Showing papers by "Robin M. Murray published in 2002"
TL;DR: This is the first prospective longitudinal study of adolescent cannabis use as a risk factor for adult schizophreniform disorder, taking into account childhood psychotic symptoms, and the Dunedin multidisciplinary health and development study has a 96% follow up rate at age 26.
Abstract: Papers pp 1195, 1199
The strongest evidence that cannabis use may be a risk factor for later psychosis comes from a Swedish cohort study which found that heavy cannabis use at age 18 increased the risk of later schizophrenia sixfold. 1 2 This study could not establish whether adolescent cannabis use was a consequence of pre-existing psychotic symptoms rather than a cause. We present the first prospective longitudinal study of adolescent cannabis use as a risk factor for adult schizophreniform disorder, taking into account childhood psychotic symptoms3 antedating cannabis use.
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Association between cannabis use in adolescence and schizophrenia and depressive symptoms and disorders at age 26 (n=759), controlling for childhood psychotic symptoms and use of other drugs in adolescence
The Dunedin multidisciplinary health and development study (a study of a general population birth cohort of 1037 individuals born in Dunedin, New Zealand, in 1972-3)4 has a 96% follow up rate at age 26. It obtained information on psychotic symptoms at age 11 and drug use at ages 15 and 18 from self reports and assessed …
1,315 citations
TL;DR: Current methods of investigating the relationship between obstetric complications and schizophrenia are reaching the limit of their usefulness, and a combination of disciplines and approaches will be needed to elucidate the mechanisms underlying these small but important associations.
Abstract: OBJECTIVE: This paper reviews the literature on obstetric complications as a risk factor for schizophrenia. The authors trace the evolution of this literature through different methods and carry out a quantitative review of the results from prospective, population-based studies. METHOD: Relevant papers were identified by a MEDLINE search, by examination of reference lists of published papers, and through personal contact with researchers in the field. Studies were grouped in chronological order according to common themes or methods. Meta-analytic techniques were used to summarize the findings of prospective population-based studies. RESULTS: The meta-analytic synthesis of the prospective population-based studies revealed that three groups of complications were significantly associated with schizophrenia: 1) complications of pregnancy (bleeding, diabetes, rhesus incompatibility, preeclampsia); 2) abnormal fetal growth and development: (low birthweight, congenital malformations, reduced head circumference),...
1,048 citations
TL;DR: Evidence is provided for an early-childhood, persistent, pan-developmental impairment that is specifically associated with schizophreniform disorder and that predicts psychotic symptoms in childhood and adulthood.
Abstract: Background Childhood developmental abnormalities have been previously described in schizophrenia. It is not known, however, whether childhood developmental impairment is specific to schizophrenia or is merely a marker for a range of psychiatric outcomes. Methods A 1-year birth cohort (1972-1973) of 1037 children enrolled in the Dunedin Multidisciplinary Health and Development Study was assessed at biennial intervals between ages 3 and 11 years on emotional, behavioral, and interpersonal problems, motor and language development, and intelligence. At age 11 years, children were asked about psychotic symptoms. At age 26 years, DSM-IV diagnoses were made using the Diagnostic Interview Schedule. Study members having schizophreniform disorder (n = 36 [3.7%]) were compared with healthy controls and also with groups diagnosed as having mania (n = 20 [2%]) and nonpsychotic anxiety or depression disorders (n = 278 [28.5%]) on childhood variables. Results Emotional problems and interpersonal difficulties were noted in children who later fulfilled diagnostic criteria for any of the adult psychiatric outcomes assessed. However, significant impairments in neuromotor, receptive language, and cognitive development were additionally present only among children later diagnosed as having schizophreniform disorder. Developmental impairments also predicted self-reported psychotic symptoms at age 11 years. These impairments were independent of the effects of socioeconomic, obstetric, and maternal factors. Conclusions The results provide evidence for an early-childhood, persistent, pan-developmental impairment that is specifically associated with schizophreniform disorder and that predicts psychotic symptoms in childhood and adulthood.
768 citations
TL;DR: If diagnostic hierarchies are relaxed, there is a degree of overlap in the genes contributing to RDC schizophrenic, schizoaffective, and manic syndromes, and Supplementing the traditional approach of assigning a single main lifetime diagnosis with information on within-person comorbidity of psychotic syndrome may provide valuable information about the familial aggregation of psychotic symptoms.
