The Test Solution “Depression - Neurocognitive Assessment” is used to assess the cognitive functional profile of individuals with depressive disorders as well as with subclinical symptoms (see chapter 6A70–73, ICD-11; WHO, 2022). The selection of dimensions for the Test Solution is based on current meta-analytic findings on cognitive changes before, during, and after depressive episodes, the diagnostic standards DSM-5-TR (American Psychiatric Association, 2022) and ICD-11 (WHO, 2022), as well as the S3 guideline for the diagnosis and treatment of unipolar depression (German Medical Association et al., 2022).
In addition to mood- and motivation-related core symptoms, both ICD-11 and DSM-5-TR describe two cognitive associated symptoms in depressive disorders: psychomotor slowing (or agitation) and concentration and decision-making problems. This is also reflected in the S3 guideline of the German Medical Association, which, in the chapter on the recognition of depression, lists memory impairments, psychomotor slowing, impairments in expressive language and language comprehension, as well as attention problems as diagnostically relevant alongside mood-related core symptoms. The diagnostic recommendations of the S3 guideline do not include psychometric ability tests, but emphasize self-assessment or targeted inquiry about concentration problems and slowing, which can be assessed objectively through testing. DSM-5-TR highlights that many patients report a markedly reduced ability to think clearly, concentrate, or make decisions during a depressive episode (criterion A8). Affected individuals often appear easily distractible or complain about memory problems, which can lead to noticeable impairments, particularly in activities with high cognitive demands. In childhood and adolescence, this may become visible through a decline in academic performance. In older individuals, pronounced memory complaints are often prominent and may be misinterpreted as “pseudodementia” (American Psychiatric Association, 2022).
In the scientific literature, cognitive performance impairments in depression are explained by two underlying models: the processing speed hypothesis and the effort hypothesis. The processing speed hypothesis states that slowing of processing speed, as a basic component of higher cognitive functions, impairs performance in more complex tasks. The effort hypothesis, on the other hand, assumes that impaired performance in executive tasks among individuals with depressive symptoms has motivational or mood-related causes, meaning that tasks requiring high cognitive effort are performed less well (see Nuño et al., 2021).
Research provides numerous, partly longitudinal meta-analyses on neurocognitive functional profiles, which can be divided into findings before, during, and after (i.e., remission) the occurrence of a depressive episode. These findings provide empirical evidence for both the processing speed hypothesis and the effort hypothesis and are discussed below across the temporal course of depressive episodes.
Before the occurrence of depressive episodes, a longitudinal meta-analysis covering k = 29 studies and n = 121,749 individuals showed that differences in cognitive and executive functions are only weakly associated with the occurrence or severity of a depressive episode (r = .09, p < .001), and that this relationship disappears completely when controlling for subclinical depressive symptoms (Scult et al., 2016). This suggests that cognitive functions are not causally involved in the development of depression.
During ongoing depressive symptoms, meta-analyses show clear impairments in executive functions. A large cross-sectional meta-analysis covering k = 113 studies comparing individuals with MDD to healthy control groups found that most executive functions were impaired, particularly inhibition (d = 0.53 [0.47–0.69]), verbal (d = 0.45 [0.34–0.56]) and visual working memory (d = 0.45 [0.30–0.59]), verbal fluency (0.55 [0.44–0.66]), processing speed (0.33 [0.15–0.50]), and cognitive flexibility (0.47 [0.39–0.55]) (Snyder, 2013). These results are consistent with a smaller meta-analysis of 13 studies and 644 individuals investigating cognitive profiles during the first depressive episode, which found small to medium executive impairments (Lee et al., 2012). Current findings also indicate that the neurocognitive profile of depressive disorders follows age-dependent patterns. A meta-analysis of adolescents and young adults (12–25 years) showed significant impairments in attention, verbal and visual memory, verbal reasoning, and general cognitive ability compared with healthy control groups (Goodall et al., 2018). In addition, several meta-analyses indicate that age and number of previous depressive episodes act as moderators of cognitive impairments, with both variables being confounded (Nuño et al., 2021; Semkovska et al., 2026).
