International Journal of Mental Health & PsychiatryISSN: 2471-4372

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Review Article, Int J Ment Health Psychiatry Vol: 4 Issue: 2

Post-psychotic Depression: A Critical Review

Zaffer Iqbal1,4*, Nicholas Stenning2, Adrian Morton3, Anjula Gupta4 and Sophie Brown1

1Department of Psychology, Navigo CiC, UK

2Department of Psychology, University of Leeds, UK

3Department of Psychology, Reigate Psychology Service, UK

4Faculty of Health Sciences, University of Hull, UK

*Corresponding Author : Zaffer Iqbal
Consultant Clinical Psychologist, Head of Psychology, NAViGO CiC NAViGO House, 3-7 Brighowgate, Grimsby, North East Lincolnshire, DN32 0QE, UK
Tel: 01472 808503
Fax: +91- 8974236218
E-mail: [email protected]

Received: April 17, 2018 Accepted: April 28, 2018 Published: May 02, 2018

Citation: Iqbal Z, Stenning N, Morton A, Gupta A, Brown S (2018) Post-psychotic Depression: A Critical Review. Int J Ment Health Psychiatry 4:2. doi: 10.4172/2471-4372.1000162


Objective: To review the literature surrounding post-psychotic depression including its prevalence, potential pathways to its emergence and deficiencies in the current understanding. Method: Electronic literature search of PubMed, PsychINFO and Web of Knowledge using search terms relating to post-psychotic depression. Results: Prevalence rates have been clouded by heterogeneous samples. Three ontological theories were present in the literature. Evidence supported a range of pathways including post-psychotic depression as intrinsic to psychosis, as resulting from neuroleptic medication or as an emotional reaction to psychosis. Further research with homogeneous samples and precise definitions of post-psychotic depression are needed to confirm these findings. Methodological problems, inconsistencies in definition and implications for the International Statistical Classification of Diseases and Related Health Problems 10th Edition (ICD-10) and the Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DSM-IV) classification are discussed. Conclusion: Better understanding of the origins and course of post-psychotic depression is required to guide future research and treatment approaches. Clearer definition and samples are crucial in this endeavour. Review of the literature public policy relevance statement: Despite it prevalence the recognition of post-psychotic depression has been varied at best. The validation of promising theoretical models has not been undertaken resulting in a delay in the development of much-needed treatments. This review argues that psychological mechanisms are central to overcoming both these issues, and also improve understanding of this highly disabling problem in post-psychosis adjustment which has significant implications for poor recovery and suicide risk.

Keywords: Depression; Psychoses; Post-psychotic depression


Psychosis is an umbrella term referring to a cluster of severe mental disturbances characterised by: a loss of touch with reality; disturbances of thought; changes in personality and often including hallucinations and delusions. Psychosis encompasses schizophrenia, schizoaffective disorder, bipolar disorder and psychotic depression. With a lifetime prevalence of approximately 3.5%, psychosis is the most common severe mental illness [1]. A number of psychiatric disorders co-occur with psychosis including obsessive-compulsive disorder, panic disorder, substance abuse and depression [2]. Psychiatric syndromes associated or co-morbid with psychosis are major factors impacting on the outcome of the disorder, often requiring treatment and management in their own right [3]. Depression may occur at any stage of psychosis [4] and there is a need to better understand how depression interacts with schizophrenia [2], especially as depression in recovered psychosis is related to an increased incidence of suicide [5]. This review focuses on a particular manifestation of depression in psychosis, observed to occur after the acute psychotic period in a ‘stable’ or ‘recovered’ phase when positive signs have abated, known as Post-Psychotic Depression (PPD). To our knowledge, PPD was first identified as a distinct clinical entity in the mid 1970s [6], however a low mood following a psychotic episode has been observed as early as the 1920s [7].

