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Department of Psychiatry, University of Cambridge and MRC Cognition and Brain Sciences Unit, Cambridge
Department of Psychiatry, University of Cambridge, UK
Correspondence: Dr B. J. Sahakian, Department of Psychiatry, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK. Tel: +44 (0) 1223 331209; fax: +44 (0) 1223 336968; e-mail: skw22{at}medschl.cam.ac.uk
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODOLOGICAL CONSIDERATIONSCOGNITIVE FUNCTIONING IN THE...GENERAL V. SPECIFIC DEFICITS:...CONCLUSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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Aims To review research of the neuropsychology of bipolar disorder, with special attention to the relationship between mood and cognitive functioning.
Method Literature review.
Results Findings generally demonstrate mania-related impairments on conventional neuropsychological tests, with direct comparisons of patients with mania and patients with depression failing to find group differences. More recent work has sought to differentiate these disorders by employing tasks with affective components. This research has demonstrated biases for processing positive and negative stimuli in patients with mania and depression, respectively.
Conclusions Future studies, employing tasks that require cognitive and emotional processing, should improve our understanding of the deficits observed in depression and mania. Neuroimaging studies of the neural regions that underlie cognitive processing of affective meaning suggest that the medial and orbitofrontal prefrontal cortex may be particularly involved.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODOLOGICAL CONSIDERATIONSCOGNITIVE FUNCTIONING IN THE...GENERAL V. SPECIFIC DEFICITS:...CONCLUSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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In this review, we offer a preliminary exploration of the neuropsychology of bipolar disorder and some suggestions for its future. We begin by considering cognitive functioning in each of the three phases of this illness, thus establishing broad links between affect and cognition. We address the complex issue of general v. specific cognitive deficits in patients with bipolar disorder, focusing on the comparative study of mania, depression and schizophrenia to establish distinct neuropsychological profiles, and conclude with an examination of some of the most interesting developments in recent studies of bipolar disorder and the scope for future research in this area.
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METHODOLOGICAL CONSIDERATIONS |
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Matching for clinical characteristics within or between patient groups presents a particularly complicated problem for research into this type of illness. Neuropsychological researchers generally attempt to minimise the effects of simpler confounds by controlling as many variables as possible; when choosing control subjects, for example, frequent attempts are made to match patients and controls for age and premorbid intelligence. Matching patients with mania and patients with depression for severity of illness, though, is more difficult, largely because assessment measures differ for each type of illness. The Young Mania Rating Scale and the Hamilton Rating Scale for Depression are often used in mania and depression, respectively, but do not allow comparison across disorders. While some investigators match patients for number of hospitalised episodes, or for some other related factor, the bases of these cross-sectional comparisons are dubious. One method of circumventing some of these problems would be to conduct longitudinal studies of patients with bipolar disorder as they enter different phases of their illness; however, as with between-subject designs, longitudinal within-subject designs cannot ensure that severity levels are equated during manic and depressed phases. In addition, potential benefits come at the price of heightened difficulty, with many researchers unable to manage the resources and lengthy time frame required by this research design.
These methodological problems, among others, make any investigation of disordered mood and cognition almost prohibitively complex, but some measures can be adopted to reduce ambiguities and confounds. For example, because knowing the stage of illness is crucial to an understanding of potential links between mood and cognitive function, this review considers only those studies that specify phase of illness. Although it is much more difficult to resolve questions posed by medication and matching for severity of illness, caution is essential, and in what follows we have attempted to be particularly sensitive to the credibility of results compromised by uncertain methodologies.
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COGNITIVE FUNCTIONING IN THE AFFECTIVE DISORDERS |
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Cognitive impairment in depression
Until fairly recently it was thought that even severe forms of depression
were associated with only minor impairments in cognitive function. An
important and comprehensive review by Miller
(1975) challenged this belief
by suggesting that both mild and severe forms of depression are associated
with pronounced deficits on cognitive, motor, perceptual and communication
tasks. Since then, many studies have demonstrated the presence of wide-ranging
neuropsychological deficits in patients with depression
(Weingartner et al,
1981; Brown et al,
1994; Beats et al,
1996; Elliott et al,
1996), with current investigation focusing on the relationship of
these now established deficits to clinical and neurobiological dimensions of
the disorder.
Although patients with depression have been studied using a wide range of neuropsychological tests, researchers have focused on memory and executive function, as the neuroanatomical regions thought to subserve these cognitive domains are fairly well specified (see Elliott, 1998). Given that patients with depression frequently complain of memory difficulties, it is perhaps not surprising that these subjects demonstrate impairments on a range of memory tasks (see Blaney, 1986; Johnson & Magaro, 1987; Burt et al, 1995, for reviews). Deficits have been reported on tests of short-term memory, verbal and visual recognition memory, spatial working memory and immediate or delayed recall (Austin et al, 1992; Brown et al, 1994; Ilsley et al, 1995; Beats et al, 1996; Elliott et al, 1996). As such a broad spectrum of findings may suggest, there has been much debate over the precise nature of memory impairment, and a number of distinct formulations have been offered to explain the observed deficits (see Robbins et al, 1992, for discussion).
