Task Force Q&A

The THINC task force have answered some of the questions they are commonly asked at THINC meetings. Click below to read or watch videos of their responses.

Answered by John Harrison
Senior Lecturer, Co-Chair

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There are a number of tests designed to assess domains of cognitive function in depression: can the panel provide guidance on which tests they use with examples of circumstances?
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Q1

Answered by John Harrison

A number of tests have been employed in patients with depression to determine the presence of cognitive deficits and to measure cognitive change. In the latter case, this has typically been in the context of determining whether a therapeutic intervention has been successful. The better measures of cognition are those that exhibit high levels of reliability, validity and sensitivity, particularly important when measuring cognitive change.
Full neuropsychological assessment with a trained expert remains the ‘gold standard’ for the evaluation of cognition in patients with depression. However, we understand and recognise that these services are not routinely available. For a quick assessment of cognitive difficulties, our inclination is to suggest the use of brief, easy to administer and easy to understand tests. We have selected the following cognitive tests for use in the forthcoming THINC screening tool and would recommend their use as a rapid screening assessment:

  1. Choice Reaction Time (CRT)
  2. One-Back Task (1BT)
  3. Digit Symbol Coding Test (DSCT)
  4. Trail Making Test (TMT)

CRT and 1BT require computers for their delivery. Versions of the DSCT can be obtained from Pearson, the owners of the Digit Symbol Substitution Test. The TMT is publically available. For the evaluation of cognitive change, we note that in a recent clinical drug trial a number of ‘pencil-and-paper’ and computerised measures captured significant effects of treatment on cognition.1 While traditional ‘pencil-and-paper’ assessments can assess cognitive change, we would suggest the use of computerised or computer-assisted measures, examples of which can be viewed at the CogStateCNS Vital SignsBracket and Cambridge Cognition websites. For further guidance on cognition test selection, see Ferris et al2 and Harrison and Maruff.3

Q1
References
  1. McIntyre RS, Lophaven S, Olsen CK. A randomized, double-blind, placebo-controlled study of vortioxetine on cognitive function in depressed adults. Int J Neuropsychopharmacol 2014; Apr 30 [Epub ahead of print].
  2. Ferris SH, Luca U, Mohs R, Dubois B, Wesnes K, Erzigkeit H, Geldmacher D, Bodick N. Objective psychometric tests in clinical trials of dementia drugs. Position paper from the International Working Group on Harmonization of Dementia Drug Guidelines. Alzheimer Dis Assoc Disord 1997; 11 (Suppl 3): 34-38.
  3. Harrison JE, Maruff P. Measuring the mind: assessing cognitive change in clinical drug trials. Expert Rev Clin Pharmacol 2008; 1: 471-473.

Answered by Bernhard Baune
Head of Psychiatry, Clinician & Researcher

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Answered by Tracy Greer
Associate Professor of Psychiatry

Is there a link between cognitive function and daily function in patients with depression?
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Q2

Answered by Bernhard Baune

Patients with depression frequently experience cognitive deficits and a decline in general, social and occupational function. Cognitive deficits are found to be a principal mediator of psychosocial impairment and workforce performance in depression. More specifically, various clinical studies show that cognitive domains such as memory (including delayed verbal recall and language), psychomotor speed (including visuo-spatial/constructional abilities) and executive function (including planning) are associated with general and occupational function.

Moreover, cognitive deficits at baseline, such as impaired working memory, verbal memory retention, visual memory, attentional switching, event-based prospective memory, executive function, non-verbal learning and motor measures, are associated with future general functioning and social and occupational functioning. Importantly, this relationship between cognitive function and general function not only holds true in acute depression but also in remitted phases of depression. Addressing these cognitive deficits provides further opportunity to prevent and treat poor daily function in patients with depression.

Q3a

Answered by Tracy Greer

Studies are beginning to link specific cognitive functions with functional outcomes, although a clear pattern is yet to be established. With respect to daily function, measures of activities of daily living and instrumental activities of daily living have been evaluated in the context of cognitive function in depression, with mixed results. For example, McCall and Dunn1 found that instrumental activities of daily living were correlated with measures of both verbal and non-verbal memory. In contrast, Baune et al2 found no relationship between cognitive performance and measures of activities of daily living.

