To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
There are few data on the profile of those with serious mental illness (SMI) admitted to hospital for physical health reasons.
To compare outcomes for patients with and without an SMI admitted to hospital in England where the primary reason for admission was chronic obstructive pulmonary disease (COPD).
This was a retrospective, observational analysis of the English Hospital Episodes Statistics data-set for the period from 1 April 2018 to 31 March 2019, for patients aged 18–74 years with COPD as the dominant reason for admission. Patient with an SMI (psychosis spectrum disorder, bipolar disorder) were identified.
Data were available for 54 578 patients, of whom 2096 (3.8%) had an SMI. Patients with an SMI were younger, more likely to be female and more likely to live in deprived areas than those without an SMI. The burden of comorbidity was similar between the two groups. After adjusting for covariates, SMI was associated with significantly greater risk of length of stay than the median (odds ratio 1.24, 95% CI 1.12–1.37, P ≤ 0.001) and with 30-day emergency readmission (odds ratio 1.51, 95% confidence interval 1.34–1.69, P ≤ 0.001) but not with in-hospital mortality.
Clinicians should be aware of the potential for poorer outcomes in patients with an SMI even when the SMI is not the primary reason for admission. Collaborative working across mental and physical healthcare provision may facilitate improved outcomes for people with SMI.
Antipsychotic treatment resistance affects up to a third of individuals with schizophrenia. Of those affected, 70–84% are reported to be treatment resistant from the outset. This raises the possibility that the neurobiological mechanisms of treatment resistance emerge before the onset of psychosis and have a neurodevelopmental origin. Neuropsychological investigations can offer important insights into the nature, origin and pathophysiology of treatment-resistant schizophrenia (TRS), but methodological limitations in a still emergent field of research have obscured the neuropsychological discriminability of TRS. We report on the first systematic review and meta-analysis to investigate neuropsychological differences between TRS patients and treatment-responsive controls across 17 published studies (1864 participants). Five meta-analyses were performed in relation to (1) executive function, (2) general cognitive function, (3) attention, working memory and processing speed, (4) verbal memory and learning, and (5) visual−spatial memory and learning. Small-to-moderate effect sizes emerged for all domains. Similarly to previous comparisons between unselected, drug-naïve and first-episode schizophrenia samples v. healthy controls in the literature, the largest effect size was observed in verbal memory and learning [dl = −0.53; 95% confidence interval (CI) −0.29 to −0.76; z = 4.42; p < 0.001]. A sub-analysis of language-related functions, extracted from across the primary domains, yielded a comparable effect size (dl = −0.53, 95% CI −0.82 to −0.23; z = 3.45; p < 0.001). Manipulating our sampling strategy to include or exclude samples selected for clozapine response did not affect the pattern of findings. Our findings are discussed in relation to possible aetiological contributions to TRS.
Neuropsychological investigations can help untangle the aetiological and phenomenological heterogeneity of schizophrenia but have scarcely been employed in the context of treatment-resistant (TR) schizophrenia. No population-based study has examined neuropsychological function in the first-episode of TR psychosis.
We report baseline neuropsychological findings from a longitudinal, population-based study of first-episode psychosis, which followed up cases from index admission to 10 years. At the 10-year follow up patients were classified as treatment responsive or TR after reconstructing their entire case histories. Of 145 cases with neuropsychological data at baseline, 113 were classified as treatment responsive, and 32 as TR at the 10-year follow-up.
Compared with 257 community controls, both case groups showed baseline deficits in three composite neuropsychological scores, derived from principal component analysis: verbal intelligence and fluency, visuospatial ability and executive function, and verbal memory and learning (p values⩽0.001). Compared with treatment responders, TR cases showed deficits in verbal intelligence and fluency, both in the extended psychosis sample (t = −2.32; p = 0.022) and in the schizophrenia diagnostic subgroup (t = −2.49; p = 0.017). Similar relative deficits in the TR cases emerged in sub-/sensitivity analyses excluding patients with delayed-onset treatment resistance (p values<0.01–0.001) and those born outside the UK (p values<0.05).
Verbal intelligence and fluency are impaired in patients with TR psychosis compared with those who respond to treatment. This differential is already detectable – at a group level – at the first illness episode, supporting the conceptualisation of TR psychosis as a severe, pathogenically distinct variant, embedded in aberrant neurodevelopmental processes.