In contrast to depression occurring in the acute phase, PPD is associated with poorer outcome and increased relapse rates [4,8-10]. Recent research has yielded PPD prevalence rates of 13.3%, 41% and 50% in individuals with psychosis [11-13]. Estimates of the prevalence of PPD vary greatly, probably because of inconsistent definition and research design [14]. In addition, the hierarchical nature of DSM classifications placing disorders such as depression lower than schizophrenia may also lead to co-occurring depression being underdiagnosed and hindering research into its validity [15]. This is an important area of research given the distress caused by psychosis to both individuals and their families. Given the number of inconsistencies and contradictions within the PPD literature, a systematic review is overdue.

The potential origin, course and theoretical explanations of PPD are disputed. Possible explanations of PPD include: Antipsychotic medication (neuroleptic) either causing depression directly or via extrapyramidal side effects; PPD as a core component of the psychosis trajectory; PPD as an emotional reaction to psychosis. Each of these theoretical perspectives will be reviewed in turn, followed by a discussion of the implications for the ICD-10 and DSM classification and suggestions for future research. This review will evaluate various definitions of PPD and discuss common methodological problems in the literature. Tentative solutions to both issues will be discussed.


Electronic databases including PubMed, PsychInfo and Web of Knowledge were searched for articles concerning the origins, course, prevalence and theoretical explanations of depression in the recovery phase. The following ICD-10/DSM-IV diagnostic terms were used in the literature search: postpsychotic depression, post-psychotic depression, postschizophrenic depression and post-schizophrenic depression. Reference lists of articles included were searched by hand to identify further relevant studies. As outlined above, there are a range of potential pathways to PPD. Consequently, longitudinal research is necessary to discern which pathway is responsible for depression in an individual at the time of assessment. Therefore an emphasis was placed on quantitative, longitudinal designs with a minimum of one assessment point in the ‘stable’ or recovery phase. Crosssectional research was only included if of theoretical importance or of particularly high quality. Research focussing upon biological mechanisms or drug treatment trials were excluded unless pertinent to a theoretical explanation of PPD. This review is concerned with the origin and course of PPD so does not aim to review treatment approaches [16]. PPD was first mentioned in the literature in 1976 therefore the date range for searches were 1976-2016 [6]. To ensure a high standard of research, only studies published in peer reviewed journals were included.

Definitions of post-psychotic depression

There is lack of consensus on a suitable definition of PPD [6,12,17]. As Leff and colleagues pointed out in the 1980s, the term post-psychotic depression has been used to describe three similar but clinically distinct groups: 1) Those with depressive symptoms at onset, with depression persisting after the decline of psychotic symptoms; 2) Those without depression at onset, with depression appearing at, or close to recovery and 3) Those without depression at onset, with depression appearing weeks or months after recovery [17]. Whilst it is possible that all of the above courses of depression may occur with psychosis, a clear definition of what constitutes PPD is required, both for consistency of research and for clinical diagnosis [18].

It should be noted that a major depressive disorder occurs less frequently than isolated depressive symptoms such as subjective feelings of sadness [19]. This is congruent with contemporary thinking, therefore a persistent negative mood may be a more appropriate definition of PPD [12,20].

To meet an ICD-10 diagnosis of post-schizophrenic depression, an individual must display prominent and distressing depressive symptoms and have fulfilled the criteria for schizophrenia within the last 12 months. Some psychotic symptoms (either positive or negative) may be present but must no longer dominate the clinical picture. There is no formal classification of PPD in DSM-IV. The criteria for depression in schizophrenia features in the Criteria Sets and Axes Provided for Further Study and is named postpsychotic depressive disorder of schizophrenia. The definition of both diagnostic manuals excludes depression occurring during the acute phase; DSM-IV excludes depression better accounted for by negative symptoms and medication side effects; ICD-10 differs in its requirement of the presence of schizophrenia within the previous 12 months. The suitability of both the DSM-IV and ICD-10 classifications of depression following psychosis have previously been assessed [21]. In this study, the majority of patients displaying depression would not match any diagnostic category in either the ICD-10 or the DSM-IV. For example, using ICD-10, depression occurring more than 12 months after the last psychotic episode, would not meet the criteria for the ICD-10 definition of PPD; therefore the authors recommended that a specific temporal relationship between the reduction in psychotic symptoms and the emergence of depression is not a useful criterion for the definition of PPD.

