Psychotic depression case studies

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In addition to the genetic and environmental correlations, it is also possible to calculate the proportion of the phenotypic correlation due to genes or environment. The cross-time associations are represented as partial regression coefficients. The value of each path is independent of the other associations addressed in the model.

Psychotic Depression: Underrecognized, Undertreated—and Dangerous

The prediction of a trait by the same trait b 11 , b 22 , as well as the prediction of a trait by another trait b 12 , b 21 , can be assessed. The value of b 11 , eg, is the contribution of time 1 depression to time 2 depression. The value of b 12 indexes the contribution of time 1 depression to time 2 paranoia independent of the within-time relationship between depression and paranoia at time 1. Descriptive statistics for all study variables at times 1 and 2 are given in table 1 and have been reported previously.

The only difference at time 2 was that females rather than males scored significantly higher for anhedonia and there were no significant sex differences in hallucinations. Note : N , number of individuals; t , t statistic; df , degrees of freedom.

Psychotic Depression: Losing Touch With Reality

Mean and SD for 1 randomly selected member of a twin pair. Within-time and cross-time correlations between specific psychotic experiences and depression are presented in table 2. Overall 3 relationships were of adequate strength to consider for twin modeling paranoia and depression; hallucinations and depression; cognitive disorganization; and depression. Note : N , number of observations; P, parent report.

Within-time correlations on diagonal; cross time correlations on off diagonal. Correlations conducted on 1 randomly selected member of a twin pair. First, as is standard twin model-fitting procedure, 33 a saturated model which allowed variances, covariances, and means to vary by zygosity group, as well as sex was run, to get a baseline index of fit.

Models which allowed for sex differences in A, C, and E parameters, and more conservative models which did not, were run. Models which allowed for sex differences had a better fit than those that did not see Supplementary Data for fit statistics ; however, as paths were similar across the sexes and Bayesian Information Criterion BIC was lower in no sex difference models, for simplicity we present results from the no sex difference model in figure 1 full sex difference models are shown Supplementary Data. Cross-twin correlations and univariate genetic and environmental estimates are presented in Supplementary Data.

All variables were moderately heritable, with low shared environmental and modest non-shared environmental influences, as reported elsewhere. Bivariate cross-lagged models for depression and psychotic experiences. Note : Hall: hallucinations; cog dis: cognitive disorganization. Additive genetic A , shared C , and non-shared environmental E influences on total variance at time 2 presented.

Is clinical depression a genetic disorder ? - Good Health FAQ

Correlations between latent factors at time 2 are presented on total, rather than residual, variances. Shared environmental correlations were generally high between the specific psychotic experiences and depression; however, as C explained very little of variance in measures this should not be over-interpreted. Patterns of genetic and environmental correlations were similar at time 2.

Shared environment accounted for little of the covariation table 3. Bivariate genetic a 2 , common environment c 2 , and unique environment e 2 estimates the proportion of the phenotypic correlation between depression symptoms and psychotic experiences due to genetic and environmental influences. The within-variable continuity paths accounted for the largest proportion of variance in variables at time 2. Specifically, within-variable continuity from time 1 to time 2 was estimated at.

Within-variable stability was also high for psychotic experiences paranoia:. Paranoia and Depression figure 2a Cross-time cross-variable paths from paranoia to depression. Hallucinations and Depression figure 2b Cross-time cross-variable paths from hallucinations to depression. Of note, the path from hallucinations to depression was stronger than the converse association although confidence intervals overlapped. This suggests hallucinations predict depression after controlling for earlier depression to a greater extent than depression predicts hallucinations after controlling for earlier hallucinations.

A case of sudden psychosis | MDedge Psychiatry

Cognitive Disorganization and Depression figure 2c Time 1 cognitive disorganization significantly predicted time 2 depression. The converse association time 1 depression to time 2 cognitive disorganization whilst significant was half the magnitude. Confidence intervals did not overlap, suggesting this difference in magnitude was significant. This suggests that cognitive disorganization impacts depression across time, after controlling for earlier levels of depression, and is a significantly stronger effect than that of depression on later cognitive disorganization after controlling for earlier levels of cognitive disorganization.