There is increasing evidence for shared genetic susceptibility between schizophrenia and bipolar disorder. Although genetic variants only convey subtle increases in risk individually, their combination into a polygenic risk score constitutes a strong disease predictor.
To investigate whether schizophrenia and bipolar disorder polygenic risk scores can distinguish people with broadly defined psychosis and their unaffected relatives from controls.
Using the latest Psychiatric Genomics Consortium data, we calculated schizophrenia and bipolar disorder polygenic risk scores for 1168 people with psychosis, 552 unaffected relatives and 1472 controls.
Patients with broadly defined psychosis had dramatic increases in schizophrenia and bipolar polygenic risk scores, as did their relatives, albeit to a lesser degree. However, the accuracy of predictive models was modest.
Although polygenic risk scores are not ready for clinical use, it is hoped that as they are refined they could help towards risk reduction advice and early interventions for psychosis.
Declaration of interest
R.M.M. has received honoraria for lectures from Janssen, Lundbeck, Lilly, Otsuka and Sunovian.
We report on the first open-label, parallel group randomised controlled trial of automated appointment reminders in a psychosis community service in the UK. Ninety-five patients were randomly allocated to receiving/not receiving automated messaging reminders 7 days and 1 day before appointments. All ‘Attended’ and ‘Missed’ appointment outcomes over 6 months were analysed using cluster regression analysis. Reminded appointments were significantly more frequently attended than non-reminded appointments (unadjusted odds ratio (OR) = 3.54, 95% CI 1.36–9.22, P = 0.01; adjusted OR = 2.95, 95% CI 1.05–8.85, P < 0.05). Automated messaging reminders can provide a robust strategy for promoting engagement with psychosis services.
Declaration of interest
The authors have no competing financial interests to declare in relation to the current work. Sarah McAllister was supported by a King's Undergraduate Research Fellowship.
Twin studies have lacked statistical power to apply advanced genetic modelling techniques to the search for cognitive endophenotypes for bipolar disorder.
To quantify the shared genetic variability between bipolar disorder and cognitive measures.
Structural equation modelling was performed on cognitive data collected from 331 twins/siblings of varying genetic relatedness, disease status and concordance for bipolar disorder.
Using a parsimonious AE model, verbal episodic and spatial working memory showed statistically significant genetic correlations with bipolar disorder (rg = |0.23|–|0.27|), which lost statistical significance after covarying for affective symptoms. Using an ACE model, IQ and visual-spatial learning showed statistically significant genetic correlations with bipolar disorder (rg = |0.51|–|1.00|), which remained significant after covarying for affective symptoms.
Verbal episodic and spatial working memory capture a modest fraction of the bipolar diathesis. IQ and visual-spatial learning may tap into genetic substrates of non-affective symptomatology in bipolar disorder.
Identifying neurocognitive subtypes in schizophrenia may help establish neurobiologically meaningful subtypes of the disorder, but is frequently confounded by differences in intellectual function between individuals with schizophrenia and controls.
To examine neuropsychological performance in individuals with epidemiologically based, first-onset schizophrenia and intellectually matched controls.
Using standard IQ and reading tests, we examined the proportions of 101 people with epidemiologically derived, first-onset schizophrenia/schizoaffective disorder and 317 community controls, falling into three a priori defined intellectual categories: ‘stable good’, ‘deteriorated poor’ and ‘stable poor’. Neuropsychological function was compared between intellectually matched participants with schizophrenia and control subgroups.
Multiple deficits in executive function, processing speed and verbal memory, but not visual/spatial perception/memory, were detected in all participant groups with schizophrenia compared with controls. The average effect size across the affected domains ranged from small to medium to large in the stable good, deteriorated poor and stable poor subgroups of participants with schizophrenia, respectively.
Compared with intellectually matched controls, people with epidemiologically derived, first-onset schizophrenia/schizoaffective disorder show multiple deficits in executive function, processing speed and verbal memory.
