Over the past six years, Alan Brown and colleagues have published an impressive series of epidemiological findings on schizophrenia in the offspring of a large cohort of carefully studied pregnant women (reviewed by Brown, 2006). Their work has confirmed and greatly extended prior findings linking maternal infection in the second trimester with increased risk for schizophrenia in the offspring. Moreover, Brown et al. found an association between anti-influenza antibodies in maternal serum and increased risk for schizophrenia, as well as a similar association with elevated levels of a cytokine in maternal serum. In a new paper (Babulas et al., 2006), this group reports a fivefold increase in risk for schizophrenia spectrum disorders in the offspring of women who experienced a genital/reproductive infection during the periconception period. The infections considered were endometritis, cervicitis, pelvic inflammatory...  Read more

Over the past six years, Alan Brown and colleagues have published an impressive series of epidemiological findings on schizophrenia in the offspring of a large cohort of carefully studied pregnant women (reviewed by Brown, 2006). Their work has confirmed and greatly extended prior findings linking maternal infection in the second trimester with increased risk for schizophrenia in the offspring. Moreover, Brown et al. found an association between anti-influenza antibodies in maternal serum and increased risk for schizophrenia, as well as a similar association with elevated levels of a cytokine in maternal serum. In a new paper (Babulas et al., 2006), this group reports a fivefold increase in risk for schizophrenia spectrum disorders in the offspring of women who experienced a genital/reproductive infection during the periconception period. The infections considered were endometritis, cervicitis, pelvic inflammatory disease, vaginitis, syphilis, condylomata, “venereal disease,” and gonorrhea. Strengths of the study include physician documentation of the infections and face-to-face assessments of schizophrenia. Although sample size was modest, these results extend a prior finding that elevated maternal anti-herpes simplex type 2 antibodies are associated with increased risk of psychotic disorders, including schizophrenia (Buka et al., 2001).

The mechanism of how maternal infection increases risk for schizophrenia could involve pathogens invading the fetus. Although this is certainly possible in the case of some of the infections studied by Babulas et al., in the case of a respiratory virus such as influenza, this explanation appears unlikely. A more parsimonious mechanism would involve activation of the maternal immune system, and action of soluble mediators such as cytokines at the level of the placenta or the fetus. Support for this hypothesis comes from animal studies. An antiviral immune response can be evoked in the absence of the pathogen by injection of synthetic double-stranded RNA (polyI:C). When this is done in pregnant rats or mice, the adult offspring display a number of behavioral abnormalities reminiscent of those observed in schizophrenia. These include deficits in prepulse inhibition, latent inhibition, and social interaction, as well as enhanced amphetamine-induced locomotion and anxiety under mildly stressful conditions (Shi et al., 2003; Zuckerman et al., 2003; Ozawa et al., 2005). Moreover, some of these deficits are ameliorated by treatment with antipsychotic drugs and exacerbated by psychotomimetics (Shi et al., 2003; Ozawa et al., 2005), and the offspring also exhibit dopaminergic hyperfunction (Zuckerman et al., 2003; Ozawa et al., 2005). Some of these abnormalities are also seen in the offspring of influenza-infected mothers or mothers injected with the bacterial cell wall component, LPS (Borrell et al., 2002; Fatemi et al., 2002; Shi et al., 2003).

The most recent advance in this growing cottage industry is the finding that there are critical periods of maternal immune activation that determine the type of adult behavioral dysfunction and neuropathology found in the offspring (Meyer et al., 2006). Injection of polyI:C during stages of mouse gestation corresponding to first-to-second versus second-to-third trimesters of human pregnancy yields different deficits in exploratory and perseverative behavior, postnatal reelin expression, and hippocampal apoptosis. Moreover, these two different stages of injection evoke diverse cytokine responses in the fetal brain. It would further be interesting to know which of these abnormalities is specific to the period corresponding to the human second trimester, as this is the key time of vulnerability for risk of schizophrenia associated with maternal infection.

