J Psychiatr Res. 2004 May-Jun;38(3):249-57. :
Extended-release venlafaxine in relapse prevention for patients with major depressive disorder.
Simon JS, Aguiar LM, Kunz NR, Lei D.
Northbrooke Research Center, 9275 North 49th Street, Suite 200, Brown Deer, WI 53223, USA.
jssimonmd@aol.com
Many studies have demonstrated that venlafaxine is an efficacious and safe treatment for major depressive disorder (MDD). This double-blind, placebo-controlled study was performed to evaluate the efficacy of venlafaxine extended-release (XR) (75-225 mg/day) in the prevention of relapse of depression. Patients with MDD who responded to an 8-week course of venlafaxine XR treatment, i.e., had a score < or = 3 on the Clinical Global Impressions scale-Severity of Illness item (CGI-S) and a 21-item Hamilton Rating Scale for Depression (HAM-D(21)) score < or = 10, were randomly assigned to receive continuation treatment (up to 6 months) with venlafaxine XR (n=161) or placebo (n=157). The main efficacy outcome measure was the number of patients who experienced a relapse of depression. Relapse was defined by either a combination of a patient meeting Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for MDD and a CGI-S score > or = 4, two consecutive CGI-S scores > or = 4, or a final CGI-S score > or = 4 for a patient who withdrew from the study. The cumulative probability of relapse was calculated using the Kaplan-Meier method of survival analysis. During the 6-month evaluation period, significantly more patients in the placebo group had a relapse of MDD than did patients who continued treatment with venlafaxine XR. Cumulative relapse rates at 3 and 6 months were 19 and 28%, respectively, for venlafaxine XR, and 44 and 52%, respectively, for placebo. This study demonstrates that venlafaxine XR is an effective and safe continuation therapy.
Pharmacotherapy. 2004 May;24(5):621-9. :
Treatment of pain syndromes with venlafaxine.
Grothe DR, Scheckner B, Albano D.
Global Medical Communications, Neuroscience, Wyeth Pharmaceuticals, Collegeville, Pennsylvania 19426, USA.
Major depressive disorder (MDD) and anxiety disorders such as generalized anxiety disorder (GAD) are often accompanied by chronic painful symptoms. Examples of such symptoms are backache, headache, gastrointestinal pain, and joint pain. In addition, pain generally not associated with major depression or an anxiety disorder, such as peripheral neuropathic pain (e.g., diabetic neuropathy and postherpetic neuralgia), cancer pain, and fibromyalgia, can be challenging for primary care providers to treat. Antidepressants that block reuptake of both serotonin and norepinephrine, such as the tricyclic antidepressants (e.g., amitriptyline), have been used to treat pain syndromes in patients with or without comorbid MDD or GAD. Venlafaxine, a serotonin and norepinephrine reuptake inhibitor, has been safe and effective in animal models, healthy human volunteers, and patients for treatment of various pain syndromes. The use of venlafaxine for treatment of pain associated with MDD or GAD, neuropathic pain, headache, fibromyalgia, and postmastectomy pain syndrome is reviewed. Currently, no antidepressants, including venlafaxine, are approved for the treatment of chronic pain syndromes. Additional randomized, controlled trials are necessary to fully elucidate the role of venlafaxine in the treatment of chronic pain
Psychosomatics. 2004 May-Jun;45(3):217-9. :
Safety and tolerability of extended-release venlafaxine in severe medical and surgical illness.
Schwartz T, Jindal S, Virk S, Wade M.
Department of Psychiatry, SUNY Upstate Medical University, Syracuse, NY 13210, USA.
schwartzresearch1@yahoo.com
OBJECTIVE: This study attempted to determine if extended-release venlafaxine is safe for use in severely medically and surgically ill depressed patients. METHOD: The charts of 16 patients who were admitted to medical and surgical inpatient services and given extended-release venlafaxine were retrospectively evaluated for dose and duration of drug treatment, blood pressure changes, medication changes, and side effects. RESULTS: There was 50%-75% improvement in depressive symptoms, with a statistically insignificant mean elevation in blood pressure. CONCLUSIONS: Extended-release venlafaxine appears to be a safe and tolerable agent for the medical-surgical depressed inpatient.
Actas Esp Psiquiatr. 2004 Mar-Apr;32(2):92-7. :
[Venlafaxine extended release for the treatment of chronic pain. A series of 50 cases]
[Article in Spanish]
Galvez R, Caballero J, Atero M, Ruiz S, Romero J.
