The economic burden of psychiatric disorders and learning disability is assessed in order to aid decisions on priorities for research funding.

A wide variety of data sources both on prevalence and on the usage and costs of relevant services were used to measure the economic burden of each condition.

Despite methodological problems and problems with the data, an attempt is made to estimate the relative economic burden imposed by each condition. No attempt is made to sum up the costs for each condition across the agencies and individuals involved.

Our findings show that learning disability, schizophrenia and neurotic conditions (including depression) are major burdens on the National Health Service; senile dementia and depression in older people impact largely on local authority social services. Senile dementia, schizophrenia and learning disability are also heavy charges on the social security system. It is also notable that the large numbers with less severely disabling neurotic disorders generate a burden that, according to our figures, is comparable to schizophrenia and other psychotic disorders.

Investigations of the Korsakoff syndrome by researchers from different disciplines have proliferated in recent years, making it apposite to review the various findings.

This review is based on the author's knowledge of reports in the major clinical and neuropsychological journals, supplemented by Medline searches to update particular subtopics.

The Korsakoff syndrome is defined as a disproportionate impairment in memory, relative to other aspects of cognitive function, resulting from a nutritional (thiamine) depletion. The initial manifestations of the disorder are variable, and a persistent memory impairment can result from a non-alcoholic aetiology, although this seems to happen much less commonly than in the past – presumably because of generally higher standards of nutrition. Although there is agreement on the underlying neuropathology, the critical lesion sites for memory disorder have been debated. Recent evidence suggests that the circuit involving the mammillary bodies, the mammillo-thalamic tract and the anterior thalamus, rather than the medial dorsal nucleus of the thalamus, is particularly critical in the formation of new memories. The relationship of these deficits to thiamine depletion remains a topic of current investigation, as does the purported role of neurotransmitter depletions in the cholinergic, glutamate/GABA and catecholamine and serotonergic systems. Neuro-imaging studies have confirmed autopsy findings of more widespread structural and metabolic abnormalities, particularly involving the frontal lobes.

The relationship of these neuropathological, neurochemical, and metabolic abnormalities to cognitive functioning, with particular reference to specific aspects of memory processing, has been considered in some detail. Whereas structural and/or neurochemical abnormalities within the limbic/diencephalic circuits account for anterograde amnesia, some other factor, such as frontal lobe dysfunction, must underlie the severe retrograde memory loss which is characteristically found in this syndrome.

A review of the efficacy of antidepressant drug treatment in patients with obsessive–compulsive disorder (OCD), using a meta-analytic approach.

Randomised double-blind clinical trials of antidepressant drugs, carried out among patients with OCD and published in peer-reviewed journals between 1975 and May 1994, were selected together with three studies currently in press. Forty-seven trials were located by searching the Medline and Excerpta Medica – Psychiatry data bases, scanning psychiatric and psychopharmacological journals, consulting recent published reviews and bibliographies, contacting pharmaceutical companies and through cross-references. Hedges' g was computed in pooled data at the conclusion of treatment under double-blind conditions or at the latest reported point of time during this treatment period. For each trial, effect sizes were computed for all available outcome measures of the following dependent variables: obsessive–compulsive symptoms considered together; obsessions; compulsions; depression; anxiety; global clinical improvement; psychosocial adjustment; and physical symptoms.

Clomipramine was superior to placebo in reducing both obsessive–compulsive symptoms considered together (g = 1.31; 95% CI = 1.15 to 1.47) as well as obsessions (g = 0.89, 95% CI = 0.36 to 1.42) and compulsions (g = 0.79; 95% CI = 0.34 to 1.24) taken separately. Also, selective serotonin re-uptake inhibitors (SSRIs) as a class were superior to placebo, weighted mean g being respectively 0.47 (95% CI = 0.33 to 0.61), 0.54 (95% CI = 0.34 to 0.74) and 0.52 (95% CI = 0.34 to 0.70) for obsessive–compulsive symptoms considered together, and obsessions and compulsions taken separately. Although on Y–BOCS the increase in improvement rate over placebo was 61.3%, 28.5%, 28.2% and 21.6% for clomipramine, fluoxetine, fluvoxamine, and sertraline respectively, the trials testing clomipramine against fluoxetine and fluvoxamine showed similar therapeutic efficacy between these drugs. Finally, both clomipramine and fluvoxamine proved superior to antidepressant drugs with no selective serotonergic properties.

Antidepressant drugs are effective in the short-term treatment of patients suffering from OCD; although the increase in improvement rate over placebo was greater for clomipramine than for SSRIs, direct comparison between these drugs showed that they had similar therapeutic efficacy on obsessive–compulsive symptoms; clomipramine and fluvoxamine had greater therapeutic efficacy than antidepressant drugs with no selective serotonergic properties; concomitant high levels of depression at the outset did not seem necessary for clomipramine and for SSRIs to improve obsessive–compulsive symptoms.