Chapter 7 176 Another query where the MoCA could be of help is whether cognitive impairment worsens after every episode. There is literature indicating that in unipolar depression, the cognitive deficits worsen with repeated episodes (Ahern and Semkovska, 2017; Riddle et al., 2017; Semkovska et al., 2019). There is evidence of a correlation between the severity of episodes and the amount of global cognitive impairment (McDermott and Ebmeier, 2009). However, in bipolar depression, studies show comparable deficits after the first episode or recurrent episodes, including late-life bipolar disease patients (Bortolato et al., 2015; Szmulewicz, Valerio and Martino, 2020). Other studies note that older patients seem to have more cognitive deficits than their younger counterparts (Hashem et al., 2017; Dols and Beekman, 2020; Mukku et al., 2021) but this can be independent of repeated episodes. Problems in concentration and attention, which are part of the diagnostic criteria of affective disorders, can influence different domains and therefore be the reason for not finding a specific profile but a more global impairment. Although information processing (processing speed), memory, and executive deficits can be prominent, apraxia, aphasia, and agnosia are rare. Lack of motivation, which is part of depression as well as of a manic episode, influences cognitive functioning. Executive dysfunction that causes impulse disinhibition is one of the diagnostic features of a manic episode. As for patients with schizophrenia, considerable data shows that cognitive impairment remains stable after onset (up to 10 years of follow-up) (Rund et al., 2016) indicating that overall cognitive impairment seems independent of the (duration of) psychotic episodes (Bortolato et al., 2015). The above-mentioned relationship between cognitive severity and number of episodes is still debated to some extent, and large longitudinal studies could further help to solve this issue. However, this should include the heterogeneity of cognitive impairment associated with these diseases. Therefore, another opportunity for the use of MoCA is to differentiate cognitive heterogeneity in these follow-up studies. A question that remains open is whether the total MoCA score or some impaired items develop or recover differently with different aetiologies. One hypothesis is that if the MoCA is impaired due to depression, this could recover to a certain amount, whereas the MoCA (if indeed impaired – as this differs greatly between individuals) of patients with schizophrenia would not recover (as much). The latter is also found in a study by Wu where the overall cognitive impairment did not recover on the MoCA during acute hospital stay and across symptoms changes with schizophrenia (Wu, Dagg and Molgat, 2017). However, the MoCA scores of patients with MCI due to neurodegenerative causes are expected to deteriorate over time. A longitudinal study can answer these important questions. A longitudinal study could also shed light on the often-used method of repeating the MoCA after the psychiatric symptoms have
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