Neither ICD-10 nor DSM-IV comment on the course, time of origin or the underlying causes of depression in the stable phase. ICD-10 does not consider the issue of time of origin of PPD, as both depression residual from the acute phase and depression originating sometime after recovery are included in its definition. This is problematic as depression occurring at different periods may have different causes and consequently will require different therapeutic approaches [18]. PPD does not feature in DSM-5.

Similarly, the ICD-10 criteria of post-schizophrenic depression implicitly assumes depression to be intrinsic to schizophrenia [12]. Whilst this may be true for depression occurring during the acute phase, research evidence points to a subgroup of patients displaying depression that is independent of psychosis and occurs after recovery [12]. The assumption of depression as intrinsic to psychosis and issues with the temporal link between psychosis and depression have led some authors to argue that the ICD-10 and DSM-IV definitions of post-schizophrenic and post-psychotic depression are in need of revision [12,21]. A comprehensive definition of depression should outline the origins and causes of PPD and must be informed by the research literature.


Theories of post-psychotic depression

Previous research suggests three hypotheses about the etiology of PPD. It may be induced by neuroleptic medication in one of two ways, either via medication directly inducing depression, known as ‘pharmacogenic’ depression, or extrapyramidal side effects mimicking depression. A second pathway to PPD in psychosis is that depression is ‘intrinsic’ to psychosis or a core component of the psychosis syndrome. This theory is supported by the presence of depression throughout every phase of psychosis from onset to recovery and beyond [4]. A third pathway to PPD is as an emotional reaction to the shame and stigma of psychosis [18]. Proponents of this theory argue that it is an individual’s appraisals of psychosis that are primary in the inception of depression rather than the psychosis itself [22].

It is important to appreciate these potential pathways to PPD to inform our understanding of the ontogeny of PPD, what it is and also to guide treatment and research appropriately. If PPD is pharmacogenic then care should be taken when prescribing medication to individuals at high risk for depression, or ‘atypical’ anti-psychotic drugs should be considered [23]. If PPD is intrinsic to psychosis then treatment should focus on the alleviation of psychotic symptoms, as one would expect the PPD to abate alongside positive and negative symptoms. If PPD is an emotional reaction to psychosis then treatment should focus on an individual’s appraisal of psychosis [18].

Medication-related depression

One explanation of PPD is that the action of neuroleptic medication on dopaminergic synapses directly causes depression. So called ‘pharmacological’ depression was observed in a number of older studies [24-26]. One study did find inflated levels of depression in ‘stable phase’ patients taking neuroleptics compared to those who were not taking medication [27]. However, a number of controlled trials of the effects of neuroleptic medication reported that patients treated with neuroleptic drugs did not display any more depression than those treated without [28,29]. Neuroleptic dose did not differ in schizophrenics with or without depression [30,31]. Similarly, depressive symptoms may persist after withdrawal of medication [32]. Given the evidence reviewed above, ‘pharmacogenic’ causes of depression seem poorly supported by the literature.

A second subtype of ‘pharmacogenic’ depression thought to result from neuroleptic medication is ‘akinetic depression’. This is characterised by extrapyramidal side effects such as loss of spontaneity in both speech and physical activity and slowness of movement (Bradykinesia). These may mimic depressive symptoms, psychomotor agitation or retardation and low mood may also be a secondary characteristic accompanying akinesia [33-35]. Akinesia is difficult to distinguish from depressive symptoms, particularly as a depressive mood may occur without the physical symptoms often associated with extrapyramidal side effects [36]. Akinesia may explain 10-15% of total cases of depression in schizophrenia [9], however its prevalence during the stable or post-psychotic period has not been explicitly researched. Future research should be designed to account for side effects of medication to avoid inflated depression scores. The Calgary Depression Scale for Schizophrenia (CDSS) may be useful in this respect as it is designed for use with schizophrenia and is not correlated with extrapyramidal side effects or negative symptoms [37,38]. One study employed the CDSS and assessed extrapyramidal symptoms as a secondary measure [12]. They reported no differences in side effects or dose of neuroleptic medication between those with PPD and those without PPD. An interesting point is that, as mentioned above, PPD has been observed as early as 1920, 30 years prior to the advent of neuroleptic medication [7].