Other fascinating questions for this increasingly popular model are, what mediates the effects of maternal immune activation (e.g., cytokines, antibodies, corticosteroids), and do they act directly on the fetus or via the placenta? Can imaging be used with the rodents to explore dopamine receptor occupancy? Which of the observed pathologies are most relevant for each of the behavioral abnormalities?

References:
Babulas V, Factor-Litvak P, Goetz R, Schaefer CA, Brown AS. Prenatal exposure to maternal genital and reproductive infections and adult schizophrenia. Am J Psychiatry. 2006 May;163(5):927-9. Abstract Borrell J, Vela JM, Arevalo-Martin A, Molina-Holgado E, Guaza C. Prenatal immune challenge disrupts sensorimotor gating in adult rats. Implications for the etiopathogenesis of schizophrenia. Neuropsychopharmacology. 2002 Feb;26(2):204-15. Abstract Brown AS. Prenatal infection as a risk factor for schizophrenia. Schizophr Bull. 2006 Apr;32(2):200-2. Epub 2006 Feb 9. Abstract Buka SL, Tsuang MT, Torrey EF, Klebanoff MA, Bernstein D, Yolken RH. Maternal infections and subsequent psychosis among offspring. Arch Gen Psychiatry. 2001 Nov;58(11):1032-7. Abstract Fatemi SH, Earle J, Kanodia R, Kist D, Emamian ES, Patterson PH, Shi L, Sidwell R. Prenatal viral infection leads to pyramidal cell atrophy and macrocephaly in adulthood: implications for genesis of autism and schizophrenia. Cell Mol Neurobiol. 2002 Feb;22(1):25-33. Abstract Meyer U, Feldon J, Schedlowski M, Yee BK. Towards an immuno-precipitated neurodevelopmental animal model of schizophrenia. Neurosci Biobehav Rev. 2005;29(6):913-47. Abstract Meyer U, Nyffeler M, Engler A, Urwyler A, Schedlowski M, Knuesel I, Yee BK, Feldon J. The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. J Neurosci. 2006 May 3;26(18):4752-62. Abstract Ozawa K, Hashimoto K, Kishimoto T, Shimizu E, Ishikura H, Iyo M. Immune activation during pregnancy in mice leads to dopaminergic hyperfunction and cognitive impairment in the offspring: a neurodevelopmental animal model of schizophrenia. Biol Psychiatry. 2006 Mar 15;59(6):546-54. Epub 2005 Oct 26. Abstract Shi L, Fatemi SH, Sidwell RW, Patterson PH. Maternal influenza infection causes marked behavioral and pharmacological changes in the offspring. J Neurosci. 2003 Jan 1;23(1):297-302. Abstract Zuckerman L, Rehavi M, Nachman R, Weiner I. Immune activation during pregnancy in rats leads to a postpubertal emergence of disrupted latent inhibition, dopaminergic hyperfunction, and altered limbic morphology in the offspring: a novel neurodevelopmental model of schizophrenia. Neuropsychopharmacology. 2003 Oct;28(10):1778-89. Abstract

Meyer and coworkers provide interesting new data on the role of the immune system in mediating the damage caused by viral infections during pregnancy on the developing nervous system of the fetus. Not just the timing of the infection appears to be critical, but the developing fetal immune system appears to play a role, too.

Polyinosinic-polycytidylic acid (polyI:C), which was employed by Meyer et al., is frequently used to mimic viral infections. It is a synthetic double-stranded RNA and has adjuvant-effects (Salem et al., 2005). PolyI:C binds to target cells via the "Toll-like receptor 3" (TLR3). TLR3 serves as a receptor in trophoblast cells and uterine epithelial cells mediating local immune activation at the maternal-fetal interface after viral infections (Abrahams et al., 2005; Schaefer et al., 2005). Glial cells like microglia and...  Read more

Meyer and coworkers provide interesting new data on the role of the immune system in mediating the damage caused by viral infections during pregnancy on the developing nervous system of the fetus. Not just the timing of the infection appears to be critical, but the developing fetal immune system appears to play a role, too.

