Background. Personality psychopathology exerts a significant and independent effect on the course of benzodiazepine (BZ) discontinuation, worsening the subjective severity of withdrawal symptoms and significantly increasing the occurrence of early taper failures.

Method. One hundred and seventy-one patients participating in a BZ discontinuation programme were administered several personality measures prior to taper. Patients were stabilized for 3 weeks at their baseline BZ dosage and then tapered off 25% per week over 4 weeks, with the option to extend up to 6 weeks if necessary.

Results. High levels of passivity and dependency as assessed by the MMPI Dependence subcluster, and at a trend level high Eysenck Neuroticism and high TPQ Harm Avoidance contributed significantly to the prediction of benzodiazepine withdrawal severity. Though there was a high correlation between personality measures, psychopathology and adjusted BZ dose, the effects of personality on withdrawal severity was significant, particularly in the initial phases of BZ taper, when taper severity was still relatively mild.

Conclusions. These findings indicate that clinical decisions on how to manage BZ tapering should be guided by personality assessments, in addition to the usual considerations of BZ dosage, residual psychopathology, duration of treatment, etc. The potential for difficulty with discontinuation related to personality traits should be one of the factors weighed in the risk–benefit assessment made in the planning of benzodiazepine treatment for patients with anxious symptomatology.

Background. Long-term low-dosage dependence on benzodiazepines is traditionally explained by withdrawal symptoms. Previous research has not given much attention to reports that suggest that many patients oppose stopping benzodiazepines long before withdrawal symptoms have developed. This study investigates the scope of and factors associated with this pre-withdrawal treatment insistence.

Methods. Patients receiving long-term low-dosage benzodiazepines in primary care were asked to take a drug-holiday of at least 3 weeks. Sociodemographic, medication, morbidity and attitudinal variables were assessed in addition to the GPs' perceptions of their patients.

Results. Two-thirds of the patients rejected the drug-holiday proposal. Patients who refused a drug-holiday were less educated and were using a higher percentage of long-acting benzodiazepines than patients who accepted the drug-holiday proposal. Those who refused were seen by their GPs as being more complaining, harder to satisfy and less co-operative.

Conclusions. These results provide evidence for drug-seeking or craving behaviour of patients who receive low-dosage benzodiazepine prescriptions. A major problem in benzodiazepine withdrawal occurs before the withdrawal programme has even begun. These data show that benzodiazepine low-dosage dependence should be considered a real form of dependence.

Background. A Dutch cohort of predominantly out-patient DSM-III-R major depressive patients was followed for 3 to 5 years after start of treatment in a psycho-neuro-endocrinological prediction study. The study design permitted description of the course of remissions, relapses and recurrences.

Methods. Pharmacological treatment was standardized, psychotherapy was tailored to the needs of the patient, follow-ups were done monthly until 3 years or more after the initial recruitment.

Results. After 9 months 49% of the patients had reached full remission and 45% were in partial remission. During the following 3 to 5 years 82% of the patients had reached a period of full remission. Sixteen per cent of the patients needed 2 years or more before full remission. A relapse or recurrence rate of 41% within 5 years was found. Patients with residual symptoms relapsed particularly in the first 4 months after remission, while patients without residual symptoms recurred mainly after 12 months after remission. Previous depressive episodes and psychoticism predicted relapse. Psychomotor retardation at inception predicted a longer time to partial remission.

Conclusion. In most cases, major depression is a seriously impairing episodic disease. This is also true for a sample of predominantly out-patients treated at a university clinic.

Background. Although many case–control studies have replicated an association between dysfunctional parenting and a lifetime diagnosis of depression, few epidemiological studies have explored the association. In addition, little is known about the association in non-western countries.

Methods. Using logistic regression analyses, additive and interactive contributions of parental child-rearing behaviours, as measured by the Parental Bonding Instrument (PBI), toward the risk for having a lifetime diagnosis of major depressive disorder were explored in 418 employed Japanese adults. The diagnosis was provided by using the Inventory to Diagnose Depression, lifetime version. The analyses were conducted for male and female subjects separately.

Results. Parental care rather than parental protection was primary in predicting lifetime depression in both male and female subjects. An interactive combination of low care and high protection (‘affectionless control’) was a significant risk factor for lifetime depression in male respondents' reporting child-rearing behaviours of both parents and female respondents' reporting paternal child-rearing behaviours. Model improvements when entering the PBI scores were larger in male subjects than in female subjects.

Conclusions. The results suggested that a combination of low care and over-protection increases a risk to lifetime depression even in a non-clinical sample; that an association between dysfunctional parenting (particularly low care) and the development of depression is independent of culture; and that Japanese boys are more sensitive than Japanese girls to dysfunctional parenting as regards the development of depression.