Executive abilities are also compromised in these patients, and it has been argued that of the neuropsychological tasks showing impairment, tests of executive function may be the most sensitive. These high-level tasks, of which the Wisconsin Card Sorting Test (WCST) (Grant & Berg, 1948) and the Tower of London test of planning ability (Shallice, 1982) are classic examples, require the coordination of cognitive processes for their successful completion, and are thought to depend on intact functioning of the prefrontal cortex. Indeed, patients with major depressive disorder have been shown to be impaired on both of these tests (Martin et al, 1991; Franke et al, 1993; Elliott et al, 1996), leading some researchers to postulate the importance of prefrontal dysfunction in the pathogenesis of clinical depression (e.g. Elliott, 1998).
Unipolar v. bipolar depression
Many studies are based on samples of patients with depression that includes
both unipolar and bipolar disorders, presupposing the essential similarity of
these conditions. Of the few studies that have directly compared the two, the
general findings suggest that, at least on some neuropsychological tasks,
deficits are more marked in bipolar than in unipolar depression. For example,
Savard et al (1980)
administered the Halstead-Reitan Category Test to acutely depressed unipolar
and bipolar groups of patients who were free of medication at the time of
testing, and found that patients in the bipolar group made significantly more
errors than either patients in the unipolar group or control subjects. On
tests of learning and verbal fluency, Wolfe et al
(1987) similarly found more
marked impairments in patients with bipolar disorder than in patients with
unipolar depression matched for age and education. It should be noted that the
conclusions drawn from both of these studies may be compromised by the
presence of confounding variables. For example, patients in the bipolar group
of Savard et al
(1980) were significantly
older than those in the unipolar group, suggesting that age alone may have
accounted for their findings. Additionally, Wolfe et al
(1987) cautioned that
differences between their unipolar and bipolar groups might actually reflect
subtle differences in severity: the rate of hospitalisation in bipolar
patients was twice that noted in the unipolar patients.
Cognitive impairment in mania
In contrast to the large amount of work devoted to the cognitive changes
accompanying depression, only a few studies have addressed the precise nature
of impairment in patients with mania. A possible explanation for this
imbalance may be the practical difficulties of using standard
neuropsychological procedures to assess mania; the nature of the illness may
prevent patients with mania from being reliable subjects, especially in tests
of cognitive functioning. Nevertheless, it has long been recognised that mania
is associated with changes in cognition as well as in affect
(Kraepelin, 1921;
Bunney & Hartmann, 1965),
and more recent empirical studies confirm this view.
Patients with mania have been studied using tasks that sample aspects of learning and memory, visuospatial ability and executive function. In a study conducted by Taylor & Abrams (1986), tests of attention, visuospatial function and memory were administered to patients with mania, approximately half of whom exhibited moderate or severe global cognitive impairment. With respect to memory processes, Bunney & Hartmann (1965) noted memory loss during manic states in a patient with regular manic-depressive cycles every 48 hours. Furthermore, Henry et al (1971) reported impaired serial word list learning during mania, with decrements in performance directly related to increasing severity of illness. More recent findings suggest that patients with bipolar disorder in the manic phase of their illness are impaired on tests of pattern and spatial recognition memory and delayed visual recognition (Murphy et al, 1999). In an attempt to explain observed memory deficits, Henry et al (1971) proposed that memory impairment may at least sometimes be owing to altered patterns of verbal association. Andreasen & Powers (1974) reached a similar conclusion with their finding that, relative to control subjects, the memory structures of patients with mania were loose, overinclusive and idiosyncratic, leading to difficulties in filtering environmental stimuli and a tendency to overgeneralise.
The notion that mania is associated with some form of ‘dysexecutive syndrome’ also seems reasonable, since patients typically exhibit disrupted social behaviour and decision-making reminiscent of that observed in patients with lesions to frontal regions of the cortex (Bechara et al, 1994). It is thus surprising that so little research assesses executive functioning in these patients. To date, this type of functioning has been studied using tests of attentional set-shifting (Morice, 1990; Clark et al, 2000), planning ability (Murphy et al, 1999) and decision-making (Clark et al, 2000; Murphy et al, 2001). Although impairments have been observed across the full range of tasks, it is not yet clear to what extent these deficits stand over and above those observed in other non-executive domains.
Residual neuropsychological impairments in euthymia
Kraepelin (1921)
distinguished manic depression from schizophrenia on the basis of its
relapsing and remitting course. Patients with affective illness, unlike those
with dementia praecox, were thought to experience remission without cognitive
impairment. Recent investigations of patients in the euthymic phase of bipolar
disorder, however, have challenged this view. Many patients continue to
experience psychological and social difficulties, and while the extent to
which neuropsychological impairment remains is less clear, most studies report
at least some degree of residual cognitive dysfunction in one or more tasks
administered.
Asarnow & MacCrimmon (1981) used a test of attention and visual information processing to compare the performance of out-patients with manic depression or schizophrenia — both groups judged by their attending psychiatrists to be free from major symptoms — with that of healthy controls. Performance of the manic depression group was midway between that of the schizophrenia and control groups, suggesting that people with bipolar disorder demonstrate cognitive impairments that are probably not entirely due to residual psychotic symptoms. Similarly, Tham et al (1997) administered an extensive range of neuropsychological tasks to patients with recurrent mood disorder (10 unipolar and 16 bipolar) who were euthymic at the time of neuropsychological assessment. Cognitive functioning was markedly impaired in a substantial number of these patients. More recently, Ferrier et al (1999) reported residual impairment of executive function in people with euthymic bipolar disorder after controlling for age, premorbid intelligence and depressive symptomatology. Rubinsztein et al (2000) found asymptomatic patients with bipolar disorder (in remission for at least 4 months) to show deficits on tests of visuospatial recognition memory; response latency, but not accuracy, on four distinct tests of executive function, was also impaired. Other investigators have reported evidence of residual impairment as well (Jones et al, 1994; McKay et al, 1995; Kessing, 1998 — but see Kerry et al, 1983).