Polyinosinic-polycytidylic acid (polyI:C), which was employed by Meyer et al., is frequently used to mimic viral infections. It is a synthetic double-stranded RNA and has adjuvant-effects (Salem et al., 2005). PolyI:C binds to target cells via the "Toll-like receptor 3" (TLR3). TLR3 serves as a receptor in trophoblast cells and uterine epithelial cells mediating local immune activation at the maternal-fetal interface after viral infections (Abrahams et al., 2005; Schaefer et al., 2005). Glial cells like microglia and astrocytes also express functional TLR3 (Farina et al., 2005; Park et al., 2006; Town et al., 2006). Thus, TLR3 plays an important role in immune responses, and its natural function appears to be immune activation in addition to cross-priming the immune system to virus-infected cells (Schulz et al., 2005). Given the expression of TLR3 at the maternal-fetal interface and on glial cells, the polyI:C-TLR3-model appears to be useful to study the basic mechanisms of viral infections and their consequences for brain development in animal models.

However, several limitations are evident: PolyI:C is not a virus, and different immunological pathways may be activated by intact viruses after binding to their appropriate receptors. Findings from the immune system of rodents cannot be directly transferred to humans, and it may be difficult to dissect—on a molecular level—the protective aspects of an immune response against a viral infection from its putative detrimental effects on human neurodevelopment. Still, such mechanisms may now be studied in the rodent models used by Meyer and coworkers and other groups, and this will help to pave the way for future studies in humans. This will hopefully lead to a better understanding of the role of the immune system and viral infections in the pathogenesis of schizophrenia.

References:

Abrahams VM, Visintin I, Aldo PB, Guller S, Romero R, Mor G. A role for TLRs in the regulation of immune cell migration by first trimester trophoblast cells. J Immunol. 2005 Dec 15;175(12):8096-104. Abstract

Farina C, Krumbholz M, Giese T, Hartmann G, Aloisi F, Meinl E. Preferential expression and function of Toll-like receptor 3 in human astrocytes. J Neuroimmunol. 2005 Feb;159(1-2):12-9. Epub 2004 Nov 11. Abstract

Park C, Lee S, Cho IH, Lee HK, Kim D, Choi SY, Oh SB, Park K, Kim JS, Lee SJ. TLR3-mediated signal induces proinflammatory cytokine and chemokine gene expression in astrocytes: differential signaling mechanisms of TLR3-induced IP-10 and IL-8 gene expression. Glia. 2006 Feb;53(3):248-56. Abstract

Salem ML, Kadima AN, Cole DJ, Gillanders WE. Defining the antigen-specific T-cell response to vaccination and poly(I:C)/TLR3 signaling: evidence of enhanced primary and memory CD8 T-cell responses and antitumor immunity. J Immunother. 2005 May-Jun;28(3):220-8. Abstract

Schaefer TM, Fahey JV, Wright JA, Wira CR. Innate immunity in the human female reproductive tract: antiviral response of uterine epithelial cells to the TLR3 agonist poly(I:C). J Immunol. 2005 Jan 15;174(2):992-1002. Abstract

Schulz O, Diebold SS, Chen M, Naslund TI, Nolte MA, Alexopoulou L, Azuma YT, Flavell RA, Liljestrom P, Reis e Sousa C. Toll-like receptor 3 promotes cross-priming to virus-infected cells. Nature. 2005 Feb 24;433(7028):887-92. Epub 2005 Feb 13. Abstract

Town T, Jeng D, Alexopoulou L, Tan J, Flavell RA. Microglia recognize double-stranded RNA via TLR3. J Immunol. 2006 Mar 15;176(6):3804-12. Abstract

This article supported absolutely what our research clinic is anecdotally experiencing. On more than several occasions we have conducted a Structured Clinical Interview for DSM-IV Axis I disorders (SCID) to find a diagnosis of schizophrenia or schizoaffective disorder. However, in contrast, the clinical chart is describing psychotic symptoms, but the clinical diagnosis is post-traumatic stress disorder alone or perhaps along with borderline personality disorder with depression. All of these cases involved younger clients (18-25 years old), either just beginning mental health services or certainly without a long history of mental health care to reflect on. They also had histories (according to primary care providers) of severe childhood abuse and trauma.