Abstract: Objective: Biometrical model fitting was applied to clinical data from twins to investigate whether operationally defined schizophrenic, schizoaffective, and manic syndromes share genetic risk factors. Method: Seventy-seven monozygotic and 89 same-sex dizygotic twin pairs in which the proband met the Research Diagnostic Criteria (RDC) for lifetime-ever schizophrenic, schizoaffective, or manic syndrome were ascertained from the Maudsley Twin Register in London. The syndromes were defined nonhierarchically. Correlations in liability were calculated for each syndrome in the monozygotic and dizygotic pairs and across the three pairings of schizophrenic-manic, schizophrenic-schizoaffective, and schizoaffective-manic syndromes both within probands and within pairs. For the three syndromes considered together, an independent pathway model was fitted. Results: The model fitting showed significant genetic correlations between all three syndromes. There was evidence of both common and syndrome-specific genetic contributions to the variance in liability to the schizophrenic and manic syndromes, but the genetic liability to the schizoaffective syndrome was entirely shared in common with the other two syndromes. In contrast, environmental liability to the schizoaffective syndrome was not shared with the other syndromes. Conclusions: If diagnostic hierarchies are relaxed, there is a degree of overlap in the genes contributing to RDC schizophrenic, schizoaffective, and manic syndromes. Supplementing the traditional approach of assigning a single main lifetime diagnosis with information on within-person comorbidity of psychotic syndromes may provide valuable information about the familial aggregation of psychotic symptoms.
452 citations
TL;DR: Individuals who were born very preterm continue to show noticeable decrements in brain volumes and striking increases in lateral ventricular volume into adolescence, and the functional significance of these abnormalities merits further investigation.
Abstract: Infants born very preterm have an increased risk of brain injury. Given the great increase in the number of such infants that are surviving, it is important to establish whether any resultant brain abnormalities persist into adolescence and adult life. We therefore examined in vivo whole brain, grey matter, white matter and hippocampal volumes, ventricular size and grey/white matter ratios in a series of adolescents who had been born very preterm, and an age-matched full-term control group. Structural MRI was carried out on a cohort of 72 adolescents (mean age 15 years) who were born before 33 weeks, and 48 age-matched full-term controls. Brain measurements were made blind to group affiliation using stereological principles. After controlling for gender and height, the very preterm subjects showed a 6.0% decrease in whole brain volume, and an 11.8% decrease in cortical grey matter volume, as well as a 15.6% decrease in right and a 12.1% decrease in left hippocampal volumes; they also had a 42.0% increase in the size of the lateral ventricles. Therefore, individuals who were born very preterm continue to show noticeable decrements in brain volumes and striking increases in lateral ventricular volume into adolescence. The functional significance of these abnormalities merits further investigation.
406 citations
01 Jan 2002
TL;DR: The implications of epidemiology for service planning in schizophrenia and gene-environment interaction in schizophrenia using neuroimaging are discussed, as well as the relationship between substance abuse and schizophrenia.
Abstract: Foreword William Carpenter Preface Part I. The Social Epidemiology of Schizophrenia: Introduction 1. Investigating socio-environmental influences in schizophrenia: conceptual and design issues Michaeline Bresnahan and Ezra Susser 2. Geographical variation in incidence, course and outcome in schizophrenia: a comparison of developing and developed countries Michealine Bresnahan, Paulo Menezes, Vijoy Varma and Ezra Susser 3. Temporal variation in the incidence, course and outcome of schizophrenia Michaeline Bresnahan, Jane Boydell, Robin Murray and Ezra Susser 4. Urbanisation, migration and risk of schizophrenia Jane Boydell and Robin Murray Part II. The Developmental Epidemiology of Schizophrenia: Introduction 5. Prenatal and perinatal risk factors for schizophrenia Mary Cannon, Robert Kendell, Ezra Susser and Peter Jones 6. Childhood development and later schizophrenia: evidence from genetic high risk and birth cohort studies Mary Cannon, C. Jane Tarrant, Matti O. Huttunen and Peter Jones 7. Prodrome, onset and early course of schizophrenia Heinz Hafner 8. The value of first-episode studies of schizophrenia Mary Clarke and Eadbhard O'Callaghan 