Diagnosing Alzheimer's disease.
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Biomedical subjects
Publications and source records attributed to C L Katona.
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beta-Adrenoceptors were measured by saturation binding of [3H]CGP 12177 in nine brain regions and pineal from suicides, with a firm retrospective diagnosis of depression, and age and sex matched controls. Twenty one suicides had not recently received antidepressant drugs, 17 had been receiving drugs prior to death. In antidepressant drug-free suicides, the number of total beta-adrenoceptors was significant lower in temporal cortex (Brodmann area 38) and beta 1-adrenoceptors (Brodmann areas 21/22) was significant lower than matched controls. Suicides who died by violent means had significantly lower numbers of total beta- and beta 1-adrenoceptors in the frontal cortex and lower numbers of beta 1-adrenoceptors in temporal cortex (Brodmann areas 21/22) than matched controls. Suicides who died by non-violent means had lower numbers of total beta-adrenoceptors in occipital cortex controls and lower numbers of total beta- and beta 1-adrenoceptors in temporal cortex (Brodmann area 38) than matched controls. In antidepressant drug-treated suicides, significantly lower number of beta-adrenoceptor binding sites were found in temporal cortex (Brodmann area 38) and thalamus compared to matched controls. The lower number of beta-adrenoceptors binding sites in the thalamus appeared to be related to drug treatment. There were no differences in beta-adrenoceptor binding in the pineal gland between antidepressant-free and antidepressant-treated suicides and controls, although there were apparent differences between suicides and controls related to the time of death and season of death.
STUDY OBJECTIVE: The aim was to assess the relationship between social deprivation, as measured by the Jarman under-privileged area score (UPA score), and psychiatric admission rates and length of stay within an inner London borough. DESIGN: The study was a retrospective survey of psychiatric admission rates for electoral wards in the London borough of Islington in relation to Jarman UPA scores and subscores. SETTING: Islington Health Authority psychiatric admission wards at the Whittington and Friern Hospitals. PATIENTS: All admissions during the year of 1985 were studied (n = 778). MAIN RESULTS: No correlation was found between the total Jarman UPA score and either admission rates or length of stay. There was, however, a correlation between the Jarman UPA subscore for ethnic minorities and admission rates (r = 0.409, p less than 0.05), and between the Jarman UPA subscore for lone parents and length of stay (r = 0.390, p less than 0.05). CONCLUSIONS: The Jarman UPA score at electoral ward level is not related to psychiatric morbidity, and should not therefore be used for planning local service provision.
The authors' study confirmed the high prevalence of depressive symptoms in elderly medical inpatients but found no relationship between the diagnosis of or symptoms of depression and mortality or hospital use. Other studies examining the impact of depression on outcome for elderly patients may not have adequately controlled for the severity of the accompanying physical illness, which may perhaps have been responsible for the reported adverse effects of depression on outcome. An alternative explanation is that the authors' study involved a 1-year follow-up and a longer period of time may be necessary. The study demonstrated that routine screening for depression in acute elderly medical inpatients may be a useful way of detecting coexisting psychiatric morbidity. The routine screening measures were acceptable to patients and may be of considerable potential value in alerting staff to accompanying psychological distress. This study also illustrated the high prevalence of depression in patient samples and the importance and usefulness of screening geriatric inpatients. There are, however, several questions that remain unanswered both in studies reviewed in this article and in the authors' own work. The etiology and mechanism of the association between physical illness and depression are unknown, and there has been a dearth of studies assessing the feasibility and utility of specific treatments for depression in the elderly physically ill.
beta-Adrenoceptor binding sites were measured by saturation binding of [3H]CGP 12177 in nine brain regions from 13 suicides, with a firm retrospective diagnosis of depression, who had been receiving antidepressant drugs, and 11 matched controls. Significantly lower numbers of beta-adrenoceptor binding sites were found in thalamus and temporal cortex (Brodmann area 38), but not in other brain regions, of antidepressant-treated suicides compared to controls. The lower number of beta-adrenoceptor binding sites in thalamus appeared to be related to drug treatment, whereas lower numbers of beta-adrenoceptors in temporal cortex were also found in antidepressant-free suicides.
Capgras syndrome in association with lithium toxicity is described in a 74-year-old woman. Lithium toxicity should be considered when new delusions occur during lithium therapy.
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Brain serotonin (5-HT) uptake sites were quantitated, by saturation binding of [3H]paroxetine, in 10 brain regions from 22 suicide victims and 20 control subjects. Suicide victims were restricted to those subjects in whom a firm retrospective diagnosis of depression was established and who had not recently been prescribed antidepressant drugs. The Kd and Bmax of [3H]paroxetine did not differ significantly between controls and depressed suicides in any of the brain regions. In putamen, Bmax values of suicides who died non-violently were lower than controls, whereas those who died by violent methods did not differ from controls. No significant differences between violent or non-violent suicides and their matched controls were found in other brain areas. These results offer little support for the view that suicide/depression is associated with an abnormality in 5-HT uptake.