View all comments by Margaret Almeida

This is a fascinating study investigating the relationship between psychological trauma and the development of psychotic symptoms using data from the Early Developmental Stages of Psychopathology (EDSP) study conducted in Munich, Germany.

There are a number of interesting findings: 1) Self-reported trauma (any) was associated with experiencing one (OR 1.40; 95 percent CI 1.09, 1.78), two (OR 1.88; 95 percent CI 1.35-2.62) and three or more (OR 2.60; 95 percent CI 1.66-4.09) psychotic symptoms during the follow-up period. While these odds ratios increase linearly with number of psychotic symptoms, when potential confounders, such as urbanicity and psychosis proneness, were controlled for, only the association with three or more psychotic symptoms remained significant (Adj. OR 1.89, 95 percent CI 1.16-3.08); 2) Most specific categories of trauma showed positive associations with psychotic symptoms, particularly at the level of three or more, though only physical threat, natural catastrophe and terrible event to other reached statistical significance (though this may be...  Read more

This is a fascinating study investigating the relationship between psychological trauma and the development of psychotic symptoms using data from the Early Developmental Stages of Psychopathology (EDSP) study conducted in Munich, Germany.

There are a number of interesting findings: 1) Self-reported trauma (any) was associated with experiencing one (OR 1.40; 95 percent CI 1.09, 1.78), two (OR 1.88; 95 percent CI 1.35-2.62) and three or more (OR 2.60; 95 percent CI 1.66-4.09) psychotic symptoms during the follow-up period. While these odds ratios increase linearly with number of psychotic symptoms, when potential confounders, such as urbanicity and psychosis proneness, were controlled for, only the association with three or more psychotic symptoms remained significant (Adj. OR 1.89, 95 percent CI 1.16-3.08); 2) Most specific categories of trauma showed positive associations with psychotic symptoms, particularly at the level of three or more, though only physical threat, natural catastrophe and terrible event to other reached statistical significance (though this may be largely an issue of statistical power); and 3) There was evidence that the association between trauma and psychotic symptoms varied by psychosis proneness. That is, the association between trauma and psychosis was strongest in those with pre-existing vulnerability to psychosis.

There has been recent controversy, at least in the U.K., about the role of trauma in the etiology of psychosis, largely as a consequence of a review paper published by John Read and colleagues which concluded that child abuse is a cause of schizophrenia (Read et al., 2005). Does the study by Spauwen et al. provide support for this conclusion? The findings allow interpretation both ways.

On the one hand, there is a robust association between any traumatic event and subsequent development of three or more psychotic symptoms. There are also indications that this may be a dose-response relationship. Further, this study has a number of methodological advantages over much of what has gone before. The prospective design overcomes many of the concerns regarding potential recall bias and direction of causation, as does the inclusion of a measure of psychosis proneness. The sample was large, and the analyses sophisticated.

On the other hand, it could be countered, the observed association between any trauma and psychotic symptoms was modest (Adj. OR 1.89) and much smaller than that found in other studies (e.g., Janssen et al. (2004) reported an adjusted odds ratio of 7.3 over a 2-year period). The evidence for a dose-response relationship was weak, and when confounders were adjusted for, only the association with the most severe level of psychotic symptoms remained significant. Furthermore, and issues of statistical power notwithstanding, it is important to note that only a small number of specific types of trauma were significantly associated with risk of developing psychotic symptoms, and these did not include sexual abuse. And there remains the ongoing issue of the relationship, if any, between psychotic-like symptoms reported in general population samples and the clinical syndromes of psychosis, particularly schizophrenia.