Depressive symptoms were moderately correlated with paranoia, hallucinations, and cognitive disorganization in adolescence. Largely the same genetic influences make individuals vulnerable to traits of depression and positive and cognitive psychotic experiences in adolescence, suggesting that the pleiotropic genetic effects reported in adult clinical samples 21—24 between major depression and psychotic disorders are also true of psychotic experiences and depression symptoms in the community in adolescence.

Strong correlations were found between positive psychotic experiences and depressive symptoms in line with previous literature. Different raters were used to assess negative symptoms parent-rated and depression symptoms self-rated in line with recommendations in the field regarding the optimal rater for these domains observer ratings for negative symptoms, self-ratings for depression.

However the use of different raters for these scales will have led to reduced observed correlation between them. Our measure of anhedonia focused on the anticipatory aspect of anhedonia inability to experience pleasure for future events rather than its consummatory component inability to experience pleasure in the moment.

Anticipatory anhedonia has been shown to be more important in schizophrenia as opposed to depression. This may explain the low correlation between anhedonia and depression.


We found that symptoms of depression and positive and cognitive psychotic experiences impact each other over time, even after taking into account the shared genetic propensity that exists between them and existing associations at earlier ages. For both hallucinations and cognitive disorganization, the strength of the path from psychotic experiences to depression was stronger than the opposite direction. This is in contrast to findings in adult clinical samples which suggest the direction of effects is from depression to psychosis but not vice-versa. The high genetic correlations observed between psychotic experiences and depression suggests that 1 reason that psychotic experiences and depression co-occur in adolescence is due to shared aetiological influences which make individuals vulnerable to both sets of traits.

The results suggest that the genetic relationship between psychotic experiences and symptoms of depression is established prior to adulthood. Although the same genetic and familial influences appear to operate across the continuum for psychotic experiences, 15 , 41 the 2 studies thus far have not found that a schizophrenia polygenic risk score predicts having more psychotic experiences in adolescence. Non-shared environmental influences were important for psychotic experiences and depression symptoms in line with previous research in adolescence.

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Our results also show moderate non-shared environmental correlations between depression and psychotic experiences. This suggests that some of the same environmental factors that influence depression may also influence psychotic experiences. Such environments could include childhood adversity 44—46 and stressful life events, 47 , 48 which have been shown to be risk factors for both depressive and psychotic disorders.

The twin design is based on several assumptions and ideally findings should be replicated across multiple study designs see Plomin et al 49 for detail. Measures of psychotic experiences and depression were collected using self-report questionnaires: although the measures are well validated and show good internal consistencies, it is possible that they fail to capture the full complexities of the phenotypes.

It is also possible that some individuals may interpret questions in alternative ways from that intended.

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Self-report data of psychotic experiences have also been shown to give higher means than interview data. The use of self-report measures allowed us to investigate the full range of positive eg, grandiosity , negative eg, lack of affect and cognitive psychotic experiences eg, disordered thinking in a large sample with a narrow age range.

As the current study was conducted in a community sample, our results were not confounded with effects of treatment and are not biased towards the most severe and comorbid cases. Limitations associated with the cross-lagged model need to be taken into account including stationarity, the assumption that causal processes influencing variables do not change over the time period in question see Kenny All models fitted less well than the saturated model, however, poor fits are commonly found within all cross-lagged models in large samples.

Psychotic experiences, in particular positive and cognitive types, are strongly related to depressive symptoms in adolescence. Our study shows that the co-occurrence of depression and psychotic experiences is due to high genetic overlap and modest overlap in environmental influences, yet in addition, psychotic experiences and depression directly impact each other over time.

While adolescent depression and paranoia predict each other bidirectionally over time, hallucinations and cognitive disorganization appear to impact later depression more so than vice-versa. The results of this study illustrate the way in which symptoms of depression and psychotic experiences in adolescence, both known risk factors for later psychiatric disorders, may develop and persist. Medical Research Council G to A. We thank the participants of TEDS for making this research possible.

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