This study examines the properties of the Child and Adolescent Psychiatric Screening Inventory-Retrospect, CAPSI-R, a self-report 146-item questionnaire for adults concerning earlier child psychiatric symptoms, comprising both DSM-IV categories and functional impairment. The instrument was mailed to 359 former child psychiatric patients born between 1951 and 1977 (164 of whom responded) and to a matched control group (193 of whom responded). There was good internal consistency (Cronbach’s alpha ranged between 0.62–0.93, and between 0.76–0.93 after elimination of one item). The lifetime prevalence of a mental disorder was 87.8% in the former patients' without considering impairment and 76.8% when impairment was considered. The corresponding figures for the control group were 49.7% and 10.4%, respectively. When the former patients' CAPSI-R diagnoses (with incorporation of the impairment criterion) were validated against the DSM-IV diagnoses based on information in their medical records, generally, an acceptable sensitivity and specificity were obtained. The overall kappa between CAPSI-R diagnoses and those from medical records was 0.79. The CAPSI-R shows promise for further evaluation and may be useful in recognising child and adolescent mental disorders in adults.

In the case of a first episode of psychosis among members of different associations of families of mentally ill people, little is known about their priorities and how satisfied they are with the help provided to them. A survey was conducted in five European family associations. Respondents emphasized the need for early (ambulant) intervention through outreach with very practical goals directed at creating stability and social functioning. About one-third of the respondents are unsatisfied or very unsatisfied. The highest percentage of unsatisfied respondents was in the following five areas of care: advice on how to handle specific problems; help with preserving or regaining social functioning; help with regaining structure and routine; information; prompt assistance preferably in patientˈs own environment. The agreement of these findings with findings from earlier studies underlines the importance of suggesting specific changes in the delivery of care.

Between 1986 and 1998, a review of 61 records of patients who died before the age of 53 years in eight psychiatric departments whose catchment area had a total population of 559,429 inhabitants revealed that 24 (39.3%) of those patients had a schizophrenic disorder. Of those 24 patients, one (4.17%; 95% CI: 0–21%) died from complications of self-induced water intoxication (SIWIS). Among the 37 remaining patients, two (5.4%; 95% CI: 0–18%) died from complications of SIWIS.

Neuroreceptor imaging has been used to examine dopamine function in schizophrenia. The evidence from PET and SPECT studies suggests that there is excess dopamine release subcortically, in the striatum, and that dopaminergic transmission may be abnormal in the cortex also, because of an upregulation in D1 receptors. We have found that patients with schizophrenia have higher subcortical levels of intrasynaptic dopamine (and have a greater proportion of D2 receptors occupied by dopamine) at baseline than controls. Those patients who had the highest levels of dopamine were the ones whose positive symptoms responded best to six weeks of treatment with an antipsychotic. Recent studies have also produced new evidence of dopaminergic disturbance in the cortex. When controls were compared with patients with schizophrenia, we found a significant increase in D1 receptors in patients, but only in the dorsolateral prefrontal cortex. Patients were also studied while they undertook a test of working memory. While there was no relationship between test performance and D1 binding potential for controls, those patients with the highest densities (most pathological levels) of D1 receptors performed the worst on the test. Both the D1 upregulation and the poor working memory may be secondary to a chronic, possibly neurodevelopmental deficit in dopamine innervation of the dorsolateral prefrontal cortex in schizophrenia. The D1 binding potential may prove to be a good biomarker with which to identify those patients suffering from schizophrenia who are most likely to benefit from treatment with a D1 agonist. A D1 receptor radiotracer that is sensitive to endogenous dopamine competition would be very valuable in the further exploration of this area.

The first choice group of psychotropic agents in schizophrenia is neuroleptics. However, this treatment is not effective in all patients and with every symptom. We summarize papers published on the role of antiepileptic drugs in treatment-resistant schizophrenia. We have searched the computer database system MEDLINE for relevant articles including reviews, reports of drug studies and case histories. Antiepileptic drugs can change symptoms of schizophrenia by their action on GABA-ergic neurotransmission or via anti-glutamatergic mechanisms. High doses of adjunctive benzodiazepines reduce positive symptoms, anxiety, and agitation. Carbamazepine is effective in affective symptoms of schizophrenia and influences violent behavior in psychotic patients. Its anti-kindling action may represent a promising treatment strategy for some patients with chronic course of schizophrenia. Valproate treatment leads to a decrease in positive symptoms as well as hostility. Lamotrigine is expected to influence the positive, negative, affective, and cognitive symptoms of schizophrenia. New antiepileptics (e.g., gabapentin, oxcarbazepine, topiramate, vigabatrin) present a promise as potential adjuncts to neuroleptic treatment in resistant symptoms of schizophrenia.

