Track topics on Twitter Track topics that are important to you
Primary: to identify physiologic indicators of venlafaxine treatment response using quantitative EEG (QEEG) cordance, and to determine if cordance changes are specifically associated with response to venlafaxine;
Secondary: to determine if cordance changes early in the course (i.e., prior to improvement in clinical symptoms) of venlafaxine (or another antidepressant if venlafaxine is not clinically indicated for a particular patient) are predictive of later clinical response.
After a one-week single-blind placebo lead in, subjects will be randomly assigned to either venlafaxine or placebo for 8 weeks. They will undergo 6 QEEG studies (end of wash-in, and 48 hours, 1 week, 2 weeks, 4 weeks, and 8 weeks after randomized treatment), with examiner and self-ratings of mood, anxiety, and clinical status at the time of each recording (Ham-D, MADRS, Ham-A, SCL-90, Beck, LIFE, and CGI) to assess improvement. Any subjects with significant deterioration in mood and/or suicidal ideation during the 8 week trial will be dropped from the study and placed in open treatment.
At the end of 8 weeks, code will be broken and all subjects will be maintained/re-assigned to open-label treatment with venlafaxine for an additional 10 months if they wish. However, if the subject's primary physician believes that another clinically available antidepressant would be indicated instead of venlafaxine (due to history of prior non-response to venlafaxine, etc.), the indicated antidepressant medication will be administered. The antidepressant medication recommended by the primary physician will be provided free of charge for a one-year period. Tricyclic antidepressants and monoamine oxidase inhibitors will not be included due to the greater possibility of serious clinical sequelae with these older medications. The open-label phase will consist of regular monitoring by the laboratory at intervals of three days and one week after beginning a new antidepressant medication, and then monthly clinical visits (or more frequently if clinically indicated) with QEEG recordings and assessments of mood and clinical status as above by the laboratory psychiatrist to ensure that the subject is getting appropriate care from his or her primary physician. Drug dose will be adjusted using standard clinical practice by the subject's primary physician in the community, and if the subject remains on venlafaxine, the dosage may be increased as high as 225 mg/day during this phase.
Subjects will have one additional follow-up QEEG at the end of the open-label phase or when significant clinical improvement is detected (defined as resolution of DSM-IV symptoms, or Ham-D < 9). After the subject's depression resolves, he or she will continue to be monitored and given medication free of charge for the remainder of the one-year period, but will be seen clinically only by the primary physician in the community. A study psychiatrist will be available for consultation in cases of clinical necessity until the primary physician can be contacted. Subjects for whom venlafaxine is not clinically indicated and/or subjects who refuse the placebo portion of the study may be allowed to bypass the placebo-controlled phase and proceed directly to the open-label phase.
Allocation: Randomized, Control: Placebo Control, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Outcomes Assessor), Primary Purpose: Treatment
venlafaxine (Effexor), placebo
University of California
University of California, Los Angeles
Published on BioPortfolio: 2014-08-27T03:26:14-0400
There are two specific aims of this project: 1. To identify physiologic indicators of venlafaxine treatment response using quantitative EEG (QEEG) cordance, and to determine if cor...
This 4-8 month study, with a 2-year follow up period, will compare sertraline (Zoloft®), venlafaxine (Effexor®), supportive-expressive psychotherapy, and placebo to determine which is mo...
The purpose of this study is to demonstrate a lack of effect of venlafaxine (Effexor XR) on QTc intervals relative to time matched placebo in healthy volunteers
The objective of this study is to compare the rate and extent of absorption of venlafaxine 25 mg tablets (test) versus Effexor® (reference) administered as 1 x 25 mg tablet under fed cond...
The objective of this study is to compare the rate and extent of absorption of venlafaxine 25 mg tablets (test) versus Effexor® (reference) administered as 1 x 25 mg tablet under fasting ...
This post-hoc analysis evaluated long-term psychosocial outcomes in patients with recurrent major depressive disorder treated with venlafaxine extended release (ER) 75-225 mg/day or placebo. Patient...
This post hoc meta-analysis evaluated the efficacy and safety of desvenlafaxine 50 and 100 mg versus placebo across age groups and severity of depression at baseline in patients with major depressive ...
Epidemiological studies strongly support the theory that stressful life events play an important role in the etiology of depression. The mechanism of chronic stress induced depression involves a numbe...
This post hoc analysis examined the time point at which clinically significant improvement in major depressive disorder (MDD) symptoms occurs with desvenlafaxine versus placebo.
The placebo effect is usually studied in clinical settings for decreasing negative symptoms such as pain, depression and anxiety. There is interest in exploring the placebo effect also outside the cli...
Depressive states usually of moderate intensity in contrast with major depression present in neurotic and psychotic disorders.
The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group.
A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders. (From AMA Drug Evaluations Annual, 1994, p311)
An MAO inhibitor that is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in the treatment of panic disorder and the phobic disorders. (From AMA, Drug Evaluations Annual, 1994, p311)
Decompression external to the body, most often the slow lessening of external pressure on the whole body (especially in caisson workers, deep sea divers, and persons who ascend to great heights) to prevent DECOMPRESSION SICKNESS. It includes also sudden accidental decompression, but not surgical (local) decompression or decompression applied through body openings.
Anxiety is caused by stress. It is a natural reaction, and is beneficial in helping us deal with tense situations and pressure. It is deterimental when is becomes an excessive, irrational dread of everyday situations. The most common types of anxiety di...
Pharmacy is the science and technique of preparing as well as dispensing drugs and medicines. It is a health profession that links health sciences with chemical sciences and aims to ensure the safe and effective use of pharmaceutical drugs. The scope of...