In summary, the evidence that neuroleptic medication directly causes PPD is weak; therefore ‘pharmacogenic’ theories may be an unsatisfactory explanation of PPD. ‘Akinetic’ depression theories may provide a partial explanation of PPD as it is probable that some individuals in the stable phase experience depression of this type [23].

Post-psychotic depression as a core component of psychosis

It has been suggested that depression may be part of the psychosis syndrome. If an ‘intrinsic’ theory of PPD is at work in an individual then depression should follow the course of psychotic symptoms and its intensity should reduce alongside psychotic symptoms as they respond to treatment [39]. This theory finds some support in the literature: An early study following patients for eight weeks found a reduction in depressive symptoms alongside reduction in psychotic symptoms however the study did not follow participants beyond two months after recovery [40]. In a later study, participants with schizophrenia only began to exhibit depression three months after the abatement of psychotic symptoms [10]. Therefore the earlier study may not have followed participants for sufficient time for PPD to emerge [40]. This has been a deficiency in the literature and will be outlined below.

Compelling evidence suggesting that remission of depression in acute psychosis occurs following the treatment of psychotic symptoms [41-43]. However none of these studies provide follow-up data from the stable or non-psychotic period, and so the recognition of depression following recovery from psychosis has been suggested in these cohorts to result from residual symptoms from the acute phase [41] or, due to the lack of assessment of extrapyramidal symptoms, it was impossible to determine whether this increase was due to the influence of neuroleptic medication or other factors [43].

Almost identical findings were reported in a separate study [17]. Depressive symptoms in the acute phase were observed to decrease with treatment of psychotic symptoms, remaining low or absent in the stable phase. Data was reported from three groups of patients; two groups were followed up 12-14 weeks after admission and both groups demonstrated a significant drop in depressive symptoms at the second interview. A third group, followed up after 6 months, reported no overall change in depressive symptoms from prior to discharge. Interestingly, 16% of the this group reported an increase in depressive symptoms. The authors acknowledge that for some individuals PPD may be a reaction to psychosis, but argue that this position is weak and cannot explain why depression decreased with psychotic symptoms for the majority of participants. This postpsychotic increase in depression for a subgroup of patients at six months is especially important to note given that the average time for PPD to emerge in the stable phase is around 8 months after onset [12]. It may be that for the majority of patients depressive symptoms abate alongside the psychotic, in which case depression could be considered intrinsic to psychosis. However, in a subgroup of patients, depression in the stable phase may be of different origin to depression in the acute phase.

Interestingly, in the acute phase a negative correlation was observed between positive symptoms and depression in a cohort of 211 community patients with a diagnosis of schizophrenia [10]; this relationship held even when accounting for negative signs, level of medication and subjective experience of extrapyramidal symptoms. This finding is in contrast to other research and is problematic to the theory that PPD and indeed depression in general is intrinsic to psychosis. A potential explanation of this finding may be that PPD is an independent syndrome and an emotional reaction to psychosis. Loss of perceived social standing and the individual’s appraisal of psychosis may be important processes in the emergence of PPD [20]. Although depression in the acute phase is thought to arise from a separate mechanism to depression in the stable phase [6], it may be worth considering the following: It is possible that during the acute phase, a patient may be too preoccupied with coping or understanding their positive signs to have any concern with social standing. Similarly, the hallucinations and delusions experienced by an individual may foster a sense of security or increase feelings of self-worth, in which case positive signs may be negatively related to depression in the acute phase. By appraising psychotic symptoms positively, depression may be inversely related to positive symptoms. This may support the notion that an individual’s appraisals are important to the development of depression in psychosis.

In a study of ‘pure’ PPD sufferers, defined as having depression in the ‘stable phase’ after psychotic symptoms have abated, no relationship was found between depression and negative symptoms but a highly significant relationship between residual positive symptoms and depression was evident [11]. The highly significant relationship found between residual positive symptoms and depression provides some support for intrinsic theories of PPD [17]. However, if depression is intrinsic to psychosis, a relationship between negative symptoms and depression would also be expected. In addition, the presence of positive symptoms is consistent with the ICD-10 definition of post-schizophrenic depression but incompatible with the proposed definition of depression as being post-psychotic only when positive symptoms have completely subsided [12].

