psychological tests to find their interrelationship with insight in 32 patients with schizophrenia. They found that a global measure of insight, the Insight and Treatment Attitudes Questionnaire (ITAQ) was related to performance on a test of left parietal lobe function. In addition, the responses to one of the ITAQ items (the one that best reflected current awareness of mental illness in patients at the time of discharge) was related to performance on prefrontal lobe tests and right and left parietal lobe tests. They concluded that at least some of the deficits in awareness of illness in schizophrenia are related to neuro-psychological dysfunction.
Contrary to the findings of all the above studies, Cuesta and Peralta (1994), in a study of 40 DSM-IIIR schizophrenia inpatients admitted with a recrudescence of symptoms, examined the relation of frontal neurologic signs, abnormal involuntary movements, soft neurologic signs and a neuro-psychological battery results with lack of insight. No correlation between poor performance and lack of insight was found on any test. On the contrary, lack of insight was associated with better performance on immediate verbal, immediate visual and delayed visual memory tasks. The same authors, in another study (1995) administered the Wisconsin Card Sorting test to 52 psychotic patients (35 of whom had schizophrenia), and concluded that poor insight may not be associated with poor performances on the WCST. These authors concluded that the neuro-psychological hypothesis of lack of insight could not be supported.
Similarly, in a study of 74 consecutive acutely psychotic inpatients who were given a controlled trial of compliance therapy, Kemp and David found that neuro-psychological test performance improved during the patient’s admission and treatment in the hospital, as did the levels of insight. Cognitive function showed no relationship to insight and compliance initially, and very little after the intervention. Hence they concluded that clinical variables were more relevant to development of insight in acute psychosis than neuro-psychological impairment. Here again, the fact that this study had patients with various types of psychoses, not just schizophrenia, should be considered before conclusions are drawn.
Amador et al, in a detailed review of awareness of illness in schizophrenia, have proposed that the many similarities between lack of insight in schizophrenia and anosognosia in neurological disorders hint that poor insight may have a neurological basis. The subsequent portion of our article enlists the arguments put forward in support of this hypothesis by Amador et al, along with some citations of the reports on anosognosia by other workers as quoted by Amador et al.
Affective unawareness has been described in neurological patients, e.g. lack of adequate emotional reactions to neurological deficit, the condition Babinski named “anosodiaphoria”. A similar state can be postulated in schizophrenia, i.e. the apparent indifferent reaction that schizophrenics show towards their illness.
Unawareness of illness in neurological disorders (i.e. anosognosia), first described by Babinski, bears a striking resemblance to poor insight in schizophrenia. Babinski described the anosognostic patient as displaying a lack of knowledge, awareness or recognition of disease. This has most frequently been observed in patients suffering from hemiplegia and hemianopia, following stroke. Gerstmann, offers the following description: “The hemiplegia is usually on the left side of the body. The patient behaves as though he knew nothing about his hemiplegia, as though it had not existed, as though his paralyzed limbs were normal, and insists that he can move and walk as well as he did before”.
As in schizophrenia, unawareness of illness in neurological disorders is largely intractable to direct confrontation. For example when such a patient is shown the affected limb, he or she will be indifferent to it (Gerstmann 1942). In other instances, the patient will reveal delusional ideas (insisting, for e.g., that the limb is someone else’s), presumably to explain the dissociation between his or her experience of self and his or her perceptions.
As with unawareness of illness in schizophrenia, anosognosia has been understood in various ways. It is most often distinguished from motivated denial (psychological defense) in that anosognosia is thought to stem from a neuro-psychological deficit that leaves a patient unable to become aware of the signs of their illness. Regardless of the aetiology, one thing is certain: Anosognosia in neurological disorders arises directly following injury to the brain.
In neurological disorders, neuroanatomically based theories of anosognosia can be broadly divided into those that attribute this deficit to focal brain lesions, and those that attribute it to diffuse brain damage. Researchers subscribing to the focal lesion viewpoint generally attribute anosognosia to right hemisphere lesions of the parietal area and its connections. Several theories for anosognosia due to right hemisphere involvement have been suggested, e.g. 1) isolation of cortical speech areas may cause anosognosia, 2) a disconnection from awareness of body scheme or image representation may cause anosognosia, or 3) a neurologically-based affective disturbance may lead to the anosognosia. Apart from these, the frontal lobes have also been implicated as a part of the focal lesion theory. According to Stuss and Benson, unawareness deficits have in common an inability to be self-monitory or to self-correct, and that self awareness demands an intact prefrontal function. These authors note the similarities between different forms of anosognosia - Capgras syndrome, reduplicative paramnesia, and confabulations frequently seen in Korsakoff syndrome. They suggest that the deficit of self-monitoring and self-correction results in a general deficiency in reality testing. They also suggest that although frontal structural damage has not been demonstrated in most reported disorders of awareness, an argument can be made that a functional disturbance exists. Hence they theorize that intact prefrontal function is necessary for the capacity of self awareness. A similar theory has been put forward by Price et al who described two adult patients who suffered bilateral prefrontal damage early in life and subsequently came to psychiatric attention because of severely aberrant behaviour. The authors stated that frontal damage acquired early in life appears to provide the neurological substrate for a special type of learning disability which includes the impairment of insight in addition to that of foresight, social judgement, empathy, and complex reasoning.