Q3b
References
  1. McCall WV, Dunn AG. Cognitive deficits are associated with functional impairment in severely depressed patients. Psychiatry Res 2003; 121: 179-184.
  2. Baune BT, Miller R, McAfoose J, Johnson M, Quirk F, Mitchell D. The role of cognitive impairment in general functioning in major depression. Psychiatry Res 2010; 176: 183-189.

Answered by Harry Barry
Head of Psychiatry, Clinician & Researcher

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Answered by Esther Klag
Consultant Clinical Psychologist & Neuropsychologist

How can cognitive dysfunction in patients with depression be easily assessed in routine clinical practice?
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Q3

Answered by Harry Barry

Depression is a multidimensional disorder involving a combination of physical, emotional and cognitive symptoms. Cognition can be categorised as having affective ‘hot’ and logic-based ‘cold’ components. Many clinicians will identify ‘hot’ cognitions (associated with emotions) in depression, such as shame, anxiety and guilt, but are less likely to identify ‘cold’ cognitive dysfunction. Clinicians are more likely to identify daily functional difficulties, the cause of which may be unrecognised ‘cold’ cognitive dysfunction. The following five simple questions are useful to screen for such functional difficulties and the most likely cognitive domain involved.

  • Do you have difficulties making decisions either at home or work and, if so, why? (Decision making)
  • Do you have difficulties reading newspapers, lecture notes or data at work, or following TV programmes or conversations? (Concentration/attention)
  • Do you find yourself misplacing items such as keys, or have difficulties remembering names or shopping items, or lose track of tasks at home or at work? (Memory)
  • Do you struggle to start or, in particular, finish common tasks, either at home or at work, due to these problems? (Motivation, problem solving, indecision, organisation)
  • How do all of above affect you in your day-to-day life? (Consequences of cognitive dysfunction)

Answered by Esther Klag

Through questions put to the patient, the clinician can elicit descriptions of symptoms indicating cognitive dysfunction. However, the aetiology and severity of the cognitive dysfunction are not easily assessed clinically and require careful questioning, observation and clinical judgement.

Some patients suffering with depression will readily describe cognitive difficulties, e.g. older patients concerned about dementia. Most other patients will tend to describe mood disturbance – ‘I’m not myself’ – behavioural difficulties and/or external stressors.
If you are a clinical practitioner who knows your patient, you will, of course, develop hypotheses in terms of changes in functioning but if this is not the case, it is important to ask questions that may reflect cognitive dysfunction. Some of these questions will be direct; others will be more subtle, indirect and often less threatening to the patient.

Direct enquiries can refer to relevant cognitive functions in the domains of attention, working memory, executive function and processing speed.1 (See also Diagnosis and assessment) Indirect enquiries can focus on functioning abilities, habits and quality of life in areas relevant to the patient such as occupational or academic progress, organisation within the home and family, and relationships. All these may be associated with, or reflect, cognitive impairment associated with depression.

Diagnosis and treatment are all the more challenging since various conditions other than depression, as well as co-morbidities, can also affect cognitive functions. Clinical judgement can, of course, be aided by identifying cognitive dysfunction within the specific context of an individual patient’s life (age, profession, background, medical history, etc). A simple, quick initial screening tool would be helpful and the THINC group is working on developing this.

References

 

  1. McIntyre RS, Cha DS, Soczynska JK, Woldeyohannes HO, Gallaugher LA, Kudlow P, Alsuwaidan M, Baskaran A. Cognitive deficits and functional outcomes in major depressive disorder: determinants, substrates, and treatment interventions. Depress Anxiety 2013; 30: 515-527.

Answered by Philippe Fossati
Professor of Psychiatry

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To what degree can ‘hot’ cognition also be categorised as social cognition and how can we assess this?
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Q4

Answered by Philippe Fossati

‘Hot’ cognition is related to the processing of emotional signals. Among these signals, social stimuli are powerful triggers of emotion. Social processes refer to a set of cognitive and neural mechanisms involved in our ability to interact with others and navigate the social world, encompassing processes of face perception, self/other representation, theory of mind, social inclusion and motor resonance among others. The ‘social brain’ overlaps with the ‘emotional brain’ and includes a set of distributed cortical, subcortical and limbic regions (ie the amygdala, anterior cingulate, insula, basal ganglia, medial and lateral prefrontal cortices, and hippocampus). Social abilities can be assessed with several tasks such as the theory of mind task, identification of emotional faces and memory for words encoded in a self-referential mode, among others.

