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Neurocognitive deficits in schizophrenia are likely to be less severe and less

related to the disorder than previously thought

Article  in  World psychiatry: official journal of the World Psychiatric Association (WPA) · June 2020
DOI: 10.1002/wps.20759

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Neurocognitive deficits in schizophrenia are likely to be less severe 1
2
3 and less related to the disorder than previously thought 3
4 4
5 Even according to Kraepelin’s observations more than one being labelled with the diagnosis of schizophrenia, are associ- 5
6 hundred years ago1, the term dementia praecox was an exag- ated with poor performance4,5. 6
7 geration, if not a misnomer. Not all of his patients showed signs Another potential source of bias that may contribute to an 7
8 of dementia, and a subgroup even recovered. Kraepelin also overestimation of deficits is the lack of representativeness of 8
9 acknowledged that memory impairment, the core symptom of control participants. In some studies where psychiatric patients 9
10 dementia, at times reflected lack of interest rather than faulty performed significantly worse than non-clinical controls, despite 10
11 “impressibility of memory”. non-significant baseline differences on age or years of education, 11
12 While the term was soon replaced by that of schizophrenia(s), the performance of controls was in fact above average, rather than 12
13 the claim that the disorder is marked by global neurocognitive patients performing below average according to norm scores6. 13
14 impairment lingers on. In fact, all major meta-analyses and re- Apart from the aforementioned state factors compromising 14
15 views converge on the conclusion that patients with schizophre- neurocognitive assessment, there are some conditions that can 15
16 nia display large and global neurocognitive impairment, which cause real and more lasting impairment, but do not reflect patho- 16
17 many experts view as a core vulnerability factor for the disorder. genetic factors of schizophrenia. Perhaps most importantly, pa- 17
18 Yet, the magnitude of these deficits – usually one standard devia- tients more often than controls suffer from obesity and diabetes 18
19 tion below the mean2 – is far less than the extent of impairments (which can be independent of and/or related to treatment with 19
20 seen in patients with primary dementia, which is inconsistent with antipsychotic medication) as well as cardiovascular disease (e.g., 20
21 the idea that schizophrenia is a (praecox) form of dementia. hypertension), and these factors compromise neurocognitive 21
22 We do not dispute that a large subgroup of patients display performance in both schizophrenia patients and the general pop- 22
23 deficits on neurocognitive tests. Yet, we would like to emphasize ulation. In addition, hospitalization and loneliness have also been 23
24 that the degree to which these deficits can be attributed to schizo­ associated with poor neurocognitive performance7. 24
25 phrenia itself is likely overestimated, whereas the degree to which One may argue that neurocognitive deficits were observed 25
26 they are due to medical and psychological factors that are often also in the pre-neuroleptic era and have been found even in at- 26
27 associated with schizophrenia, but that do not form part of the risk individuals. However, the effects of, for example, defeatist 27
28 syndrome itself, has not been fully appreciated. beliefs (which are high in at-risk subjects, too) and hospitaliza- 28
29 These two classes of bias at times overlap, but should be dis- tion (at least in manifest patients) may have contributed to this. 29
30 tinguished for heuristic purposes. Importantly, this distinction Poor neurocognitive performance may also represent an epi- 30
31 is not just an academic issue. It has significant implications for: phenomenon of perceptual problems8. Furthermore, patients 31
32 a) understanding why many people with schizophrenia appear are often prescribed anticholinergic medications (clozapine or 32
33 to be cognitively impaired; b) understanding why the extent of drugs aimed to reduce extrapyramidal symptoms) that compro- 33
34 observable cognitive impairment in people with schizophrenia mise attention and memory. Finally, motor side effects, which 34
35 can fluctuate widely depending on the environmental and inter- are common with first-generation antipsychotics but can also 35
36 personal context; and c) choosing interventions to address the occur with second-generation medications, can reduce perfor- 36
37 impairment. mance on timed tests. 37
38 With respect to overestimation, an emerging literature indi- Experienced neuropsychologists will be well aware of the 38
39 cates that poor performance is partly due to confounds during aforementioned biases and confounds. In written individual re- 39
40 neurocognitive assessment. Most obviously, disorganization and ports, these may be acknowledged and perhaps even adjusted for. 40
41 derailed thinking, frequent symptoms in the disorder – especially In group comparisons, however, these influences are traditionally 41
42 under stress – may prevent proper understanding of task instruc- ignored, as they are hard (e.g., motivation) or even impossible to 42
43 tions and/or lead to avoidance of full engagement, with subsequent control for (e.g., medication when the control group is not medi- 43
44 failure in more difficult tests. cated at all). 44
45 Patients may also experience interference from symptoms We advise researchers to either control/adjust for these fac- 45
46 such as hallucinations, rumination and delusional ideas during tors where possible, for example through mediation analyses3, or 46
47 assessment, further distracting them from the task at hand3. to acknowledge possible sources of exaggeration of deficits in the 47
48 Moreover, patients’ motivation for assessment is often lowered, abstract and discussion of their manuscripts. We also advise re- 48
49 while anxiety and stress are higher compared to controls, and searchers not only to report mean values, but also the percentage 49
50 both of these factors are known to compromise performance3. of patients performing one and two standard deviations below 50
51 According to A. Beck and colleagues4,5, poor effort can explain be­ the norm, to more fully describe the level of impairment in the 51
52 tween one-quarter to one-third of the variance in test results. sample. Often, only a minority of patients drives group differ- 52
53 So far, the role of stigma related to diagnosis remains elusive. ences that are then extrapolated to the entire population. 53
54 However, defeatist beliefs, which are a common consequence of Some aforementioned biases resulting in overestimation of 54
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World Psychiatry 19:2 - June 2020 1