9. Schizophrenia at the extremes of life Kenneth G. D. Orr and David J. Castle Part III. The Genetic Epidemiology of Schizophrenia: Introduction 10. The 'classical' genetic epidemiology of schizophrenia Alastair Cardno and Robin Murray 11. Molecular genetics and epidemiology in schizophrenia: a necessary partnership Stanley Zammit, Glyn Lewis and Michael J. Owen 12. Gene-environment correlation and interaction in schizophrenia Jim van Os and Pak Sham 13. Investigating gene-environment interaction in schizophrenia using neuroimaging Theo G. M. van Erp, Timothy L. Gasperoni, Isabelle M. Rosso and Tyrone D. Cannon Part IV. Special Issues in the Epidemiology of Schizophrenia: Introduction 14. Mortality and physical illness in schizophrenia Preben Bo Mortensen 15. The clinical epidemiology of suicide in schizophrenia Hannele Heila and Jouko Loennqvist 16. What is the relationship between substance abuse and schizophrenia? Robin Murray, Anton Grech, Peter Phillips and Sonia Johnson 17. Criminal and violent behaviour in schizophrenia Elizabeth Walsh and Alec Buchanan Part V. Future Directions and Emerging Issues: Introduction 18. Diagnosis and classification of schizophrenia: categories vs dimensions, distributions vs disease Jim van Os and Helene Verdoux 19. The implications of epidemiology for service planning in schizophrenia Graham Thornicroft and Michele Tansella 20. Prevention of schizophrenia - not an impossible dream John McGrath Glossary Index.
254 citations
TL;DR: Conventional antipsychotic medications cause significant levels of sexual dysfunction and Clinicians should routinely enquire about sexual symptoms prior to the prescription of antipsychotics and on follow-up.
Abstract: Background Antipsychotic drugs are associated with sexual dysfunction but the mechanisms are poorly understood.
Aims To ascertain the frequency of sexual dysfunction in patients taking conventional antipsychotics and to determine the possible underlying mechanisms.
Method Sexual dysfunction was assessed in 101 patients receiving conventional antipsychotic medication, 57 normal controls and 55 controls attending a sexual dysfunction clinic.
Results Sexual dysfunction occurred in 45% of patients taking antipsychotic medication, 17% of normal controls and 61% of controls attending a sexual dysfunction clinic. Sexual dysfunction was associated with autonomic side-effects in normoprolactinaemic males, but the presence of hyperprolactinaemia overrode other causes of sexual dysfunction. For women, hyperprolactinaemia was the main cause of sexual dysfunction.
Conclusions Conventional anti-psychotic medications cause significant levels of sexual dysfunction. Clinicians should routinely enquire about sexual symptoms prior to the prescription of antipsychotics and on follow-up.
237 citations
Journal Article•
232 citations
TL;DR: Patients with first-episode psychosis show an excess of Neurological soft signs, particularly in the areas of motor coordination and sequencing, sensory integration and in developmental reflexes, and the role of NSS as markers of cognitive dysfunction is clarified.
Abstract: Background Neurological soft signs (NSS) are minor neurological signs indicating non-specific cerebral dysfunction. Their presence has been documented extensively in schizophrenia but not during the first psychotic episode. Aims To review studies that have specifically investigated NSS atthe time of the first psychotic episode. Method A review of studies investigating neurological function in first-episode psychosis, using a clinical examination. Results Patients with first-episode psychosis show an excess of NSS, particularly in the areas of motor coordination and sequencing, sensory integration and in developmental reflexes. Furthermore, NSS may be associated with a specific laterality pattern. Conclusions More studies on first-onset schizophrenia are needed, evaluating both sensory and motor neurological domains (scoring separately for the two sides ofthe body), integrating this knowledge with neuroimaging findings and clarifying the role of NSS as markers of cognitive dysfunction. Declaration of interest None. Funding from the Stanley Foundation and the Medical Research Council (UK).
223 citations
TL;DR: It is concluded that large samples are required for powerful investigation of genetic effects in imaging data from twins and that genetic effects on structure of the human brain are regionally variable and predominantly symmetric in paralimbic structures and lateral temporal cortex.
211 citations
TL;DR: The results of this study indicate that neuroleptic-induced prolactin secretion is a dose-related side effect and, in females, the level of hyperprolactinaemia is correlated with the degree of suppression of the HPG axis.