So, there are reasons to retain a healthy skepticism, particularly in relation to claims that child abuse causes schizophrenia. But equally, the emerging evidence suggests it would be wrong to reject a possible role for psychological trauma out of hand. Studies are becoming more methodologically robust, and that by Spauwen et al. is an example of this. There is, however, clearly a need for much more research. Until this is available, we should remain open-minded.

References:

Janssen I, Krabbendam L, Bak M, Hanssen M, Vollebergh W, de Graaf R, van Os J. Childhood abuse as a risk factor for psychotic experiences. Acta Psychiatr Scand. 2004 Jan;109(1):38-45. Abstract

Read J, van Os J, Morrison AP, Ross CA. Childhood trauma, psychosis and schizophrenia: a literature review with theoretical and clinical implications. Acta Psychiatr Scand. 2005 Nov;112(5):330-50. Review. Abstract

I agree with most of the comments already posted by others on the very interesting paper by Spauwen et al on psychological trauma and psychotic symptoms. I'd like to raise just one additional point. This pertains to the specificity for psychotic symptoms. It appears that the study found no relation of these psychological traumas to depression or bipolar disorder, but it isn't clear whether there was any relation to depressive symptoms. It's worth considering this point in the interpretation of the results, because psychological traumas have been related to a number of other conditions in previous studies.

View all comments by Ezra Susser

We read the paper by Spauwen et al. (2006) with great interest. Their findings suggest a specific relationship between psychological trauma and psychosis. Previous studies already showed that psychological trauma is clearly associated with depression and other symptoms of post-traumatic stress disorder, but the link between childhood trauma and psychosis was controversial. The current finding is very interesting and based on a study with a large data set and a good methodology. However, more research on this topic needs to be done. This research should measure the type of trauma in greater detail since this could give a better understanding of the exact link between trauma and psychosis. Moreover, the focus of future research should be more on the underlying neurological mechanisms by which childhood trauma increases the risk of psychosis. For instance, it would be interesting to conduct neuroimaging studies (Ni Bhriain et al., 2005), that focus on dopamine abnormalities (  Read more

We read the paper by Spauwen et al. (2006) with great interest. Their findings suggest a specific relationship between psychological trauma and psychosis. Previous studies already showed that psychological trauma is clearly associated with depression and other symptoms of post-traumatic stress disorder, but the link between childhood trauma and psychosis was controversial. The current finding is very interesting and based on a study with a large data set and a good methodology. However, more research on this topic needs to be done. This research should measure the type of trauma in greater detail since this could give a better understanding of the exact link between trauma and psychosis. Moreover, the focus of future research should be more on the underlying neurological mechanisms by which childhood trauma increases the risk of psychosis. For instance, it would be interesting to conduct neuroimaging studies (Ni Bhriain et al., 2005), that focus on dopamine abnormalities (McGowan et al., 2004) in patients with traumatic experiences early in life.

References:

McGowan S, Lawrence AD, Sales T, Quested D, Grasby P. Presynaptic dopaminergic dysfunction in schizophrenia: a positron emission tomographic [18F]fluorodopa study. Arch Gen Psychiatry. 2004 Feb;61:134-142. Abstract

Ni Bhriain S, Clare AW, Lawlor BA. Neuroimaging: a new training issue in psychiatry? Psychiat Bull. 2005 May;29:189-192.

Spauwen J, Krabbendam L, Lieb R, Wittchen HU, van Os J. Impact of psychological trauma on the development of psychotic symptoms: relationship with psychosis proneness. Br J Psychiatry. 2006 Jun;188:527-33. Abstract

Spauwen and colleagues add further weight to research linking traumatic experiences and psychotic symptoms (Spauwen et al., 2006). There are now a number of studies showing an association between trauma and psychotic symptoms (Bebbington et al., 2004; Janssen et al., 2004; Sareen et al., 2005; Shevlin et al., 2006; Whitfield et al., 2005). There are also a number of large community-representative studies showing that psychotic symptoms are highly prevalent in community populations (Eaton et al., 1991;   Read more

Spauwen and colleagues add further weight to research linking traumatic experiences and psychotic symptoms (Spauwen et al., 2006). There are now a number of studies showing an association between trauma and psychotic symptoms (Bebbington et al., 2004; Janssen et al., 2004; Sareen et al., 2005; Shevlin et al., 2006; Whitfield et al., 2005). There are also a number of large community-representative studies showing that psychotic symptoms are highly prevalent in community populations (Eaton et al., 1991; Scott et al., 2006; van Os et al., 2000).