Q5

Answered by Hans-Ulrich Wittchen
Chair of the Institute of Clinical Psychology and Psychotherapy

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How important is the distinction between hot and cold cognition?
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Q5

Answered by Hans-Ulrich Wittchen

The current status of basic research does not allow us to pinpoint with sufficient precision which complex mechanisms are involved in these two types of cognition. The differentiation of ‘hot’ and ‘cold’ cognition, which are in fact interacting, is at this point an imperfect heuristical model. It is likely that increased research activities will gradually identify potential differences between these two classes of cognition.

Q6

Answered by Hans-Ulrich Wittchen
Chair of the Institute of Clinical Psychology and Psychotherapy

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What impact do antidepressants have on ‘hot’ and ‘cold’ cognition?
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Q6

Answered by Hans-Ulrich Wittchen

The broad effects of antidepressants seem to affect both ‘hot’ and ‘cold’ cognition; however, the specific pathways and mechanisms regulating these domains remain, at this point, unclear.

Q7

Answered by Catherine Harmer
Professor of Cognitive Neuroscience

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To what degree is response to negative feedback state-related? Could the effects of antidepressants on cognitive function in patients with depression be due to effects on negative cognitive biases?
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Q7

Answered by Catherine Harmer

Abnormal response to negative feedback is specifically associated with depression, meaning that patients with depression tend to show worse performance on cognitive tests after receiving negative feedback, and this performance is lower than in patients with other conditions where overall performance is impaired (such as Parkinson’s disease or schizophrenia). This suggests that receiving negative feedback can particularly affect how patients with depression perform on a cognitive task and illustrates the potential for negative biases, even on ‘cold’ cognitive task performance. Although abnormal response to negative feedback is most commonly investigated in patients with depression, there is some recent evidence that risk factors for depression (in this case, serotonin transporter genotype and childhood adversities) can also lead to the same pattern.1 This suggests that the abnormal response to negative feedback may not be purely state (or mood) related but involved in predisposition to depression.

Q8a

Antidepressants can reduce negative biases in both depressed patients and healthy control individuals. These effects would be predicted to also improve aspects of ‘cold’ cognitive function by reducing the potential for negative response to failure. However, it is currently unclear to what extent the effects of antidepressants on ‘cold’ cognition are mediated by changes in emotional factors and this is the subject of on-going research.

Q8b
References
  1. Owens M, Goodyer IM, Wilkinson P, Bhardwaj A, Abbott R, Croudace T, Dunn V, Jones PB, Walsh ND, Ban M, Sahakian BJ. 5-HTTLPR and early childhood adversities moderate cognitive and emotional processing in adolescence. PLoS One 2012; 7: e48482.

Answered by Philippe Fossati
Professor of Psychiatry

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Anxiety is a co-morbidity frequently observed with depression. How does anxiety impact on executive functions and what are the implications of this in depression?
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Q8

Answered by Philippe Fossati

Executive functions involve a set of cognitive processes that are affected by depression, such as inhibition, updating and set-shifting. Anxiety co-morbid disorders and anxiety symptoms associated with depression may impact on these executive processes. Few studies have directly evaluated the contribution of anxiety to executive impairment in depression.1 However, we can assume that anxiety contributes to dampen executive resources in depressed patients by increasing the severity of depression. Treating the depression, anxiety symptoms and anxiety disorders is essential to reduce cognitive problems in depressed patients.

Q9
References
  1. Snyder HR. Major depressive disorder is associated with broad impairments on neuropsychological measures of executive function: a meta-analysis and review. Psychol Bull 2013; 139: 81-132.

Answered by Hans-Ulrich Wittchen
Chair of the Institute of Clinical Psychology and Psychotherapy

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What is the impact of insomnia on cognitive function in depression, both during the acute phase and on residual cognitive symptoms during remission?
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Q9

Answered by Hans-Ulrich Wittchen

The effects of insomnia – both as a core symptom of depression and as a separate clinical condition – are substantial and have been broadly described (e.g. in the most recent Fifth Edition of the Diagnostic and Statistical Manual of Mental Disorders). There are considerable general (i.e. arousal) and specific (i.e. attention, memory consolidation) effects of insomnia that can impair a broad range of cognitive functions, both in the acute and residual phases of depression.

Q10

Answered by Roger McIntyre
Professor of Psychiatry & Pharmacology, Co-Chair

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Are cognitive symptoms in patients with depression associated with the development of dementia?
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Q10

Answered by Roger McIntyre

Epidemiological and clinical data provide convergent evidence of association between multi-episode depression and incident dementia. The mechanistic basis of this association is unclear. It is also unclear whether cognitive impairment in younger people with depression identifies a sub-population at greater risk for incident dementia.