While the jury is still out on the precise neuropsychological profile found in euthymic bipolar disorder, the balance of evidence from such studies supports a hypothesis of residual cognitive impairment. It is important to note that the bulk of these studies employ cross-sectional, between-subject designs that compare euthymic patients with bipolar disorder with healthy controls. As mentioned above, longitudinal, within-subject designs are more effective in assessing how cognitive performance changes with symptomatic recovery. Clearly, both types of study are necessary if we are to address whether performance of euthymic patients with bipolar disorder is inferior to that of healthy controls, and to demonstrate deterioration or improvement of cognitive functioning within a single subject group. One final note of caution is that some studies do not measure manic or depressive symptomatology during the euthymic phase under study (see Rubinsztein et al, 2000, for a notable exception). It is therefore possible that subclinical psychopathology may at least partially account for the residual deficits observed.
Thus, while recent experiments have established the range and depth of cognitive impairments associated with depression, mania is clearly suffering from a lack of attention. Preliminary results suggest wide-ranging deficits in patients with mania; but a comprehensive investigation of cognitive functioning across a full spectrum of tasks should still be undertaken. Comparisons of unipolar and bipolar forms of depression have revealed interesting findings; they suggest that studies presupposing the essential similarity of unipolar illness with bipolar illness may be too simplistic. Likewise, the presumption that (bipolar) mania and unipolar depression represent opposite emotional pales in a cognitive—affective continuum may also be an over-simplified model. It is also possible that the cognitive deficits observed in bipolar disorder (depressed phase) could stem from a source unrelated to that of similar impairments in unipolar depression, and that the relationship of affect to all these impairments might be more complicated.
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GENERAL V. SPECIFIC DEFICITS: DISTINGUISHING MANIA FROM SCHIZOPHRENIA AND DEPRESSION |
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TOPABSTRACTINTRODUCTIONMETHODOLOGICAL CONSIDERATIONSCOGNITIVE FUNCTIONING IN THE...GENERAL V. SPECIFIC DEFICITS:...CONCLUSIONClinical Implications and...ACKNOWLEDGMENTSREFERENCES |
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Comparing mania and schizophrenia
Several studies have compared performance in mania and schizophrenia
(Andreasen & Powers, 1974;
Oltmanns, 1978;
Strauss et al, 1984; Morice, 1990;
Goldberg et al,
1993). Findings from these studies indicate that on tests of
selective attention (Oltmanns,
1978), perceptual span
(Strauss et al, 1984)
and shifting attentional set (measures by the WCST
(Morice, 1990), the deficits
in patients with mania are indistinguishable from those in patients with
schizophrenia. Oltmanns (1978)
found that although both sets of patients were more distractable than normal
controls, they did not differ from each other. Other investigators have also
demonstrated the non-specific nature of mania-related deficits. Otteson &
Holzman (1976) studied
patients with schizophrenia, patients with psychosis but without schizophrenia
and non-psychotic patients and compared them to one another and to healthy
controls on a variety of cognitive measures. While group differences emerged
between psychiatric patients and control subjects, and also between patients
with and without psychosis, there were no differences between the
schizophrenia and mania groups. Any group differences appeared to be related
to degree, rather than type, of disorganisation.
In contrast to the above, differences between patients with mania and schizophrenia have also been reported. For example, Andreasen & Powers (1974) found overinclusive thinking to be more prominent in mania than in schizophrenia. Similarly, Goldberg et al (1993) reported that patients with schizophrenia consistently performed at lower levels than those with affective disorder (unipolar depression, bipolar depression and bipolar mania) on tests of psychomotor speed, attention, memory and attentional set-shifting. It is perhaps noteworthy that generalised intellectual deterioration was more marked in schizophrenia than in the affective disorders, and when intelligence was controlled for, group differences emerged only on a test of memory and the WCST. Thus, the balance of evidence suggests marked similarities between the neuropsychological profiles in mania and schizophrenia.
Comparing mania and depression
Similar findings have been reported from work on comparative cognitive
performance in mania and depression. Bulbena & Berrios
(1993) assessed performance of
patients during acute episodes of major depression and mania using tests of
attention, memory, visuospatial function and choice reaction time. Relative to
controls, patients were impaired on most cognitive measures, but no
differences between mania and depression were found. Moreover, Goldberg et
al (1993) found that in
bipolar disorder, patients in manic and depressed episodes did not differ on
the Wechsler Adult Intelligence Scale — Revised (WAIS—R), WCST, or
on neuropsychological tests of reading, line orientation and facial
recognition.