beta-Adrenoceptor binding sites were quantitated by saturation binding of [3H]CGP 12177 in 9 brain regions from 21 suicide victims, with a firm retrospective diagnosis of depression, who had not recently received antidepressant drugs, and 20 age- and sex-matched controls. In depressed suicides the number of total beta-adrenoceptors was significantly lower in temporal cortex (Brodmann area 38, by 19%) and beta 1-adrenoceptors (Brodmann area 21/22, by 17%) compared to controls. Suicides who died by violent means had significantly lower numbers of total beta- and beta 1-adrenoceptors in frontal cortex than matched controls (by 23 and 25%, respectively) and than non-violent suicides (by 20 and 22%, respectively) and lower numbers of beta 1-adrenoceptors in temporal cortex (Brodmann area 21/22) than matched controls (by 16%). Depressed suicides who died by non-violent means had lower numbers of total beta-adrenoceptors in occipital cortex than matched controls (by 24%) and than violent suicides (by 18%), and lower numbers of total beta- and beta 1-adrenoceptors in temporal cortex (Brodmann area 38) than matched controls (by 27 and 24%, respectively). Depression in suicide victims is associated with deficits in beta-adrenoceptor binding sites, largely restricted to cortical areas.
5-HT1 and 5-HT1A binding sites were measured in brain tissue obtained at postmortem from 19 suicides, with definite evidence of depression, and 19 sex and age-matched controls. Thirteen of the depressed suicides had not been prescribed psychoactive drugs recently (drug-free suicides); six had been receiving antidepressant drugs, alone or in combination with other drugs (antidepressant-treated suicides). No significant differences were found in the number or affinity of 5-HT1 and 5-HT1A binding sites in frontal or temporal cortex between drug-free suicides and controls. The number of 5-HT1 sites was significantly lower (by 20%), affinity unaltered, in hippocampus and the affinity significantly lower (by 33%), number unaltered, in amygdala of drug-free suicides than controls. The number of 5-HT1 binding sites tended to be higher and the affinity lower in the antidepressant-treated compared to drug-free suicides, and significantly so in hippocampus. The present results, together with our previous studies, provide no evidence of altered cortical 5-HT markers in depressed suicides, but further emphasise abnormalities in the hippocampus.
Benzodiazepine binding was measured in amygdala and hippocampus from 19 suicides in whom a firm diagnosis of depression was established retrospectively, and 19 well-matched controls. The number and affinity of benzodiazepine binding sites did not differ significantly between the drug-free or drug-treated suicides and controls.
Regional variations across Hungary in suicide rate and in rate of treated depression were examined. Regional differences in suicide rate as well as psychiatric morbidity were consistent over the 3 years examined (1985, 1986 and 1987). The suicide rate showed a significant negative correlation with the rate of treated depression in each of the 3 years, and weaker negative correlations with perinatal mortality and divorce rate. No correlation between suicide rate and rate of schizophrenia was found. The results suggest that underdiagnosis of depression may contribute to Hungary's very high suicide rate. The implications of this for medical education and psychiatric practice are discussed.
5-Hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations and 5-HT turnover (5-HIAA/5-HT) were determined in 6 brain regions from 19 suicide victims in whom a retrospective diagnosis of depression was established, and 19 age- and sex-matched control subjects. Thirteen of the suicides were free of psychoactive drugs at the time of death; 5 were receiving antidepressant drugs. 5-HT, 5-HIAA and 5-HT turnover did not differ significantly between the total, drug-free and antidepressant-treated suicides and controls in frontal and temporal cortex, caudate and hippocampus. 5-HIAA concentration was significantly higher in amygdala of drug-free suicides than controls, whereas 5-HT and 5-HT turnover did not differ. 5-HT concentration was significantly lower in putamen of the total and antidepressant-treated suicides and a similar reduction was also apparent in the drug-free suicides. 5-HT turnover in putamen was significantly higher in the total and drug-free suicides compared to controls. 5-HT and 5-HIAA concentrations in putamen were significantly lower in drug-free suicides who died by non-violent means than in those who died by violent means. Differences between controls and suicides could not be attributed to age, sex or postmortem delay. These results offer no support for the view that 5-HT turnover is reduced in depressed subjects who commit suicide.
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3H-Imipramine binding was measured in freshly prepared platelet membranes from 47 drug-free major depressives and 46 healthy controls. Where possible, platelet binding in depressed subjects was repeated following treatment. A significant negative correlation was found between Bmax and assay protein concentration and Bmax values were corrected for this effect. Adjusted Bmax was significantly lower (by 14%) in female depressed patients than in female control subjects, and the difference was of similar magnitude premenopausally and postmenopausally. No such difference was found in males. Kd did not differ significantly between depressed and control subjects. Multiple regression analysis confirmed significant effects on Bmax of presence of depressive illness, age (positive correlation), and season (higher in summer). Within the depressed sample, Bmax was significantly lower in those subjects with obsessional features. Endogenicity (Research Diagnostic Criteria or Newcastle), dexamethasone suppression test result, drug-free interval, family history of depression, depressive psychosis, suicidal ideation, and past history of suicide attempts were not significantly related to Bmax. Paired comparisons revealed no significant effect on Bmax of 6 weeks' treatment with imipramine, maprotiline, or BRL 14342 or of a course of electroconvulsive therapy.
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