Efficacy Of Antidepressant Treatment Research Articles

Treatment of acute bipolar depression: a review of the literature.

Our goal was to ascertain the efficacy of various antidepressant treatments for acute bipolar depression. English articles that reported on the efficacy of antidepressant treatments in bipolar depression were located by computerized Medline and manual search. These studies were systematically reviewed and response rates for each treatment were computed. The available data suggest that mood stabilizers, MAOIs, cyclic antidepressants, and ECT are all effective in treating bipolar depression. All antidepressant treatments with the exception of mood stabilizers have been reported to induce a manic/hypomanic switch. It is recommended that mood stabilizers may be the first step of treatment, followed by the addition of an antidepressant, especially a cyclic antidepressant. The specific symptoms profile of individual patients, such as anergic or psychotic features, may indicate more specific treatment options. ECT is an important measure for those who are pharmacotherapy-resistant or psychotic.

Attenuation of sucrose consumption in mice by chronic mild stress and its restoration by imipramine.

Chronic exposure to mild unpredictable stressors (CMS) has previously been found to reduce the consumption of palatable, sweet solutions in rats. In the present study, the utility of this procedure was assessed in mice. Male AP mice subjected to CMS showed reduced consumption of a 2% or 4% sucrose solution. This effect was reversed by chronic (3 weeks) treatment with the tricyclic antidepressant imipramine (20 mg/kg per day). These results extend previous reports of a generalized decrease in sensitivity to reward (anhedonia) in rats caused by CMS and the efficacy of antidepressant treatment in this paradigm. Chronic unpredictable mild stress in mice appears to provide a realistic animal model of depression.

Endocoids in depression: Do antidepressants alter endocoids that affect the serotonergic system?

1. Studies undertaken over the last decade have shown that factors are present in in brain extacts, cerebrospinal fluid and plasma that impede the transport of tritiated 5HT into cortical tissue and platelets. 2. While the precise nature of these substances is presently unknown, it has been hypothesized that they may play a role in the aetiology of the affective disorders. 3. A preliminary study is described in which the plasma from untreated depressed patients was shown to impair the 5HT induced platelet aggregation, and 3H-5HT uptake, of control subjects. The effect of this factor on platelet 5HT aggregation appears to be diminished following the recovery of the depressed patients. 4. The results of these and other studies suggest that endocoids are present in the depressed patient that could be causally responsible for the defects in serotonergic function that is commonly associated with the disease. 5. The efficacy of antidepressant treatments may therefore be related to their ability to counteract the effect of such endocoid(s).

Depression in Alzheimer's Disease Significantly Improved under Treatment with Mianserine

To the Editor:—Depression is a frequent unspecific behavioral concomitant of Alzheimer's disease. Typically, the mood disorder is shortlived and fluctuating but may meet the diagnostic criteria for major depression in up to 30% of all cases.1 The efficacy of antidepressant treatment in demented patients has been observed using compounds such as monoamine-oxidase inhibitors2,3 or imipramine.4 There are no reports on the effects of the tetracyclic antidepressant mianserine on depression in Alzheimer's disease although this compound, a dipyrazinoazepine derivate, may be particularly useful in elder patients because it shows little vegetative and almost no anticholinergic side effects. In our outpatient clinic a 79-year-old woman, with clinically diagnosed moderate Alzheimer's disease (NINCDS-ADRDA), complaining of depressed mood, low self-esteem, and anxiety showed markedly reduced drive and mentioned occasional suicidal thoughts. She had lost interest in social activities during the past 4 weeks. The criteria for major depression (DSM-III-R) were fulfilled. Treatment was begun with mianserine 10 mg/day and after 1 week was raised to 20 mg/day. Two weeks after initial treatment, her symptoms of anxiousness, depression, drive, and self-esteem had improved clinically. According to her husband, suicidal thoughts were no longer present, and she had even started to participate in some activities (taking a walk, visiting friends). Six weeks after initial treatment, further substantial improvement of depression was clinically demonstrable. The patient could enjoy social activities in daily living. During the follow-up assessment over 6 weeks, no relevant side effects, such as tiredness, sedation or orthostatic hypotension, occurred. There was no change in cognitive impairment during these 6 weeks. The clinical observations were confirmed by baseline and follow-up assessments (Table 1) at 2 and 6 weeks with the Dementia Mood Assessment Scale,5 the Nurses' Observation Scale for Geriatric Patients,6 and the Cambridge Cognitive Examination.7 This case report suggests that treatment with mianserine can substantially improve major depression in Alzheimer patients. We did not find relevant side effects during treatment. In contrast to that, postural hypotension, drowsiness, and dizziness have been reported during treatment of depression in Alzheimer patients with tricyclic antidepressants4 and monoamino-oxidase inhibitors.3 Furthermore, treatment with monoamino-oxidase inhibitors requires dietary precautions to prevent potential hypertensive reactions.8 We therefore suggest that the tetracyclic antidepressant mianserine should be considered as a valuable alternative in the pharmacological treatment of depression in Alzheimer's patients.

5-HT uptake inhibitors and tricyclic antidepressants: relation between trytophan availability and clinical response in depressed patients

The amount of tryptophan (TrP) available for transport from plasma into the brain was estimated in patients with major depression before treatment for 4 weeks with a 5-HT potentiating tricyclic antidepressant (TCA), amitriptyline ( n = 21) or clomipramine ( n = 17), or a selective 5-HT uptake inhibitor, citalopram ( n = 14) or paroxetine ( n = 27). The ratio in plasma of Trp to the sum of the other large neutral amino acids (LNAA) was significantly inversely correlated with improvement on TCA, and patients with ratio Trp/LNAA below the mean improves significantly more than patients with a higher ratio but with comparable serum steady-state drug levels. The Trp concentration was a bit stronger inversely correlated with improvement on 5-HT uptake inhibitors than the ratio Trp/LNAA, and patients with Trp level below the mean improved significantly more than those with a higher level butwith comparable serum steady-state drug levels. Plasma amino acid variables may be a useful tool for increasing the efficacy of antidepressant treatment.