PubMed Health⌕ Search

Biomedical subjects

C Berlanga

Publications and source records attributed to C Berlanga.

9 recordsLinked to original sources
PubMed1999

Personality and clinical predictors of recurrence of depression.

OBJECTIVE: To help clinicians more accurately predict outcomes of treatment for depression, variables associated with recurrence of depression in the year after treatment were examined in a group of patients who completed treatment for an index episode of depression. METHODS: Forty-two depressed patients who participated in a double-blind pharmacological treatment study were followed for one year after treatment was discontinued. Length of treatment for the index episode was determined by clinicians and ranged from eight to 76 consecutive weeks. Eighteen patients who had a recurrent episode (43 percent) and 24 patients who did not (57 percent) were compared on sociodemographic and clinical variables, including scores on the Eysenck Personality Questionnaire (EPQ). RESULTS: A combination of three variables predicted recurrence of depression in 90 percent of cases. They were an elevated EPQ score on the neuroticism subscale, a short duration of treatment of the index episode, and a slow onset of response to treatment of the index episode. CONCLUSIONS: The findings suggest that personality traits, treatment duration, and variations in response to treatment might have an impact on long-term treatment outcome. Clinicians should consider these factors when making treatment decisions for depressed patients.

Adult↗
PubMed1995

A 3-year follow-up of a group of treatment-resistant depressed patients with a MAOI/tricyclic combination.

Treatment-resistant depression is a clinical complication that not infrequently affects a certain number of patients. Within the treatment strategies proposed for this condition, the association of a MAO inhibitor (MAOI) with a tricyclic antidepressant has gained reputation both for its unusual efficacy, as for its potential toxicity. However, when cautions are taken, it may be safely administered. Most reports on this combination have been carried in nonresistant patients and, when resistant patients are included, only the acute phase of the treatment is reported. In this study, a group of well-defined resistant patients received an open trial with the association of isocarboxazide and amitryptiline (n = 25). Those who responded were followed during the next 3 years (n = 12) and every 6 months an attempt was made to discontinue the MAOI and continue only with amitryptiline. At the end of the study, 4 patients maintained response with single medication, 6 still required both drugs and 2 relapsed. No clinical differences were apparent between the outcome groups, except that those who maintained their response only with the 2 combined drugs had more previous depressive episodes than the others. The isocarboxazide/amitryptiline combination may be a good treatment option for at least some forms of resistant depression. The safety of this treatment modality is confirmed, even when given for long periods of time. The study also suggest that there are no clinical characteristics in resistant depression that may predict the treatment outcome but, perhaps in some patients, a combined treatment is required to obtain a broader biochemical effect that could convert them from nonresponders to responders.

Adolescent↗
PubMed1992

Efficacy of S-adenosyl-L-methionine in speeding the onset of action of imipramine.

A double-blind clinical trial was carried out to evaluate the efficacy of S-adenosyl-L-methionine (SAMe) in speeding the onset of action of imipramine (IMI). SAMe is a naturally occurring substance that has been shown to possess antidepressant activity with a rapid mode of onset and minimal side effects. Sixty-three outpatients with moderate to severe depression were included in the study. After an initial 1-week placebo period, only 40 patients entered the active treatment phase. During the first 2 weeks of the trial, half of these patients received 200 mg/day of SAMe intramuscularly, while the other half received placebo. Simultaneously, oral IMI was administered to all patients at a fixed dose of 150 mg/day. The onset of clinical response was determined by evaluating patients every second day. By the end of week 2, the parenteral treatment was suppressed and IMI was adjusted according to individual needs. Depressive symptoms decreased earlier in the patients who were receiving the SAMe-IMI combination than in those who were receiving the placebo-IMI combination.

Adult↗
PubMed1985

[In search of biological markers of affective disorders].

The field of biological markers of affective disorders is defined on its conceptual and methodological basis, and the results of some studies in this area conducted at the Mexican Institute of Psychiatry are reported. Urinary MHPG levels greater than 2800 micrograms/24 hs, suggest a poor response to conventional drug treatment. Allnight EEG recordings, showed that sleep architecture of depressed patients is substantially different from that of normal subjects; particularly REM sleep latency, which can reliably discriminate between patients and controls. The dexamethasone suppression test showed a diagnostic confidence of 77% which is similar to that reported from other centers. The author suggests caution on interpreting these results, as further prospective longitudinal studies are needed before firm conclusions can be drawn.

Adolescent↗
PubMedDate not supplied

[Early and intermediate responses as factors predicting efficiency of antidepressive agents].

An important limitation in the treatment of depression is the lack of reliable factors for predicting treatment response. Most of these factors have been related to biological and clinical aspects. A clinical aspect that has proved to reasonably predict long-term efficacy is early response. An adequate early response predicts a good outcome at the long term. The purpose of this study was to quantify the proportion of patients who show no response to a fixed dose of antidepressants after 2,4, and 6 weeks of treatment, and then respond by week 8. Additionally, a subgroup of patients was followed using the same methodology until 12 weeks of treatment. A lack of response by weeks 4 and 6 predicted a final lack of response both at weeks 8 and 12 of treatment. Alternatively, a robust response as early as week 2 predicted a good response by the end of the two treatment periods. These findings should help clinicians revalorate treatment when finding no response after 4 or 6 weeks of treatment.

Adult↗