1 deficits can be mitigated through creating a kind and motivat- 1. Kraepelin E. Psychiatrie: Ein Lehrbuch fur Studierende und Arzte, 8th ed. 1
Leipzig: Barth, 1913.
2 ing atmosphere during assessment9. In addition, it would help 2. Fatouros-Bergman H, Cervenka S, Flyckt L et al. Schizophr Res 2014;158:
2
3 to test patients when distracting symptoms (e.g., hallucinations) 156-62. 3
4 are at a minimum. Change in medication might be sought, espe- 3. Moritz S, Klein JP, Desler T et al. Psychol Med 2017;47:2602-12. 4
4. Beck AT, Himelstein R, Bredemeier K et al. Psychol Med 2018;48:2776-85.
5 cially lower doses and minimization of drugs with anticholinergic 5
5. Grant PM, Best MW, Beck AT. World Psychiatry 2019;18:163-4.
6 properties. 6. Moritz S, Kloss M, Jacobsen D et al. J Clin Exp Neuropsychol 2005;27:795- 6
7 Addressing lifestyle factors related to hypertension, obesity 814. 7
7. Badcock JC, Shah S, Mackinnon A et al. Schizophr Res 2015;169:268-73.
8 and diabetes (e.g., weight loss, physical exercise) may reduce 8
8. Silverstein SM, Fradkin SI, Demmin DL. Schizophr Res (in press).
9 neurocognitive-relevant somatic risk factors, and there is ten- 9. Park S, Lee J, Folley B et al. Behav Brain Sci 2003;26:98-9. 9
10 tative evidence that such interventions indeed enhance neuro- 10. Maurus I, Röh A, Falkai P et al. Dialogues Clin Neurosci 2019;21:261-9. 10
11 cognition10. Future consideration of these factors may open new DOI:10.1002/wps.20759
11
12 windows for therapy beyond cognitive remediation, the tradi- 12
13 tional way to enhance neurocognition. 13
14 14
15 Steffen Moritz1, Stephen M. Silverstein2, Mona Dietrichkeit1, 15
Jürgen Gallinat1
16 1
Department of Psychiatry and Psychotherapy, University Medical Center Hamburg- 16
17 Eppendorf, Hamburg, Germany; 2Department of Psychiatry, University of Rochester 17
18 Medical Center, Rochester, New York, NY, USA 18
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