While direct statistical comparison between patients with mania and depression is clearly the best approach in searching for distinct neuropsychological profiles, indirect comparison between patient groups who have been assessed using standardised neuropsychological tasks can also be informative. In a study by Murphy et al (1999), patients in the manic phase of bipolar illness were given tests of memory and executive function taken from the Cambridge Neuropsychological Test Automated Battery (CANTAB, CeNes Plc, Cambridge, UK). These tests are reliable and valid (Robbins et al, 1994, 1998), and had been previously administered as part of a much larger test battery to a sample of patients with major depressive disorder (Elliott et al, 1996). Patients with mania demonstrated substantial impairments on tests of pattern and spatial recognition memory, and delayed visual recognition. This pattern of impairment was strikingly similar to that previously observed in patients with depression (Table 1). Executive function, as assessed by the computerised one-touch Tower of London test of planning ability, was also similarly impaired in the two patient groups (Fig. 1).
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The cognitive impairments observed in both groups of patients in these studies were interpreted as evidence for relatively global neuropsychological dysfunction (Elliott et al, 1996; Murphy et al, 1999). The deficits observed in patients with mania and depression when tested on object recognition memory were comparable to those previously reported in patients with posterior dysfunction, such as temporal lobe lesions (Owen et al, 1995a) or mild Alzheimer's dementia (Sahakian et al, 1988). The deficits seen on tests of spatial recognition memory and planning ability, however, were similar to those in patients with frontal dysfunction (Owen et al, 1995b) or basal ganglia disorders such as Parkinson's disease (Owen et al, 1995b), in which there is disrupted functioning of frontostriatal ‘loops’ (Alexander et al, 1986). At first glance, these findings suggest that patients with mania and depression are similarly impaired on a range of cognitive tasks subserved by different neural regions, and that a single common underlying mechanism may account for the noted deficits in both groups. Investigators of depression have suggested that the pervasive deficits observed could be due to reduced motivation (Miller, 1975; Seligman, 1975; Richards & Ruff, 1989), a conservative response style (Johnson & Magaro, 1987; Williams et al, 1997), diminished cognitive capacity and processing resources (Hasher & Zacks, 1979), or a narrowing of attentional focus to depression-relevant or task-irrelevant thoughts (Ellis & Ashbrook, 1988). To date, few investigators have considered mania-related deficits within these or similar frameworks.
The bulk of research suggests that in both mania and depression, patients are impaired on a range of cognitive tasks subserved by different neural regions. In addition, although the few studies that actually compare mania and depression employ a limited range of tasks, it appears that conventional neuropsychological tests of attention, memory and executive function are unable to discriminate between patients with mania and depression. Together, these findings suggest that global pathological change, rather than factors unique to either disorder, may account for the observed deficits, and that similar processes may be involved despite markedly different clinical presentations.
New approaches to distinct profiles: biases in information
processing
So far, this review has focused on the performance of cognitive and
neuropsychological tasks employing neutral materials — those that are
not emotionally relevant to the patient's condition, i.e. materials not
seemingly positive or negative in affective or emotional tone. This exclusion
of affective material effectively removes mood from the experimental dynamic;
in order to assess the possible relationship between mood and cognition in the
affective disorders, we must consider studies incorporating affective material
in the experimental design. In patients with depression, empirical studies of
mood-congruent biases in information processing are abundant, with biases
reported in evaluative processes, social judgements, decision-making,
attention and memory (Clark &
Teasdale, 1982; Blaney,
1986; Gotlib & Cane,
1987; Mogg et al,
1995; Bradley et al,
1996). One of the earliest studies examined the recall of past
experiences in patients who were clinically depressed and healthy control
participants (Lloyd & Lishman,
1975). The results indicated that when patients with depression
were required to recall pleasant or unpleasant experiences from their past in
response to various cue words (e.g. ‘house’, ‘table’),
patients recalled unpleasant memories more quickly than pleasant ones as the
severity of depression increased.
In light of these findings, it seemed reasonable to suppose that if differences in cognitive functioning in mania and depression do indeed exist, they will emerge on tasks involving the interaction between cognitive and affective (or emotional) processing. We attempted to address this hypothesis by administering a novel ‘affective go/no-go’ task to patients with mania and depression, and to healthy controls matched for age and premorbid intelligence (Murphy et al, 1999). This task required both attentional and affective processes for its successful completion. Specifically, subjects were required to respond to target words of either positive or negative affective tone by tapping the space bar of a computer keyboard as quickly as possible, and to inhibit this response to words of the competing affective category. As shown in Fig. 2, both groups of patients exhibited attention and response biases — in mania towards the positive stimuli and in depression towards the negative stimuli. In addition, patients with mania — but not those with depression — were impaired in their ability to inhibit behavioural responses and focus attention. These findings were particularly interesting against a background of similar impairments on conventional neuropsychological tests of memory and executive function (see above).
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Neuroimaging studies of the neural regions that underlie cognitive processing of affective meaning suggest that medial and orbitofrontal prefrontal cortex (PFC) are particularly involved (Beauregard et al, 1997; Teasdale et al, 1999). In line with these findings, Murphy et al (1999) concluded that performances in mania and depression were most likely to differ on cognitive tasks subserved by functioning of the orbital/ventromedial regions of PFC. Indeed, Drevets et al (1997) found that the subgenual PFC, which lies in the ventromedial PFC, is differentially activated during periods of mania and depression. The disinhibited response often observed in mania, but not in depression, provides further evidence for differential performance on tasks requiring ventromedial prefrontal functioning, as patients with medial or ventral prefrontal damage are similarly impaired on ‘go/no-go’ tasks (Drewe, 1975; Malloy et al, 1993).