Read and colleagues have argued that child abuse may be an etiological factor for schizophrenia in some individuals (Read et al., 2001; Read et al., 2005). In a clinical study of adolescent inpatients who hallucinated, we found using a structured questionnaire and structured clinical interview (K-SADS) that the hallucinations of schizophrenia and those of post-traumatic stress disorder (PTSD) were very similar in form and content (Scott et al., 2006, in press). Thus, clinicians and researchers need to remain mindful of the overlap of psychotic symptoms in these disorders.

A possible explanation for the above is that psychotic symptoms are non-specific experiences. Perhaps they represent a final common pathway to a range of stressors including unemployment, social isolation, migration, substance use and trauma. From a different perspective in relation to trauma, psychotic symptoms may be part of a dissociative process (van der Kolk et al., 1996), and the positive psychotic symptoms in PTSD are phenomenologically difficult to distinguish from those of schizophrenia.

The association between trauma and psychotic symptoms is a fascinating one requiring further objective, open-minded research.

References:

Bebbington PE, Bhugra D, Brugha T, Singleton N, Farrell M, Jenkins R, Lewis G, Meltzer H. Psychosis, victimisation and childhood disadvantage: evidence from the second British National Survey of Psychiatric Morbidity. Br J Psychiatry. 2004 Sep;185:220-6. Abstract

Eaton WW, Romanoski A, Anthony JC, Nestadt G. Screening for psychosis in the general population with a self-report interview. J Nerv Ment Dis. 1991 Nov;179(11):689-93. Abstract

Janssen I, Krabbendam L, Bak M, Hanssen M, Vollebergh W, de Graaf R, van Os J. Childhood abuse as a risk factor for psychotic experiences. Acta Psychiatr Scand. 2004 Jan;109(1):38-45. Abstract

Read J, Perry BD, Moskowitz A, Connolly J. The contribution of early traumatic events to schizophrenia in some patients: a traumagenic neurodevelopmental model. Psychiatry. 2001 Winter;64(4):319-45. Review. Abstract

Read J, van Os J, Morrison AP, Ross CA. Childhood trauma, psychosis and schizophrenia: a literature review with theoretical and clinical implications. Acta Psychiatr Scand. 2005 Nov;112(5):330-50. Review. Abstract

Sareen J, Cox BJ, Goodwin RD, J G Asmundson G. Co-occurrence of posttraumatic stress disorder with positive psychotic symptoms in a nationally representative sample. J Trauma Stress. 2005 Aug;18(4):313-22. Abstract

Scott J, Chant D, Andrews G, McGrath J. Psychotic-like experiences in the general community: the correlates of CIDI psychosis screen items in an Australian sample. Psychol Med. 2006 Feb;36(2):231-8. Epub 2005 Nov 23. Abstract

Scott J, Nurcombe B, Sheridan J, et al. (2006) Hallucinations in Adolescents with Post-traumatic Stress Disorder and Psychotic Disorder. Australasian Psychiatry, In press.

Shevlin M, Dorahy M, Adamson G. Childhood traumas and hallucinations: An analysis of the National Comorbidity Survey. J Psychiatr Res. 2006 Apr 24; [Epub ahead of print] Abstract

Spauwen J, Krabbendam L, Lieb R, Wittchen HU, van Os J. Impact of psychological trauma on the development of psychotic symptoms: relationship with psychosis proneness. Br J Psychiatry. 2006 Jun;188:527-33. Abstract

van der Kolk BA, Pelcovitz D, Roth S, Mandel FS, McFarlane A, Herman JL. Dissociation, somatization, and affect dysregulation: the complexity of adaptation of trauma. Am J Psychiatry. 1996 Jul;153(7 Suppl):83-93. Review. Abstract

van Os J, Hanssen M, Bijl RV, Ravelli A. Strauss (1969) revisited: a psychosis continuum in the general population? Schizophr Res. 2000 Sep 29;45(1-2):11-20. Abstract