After a depressive episode, small group differences remain between remitted individuals and those never affected by depressive episodes. A large meta-analysis of 244 studies with more than 10,000 individuals per group showed that differences in processing speed, inhibition, cognitive flexibility, numerical and verbal fluency, planning ability, and working memory persist even in remission. A moderator analysis from the same study showed that all these differences, except working memory, could be fully explained by processing speed, providing strong empirical evidence for the processing speed hypothesis. In working memory, small differences were observed (e.g., digit span forward: g = –0.28 [–0.41 to –0.14]; 53 studies, n = 3180 vs. 2307) (Semkovska et al., 2026). These findings replicate and extend results from the preceding study, which additionally found that differences in general cognitive ability were negligible and that recognition of emotional expressions in others was significantly better in remitted individuals (d = –0.83 in favor of the remitted group) (Semkovska et al., 2019). A meta-analysis of longitudinal data from individuals with depressive symptoms before and after treatment (k = 16 studies, n = 859 individuals) showed significant improvements in working memory, verbal memory, and verbal fluency, while processing speed and non-verbal memory remained unchanged, although retest effects could not be ruled out (Bernhardt et al., 2019). A prospective long-term study with n = 267 individuals found that cognitive symptoms persisted in about half of the affected individuals even after three years, whereas mood- and motivation-related aspects showed significantly stronger improvement (Conradi et al., 2010).
These findings underline the importance of monitoring depressive symptoms, which is also recommended by the S3 guideline. The guideline notes that monitoring is often not frequent enough and that psychometrically validated instruments should be used. The focus is on self- and observer ratings, particularly the PHQ-9. Executive functions may also be relevant for treatment planning. A systematic review of 39 studies showed that baseline cognitive function can, in some cases, predict the effectiveness of psychopharmacological treatment options (Groves et al., 2018). Although cognitive ability tests and training procedures are not currently part of the S3 guideline recommendations, these results indicate that executive functions may play a role not only in diagnostics but also in treatment planning and prognosis in depression. Initial findings also suggest that cognitive remediation, a combined method integrating cognitive training with other psychotherapeutic approaches, can lead to moderate improvements in executive functions, working memory, attention, and global cognition in patients (Thérond et al., 2021). Furthermore, although general cognitive ability in remitted individuals is on average not impaired compared to healthy individuals (Semkovska et al., 2019; 2025), it may still be relevant for individual therapy planning and prognosis, as cognitive ability is associated with short- and long-term treatment outcomes (see Knekt et al., 2014).
In summary, depression is associated with impairments in many areas of executive functions, which often persist during remission, and these effects can largely be explained by processing speed. The Test Solution “Depression - Neurocognitive Assessment” for acute depressive episodes therefore includes the following cognitive domains (see DSM-5-TR; APA, 2022):
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Attention
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Processing speed (TMT-S, Part A)
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Ability to concentrate (TACO)
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Executive Functions
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Cognitive flexibility (TMT-S, Part B)
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Interference (STROOP)
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Verbal working memory (SPAN, digit span backward)
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Learning and memory
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Verbal short-term memory (SPAN, digit span forward)
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Logical reasoning (BMT)
For monitoring neurocognitive impairments and resources in remission, the literature discussed above recommends assessing the central cognitive dimensions processing speed and working memory (TMT-A, SPAN). Multiple parallel forms and adaptive administration are available to avoid practice effects.
Depending on the assessment question, additional tests outside the SCHUHFRIED Selection may be added to the Test Solutions, for example to assess verbal fluency (WIWO). In addition, the PHQ-9 (Patient Health Questionnaire-9) is available as a free supplementary questionnaire for assessing depressive symptoms (see Open access tests ). Please note that when configuring the test sequence and adding tests that are not part of the SCHUHFRIED Selection, the combined results overview is no longer automatically available (see Notes on evaluation and interpretation ).
The test duration of the standard form is approximately 55 minutes.
References can be found here: Literature