Evidence for an intrinsic theory of PPD is mixed with limited support from the literature, however a number of unexpected findings are left unexplained. The majority of studies supporting the intrinsic theory of PPD failed to follow participants for sufficient time for PPD to emerge, which is on average 8 months after recovery [12]. Depression may be related to psychotic symptoms in these studies due to a subgroup of participants with intrinsic depression yielding depression scores that are associated with residual psychotic symptoms after recovery. Research with better defined samples or assessing depression for longer time periods tends to support the notion that PPD is independent of psychosis [11,43]. Taken with findings that depression may be negatively related to psychotic symptoms, it seems unlikely that an intrinsic theory offers a complete explanation of all cases of depression in the stable phase. Higher quality longitudinal trials distinguishing between different depressive subgroups are required to further investigate the relationship between psychotic symptoms and PPD. In summary, the theory of PPD as intrinsic to psychosis is an incomplete explanation of all cases of PPD particularly as there is a burgeoning literature espousing that an individual’s cognitive appraisals of their psychosis may be important in the emergence of depressive symptoms.

Post-psychotic depression as a psychological reaction to psychosis

Four studies [12,20,44,45] explicitly investigated the course of depression in psychosis aiming to discern which of the three course patterns of depression [17] follows and which of the three pathways to depression are at work [38]. The first study [12] longitudinally measured depression, positive symptoms, negative symptoms and pharmacogenic side effects from the acute phase to 12 months after admission. This study has the advantage over previous research by regularly assessing patients from onset of psychosis for a complete year, giving a comprehensive picture of the course of depression from the acute phase and beyond.

Analysis revealed four clinically distinct sub-samples within the study, each displaying a unique course of depression. The first experienced high depression at onset, none during recovery and then a rise again after a period of no depression. The second group experienced no depression at onset and then a significant rise after recovery from the acute phase. A third group were depressed during onset, but not after recovery. The final group displayed no depression throughout the course of the study. There was no association between depression in the acute phase and PPD, implying that the two are independent of each other and may have different inception and maintaining factors. Similarly, in the stable phase, there were no differences between those with PPD and those without PPD on measures of positive and negative symptoms, again supporting the notion that PPD is independent of psychosis [12].

The finding of four distinct groups assessed during the same time period, two displaying PPD and two without PPD, may explain some of the inconsistencies in previous research. By aggregating all depressive subgroups, the true course and prevalence of PPD may have been disguised by differences in levels of depression between the subgroups at the various time points. Another study investigating individuals experiencing their first episode of psychosis (FEP) [44] following participants for one year reported the same course patterns as previous findings [12] i.e. depression was unrelated to psychotropic medication at baseline and at follow-up.

A recent study investigated the course of depression and suicidality in the prodrome, acute and recovered phases in FEP [45]. The CDSS [46] was used on first contact with services and again at 6 and 12 months. Prodromal depression was retrospectively assessed at first interview. Depression present in the prodrome was related to an increased likelihood of depression in the acute phase and in the 12 months after recovery. The researchers stressed the importance of understanding depression in the prodromal stage of FEP as they found it rare for individual’s not experiencing depression during the early stages of psychosis to later develop depressive symptoms.

If it is assumed that depression and observed during the prodrome acute psychotic phases are phenomenologically the same, the findings of the more recent study [45] differ from those of the first [12]. The former [45] proposes depression in the prodrome as a predictor of PPD, whereas the latter [12] argue that depression during acute psychosis did not predict PPD. However, if it is argued that prodromal depression and acute psychosis depression are distinctly different, one due to stressors and premorbid capacity for vulnerability and the other as an emergent affective reaction to positive symptoms such as voices and delusions, then the utility of these depressions in predicting future PPD is consistent across the two studies. This would suggest that depression in the prodrome is a predictor of PPD whereas depression in the acute phase is not. A study investigated depression prior to and during the prodrome [47], finding that 17% of patients included in their study had experienced a major depressive episode more than a year before onset of FEP. This increased to 30% during or after onset of psychosis. This study provides partial support for the finding that depression in the prodrome predicts PPD [45]. It should be noted however, that it is not clear how many participants had acute depression and/or pre-psychotic depression, either prodromal or premorbid, prior to developing PPD. Additionally, a weakness of both these papers is their reliance on subjective recall of earlier depression, prior to the onset of psychosis.