Whitfield CL, Dube SR, Felitti VJ, Anda RF. Adverse childhood experiences and hallucinations. Child Abuse Negl. 2005 Jul;29(7):797-810. Abstract

Spauwen and colleagues find that exposure to psychological trauma may increase the risk of psychotic symptoms in people vulnerable to psychoses. The experiences of war, natural disasters and child abuse cannot be good for anyone. Am I wrong to think that these add up to much more than psychological trauma or that such events would also tend to bring on and exacerbate the symptoms of myriad other conditions such as those relating to the heart, lungs and other bodily organs?

View all comments by Ella Matthews

I feel it is better to characterise the symptoms of schizophrenia as falling into two categories: "active" and "passive." None of the symptoms is "positive" in a layperson's understanding of the word, and all of them are "negative." If the APA is to change the DSM language regarding schizophrenia, they should also correct the unfortunate positive/negative terminology.

View all comments by Jane Nangle

Many patients seen in the emergency room at the hospital where I work are still calling Bipolar Spectrum Disorder by its original diagnostic designation, "manic depression." Honestly, we as a mental health care community must ask, what is in a name? Schizophrenia is well know as a term; perhaps instead of changing the name of the classification, we should spend time educating people what it means and how to live well with it.

View all comments by Christopher Holly

I would like to agree with the general concept that the categorical classifications should disappear, at least the current phenomenological classifications (DSM-IV). These kinds of classifications are a large listing of phenomenological symptoms that do not meet any neurobiological criteria according to the last scientific research data in the field of psychiatry, especially within the field of psychiatric genetics data.

The dimensional classifications are more adapted to the newest research in the neurobiology of schizophrenia, possibly a gradual combination of less categorical and more dimensional classifications, as Dr. William Carpenter explained at the ICOSR.

Summing up, I think that the central issues of the discussion are represented by the following points:

1. The inclusion of the concept of endophenotypes (see SRF Live Discussion, led by I. Gottesman) and their biomarkers in the new classifications.

2. The inclusion of dimensional classifications.

Certainly, the inclusion...  Read more

I would like to agree with the general concept that the categorical classifications should disappear, at least the current phenomenological classifications (DSM-IV). These kinds of classifications are a large listing of phenomenological symptoms that do not meet any neurobiological criteria according to the last scientific research data in the field of psychiatry, especially within the field of psychiatric genetics data.

The dimensional classifications are more adapted to the newest research in the neurobiology of schizophrenia, possibly a gradual combination of less categorical and more dimensional classifications, as Dr. William Carpenter explained at the ICOSR.

Summing up, I think that the central issues of the discussion are represented by the following points:

1. The inclusion of the concept of endophenotypes (see SRF Live Discussion, led by I. Gottesman) and their biomarkers in the new classifications.

2. The inclusion of dimensional classifications.

Certainly, the inclusion of endophenotypes, explained by Dr. Guvant Thakar, is the only real innovation. I think that the combination of all of these points will make new classifications more useful tools for both clinicians and scientific researchers.

My family is unlucky in that two members have had affective illnesses and one has schizophrenia, although there is no family history on either side. I have no difficulty in the diagnoses and no difficulty in seeing them as different entities. Perhaps the point is that observation over a degree of duration brings clarity when initial presentation or point examination does not always do that.

In the United Kingdom one other argument for keeping the diagnosis schizophrenia remains for those who are family carers—despite the present 'walk on the other side and keep your eyes down attitude,' the amount of funding that goes to the care and treatment of the those with the illness can be scrutinised, and any discrepant lack of it—when say, compared with the funding share going to less serious conditions—can be pointed out. You will get what you pay for.

View all comments by David Yates