Given that we are celebrating the 50th birthday of neuroleptics introduction in psychiatry, the author proposes to take a look at certain results related to therapeutic practice. After a brief chronological literature review of the clinical practices and theoretical models that have controlled drug treatment of schizophrenia, the author presents a critical review of four meta-analyses. Since Delay, Deniker and Harl’s initial report, the story of neuroleptics comprises several periods. In 1963, the hyper-dopaminergic theory of psychoses was proposed. Another period began with models mainly based on the serotonin/dopamine relative blockade receptor hypothesis. More recently, a new framework to understand the differential effect of antipsychotics is related to the appropriate modulation (e.g., fast dissociation) of the D2 receptor alone. The concept of atypicality has become a new vista for research and to market new compounds. However, after 50 years of neuroleptic drugs, are we able to answer the following simple questions: Are neuroleptics effective in treating schizophrenia? Is there a difference between atypical and conventional neuroleptics? How do the efficacy and safety of newer antipsychotic drugs compare with those of clozapine? Actually, the answers yielded by these simple questions by meta-analysis should elicit in us a good deal of humility. If we wish to base psychiatry on evidence-based medicine, we run a genuine risk in taking a closer look at what has long been considered fact. Each psychiatrist must continue to be critical, sceptical, optimistic (not overoptimistic) and to learn in order to integrate the positive aspects of our growing knowledge base.

Alzheimer’s disease (AD) patients often present with concurrent major depression (MD). To investigate the reasons for this comorbidity, e.g. MD being a risk factor for AD, or both diagnoses having a common neurobiology, the temporal relationship between the first onset of AD and of MD during lifetime was investigated—57 out of 146 AD patients had a lifetime diagnosis of MD. The correlation between the ages at onset of MD and dementia was calculated. The incidence of MD in AD patients in several 5-year-intervals before and after the onset of AD was compared with the average incidence of MD in the present AD sample and with the expected incidence of MD in the general population. No significant correlation between the onset of AD and of MD could be found after controlling for age, gender and the Mini-Mental-State. However, the incidence of MD 5 years before and after the onset of AD significantly exceeded the expected incidences—MD is only partially related to AD. However, the increased incidence of MD within 5 years before and after the onset of dementia may indicate that a common neurobiological process causes cognitive decline and depression in a subsample of AD patients.

This study describes service utilisation under routine clinical activity and the costs of providing mental health care for 24 months for the whole population of 330 subjects who had first contact with the Magenta Community Mental Health Centre during one year. The mean age of patients was 42.5 years, and 61% were females. According to ICD 10 criteria, 7% were diagnosed as having schizophrenia, 22% mood disorders, 37% neurotic disorders, 15% personality disorders and 19% other diagnoses. The clinical routine activity was monitored for 24 months from the first contact for each patient. The mean cost for a schizophrenic patient is more than double that of other patients. In-patient activity and community services accounted, respectively, for 49.7% and 50.3% of the total costs. Total health care costs per patient differ widely according to whether patients had been hospitalised during the observation period. Patients with a previous psychiatric contact and a longer duration of illness were more costly than the other patients. Multiple regression analysis was used to assess the association between all the individual variables and costs. For the whole population, the model explains 50% of the cost variation. Higher treatment costs were positively associated with the presence of previous psychiatric contacts and referral to the CPS by other sources than a general practitioner, and negatively associated with age.