Abstract: Hyperprolactinaemia is commonly induced by antipsychotic medications that have dopamine-blockade as their main mechanism of action. The purpose of this study was to assess the effect of antipsychotic-induced hyperprolactinaemia on hypothalamic-pituitary-gonadal axis (HPG) function.HPG axis function was assessed in 67 consecutive outpatients who were diagnosed with schizophrenia and stabilized for a period of not less than 2 years on typical antipsychotic medication, by means of clinical history, relevant questionnaires and measurement of plasma prolactin, estradiol, progesterone, testosterone, LH, FSH, sex hormone binding globulin, and TSH levels. Normative laboratory data were used to assess whether hormone levels fell within the reference range for a normal population. There was a significant correlation between dose of medication and plasma prolactin levels for the total group (P<0.001). Prolactin levels were significantly negatively associated with sex hormone levels in females (P<0.05). Males taking antipsychotic medication had a mean prolactin level of 404.1m/IU and mean gonadotrophin and sex hormone levels that fell within normal limits. The results of this study indicate that neuroleptic-induced prolactin secretion is a dose-related side effect and, in females, the level of hyperprolactinaemia is correlated with the degree of suppression of the HPG axis. Women taking long-term prolactin-raising antipsychotic medications are likely to be hyperprolactinaemic and have an associated hypogonadal state. In males, prolactin levels remain within normal limits, but at the upper end, with no apparent disturbance of reproductive hormones.
TL;DR: It is concluded that schizophrenia in the mother implies an increased risk for poor perinatal outcome, not fully explained by maternal factors, and a need to consider a common familial (probably genetic) vulnerability for pre- and per inatal stress and schizophrenia.
TL;DR: During the production of continuous speech, patients with formal thought disorder showed a reversed laterality of activation in the superior temporal cortex, consistent with findings of perturbed hemispheric interaction in schizophrenia, particularly in patients with formally thought disorder.
Abstract: Background. Formal thought disorder is a core symptom of schizophrenia. It is associated with a reversed lateralization of the superior temporal cortex volume, an area that is implicated in lexical retrieval. We investigated the neural correlates of word retrieval during continuous speech in patients with formal thought disorder using functional magnetic resonance imaging (fMRI).Methods. Blood oxygenation level dependent (BOLD) contrast was measured with fMRI while six patients with schizophrenia and six healthy control subjects spoke about seven Rorschach inkblots for 3 min each. Subjects produced varying amounts of speech during each run. In a within subject design, the number of words produced was correlated with the BOLD contrast in the two runs in each participant who showed the highest variance of speech output.Results. In control subjects, the amount of speech produced was mainly correlated with activation in the left superior temporal gyrus. In the patient group, the main correlations were in the right superior temporal gyrus.Conclusions. During the production of continuous speech, patients with formal thought disorder showed a reversed laterality of activation in the superior temporal cortex. This is consistent with findings of perturbed hemispheric interaction in schizophrenia, particularly in patients with formal thought disorder.
TL;DR: In this paper, the authors used functional magnetic resonance imaging (fMRI) to examine the relationship between activity in these areas while the rate of inner speech generation was varied experimentally, and found that the faster rate was associated with activation in the left inferior frontal gyrus, the right pre-and postcentral gyri and both superior temporal gyri.
Abstract: Monitoring one's thoughts (in the verbal modality) is thought to be critically dependent on the interaction between areas that generate and perceive inner speech in the frontal and temporal cortex, respectively. We used functional magnetic resonance imaging (fMRI) to examine the relationship between activity in these areas while the rate of inner speech generation was varied experimentally. The faster rate was associated with activation in the left inferior frontal gyrus, the right pre- and postcentral gyri and both superior temporal gyri. Thus, temporal cortical activation was associated with increasing the rate of covert articulation, in the absence of external auditory input, suggesting that there is effective fronto-temporal connectivity. Furthermore, this may provide support for the existence of feed forward models, which suggest that activity in regions responsible for verbal perception is modulated by activity in areas that generate inner speech.
TL;DR: Individuals inheriting the susceptibility to schizophrenia appear particularly prone to develop ventricular enlargement in response to obstetric complications, particularly in males.