At first glance it might seem puzzling that patients with mania and depression in the study by Murphy et al were differently impaired on the ‘affective go/no-go’ task but not on the Tower of London test of planning, tasks both thought to be subserved by PFC. This apparent inconsistency may be explained by the functional and anatomical distinctions between the dorsolateral and orbital/ventromedial regions of PFC that have been postulated in recent years. It is now known that tasks such as the WCST and the Tower of London test activate a neural network that includes important areas such as dorsolateral regions of PFC (Berman et al, 1986; Baker et al, 1996). These regions have numerous connections with cortical systems involved in information processing. In contrast, tasks that assess ability to make decisions and reverse associations between stimulus and reward are thought to be subserved by ventromedial regions (Rahman et al, 1999; Rogers et al, 1999), which are more extensively connected with limbic structures (Pandya & Yeterian, 1996). As a result, it is possible that this inconsistency is related to the different neural pathways subserving cognitive function in these two tasks.
To the best of our knowledge, no other studies have compared information processing biases in mania and depression. The mood-congruent bias observed in depression is consistent with many depression studies demonstrating biases of memory and attention (see above), but this may be the first demonstration of a positive attentional bias in mania. In this context, it is worth noting that a recent study demonstrated a bias for processing negative information in bipolar mania (Lyon et al, 1999). While such results may seem directly contradictory to the findings reported above, the authors suggested that negative bias may be limited to implicit tests of affective orientation; the ‘go/no-go’ task used by Murphy et al and described here surely taps affective bias more explicitly.
Abnormal response to performance feedback
Another concept related to cognitive processing of emotional material and
to mood-congruent bias is that of reinforcement or reward. It has been argued
that the manifold signs and symptoms of manic depression may be viewed in
terms of dysregulation of three major neurobiological systems: those that
involve reinforcement—reward functions, central pain mechanisms and
psychomotor activity (Carroll,
1994). Although research has yet to demonstrate a disturbance of
reinforcement—reward systems in bipolar disorder, a series of related
studies has suggested that such systems may be disrupted in patients with
major depression (Beats et al,
1996; Elliott et al,
1996,
1997a). Sahakian and
colleagues have suggested that an abnormal response to negative feedback may
contribute to the poor performance often observed in individuals with
depression. Specifically, Elliott et al
(1996) found that on two
CANTAB computerised neuropsychological tasks, which tap different cognitive
functions and involve different neural substrates, failure on one problem
appeared to elevate the probability of failure on the immediately subsequent
problem, suggesting that negative feedback may have a detrimental effect on
subsequent performance. This effect was specific to patients with depression
and was not observed in any of the other clinical groups examined, i.e. those
with Parkinson's disease, schizophrenia or neurosurgical legions of the
frontal or temporal lobes (Elliott et
al, 1997a). The investigators suggested that this
effect may represent an important link between negative affect and the
cognitive impairments associated with depression. Whether this type of effect
is specific to depression or extends to patients who are manic at the time of
testing, however, remains to be determined. In this regard, it is worth
mentioning that in a study investigating the neural response to performance
feedback, the presence of feedback increased blood flow in the
ventromedial/orbitofrontal cortex for a guessing but not for a planning task
(Elliott et al,
1997b,
1998).
Also relevant is a study by Corwin et al (1990) that investigated response bias (i.e. the decision rule subjects adopt when uncertain) on a task of recognition memory in patients with unipolar depression, bipolar mania and controls. An abnormally conservative response bias was associated with depression — whereas a liberal response bias was associated with mania, regardless of severity of illness. Consequently it seems that cognitive performance in depression and mania may be influenced by different emotional or affective responses to task stimuli.
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CONCLUSION |
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The establishment of such distinct profiles is crucial to our understanding of the neuropsychology of the affective disorders. Until recently, most comparative studies noted striking similarities between schizophrenia, mania and depression. However, these studies employed affectively neutral designs, eliminating emotional processing from the experimental dynamic and thus compromising their usefulness in the investigation of mood and cognition. More recent studies, based on the model of earlier investigations of mood-congruent bias in depression, have attempted to differentiate mania and depression by employing tasks with affective components. These studies have noted biases in informational processing and abnormal responses to feedback that appear to be consistent with other data obtained from neuroimaging work on mania and depression.
Historically, studies of mood disorders have made virtually no reference to basic research on emotion in healthy volunteers, and conventional neuropsychological testing has shied away from emphasising emotional components of cognition. A neuropsychological approach that incorporates both elements in experimental designs requiring both cognitive and emotional processing could go a long way towards a better characterisation of the deficits so far observed in depression and in mania (see, for example, Murphy et al, 1999). Such an integrated approach could benefit greatly by incorporating ideas from emotion theories that emphasise cognition—emotion interactions (e.g. Barnard & Teasdale, 1991; Teasdale & Barnard, 1993; Williams, 1996) and from recent advances in our understanding of the brain mechanisms that underlie emotion (e.g. Damasio, 1994; LeDoux, 1995). Studies focusing on the neural networks involved in such emotional processes in the neuropsychiatric affective disorders of depression and mania may provide the key to resolving these important issues.
