Results show very high rates of lifetime but not current major depression. Rates of current phobia and suicidal ideation in the very elderly are also high compared with other studies. The rates reported are likely to be underestimates.
There is compelling evidence that serotonin system dysfunction is associated with certain behavioral disorders, such as suicidal behavior and impulsive aggression. A functional polymorphism in the promoter region of the serotonin transporter gene (5-HTTLPR) was recently identified and the presence of the short allele found to be associated with a lower level of expression of the gene, lower levels of 5-HT uptake, suicidal behavior and anxiety-related traits. We genotyped 51 West European Caucasians who had made violent suicide attempts and 139 controls of the same ethnic origin, with no history of suicidal behavior. The frequencies of the S allele and the SS genotype were significantly higher in the violent suicide attempters than in the controls. The odds ratio for the SS genotype vs the LL genotype was 3.63 (95% CI (1.27-10.40)). This suggests that a change in expression of the gene encoding the 5-HT transporter may be involved in violent suicidal behavior. Molecular Psychiatry (2001) 6, 338-341. Since the seminal studies by Asberg and collaborators in the mid 1970s, 1 most studies have shown that impulsive aggression and suicidal behavior are correlated with low levels of 5-HT transmission.2 This association is stronger for more severe phenotypes: lethal and/or violent suicidal behavior and violent aggressive behavior.3-5 The magnitude and duration of serotonergic activity is believed to be regulated mainly by the human serotonin transporter (5-HTT), which controls the uptake of serotonin from the synaptic junction.6,7 The human 5-HTT is in a presynaptic location and Lesch et al 7 have demonstrated that it is identical in platelets and in the brain. Conflicting results have been obtained in studies of the platelet 5-HT transporter in individuals with suicidal behavior. Some studies have shown a decrease in the number of 5-HT transporter recognition sites in such individuals, as shown by the radiolabeled ligand-binding technique, and in the amount of 5-HT transporter protein, as shown by 5-HT uptake measurements. 8,9 Despite differences in the results obtained, probably due to differences in the ligands used, studies of radioligand binding in the brainstem of individuals who have committed suicide and in platelets have provided evidence that there is a negative association between serotonin dysfunction and impulsive aggression and violent or suicidal behavior. [8][9][10][11] Coccaro et al 11 studied patients with personality disorders and found a negative correlation between aggression and tritiated paroxetine binding to platelet serotonin transporter sites. Roy 9 recently reported that the affinity of the serotonin uptake protein for serotonin is lower in depressed patients displaying suicidal behavior than in depressed patients who have never attempted suicide and in controls. This lower affinity for serotonin was also found to have predictive value for subsequent suicide attempts and suicides during a 5-year follow-up period.Pharmacological studies have also provided evidence that the serotonin transport...
The percentage occupation of striatal dopamine D2 receptors has been evaluated in 25 patients using 76Br-bromospiperone positron emission tomography (PET) and prolactin plasma levels (PRL) during oral neuroleptic treatment (11 studies), 1-90 days following discontinuation of such treatment (16 studies), and 1-120 days after last intramuscular administration of depot neuroleptics (nine studies). The PET-estimated occupation was highly significantly correlated in a sigmoid-like fashion to the logarithm of the chlorpromazine-equivalent dose of oral neuroleptics (suggesting a strict dose-occupation relationship during oral neuroleptic treatment and supporting the D2-mediated hypothesis of neuroleptic action), while PRL was weakly related to daily dosage. Following withdrawal, return to normal receptor availability, as estimated by PET, occurred within 5-15 days (suggesting that protracted effects of neuroleptics after withdrawal are not due to sustained D2 receptor occupation), but PRL values fell even more rapidly. Efficient treatment with depot neuroleptics resulted in marked PET-estimated D2 receptor occupation, stable over the whole 4-week drug-administration interval, suggesting that longer intervals could be appropriate; PRL values bore no relationship to PET-estimated occupation, indicating variable intersubject tolerance to neuro-endocrine dopamine blockade. Overall, PET was much more sensitive than PRL to estimate striatal D2 receptor occupation in vivo.
Care of cancer patients may be a source of considerable stress. As part of a large scale longitudinal study of the interaction of biological, psychological and environmental factors in determining patient outcome, the mental and physical health status of 37 members of the nursing staff of a cancer hospital was examined. The study identifies risk factors for stress, professional 'burn-out' and psychiatric morbidity. An assessment questionnaire also examined work time, work organization, relationships with colleagues, identification of stressful situations, and treatment of pain. Each subject completed three scales designed to measure stress and psychiatric morbidity: the Nursing Stress Scale, the Maslasch Burnout Inventory and the General Health Questionnaire. Item analysis suggested that stress is primarily related to inadequate training, lack of time to deal with the psychological component of care giving especially terminal care, and relationship difficulties with other medical staff. Multiple analysis of correspondence indicated that in the face of stress, risk factors for professional burnout are high psychiatric symptomatology, lack of information at the time of diagnosis, poor perceived health, relationship difficulties with patients and their families, and work uncertainties.
We screened 124 individuals for single nucleotide polymorphisms of the alpha1, beta3 and gamma2 genes of the GABA(A) receptor in the regions corresponding to the ligand-binding domains on the protein level. In a patient with chronic insomnia, a missense mutation was found in the gene of the beta3 subunit. This mutation results in the substitution of the amino acid residue arginine for histidine in position 192 (beta3(R192H)). The patient was found to be heterozygous for this mutation. Functional analysis of human alpha1beta3(R192H)gamma2S GABA(A) receptors using ultra fast perfusion techniques revealed a slower rate of the fast phase of desensitization compared with alpha1beta3gamma2S GABA(A) receptors. Additionally, current deactivation [a major determinant of inhibitory postsynaptic current (IPSC) duration] was faster in the mutated receptors. This raises the possibility of decreased GABAergic inhibition contributing to insomnia, as some members of the patient's family also suffer from insomnia. The mutation beta3(R192H) might, therefore, be linked to this condition. The intron/exon boundaries of the alpha1 subunit gene were also established and three additional variants were found in the alpha1 and beta3 genes.
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