Upthegrove and colleagues suggest eight pathways to depression in psychosis [45]. Four of these are concerned with depression in the postpsychotic phase and are as follows: 1) Depression throughout; 2) Depression in prodrome, no acute depression, depression at followup; 3) No prodromal depression, depression in acute phase and follow-up and; 4) Depression in follow-up only.

These findings must be accepted with caution as a retrospective measure of prodromal depression was employed and is particularly contentious given the bias towards recalling more negative events in individuals experiencing later depression [48]. This method avoids the need for a large sample of individuals ‘at risk’ of developing psychosis, but makes it difficult to infer a direct link between prodromal depression and depression later in psychosis, and a wholly longitudinal replication of these results is warranted.

Iqbal and colleagues [20] drew on research from social ranking theory and power [49] which argues that certain life events may be depressogenic, particularly if they involve feelings of loss and humiliation. Iqbal et al. view psychosis as a potentially depressogenic life event [20]. Negative appraisals of psychosis such as feelings of entrapment may lead to a loss of perceived social standing, self-worth and social acceptance, all of which have been implicated in depression [50]. Participants’ appraisals about their psychosis were assessed using the Insight Scale [51], a measure of the conceptualisation of psychosis and the Personal Beliefs about Illness Questionnaire (PBIQ) [52]. The PBIQ assesses feelings of loss, humiliation, shame, entrapment in psychosis and attribution of behaviour to self or illness. A measure of self-concept, the Possible Selves Questionnaire (PSQ) [53], provides a score presenting how a person views themselves at present, how they view themselves in the future and how they would like to be in the future, yielding a mean score of the ‘now self’, ‘the probable self’ and the ‘like to be self’.

When participants were not depressed, insight did not differ between the PPD and non-PPD groups. During PPD, participants had better insight into their condition, a reduction of self-esteem and an increase in feelings of loss, humiliation, shame entrapment and selfblame. This replicates studies comparing individuals with depression and non-depressed controls [22,51,52]. Similarly, those with PPD were more likely to view their future selves as low status than non- PPD participants, however their scores on the ‘like-to-be self’ were identical. Therefore the PPD group had similar aspirations to the non-PPD group, but viewed themselves to have lower status in the future. In summary, participants with PPD were more likely to view their future social status as lower, had more negative appraisals about their condition, were more self-critical and had lower self-esteem. This is supported by a study of 92 participants experiencing acute FEP, followed-up a year later, which revealed that those experiencing PPD had greater appraisals of loss, shame and entrapment by the psychosis than non-PPD participants, and that negative appraisals of psychosis were a significant contributor to PPD severity [54]. Although a single 12-month follow up may reduce the identification of PPD cases, the study places a focus on the cognitive appraisals that may be implicated in PPD onset. Both studies support the notion that an individual’s appraisals of their psychosis may be important in the development of PPD.

Several studies [45,47,55] support the notion that an emotional reaction to psychosis is a potential cause of PPD. By grouping patients according to depressive course, Birchwood and colleagues overcame a weakness of many studies by avoiding the aggregation of depression scores which in previous research may have disguised a number of distinct courses of depression within a particular sample [12]. The differences in cognitive appraisals between those with PPD and those without PPD bolster the emotional reaction theory; lower self-esteem, lower perceived social rank and more negative appraisals differentiated those with PPD and those without PPD. There was no difference in levels of extrapyramidal side effects and neuroleptic dose between those with or without PPD. This effectively rules out ‘pharmacogenic’ or ‘akinetic’ explanations of PPD. Similarly, as there were no differences between positive and negative symptoms in those with and those without PPD, it seems unlikely that PPD is intrinsic to psychosis, rather it is an independent disorder. This finding, combined with the differing cognitive appraisals between those with PPD and those without PPD, highlights that depression as an emotional reaction to psychosis is a reasonable suggestion.