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Clinical Implications and Limitations |
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LIMITATIONS
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ACKNOWLEDGMENTS |
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American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM—IV). Washington, DC: APA.
Andreasen, N. J. C. & Powers, P. S. (1974)
Overinclusive thinking in mania and schizophrenia. British Journal
of Psychiatry, 125, 452
-456.
Asarnow, R. F. & MacCrimmon, D. J. (1981) Span of apprehension deficits during the postpsychotic stages of schizophrenia. Archives of General Psychiatry, 38, 1006 -1011.[Abstract]
Austin, M. P., Ross, M., Murray, C., et al (1992) Cognitive function in major depression. Journal of Affective Disorders, 25, 21-30.[CrossRef][Medline]
Baker, S. C., Rogers, R. D., Owen, A. M., et al (1996) Neural systems engaged by planning: a PET study of the Tower of London task. Neuropsychologia, 34, 515 -526.[CrossRef][Medline]
Barnard, P. J. & Teasdale, J. D. (1991) Interacting cognitive subsystems: a systemic approach to cognitive—affective interaction and change. Cognition and Emotion, 5, 1 -39.
Beats, B. C., Sahakian, B. J. & Levy, R. (1996) Cognitive performance in tests sensitive to frontal lobe dysfunction in the elderly depressed. Psychological Medicine, 26, 591 -603.[Medline]
Beauregard, M., Chertkow, H., Bub, H., et al (1997) The neural substrate for concrete, abstract, and emotional word lexica: a positron emission tomography study. Journal of Cognitive Neuroscience, 9, 441-461.[Abstract]
Bechara, A., Damasio, A. R., Damasio, H., et al (1994) Insensitivity to future consequences following damage to human prefrontal cortex. Cognition, 50, 7-15.[CrossRef][Medline]
Berman, K. F., Randolph, C., Gold, J., et al (1986) Physiological activation of a cortical network of the Wisconsin Card Sorting Test: a positron emission tomography study. Neuropsychologia, 33, 1027 -1046.
Blaney, P. H. (1986) Affect and memory: a review. Psychological Bulletin, 99, 229 -246.[CrossRef][Medline]
Bradley, B. P., Mogg, K. & Millar, N. (1996) Implicit memory bias in clinical and non-clinical depression. Behaviour Research and Therapy, 34, 865 -879.[CrossRef][Medline]
Brown, R. G., Scott, L. C., Bench, C. J., et al (1994) Cognitive function in depression: its relationship to the presence and severity of intellectual decline. Psychological Medicine, 24, 829 -847.[Medline]
Bulbena, A. & Berrios, G. E. (1993) Cognitive function in the affective disorders: a prospective study. Psychopathology, 26, 6 -12.[Medline]
Bunney, W. E. J. & Hartmann, E. L. (1965) A study of a patient with 48-hour manic—depressive cycles, I. An analysis of behavioural factors. Archives of General Psychiatry, 12, 611 -618.
Burt, D. B., Zembar, M. J. & Niederehe, G. (1995) Depression and memory impairment: a meta-analysis of the association, its pattern, and specificity. Psychological Bulletin, 117, 285 -305.[CrossRef][Medline]
Carroll, B. J. (1994) Brain mechanisms in manic
depression. Clinical Chemistry,
40, 303
-308.
Clark, D. M. & Teasdale, J. D. (1982) Diurnal variation in clinical depression and accessibility of memories of positive and negative experiences. Journal of Abnormal Psychology, 91, 87 -95.[CrossRef][Medline]
Clark, L., Iversen, S. D. & Goodwin, G. M. (2000) A neuropsychological investigation of prefrontal cortex function in acute mania. Journal of Psychopharmacology, 14 (suppl.), A22 .
Corwin, J., Peselow, E., Feenan, K., et al (1990) Disorders of decision in affective disease: an effect of B-adrenergic dysfunction? Biological Psychiatry, 27, 813 -833.[CrossRef][Medline]
Damasio, A. R. (1994) Descartes' Error. New York: Putnam.
Drevets, W. C., Price, J. L., Simpson, J. R. et al (1997) Subgenual prefrontal cortex abnormalities in mood disorders. Nature, 386, 824 -827.[CrossRef][Medline]
Drewe, E. A. (1975) Go—no go learning after frontal lobe lesions in humans. Cortex, 11, 8-16.[Medline]
Elliott, R. (1998) The neuropsychological profile in unipolar depression. Trends in Cognitive Sciences, 2, 447 -454.
Elliott, R., Sahakian, B. J., McKay, A. P., et al (1996) Neuropsychological impairments in unipolar depression: the influence of perceived failure on subsequent performance. Psychological Medicine, 26, 975 -989.[Medline]
Elliott, R., Sahakian, B. J., Herrod, J. J., et al
(1997a) Abnormal response to negative feedback in
unipolar depression: evidence for a diagnosis specific impairment.
Journal of Neurology, Neurosurgery and Psychiatry,
63, 74-82.