Abstract: Structural brain abnormalities are consistently reported in schizophrenic subjects but the etiology of these abnormalities remains unclear. We tested the contribution of genetic predisposition and obstetric complications to the structural brain abnormalities found in schizophrenic probands and their relatives. MRI scans were carried out on 35 schizophrenic probands from families multiply affected with the disorder, and 63 of their unaffected relatives, including 10 parents who appeared to transmit genetic risk to their children; as well as 31 schizophrenic probands from families with no other affected members, 33 of their unaffected relatives; and finally 68 controls. Volumetric measurements of whole brain, lateral ventricles, third ventricle, cerebellum, and temporal lobes were completed for each subject. The impact of obstetric complications on brain structure was assessed across the gradient of presumed genetic predisposition. Both groups of schizophrenic probands displayed enlargement of the lateral and third ventricles, and there was a gradient of ventricular enlargement amongst the unaffected relatives in proportion to their likelihood of carrying schizophrenic genes. Ventricular enlargement was largely confined to males in both probands and unaffected relatives. Obstetric complications were associated with ventricular enlargement only in the familial probands. Non-familial probands displayed reduced volume of the temporal lobes bilaterally. In families with several schizophrenic members, ventricular enlargement is a marker for genetic liability, particularly in males. Individuals inheriting the susceptibility to schizophrenia appear particularly prone to develop ventricular enlargement in response to obstetric complications.
TL;DR: During the production of continuous speech, patients with formal thought disorder showed a reversed laterality of activation in the superior temporal cortex, consistent with findings of perturbed hemispheric interaction in schizophrenia, particularly in patients with formally thought disorder.
TL;DR: A plasticity of function compensating for early damage to the corpus callosum is revealed, possibly because the task was accomplished by storing information in working memory.
Abstract: We used functional MRI (fMRI) to establish the functional significance of corpus callosum damage in young adults who had been born very preterm. Seven subjects from a cohort of individuals who had been born at <33 weeks gestation and who had sustained callosal damage visualized on structural MRI were compared while they carried out auditory and visual tasks requiring callosal transfer with nine very preterm subjects with corpora callosa of normal appearance on structural MRI, and with seven full-term controls. The very preterm subjects with damaged corpora callosa had significantly different activation patterns compared with the two control groups. In the visual task, additional activity was seen in the right dorsolateral prefrontal cortex of the damaged callosum group, possibly because the task was accomplished by storing information in working memory. On the auditory task, a deficit of activity was seen in the right temporal lobe of the callosum group. The findings reveal a plasticity of function compensating for early damage to the corpus callosum.
TL;DR: Poor educational attainment, poor grades for attention at school, higher birth weight and larger head circumference were significantly associated with the risk of criminal offending in adulthood in this sample of patients with schizophrenia.
Abstract: Background Individuals with schizophrenia appear to be at increased risk for violent and criminal behaviour. Obstetric complications, neuromotor problems and intellectual deficits have variously been reported as increasing the risk for criminality in the general population.
Aims To investigate whether such risk factors are associated with criminal behaviour in an epidemiological cohort of patients with schizophrenia.
Method We identified from health care registers all individuals with schizophrenia born in Helsinki between 1951 and 1960, and used the national criminal register to identify those with a criminal record by 1995. Childhood information was obtained from archived birth and school records.
Results Poor educational attainment, poor grades for attention at school, higher birth weight and larger head circumference were significantly associated with the risk of criminal offending in adulthood in this sample of patients with schizophrenia. An association between labour/delivery complications and later violent offending among male patients was of borderline significance.
Conclusions Our hypotheses that birth complications and childhood neuromotor problems would increase the risk of criminal offending in schizophrenia were not upheld.
Journal Article•
TL;DR: Genes involved in early cortical development and early neurodevelopmental insults causing developmental impairment may put individuals on a trajectory towards schizophrenia rather than bipolar illness, which is the most plausible explanation.
Abstract: Over the past 100 years, the Kraepelinian classification of psychoses has dominated our approach to schizophrenia and bipolar disorder However, controversy as to the nature of the illnesses--whether they can be viewed as completely distinct, essentially the same, or occupying different points along a psychosis spectrum--has intensified in recent years This paper reviews the evidence for these differing opinions, examining both the commonalities between the two diseases and the distinctions A genetic propensity towards psychotic disorders is widely acknowledged; more recent studies suggest a considerable overlap in genetic susceptibility to schizophrenia and bipolar disorder The influence of early environmental effects, such as obstetric complications, on schizophrenia is also established but little such evidence exists for bipolar disorder Structural abnormalities of the brain of developmental origin as well as neuropsychological deficits have been clearly identified in schizophrenia but less evidence has been found in bipolar disorder The most plausible explanation is that one or more susceptible genes are shared between schizophrenia and bipolar illness, and can be thought of as predisposing individuals to psychosis, perhaps by producing a dysregulation of the dopaminergic response to stress Other genes and environmental factors are likely to have more specific effects and contribute to producing the patterns that psychiatrists recognize as 'classical' schizophrenia and mania In particular, genes involved in early cortical development and early neurodevelopmental insults causing developmental impairment may put individuals on a trajectory towards schizophrenia rather than bipolar illness
TL;DR: Preschizophrenic children who merit psychiatric referral are claimed to have a particularly malevolent illness when the psychosis develops later, and the 21-year outcome of a sample of such children was investigated.
