Reduced Capacity

The notion of reduced capacity in depression was first proposed by Hasher and Zacks (1979). The main assumption of resource allocation theory is that encoding operations vary in the demands they make on limited attentional resources, and that individuals vary in the amount of attentional resources they have available (see section 2.2.5.1.). Hasher and Zacks (1979) suggested the pattern of cognitive deficits associated with depression was compatible with reduced attentional resources, that is, deficits are more likely on tasks which make high demands on attentional resources. While Hasher and Zacks (1979) did not specify the means by which resources might be reduced in depression, others have suggested biological mechanisms might be implicated. For example, Roy-Byme et al. (1986) suggested depression may selectively impair effortful processes as opposed to automatic processes by interfering with the effects of the neurotransmitter dopamine.

Ellis and Ashbrook (1988) proposed a model which built on the ideas posited by Hasher and Zacks (1979). Like Hasher and Zacks, Ellis and Ashbrook (1988) assumed tasks vary in the demands they place on attentional resources, and depression might be a factor in regulating the amount of available resources. They introduced the idea that increased processing of irrelevant aspects of the task, or processing of non-task material, such as material relating to personal concerns, might be one mechanism by which depression reduces available resources. Thus, Ellis and Ashbrook suggest resources might be diverted as well reduced in depression, but the overall effect will be one of reduced availability of attentional resources. This model has strong links with the cognitive models of depression reviewed in section 2.1.3.3.6 (e.g. Williams et al., 1988) which posited depression is associated with biases in memory, and possibly attention, for negative material which could divert depressive allocation o f resources. Hasher and Zacks (1988) put forward a model which assumes narrowing of attentional focus to be the underlying causal mechanism. They suggested in both normal ageing and depression, normal inhibitory mechanisms may become less efficient. This would permit irrelevant information to enter WM and receive sustained activation, leading to reduced resources.

resources predicts performance should suffer with increasing task demands on attentional capacity. If processing resources are reduced or partially occupied, fewer resources are available for task performance. If the task is resource-limited (see section 2.2.5.1.3), impairment in performance may occur, and the extent o f this should be related to the amount of resources needed for its performance, so it is predicted depressed Ss should not show deficits on tasks which make no, or only minimal demands on processing resources. Hypotheses of both reduced and diverted resources make identical predictions in most instances, although Hartlage, Alloy, Vazquez and Dykman (1993) have suggested some ways in which they could best be distinguished in future research.

The evidence reviewed in section 2.3 suggests depressed Ss are differentially impaired on effortful relative to automatic tasks consistent with the prediction o f a reduced resources model, although the inconsistency of the findings in relation to implicit memory tasks (see section 2.3.6.2) suggest this conclusion cannot yet be fully accepted. Studies which have varied task demands have frequently reported depressed Ss show relatively more impairment as demands increase (see section 2.3). However, Robbins, Joyce and Sahakian (1992) postulate studies may have confounded task demands with task difficulty, so that, for example, differential performance on automatic and effortful tasks might simply be a function o f task difficulty. They suggest difficult tasks might be more discriminating in separating patients and controls, but the concept of resource allocation may not have any additional explanatory power.

The theories o f reduced and/or diverted resources in depression (Ellis & Ashbrook, 1988; Hasher & Zacks, 1979) outlined above seem to assume a single pool of attentional resources. However, as noted in section 2.2.5.1.4, theorists (e.g. Navon & Gopher, 1979; Wickens, 1984) have argued multiple resources may exist, each with its own capacity. It is therefore important to consider the implications o f this type o f attentional system for current theories of reduced/diverted resources in depression. The assumption of a single pool of resources predicts the effects of a reduction/diversion of resources will be determined simply on the basis o f the total demands made on resources. In contrast, the predictions of a multiple resource model o f attention would be far more complex, since any deficits would depend on which of the resources were reduced/diverted in depression and which were required by the current task, as well as whether the available resources were exceeded. In section 2.3.7, the evidence o f depressive task performance was

assessed in relation to one model of multiple resources: the WM model posited by Baddeley and Hitch (1974). While there was some evidence of depressive impairment on measures of the CE component, the two slave systems, the PL and the VSSP, appeared relatively intact. Other models of multiple resources are not yet sufficiently well-defined to permit this type of detailed assessment, although this is likely to change in the future.

2.3.9.2 Response Style v r /

Other models have challenged the notion^epression is associated with reduced availability o f resources, and have suggested instead their style of performance differs from non­ depressed Ss in ways that lead to the appearance of reduced resources. Johnson and Magaro (1987) proposed,depressed Ss recall as much as controls, but are less willing to

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report the information. The evidence for the hypothesis that depressed Ss are characterised by a conservative response bias was examined in section 2.3.4.3, and on the whole it seemed to suggest depressed Ss do have a tendency to respond in a conservative manner, but nevertheless they also exhibit true deficits on some tasks.