Elliott, R., Frith, C. D. & Dolan, R. J. (1997b) Differential neural response to positive and negative feedback in planning and guessing tasks. Neuropsychologia, 35, 1395 -1404.[CrossRef][Medline]
Elliott, R., Sahakian, B. J., Michael, A., et al (1998) Abnormal neural response to feedback on planning and guessing tasks in patients with unipolar depression. Psychological Medicine, 28, 559 -571.[CrossRef][Medline]
Ellis, H. C. & Ashbrook, P. W. (1988) Resource allocation model of the effects of depressed mood states on memory. In Affect, Cognition, and Social Behavior (eds K. Fiedler & J. Forgas). Gottingen: Hogrefe.
Ferrier, I. N., Stanton, B. R., Kelly, T. P., et al
(1999) Neuropsychological function in euthymic patients with
bipolar disorder. British Journal of Psychiatry,
175, 246
-251.
Franke, P., Maier, W., Hardt, J., et al (1993) Assessment of frontal lobe functioning in schizophrenia and unipolar major depression. Psychopathology, 26, 76 -84.[Medline]
Goldberg, T. E., Gold, J. M., Greenberg, R., et al
(1993) Contrasts between patients with affective disorders
and patients with schizophrenia on a neuropsychological test battery.
American Journal of Psychiatry,
150, 1355
-1362.
Gotlib, I. H. & Cane, D. B. (1987) Construct accessibility and clinical depression: a longitudinal investigation. Journal of Abnormal Psychology, 96, 199 -204.[CrossRef][Medline]
Grant, D. A. & Berg, E. A. (1948) A behavioural analysis of degree of reinforcement and ease of shifting to new responses in a Weigl-type card sorting problem. Journal of Experimental Psychology, 38, 404 -411.[CrossRef]
Hasher, L. & Zacks, R. T. (1979) Automatic and effortful processes in memory. Journal of Experimental Psychology: General, 108, 356 -388.[CrossRef]
Henry, G., Weingartner, H. & Murphy, D.
(1971) Idiosyncratic patterns of learning and word
association during mania. American Journal of
Psychiatry, 128, 564
-573.
Ilsley, J. E., Moffoot, A. P. R. & O'Carroll, R. E. (1995) An analysis of memory dysfunction in major depression. Journal of Affective Disorders, 35, 1-9.[CrossRef][Medline]
Johnson, M. H. & Magaro, P. A. (1987) Effects of mood and severity on memory processes in depression and mania. Psychological Bulletin, 101, 28-40.[CrossRef][Medline]
Jones, B. P., Duncan, C. C., Mirsky, A. F., et al (1994) Neuropsychological profiles in bipolar affective disorder and complex partial seizure disorder. Neuropsychology, 8, 55 -64.
Kerry, R. J., McDermott, C. M. & Orme, J. E. (1983) Affective disorders and cognitive performance. Journal of Affective Disorders, 5, 349-352.[CrossRef][Medline]
Kessing, L. V. (1998) Cognitive impairment in the euthymic phase of affective disorder. Psychological Medicine, 28, 1027 -1038.[CrossRef][Medline]
Kraepelin, E. (1921) Manic—depressive Insanity and Paranoia. Edinburgh: Livingstone.
LeDoux, J. E. (1995) In search of an emotional system in the brain: leaping from fear to emotion and consciousness. In The Cognitive Neurosciences (ed. M. S. Gazzaniga), pp. 1153 -1164. Cambridge: MIT Press.
Lloyd, G. G. & Lishman, W. A. (1975) Effect of depression on the speed of recall of pleasant and unpleasant experiences. Psychological Medicine, 5, 173-180.[Medline]
Lyon, H. M., Startup, M. & Bentall, R. P. (1999) Social cognition and the manic defense: attributions, selective attention, and self-schema in bipolar affective disorder. Journal of Abnormal Psychology, 108, 273 -282.[CrossRef][Medline]
Malloy, P., Bihrle, A., Duffy, J., et al (1993) The orbitomedial frontal syndrome. Archives of Clinical Neuropsychology, 8, 185 -201.
Martin, D. J., Oren, Z. & Boone, K. (1991) Major depressives' and dysthymics' performance on the Wisconsin card sorting test. Journal of Clinical Psychology, 47, 684 -690.[Medline]
McKay, A. P., Tarbuck, A. F., Shapleske, J., et al
(1995) Neuropsychological function in manic—depressive
psychosis. Evidence for persistent deficits in patients with chronic, severe
illness. British Journal of Psychiatry,
167, 51-57.
Miller, W. R. (1975) Psychological deficit in depression. Psychological Bulletin, 82, 238 -260.[CrossRef][Medline]
Mogg, K., Bradley, B. P. & Williams, R. (1995) Attentional bias in anxiety and depression: the role of awareness. British Journal of Clinical Psychology, 34, 17-36.
Morice, R. (1990) Cognitive inflexibility and
pre-frontal dysfunction in schizophrenia and mania. British Journal
of Psychiatry, 157, 50
-54.