The first effective antidepressants (monoamine oxidase inhibitors and tricyclic antidepressants) relied on their ability to augment serotonin and noradrenaline levels at the synapse. Forty years later, the same biological model led to the supremacy of the serotonergic hypothesis to explain not only the pathophysiology of depressive illness, but also the neuropharmacological basis for obsessive compulsive disorder, phobias, posttraumatic stress disorder, and even generalized anxiety disorder. It could be argued that the blinkered view of depression as a solely serotonergic phenomenon has not only restrained and limited research into other potential systems, but has also slowed down the discovery of putative antidepressant drugs. While some might argue that the hypothalamic-pituitary-adrenal (HPA) axis explains an individual’s sensitivity to depression, there are others who equally claim that the most likely explanations are to be found in the neuropsychopharmacology of the immune system or even through reductions in hippocampal volume. There is a richness of possibilities regarding the mechanisms for antidepressant activity embracing theoretical, pharmacological and clinical data. However, the methods by which putative antidepressants are assessed and their clinical efficacy demonstrated are not always robust. That current clinical comparisons of antidepressants rarely show major differences in efficacy between existing molecules could be taken as an indication that “all drugs are the same” or perhaps, more insightfully, as an indication that the ubiquitous Hamilton depression (HAM-D) rating scales are not sensitive to inter-drug differences, even though pronounced pharmacodynamic differences between molecules are easily demonstrated. Any advances in the development of new antidepressants will have to find not only original compounds but also unique psychometric tests by which the drugs can be assessed in a sensitive, reliable, and valid manner.

In Sweden, a psychiatry reform, aimed at improving the living conditions of the psychiatrically disabled, came into force in 1995. The aim of the present study was to evaluate the impact of the reform by investigating quality of life and standard of living 2 years later in a randomly selected group of people with longstanding psychiatric disability. Self-ratings and interviews were conducted in a study group and a control group. The study group consisted of 19 women and 18 men (mean age 46.1 years) diagnosed with neurosis, schizophrenia or affective disorder. The control group consisted of 19 women and 17 men (mean age 48.7 years). Self-rated quality of life was significantly poorer in the study group (P < 0.0001, unpaired t-test), and so was housing (P < 0.001, test of similar proportions in independent samples). We found no significant positive correlation between subjective quality of life and standard of living in either group but a significant negative correlation in the control group (P < 0.05; r = 0.40, Pearson correlation coefficient). The results suggest that, in 1997, people with longstanding psychiatric disability still had poorer quality of life than the general population. This may be due to factors other than outward standard of living.

Dopamine is implicated in the pathogenesis of both the positive and the negative symptoms of schizophrenia. Clinical efficacy of antipsychotic drugs, without the production of side-effects, may be achieved by a dose–response separation of pharmacological function, regional (i.e., anatomical) selectivity of action, or by the selective targeting of neuroreceptors. The atypical antipsychotics have many different ways of acting on receptors in the brain, but they have in common a decreased likelihood of producing extrapyramidal side-effects. Patients respond well to them by showing improvements of both positive and negative symptoms. The preclinical profile of amisulpride shows specificity for D2/D3 dopamine receptors and selective activity in the limbic system. There is evidence that amisulpride is effective in treating both the negative and positive symptoms of schizophrenia, and that it has a low propensity to induce motor side-effects. Therefore, both positive and negative symptoms can be treated, without inducing these side-effects, by selectively targeting dopamine receptors.

Dysfunction of central dopaminergic neurotransmission has been implicated in the pathogenesis of schizophrenia as well as drug and alcohol dependence. Different drugs of abuse stimulate dopamine release in the ventral striatum and thus reinforce drug consumption. Increased subcortical dopamine release has also been associated with the pathogenesis of positive symptoms in schizophrenia and may be driven by a prefrontal dopaminergic dysfunction. These seemingly heterogeneous findings may be explained by recent research in non-human primates. According to these studies, reward anticipation but not anticipated reward consumption is accompanied by a phasic dopamine release in the striatum and prefrontal cortex. In the striatum, phasic dopamine release primarily affects motivation, psychomotor activation and reward craving, while in the prefrontal cortex, dopaminergic stimulation is involved in the activation of working memory and reward anticipation. In alcoholism, previously neutral stimuli that have been associated with alcohol intake can become conditioned cues which activate phasic dopamine release and reward craving. In schizophrenia, stress-induced or chaotic activation of dopamine release may attribute incentive salience to otherwise irrelevant stimuli and thus be involved in the pathogenesis of delusional mood and other positive symptoms. Studies in humans and non-human primates emphasize the role of dopaminergic neurotransmission in reward anticipation and its dysfunction in different neuropsychiatric diseases.