Answered by Roger McIntyre
Professor of Psychiatry & Pharmacology, Co-Chair

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Is there any evidence that treating cognitive dysfunction in depression may reduce this risk?
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Q11

Answered by Roger McIntyre

There is no evidence at this point that treating cognitive dysfunction in depression reduces incident dementia.

Answered by Roger McIntyre
Professor of Psychiatry & Pharmacology, Co-Chair

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How can we differentiate between cognitive impairment and initial dementia in patients with depression?
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Q12

Answered by Roger McIntyre

Cognitive disturbance in mild cognitive impairment and dementia is primarily characterised by profound deterioration in performance in both learning and memory. This is typically of a greater magnitude than that observed with depression.

Q13

Answered by Bernhard Baune
Head of Psychiatry, Clinician & Researcher

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Is there any difference in the type of cognitive dysfunction observed in unipolar, bipolar and psychotic depression?
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Q13

Answered by Bernhard Baune

It has been suggested that a number of clinical and demographic factors are related to cognitive performance in depression. Studies have investigated whether the type of depression (unipolar, bipolar, psychotic, melancholic) contributes to cognitive deficits and it is not surprising that complex mood disorders tend to be associated with more severe cognitive deficits. For example, existing research demonstrates that bipolar disorder patients show stronger cognitive deficits compared to unipolar depressed patients.1

However, results are somewhat inconsistent among the literature, as research has also shown that cognitive deficits are similar between bipolar and unipolar depressed patients, or that differences in cognitive functioning rather relate to the profile of cognitive deficits. Among bipolar patients, patients with bipolar disorder Type I demonstrated stronger cognitive impairment than patients with bipolar disorder Type II. Along these lines, other studies have shown that patients with depression have more severe cognitive deficits compared to those with dysthymia.

The view that subtypes of depression with additional psychopathological symptoms are associated with poorer cognitive functioning is also supported by research. Specifically, poorer cognitive functioning has been reported for depressed patients with the melancholic or psychotic sub-types of depression when compared to depressed patients without these sub-type specifiers. Finally, it was found that patients with melancholic subtypes of depression not only show poorer performance but also a longer time for cognitive recovery compared to patients with non-melancholic sub-types.

References
  1. Baune BT, Fuhr M, Air T, Hering C. Neuropsychological functioning in adolescents and young adults with major depressive disorder – a review. Psychiatry Res 2014; 218: 261-271.

Answered by Hans-Ulrich Wittchen
Chair of the Institute of Clinical Psychology and Psychotherapy

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Is cognitive behavioural therapy (CBT), which requires complex cognitive processes, appropriate for depressed patients with severe cognitive dysfunction?
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Q14

Answered by Hans-Ulrich Wittchen

Currently, according to the results of randomised controlled trials, there is no significant difference regarding the efficacy of various forms of CBT for severe and less severe forms of depression. However, as a general rule of CBT as a personalised intervention tool, the speed and range of therapeutic interventions need to be adapted to the patient’s state. This may include tailoring the amount of psychoeducation and the length of sessions to ‘meet the patient where he/she is’.

 

Q15

Answered by Bernhard Baune
Head of Psychiatry, Clinician & Researcher

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What is the difference between multimodal and monomodal?
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Q15

Answered by Bernhard Baune

The pharmacological difference between monomodal and multimodal drug action is based on the number of different modes of action involved. For example, when a drug acts as a reuptake inhibitor only (regardless of the monoamine blocked) then this is a single mode of action and defined as a monomodal drug. In contrast, when more than one mode of action is involved (e.g. reuptake inhibition and receptor activity as pharmacological targets) then this is defined as multimodal drug action (see Figure 1). It appears that combining multiple modes of monoaminergic action may enhance the efficacy of antidepressant treatment for some patients.

Figure 1: Monomodal and multimodal antidepressant actions on the reuptake of monoamine neurotransmitters at synapses and modulation of the reactivity of serotonin receptors on the post-synaptic dendritic membrane.

Multimodal antidepressants may have greater efficacy against depression due to their multimodal effects of reducing the reuptake of monoamines as well as decreasing their movement into the post-synaptic neuron.

Disclaimer: The views and opinions expressed on this page are those of the authors and do not necessarily reflect those of Lundbeck.
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