Murphy, F. C., Sahakian, B. J., Rubinsztein, J. S., et al (1999) Emotional bias and inhibitory control processes in mania and depression. Psychological Medicine, 29, 1307 -1321.[CrossRef][Medline]
Murphy, F. C., Rubinsztein, J. S., Michael, A. (2001) Decision-making cognition in mania and depression. Psychological Medicine, 31, 679 -694.[CrossRef][Medline]
Oltmanns, T. F. (1978) Selective attention in schizophrenic and manic psychosis: the effect of distraction on information processing. Journal of Abnormal Psychology, 87, 212 -225.[CrossRef][Medline]
Otteson, J. P. & Holzman, P. S. (1976) Cognitive controls and psychopathology. Journal of Abnormal Psychology, 85, 125 -139.[CrossRef][Medline]
Owen, A. M., Sahakian, B. J., Semple, J., et al (1995a) Visuo-spatial short-term recognition memory and learning after temporal lobe excisions, frontal lobe excisions or amygdalo-hippocampectomy in man. Neuropsychologia, 33, 1-24.[CrossRef][Medline]
Owen, A. M., Sahakian, B. J., Hodges, J. R., et al (1995b) Dopamine-dependent frontostriatal planning deficits in early Parkinson's disease. Neuropsychology, 9, 1 -15.
Pandya, D. N. & Yeterian, E. H. (1996) Morphological correlations of human and monkey frontal lobe. In Neurobiology of Decision-Making (eds A. R. Damasio, H. Damasio & Y. Christen), pp. 13-45. Berlin: Springer.
Rahman, S., Sahakian, B. J., Hodges, J. R., et al
(1999) Specific cognitive deficits in mild frontal variant
frontotemporal dementia. Brain,
122, 1469
-1493.
Richards, P. M. & Ruff, R. M. (1989) Motivational effects on neuropsychological functioning: comparison of depressed versus nondepressed individuals. Journal of Consulting and Clinical Psychiatry, 57, 396 -402.[CrossRef]
Robbins, T. W., Joyce, E. M. & Sahakian, B. J. (1992) Neuropsychology and imaging. In The Handbook of Affective Disorders (ed E. S. Paykel), pp. 289 -309. London: Churchill Livingstone.
Robbins, T. W., James, M., Owen, A. M., et al (1994) Cambridge Neuropsychological Test Automated Battery (CANTAB): a factor analytic study of a large sample of normal elderly volunteers. Dementia, 5, 266 -281.
Robbins, T. W., James, M., Owen, A. M., et al (1998) A study of performance on tests from the CANTAB battery sensitive to frontal lobe dysfunction in a large sample of normal volunteers: implications for theories of executive functioning. Journal of the International Neuropsychological Society, 4, 474 -490.
Rogers, R. D., Everitt, B. J., Baldacchino, A., et al (1999) Dissociable deficits in the decision-making cognition of chronic amphetamine abusers, opiate abusers, patients with focal damage to prefrontal cortex, and tryptophan-depleted normal volunteers: evidence for monoaminergic mechanisms. Neuropsychopharmacology, 20, 322 -339.[CrossRef][Medline]
Rubinsztein, J. S., Michael, A., Paykel, E. S., et al (2000) Cognitive impairment in remission in bipolar affective disorder. Psychological Medicine, 30, 1025 -1036.[CrossRef][Medline]
Sahakian, B. J., Morris, R. G., Evenden, J. L., et al
(1988) A comparative study of visuospatial memory and
learning in Alzheimer-type dementia and Parkinson's disease.
Brain, 111, 695
-718.
Savard, R. J., Rey, A. C. & Post, R. M. (1980) Halstead—Reitan Category Test in bipolar and unipolar affective disorders. Journal of Nervous and Mental Disease, 168, 297 -304.[CrossRef][Medline]
Seligman, M. E. P. (1975) Helplessness: On Depression, Development, and Death. San Francisco, CA: Freeman.
Shallice, T. (1982) Specific impairments of planning. Philosophical Transactions of the Royal Society of London (Biol.), 298, 199 -209.
Strauss, M. E., Bohannon, W. E., Stephens, J. H., et al (1984) Perceptual span in schizophrenia and affective disorders. Journal of Nervous and Mental Disease, 172, 431 -435.[Medline]
Taylor, M. A. & Abrams, R. (1986) Cognitive dysfunction in mania. Comprehensive Psychiatry, 27, 186 -191.[CrossRef][Medline]
Teasdale, J. D. & Barnard, P. J. (1993) Affect, Cognition, and Change. Hove: Lawrence Erlbaum.
Teasdale, J. D., Howard, R. J., Cox, S. G., et al
(1999) Functional MRI study of the cognitive generation of
affect. American Journal of Psychiatry,
156, 209
-215.
Tham, A., Engelbrektson, K., Mathe, A. A., et al (1997) Impaired neuropsychological performance in euthymic patients with recurring mood disorders. Journal of Clinical Psychiatry, 58, 26 -29.
Weingartner, H., Cohen, R. M., Murphy, D. L., et al (1981) Cognitive processes in depression. Archives of General Psychiatry, 38, 42 -47.[Abstract]
Williams, J. M. G. (1996) Depression and the specificity of autobiographical memory. In Remembering our Past: Studies in Autobiographical Memory (ed. D. C. Rubin), pp. 244 -267. New York: Cambridge University Press.
Williams, J. M. G., Watts, F. N., MacLeod, C., et al (1997) Cognitive Psychology and Emotional Disorders. Chichester: Wiley.
Wolfe, J., Granholm, E., Butters, N., et al (1987) Verbal memory deficits associated with major affective disorders: a comparison of unipolar and bipolar patients. Journal of Affective Disorders, 13, 83 -92.[CrossRef][Medline]
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