One of the earliest hypotheses regarding depressive deficits was the proposal that depressed individuals are simply not motivated to do well when given tasks to perform, or that, even though motivated, depressed individuals may be unable to sustain any prolonged motivation. This is consistent with the reduction in motivation identified as a salient feature of depression by several theorists (e.g. Abramson, Seligman & Teasdale, 1978; Beck, 1967). In his early review of the field of cognitive function in depression Miller (1975) identified reduced motivation as one possible explanation o f the pattern of findings, and this was supported by McAllister (1981) in his review. Subsequently, the simple motivation explanation became less popular, and little research effort has been expended to test the specific predictions of this position. One exception was reported by Richards and Ruff (1989) who compared depressed patients and normal controls on a range o f cognitive tasks in motivation and non-motivation conditions. They found a manipulation designed to increase motivation did not differentially improve performance in the depressed Ss, even though the manipulation enhanced speed of responding to the same degree as in normal Ss. The authors concluded depressive deficits were not attributable to motivational factors. The findings of studies described in section 2.3.7.3 that the addition of a secondary task does not necessarily impair performance in depressed

Recently, Elliott et al. (1996) have proposed that depressive performance on measures of cognitive function may be influenced by a highly specific form o f motivational deficit involving the response of patients to perceived failure. They reported that on two tasks, negative feedback given immediately following an experimental test trial, increased the likelihood that depressed patients would fail the next item. Elliott et al (1996) speculate that the depressed Ss' response to the negative feedback interfered with their performance on the next test item. However, this explanation cannot account completely for depressive deficits since depressed Ss were significantly impaired relative to controls after controlling for the effects of failure.

In a more sophisticated version of the motivational hypothesis, Hertel and her colleagues (e.g. Hertel & Hardin, 1990; Hertel & Rude, 1991b) have challenged the processing resources account of depression. They argue depressed Ss are characterised by reduced initiative, leading to failure to use strategies spontaneously or engage in elaborative thinking, but they are capable of this when directed. They emphasise .depression impairs

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initiative to use strategies, but not the ability to do so. On many tasks, the initiative hypothesis makes predictions which are similar to the processing resources model. For example, reduced initiative would also predict depressed Ss should be unimpaired on automatic tasks which do not require the use of a strategy.

In order to test their model, Hertel and her colleagues have conducted a series of experiments in which they manipulated whether the appropriate strategy was implicit in the task, or had to be generated spontaneously. They found any deficits shown by depressed Ss relative to controls tended to show improvement with specific direction as to the use of an appropriate strategy. They therefore suggested tasks sensitive to

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depressive deficits would be those which permit but do not specify the spontaneous use o f strategies, rather than those which direct or bypass the use of strategies. Hertel and Knoedler (1996) demonstrated this lack of initiative can be beneficial when attempts to use a strategy interfere with task performance (see section 2.3.8.2.4.2). Hertel and her colleagues contend that an account in terms of reduced or unavailable processing resources alone is inadequate, since performance of their tasks under directed strategy conditions was in some cases likely to be at least as effortful as undirected conditions. However, their findings were not clear-cut since directed strategy manipulations did not always prove to be completely effective in removing performance deficits. Thus, Hertel and Rude

(1991b) found depressive Ss remained slower than controls on a secondary probe latency task, although primary task performance improved to normal levels. Hertel and Rude (1991b) acknowledged that impairment in initiating strategies may reflect either motivational deficiencies, or a true cognitive deficit in planning and generating appropriate performance strategies (which may in turn require processing resources).

In summary, there are a number of competing models of depressive deficits, and on the basis o f current evidence it is difficult to conclude which model is best supported. This situation has in part arisen from the fact that predictions made by the models are indistinguishable for many of the tasks which have been utilised, while only a small number o f studies have attempted to test hypotheses which would separate the models. Furthermore, since the models are not incompatible with each other, it is possible the current situation has arisen because more than one o f the models is correct. For example, Watts (1993) concluded both reduced processing resources and under-deployment of remaining resources may characterise depressed Ss.

The models of cognitive function in depression outlined above have given some attention to the possible biological mechanisms which might underlie any deficits in cognitive function associated with depression (e.g. Roy-Byrne et al., 1986). However, the recent work using neuro-imaging techniques to investigate physical changes in depression which was reviewed in section 2.1.3.2.2 is likely to inform theories o f cognitive function to a far greater degree in the future. Furthermore, this work may potentially provide a link between the competing theories. For example, it is possible both reduced capacity and a particular response style might result from impaired brain function. The studies reviewed in section 2.1.3.2.2 suggested impairments in frontal lobe function have most consistently been associated with depression. Frontal lobe function was reviewed in section 2.2.3. The evidence links the frontal lobes with executive function, postulating a role in both the allocation o f attentional capacity and in the implementation of strategies. While hypotheses about possible links between depression and brain function must remain tentative at present, this is likely to be a fruitful direction for future research, and needs to be taken into consideration.