We analysed Stroop (neuropsychological screening test) measures of response
inhibition in 18 twin pairs discordant for bipolar I disorder compared with
17 healthy control pairs, as well as 40 singletons with bipolar disorder
with psychotic features and a family history of psychosis, 46 of their
first-degree relatives without bipolar disorder or psychosis and 48
controls. In both studies, individuals with bipolar disorder showed Stroop
deficits and their first-degree relatives showed intact performance. In the
twin patients, an interference score was associated with depressive
symptoms. Having a first-degree relative with bipolar disorder, even a
familial, psychotic form, did not confer risk for enhanced susceptibility to
interference in our studies.
We assessed premorbid functioning during childhood and adolescence in 50 people with schizophrenia from multiply affected families, 39 of their unaffected siblings, 69 people with schizophrenia with no family history of psychosis, 67 of their unaffected siblings and 83 controls. People with schizophrenia had poorer premorbid social and academic adjustment and exhibited a decline between childhood and adolescence compared with controls. Unaffected siblings from multiply affected families also had poor academic functioning in adolescence, with a decline between childhood and adolescence. This may represent a familial (presumed genetic) effect.
Background. Electrophysiological endophenotypes are far less explored in bipolar disorder as compared to schizophrenia. No previous twin study of event-related potentials (ERPs) in bipolar illness has been reported. This study uses a twin design and advanced genetic model fitting analyses aiming to (1) assess and quantify the relationship of a range of ERP components with bipolar disorder with psychotic features, and (2) examine the source of the relationship (due to genetic or environmental factors).
Method. P300, P50 suppression and mismatch negativity (MMN) were recorded in 10 discordant monozygotic (MZ) bipolar twin pairs, six concordant MZ bipolar twin pairs and 78 control twin pairs. Statistical analyses were based on structural equation modelling.
Results. Bipolar disorder was significantly associated with smaller P300 amplitude and decreased P50 suppression. Genetic correlations were the main source of the associations, estimated to be −0·33 for P300 amplitude and 0·46 for P50 ratio. Individual-specific environmental influences were not significant. MMN and P300 latency were not associated with the illness.
Conclusions. The results provide supporting evidence that P300 amplitude and P50 suppression ratio are ERP endophenotypes for bipolar disorder.
Intellectual asymmetry with superiority of verbal skills to spatial skills
frequently characterises patients with schizophrenia, but it is unclear
whether this pattern also reflects genetic susceptibility to the disorder.
We examined the association of a continuous measure of genetic liability to
schizophrenia with Verbal-Spatial Contrast IQ (an index of intellectual
asymmetry) in 108 first-degree relatives without psychosis of probands with
schizophrenia. Higher genetic liability was significantly associated with
greater intellectual asymmetry in favour of verbal skills. Intellectual
asymmetry with a relative superiority of verbal skills to spatial skills
represents a putative endophenotype of schizophrenia.
We report cognitive performance of a group of individuals who are likely to have transmitted liability to psychosis to their offspring. Out of 230 relatives of patients with psychosis, 27 met our criteria for a presumed obligate carrier, that is a non-psychotic individual who had a parent or a sibling as well as an offspring with psychosis. The presumed obligate carriers showed impairments in verbal memory and in visuospatial manipulations, suggesting that these individuals transmit vulnerability for psychosis to their offspring in terms of a disability to recall verbal information and an impaired capacity to perceive spatial relations.
Eugenia Kravariti, Institute of Psychiatry, King's College, London, UK,
Paola Dazzan, Institute of Psychiatry, King's College, London, UK,
Paul Fearon, Institute of Psychiatry, King's College, London, UK,
Robin M. Murray, Institute of Psychiatry, King's College, London, UK
Childhood antecedents of schizophrenia may variably reflect integral components of the schizophrenia diathesis, non-specific factors that potentiate this predisposition, or early manifestations of the disorder itself. This chapter explores the nature of the childhood antecedents of schizophrenia. It explores whether children who develop schizophrenia in adulthood are distinguishable from control children. The chapter examines how strong the association between the distinguishing features of preschizophrenia children as a group and the later development of the disorder is. It also explains ways we can identify preschizophrenia children on the basis of these characteristics. The early risk factors that flag the preschizophrenia status are also considered. Particular emphasis is on prospective population-based, high-risk, and follow-back studies. The measures investigated by the high-risk paradigm can aid in identification of truly vulnerable individuals within the high-risk population.
Email your librarian or administrator to recommend adding this to your organisation's collection.