Anosognosia has also been observed in patients who have had diffuse brain damage, usually following a stroke. In these patients self-awareness deficits are most often understood as stemming from an overall decline in cognitive function. But according to Babinski and Gerstmann1, this seems unlikely, since anosognosia has been observed in patients without general intellectual impairment, and in patients with unawareness of specific dysfunctions coinciding with intact awareness of other deficits.
Of interest is the finding of domain-specificity for anosognosia. For example, a case described by Von Hagen and Ives involved a 76 year old patient who denied paralysis of the left leg and yet was aware of the paralysis of the left upper limb and of severe memory impairment. Such observations have led some investigators to postulate that these deficits involve “modality-specific disorders of thought” that arise from a dysfunction of a modular central processing system rather than of a single higher order system responsible for self awareness.
The literature on unawareness of tardive dyskinesia in schizophrenia suggests that self awareness deficits in schizophrenia may also be domain-specific. Caracci et al, found that fifteen of twenty (75%) of the schizophrenic patients with tardive dyskinesia(TD) in their study were unaware of their involuntary movements. Moreover, when the relation between unawareness of TD and unawareness of psychiatric disorder was examined, it was found that thirteen patients were unaware of their psychiatric disorder, indicating that although the two measures were strongly correlated, there was not complete overlap.
From the varied literature on the subject including the above reports, Amador et al have suggested that certain parallels may be drawn between unawareness phenomena described in neurological disorders and schizophrenia. They also note that there are numerous reports of the presence of neurological soft signs and neuro-psychological deficits in schizophrenic patients. They quote Matthysse et al who have proposed that schizophrenia and eye-tracking dysfunction are independent expressions of an underlying latent trait, some nervous system disease process that affects different regions and systems of the brain independently. This model is consistent with the explanations for anosognosia offered by Mcglynn and Schacter and Stuss and Benson. That is, schizophrenia in all its varied forms may result from deficits in multiple brain regions resulting in disorders of thought, perception, attention, affect, eye movement, and /or insight.
Bear has drawn attention to the therapeutic implications of recognition of the presence of unawareness of illness. He says that in the rehabilitation of aphasic patients with left-hemispheric injuries, the use of melodic intonation or visuo-gestural association may enlist the abilities of the right hemisphere. After right hemispheric injury, he suggests that the verbal hemisphere must be repeatedly reminded about the tendency to neglect, minimise and socially misperceive, and verbal strategies that the patient may apply for correction must be repeatedly presented to the patient. Steps in emotional perception and communication may have to be explicitly rehearsed. Techniques to maximise alertness and attention might improve therapy.
Bellack et al administered the Wisconsin Card Sorting test to sixteen schizophrenic patients with standard instructions as compared to a second cohort of twelve schizophrenic patients who were given the WCST after a brief training which included instructions plus rehearsal and feedback. The performance of the second cohort was better, which led the authors to conclude that deficits in performance of schizophrenic patients on the WCST are remediable with training. They further elaborated on the difference in WCST performance deficits between patients of focal frontal dysfunction (neurologic) versus schizophrenic patients. They said that the neurologic frontally impaired patients do poorly on the WCST because of perseveration and impaired set shifting when the rule for correct responses changes, while the schizophrenic patients have an impaired ability to develop a plan rather than being unable to shift from an incorrect plan. They suggest that their training may have compensated for such a deficiency in the second cohort. However, they do agree that it is not clear how durable or generalizable the results of training are and so recommend studying the effect of a more extensive training regime on cognitive processes that affect daily living.
All these may apply to those efforts, which are taken to improve insight in schizophrenia.
The theories and the research reports reviewed above do hold some substance and therefore cannot be ignored. However, further research with methodologies devoid of the limitations of the above studies (for example, use of uniform samples with only patients with schizophrenia rather than various types of psychosis) is necessary before valid conclusions can be drawn about the neurocognitive basis of poor insight in schizophrenia. Despite this, attempts to improve cognitive processes, which affect insight, may be done to improve the therapeutic outcome in schizophrenia.