Methodological limitations

As mentioned in previous section, lack of consensus of a precise definition of PPD may have led to the inconsistent prevalence rates reported in the literature. Additionally, heterogeneous samples may have clouded some findings; of the 81 participants who participated in the longitudinal study by Birchwood and colleagues [12] only 39 displayed ‘pure’ PPD, with depression emerging after recovery. By aggregating depression scores across all subgroups each with a differing course of depression, it is impossible to distinguish those who are suffering PPD from those with residual depression from the acute phase. Use of a retrospective measurement of depression is also problematic as it is open to recall bias. This is especially important given the tendency towards recalling more negative information that is well documented in those experiencing low mood [48].

PPD research has typically employed one or more of the following depression measures: The Hamilton Depression Rating Scale (HDRS) [56]; The Beck Depression Inventory (BDI) [57] and the depression sub-scale of Positive and Negative Symptoms Scale (PANSS-D) [58]. None of these measures were designed specifically for use in populations with psychosis. Consequently, these measures may overlap with depressive symptoms, negative symptoms and extrapyramidal symptoms, which may have yielded inflated depression scores in many studies. An alternative to the previous measures is the CDSS which was developed to overcome the weaknesses inherent in other measures of depression when used in psychosis and is uncorrelated with extrapyramidal symptoms or negative symptoms [37,59]. The CDSS is significantly correlated with both the PANSS-D and the HDRS and is recommended for research into depression and psychosis [60].

The assessment period of research in the literature is also variable with some studies following participants only during the acute phase, others for 12 weeks [43] or up to a year [12,44]. As noted earlier, the average time for onset of PPD is 8 months, so many studies stopped short of the minimum time period for the emergence of PPD. Similarly, irregular measurement points between studies are also common, making direct comparison between studies more difficult.

Further Research

Future research would benefit from using a consistent definition of PPD. As suggested by a number of researchers [6,12] a suitable definition of PPD may be: Depression unexplained by neuroleptic side effects, occurring independently of psychosis that is itself in a stable phase following an acute psychotic episode, with the depressive symptoms only commencing after psychotic symptoms have abated or stabilized.

In light of the methodological shortcomings in many of the papers discussed above, further research requires longitudinal designs of at least 8 month duration and clear identification of the differing subgroups of individuals (pathways) to avoid confounding relationships between heterogeneous samples.

In terms of depression psychometrics, the CDSS is the most appropriate measure of depression in psychosis. As outlined previously, the CDSS is a superior measure of depression in psychosis and may overcome the limitations of other measures by assessing depression independently of negative and extrapyramidal symptoms.

By recognising the impact of an individual’s appraisals, the notion that PPD may be caused by an emotional reaction to psychosis represents an important step in PPD research [12,20]. The next stages of research should include more detailed exploration of the thoughts, feelings and emotions of an individual with psychosis and their appraisals of psychosis.

Researching the impact of prodromal depression as a predictor of PPD and depression in acute psychosis is also required. To ensure adequate statistical power, longitudinal designs following the course of depression from the prodrome to recovery may require large samples of at high risk of transition to psychosis cohorts [61]. Future research could follow individuals who have already experienced their first episode, though this would not allow elucidation of the eight pathways suggested by Upthegrove and colleagues [45].

Summary and Conclusion

It is likely that a number of clinically distinct courses of depression are present in individuals in recovery from psychosis, ranging from medication induced dysphoria or akinesia to an emotional reaction to psychosis. If PPD is defined as a persistent low mood arising weeks or months after psychotic symptoms have abated, then the evidence supporting intrinsic theories of depression in psychosis are supported within the literature. However, these have been limited by variables such as: heterogeneous samples; inappropriate assessment scales and criteria; varied and often contradictory definitions of PPD, small sample sizes and occasionally negative or inverse findings. On the other hand, the psychological reaction theory is supported by a small but high quality evidence base that overcomes many of the limitations in the wider literature.


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