Abstract: Objective: Preschizophrenic children who merit psychiatric referral are claimed to have a particularly malevolent illness when the psychosis develops later. The 21 years outcome of a sample of such children was investigated.
Method: Fifty-one children who attended psychiatric services, and were later diagnosed as having schizophrenia, were followed up a mean of 21 years later. Baseline childhood demographic, clinical and putative aetiological characteristics were identified from the case notes. Follow-up assessment evaluated clinical symptoms, social functioning and service utilization. The predictive value of baseline factors on outcome was examined.
Results: Outcome was poor, and seven (14%) of the subjects were deceased. Childhood IQ was strongly predictive of social outcome (F=5.1, P=0.01) and service utilization (F=5.2, P=0.01), but not clinical symptoms. No other factors predicted outcome.
Conclusion: Low childhood IQ had an unfavourable impact on social outcome and service utilization once schizophrenia developed.
TL;DR: These results indicate that the nuclear syndrome shows substantial heritability, although this is slightly lower than that for schizophrenia as defined by the DSM and ICD systems.
Abstract: Background Schneider's first-rank symptoms are given particular weight when making a diagnosis of schizophrenia, but the nuclear syndrome, characterised by one or more first-rank symptoms, has been found previously to have no heritability.
Aims To estimate the heritability of the nuclear syndrome.
Method A total of 224 twin pairs (106 monozygotic, 118 same-gender dizygotic) were ascertained from the Maudsley Twin Register in London via probands with any psychosis. Lifetime-ever first-rank symptoms were rated using the OPCRIT checklist. Probandwise concordance rates were calculated for the nuclear syndrome and a heritability estimate was derived from biometric model fitting.
Results Probandwise concordance rates were 13/49 (26.5%) for monozygotic and 0/45 to 2/46 (0.0-4.3%) for dizygotic pairs. The heritability estimate for the best-fitting model was 71% (95% CI 57-82).
Conclusions These results indicate that the nuclear syndrome shows substantial heritability, although this is slightly lower than that for schizophrenia as defined by the DSM and ICD systems.
TL;DR: The question is whether schizophrenia is a) simply the final consequence of a cascade of increasing developmental deviance (Bramon et al., 2001), or b) whether there is an additional brain degeneration following onset of psychosis which is superimposed on the developmental impairment (Lieberman, 1999).
Abstract: The debate as to whether schizophrenia is a neurodevelopmental or a neurodegenerative disorder has its roots in the latter part of the 19th century when authorities such as Clouston (1891) posited that at least some insanities were “developmental” in origin. These views were soon eclipsed by Kraepelin’s (1896) concept of dementia praecox as a degenerative disease, and the latter view carried not only the day but also much of the 20th century. Then, in the 1980s several research groups again began to speculate that schizophrenia might have a significant developmental component (Feinberg, 1982–1983; Schulsinger et al, 1984; Murray et al., 1985; Murray and Lewis, 1987; Weinberger et al., 1987). What became known as the “neurodevelopmental hypothesis” received support from neuropathological studies implicating anomalies in early brain development such as aberrant migration of neurons. Unfortunately, these studies proved difficult, if not impossible, to replicate (Harrison, 1999).
TL;DR: New reports implicate deviant neurodevelopment, under the influence of both genetic and early environmental factors, in the aetiology of schizophrenia, however, it is still not clear how developmental impairment in childhood is transformed into frank psychosis.
Abstract: New reports implicate deviant neurodevelopment, under the influence of both genetic and early environmental factors, in the aetiology of schizophrenia. However, it is still not clear how developmental impairment in childhood is transformed into frank psychosis. Several longitudinal magnetic resonanc
TL;DR: Age of onset, course of disorder, impairment during disorder, mode of onset and premorbid functioning were shown to be familial and supports their use in the delineation of homogeneous subsets for future genetic studies.
Journal Article•
TL;DR: The most striking finding was that disorganisation appeared to arise when a familial predisposition to mania was compounded by low premorbid IQ.
TL;DR: In this paper, the diagnostic and socio-demographic differences between high-security psychiatric service users from their peers in community services were examined, and it was shown that ethnic minority patients are much more likely to have engaged in serious violence and need high security placement.
Abstract: Background Serious violence is an unusual but significant correlate of psychosis, and leads to the need for specialist secure psychiatric services. Most such service users have previously used general psychiatric services.
Aims To examine diagnostic and socio-demographic differences between high-security psychiatric service users from their peers in community services.
Method Two groups of patients with psychosis were compared: a national sample of high-security hospital residents, and a sample of patients in contact with general psychiatric services.
Results Schizophrenia was the almost invariable diagnosis for all special hospital patients. White patients in the community sample were significantly more likely to have affective components to their illness compared with African—Caribbean patients; unlike those in special hospitals. There was a small excess in the proportion of African—Caribbean patients in the special hospital group, controlling for diagnosis, gender and locality. Men were overrepresented in this group.
Conclusions Among patients with psychosis, having a diagnosis of schizophrenia and being male increase the likelihood of special hospital admission. Suggestions that ethnic minority patients are much more likely to have engaged in serious violence and need high-security placement were not borne out.
TL;DR: University-educated schizophrenic patients who were functioning well enough to enter university prior to illness onset may have a non-developmental subtype of schizophrenia.
Abstract: Background Many people who develop schizophrenia have impairments in intellectual and social functioning that are detectable from early childhood However, some patients do not exhibit such deficits, and this suggests that they may have suffered less neurodevelopmental damage We hypothesized that the aetiology and form of schizophrenia may differ in such patients We therefore studied a group of schizophrenic patients who were functioning well enough to enter university prior to illness onset Methods The casenotes of 46 university-educated patients and 48 non-university-educated patients were rated on several schedules including the OPCRIT checklist, and the two groups were compared using univariate statistical techniques Principal components analysis was then performed using data from all patients, and the factor scores for each principal component were compared between groups Results Univariate analyses showed the university-educated patients had an excess of depressive symptoms, and a paucity of core schizophrenic symptoms Four principal components emerged in the principal components analysis: mania, biological depression, schizophrenic symptoms, and a reactive depression University-educated patients scored significantly higher on the reactive depression principal component, and lower on the schizophrenic symptoms principal component, than the non-university-educated patients Conclusions University-educated patients may have a non-developmental subtype of schizophrenia
TL;DR: One hundred first-degree relatives of patients with schizophrenia (SR) and 88 first degree relatives of affective psychotic patients (APR) completed the Eysenck Personality Questionnaire which measures extraversion, neuroticism, and psychoticism; they were also administered the National Adult Reading Test (NART), the Trail Making Test (TMT), and a Verbal Fluency Test (VFT) as mentioned in this paper.
TL;DR: The commonalities and the differences between schizophrenia and bipolar disorder are examined, finding that schizophrenia but not bipolar disorder is subject to additional genes or early environmental hazards causing neurodevelopmental impairment.
Abstract: This paper examines the commonalities and the differences between schizophrenia and bipolar disorder. Recent studies suggest a possible overlap in genetic susceptibility to the two conditions. However, while the influence of early environmental effects, particularly obstetric complications, has been established for schizophrenia, no such replicable association with bipolar disorder has been found. Structural abnormalities of the brain have been identified in both schizophrenia and bipolar disorder, but while the volume of the amygdala and hippocampus appears decreased in schizophrenia, this is not the case in bipolar disorder; indeed, there are some suggestions of increased volume of the amygdala. Furthermore, schizophrenia is characterised by lower IQ, executive function and verbal memory, but there is little evidence of trait neuropsychological deficits in bipolar disorder. Similarly, premanic children do not show the cognitive and neuromotor impairments characteristic of those destined to develop schizophrenia. The most plausible explanation is that the two conditions share some genetic predisposition but differ in that schizophrenia but not bipolar disorder is subject to additional genes or early environmental hazards causing neurodevelopmental impairment.