Unidad de Dolor, Servicio de Anstesia, Hospital Universitario Virgen de las Nieves, Granada.
rgalvez@fundacionhvn.org
INTRODUCTION: The objective of this study is to investigate analgesic effectiveness and safety of venlafaxine extended release in chronic pain of any etiology. METHODS: Six month, observational, open study, carried out in two pain units. Initially, a daily dose of 75 mg of venlafaxine extended release was administered, increasing it to 150 mg, following clinical criteria. Treatment response was measured using the Visual Analogue Scale (VAS), rest and mobilization, Hospital Anxiety and Depression Scale (HAD) and Eastern Cooperative Oncology Group (ECOG) and an adverse event sheet to record adverse events occurring during the study. RESULTS: The study was carried out in a 50 patient sample with a mean age of 57.1 +/- 1.8 years, with chronic pain. A total of 85-90 % of the patients was maintained with a daily dose of 75 mg of venlafaxine extended release. This produced a gradual reduction of the VAS scores at rest (significant reduction of 5.2 +/- 1.1 to 2.7 +/- 1.5 points; (p<0.0005) and mobilization (significant reduction of 5.5 +/- 0.8 to 3.1 +- 1.6 points; p<0.0005). Pain relief increased progressively. Regarding physical activity measured by the ECOG scale, there was a reduction of the percentage of patients and increase of outpatients. Tolerability to venlafaxine was "excellent", "very good" or "good" for 72% of the patients. CONCLUSIONS: Extended release venlafaxine can be an effective and well-tolerated treatment in patients with chronic pain of any etiology, although it must be investigated in depth.
J Clin Psychiatry. 2004 Mar;65(3):328-36. :
Venlafaxine versus placebo in the preventive treatment of recurrent major depression.
Montgomery SA, Entsuah R, Hackett D, Kunz NR, Rudolph RL; Venlafaxine 335 Study Group.
Imperial College School of Medicine, PO Box 8751, London W13 8WH, England, UK.
stuart@samontgomery.co.uk
BACKGROUND: Major depression is often chronic and recurrent, yet most long-term therapeutic trials are not adequately designed to assess antidepressant efficacy in recurrence prevention. Long-term efficacy and safety of prophylactic venlafaxine treatment were evaluated in outpatients with recurrent major depression. METHOD: Patients with a history of recurrent DSM-III-R major depression received open-label treatment with venlafaxine, 100 to 200 mg/day, for 6 months. Those who responded to treatment (Hamilton Rating Scale for Depression [HAM-D(21)] score < or = 12, day 56) and remained relapse-free (no more than 2 HAM-D(21) scores > 10 and no Clinical Global Impressions-Severity of Illness [CGI-S] score > or = 4, months 2-6) either continued taking venlafaxine, 100 to 200 mg/day, or were switched in a double-blind fashion to placebo for 12 months. The primary efficacy outcome was the number of patients experiencing a recurrence of major depression (CGI-S score > or = 4). The cumulative probability of recurrence was calculated using the Kaplan-Meier method of survival analysis. Data were collected from November 1992 through December 1995. RESULTS: Of the 235 patients who enrolled in the recurrence-prevention period, 225 (N = 109, venlafaxine; N = 116, placebo) provided efficacy data. Survival analysis determined a 22% cumulative probability of recurrence in venlafaxine-treated patients after 12 months compared with 55% for the placebo group (p <.001). More than twice as many placebo-treated patients (48%) as venlafaxine-treated patients (21%) discontinued treatment because of lack of efficacy (p <.001). CONCLUSION: Twelve-month maintenance venlafaxine treatment was significantly more efficacious than placebo in preventing major depression recurrence in patients who had been successfully treated with venlafaxine for 6 months.
Psychiatry Clin Neurosci. 2004 Feb;58(1):92-5. :
Venlafaxine in children and adolescents with attention deficit hyperactivity disorder.
Motavalli Mukaddes N, Abali O.
Istanbul University, Department of Child and Adolescent Psychiatry, Istanbul Medical Faculty, Istanbul, Turkey.
nmotavalli@yahoo.com
The primary purpose of this study was to describe tolerability and efficacy of venlafaxine in the treatment of children and adolescents with attention deficit hyperactivity disorder (ADHD). A 6-week open trial of venlafaxine was conducted in 13 children and adolescents (mean age 9.9 +/- 2.5 years) with ADHD, and without comorbid depression. Venlafaxine was initiated at a dose of 18.75 mg/day and flexibly titrated to 56.25 mg/day. The Conners parent scale and Clinical Global Improvement (CGI) severity item were performed at baseline and at the end of the 6-week trial. All subjects completed the trial. Mean final dose of venlafaxine was 40.3 +/- 7.0. Venlafaxine was significantly effective in reducing the total score of the Conners parent scale from baseline to endpoint (P < 0.002, Z =-3.113) and the CGI severity item (P < 0.05). Transient side-effects such as somnolence (n = 2), stomachache (n = 2), and headache (n = 1) disappeared after second week of treatment. Also three subjects complained of sedation after raising the dose to 56.5 mg/day, therefore the dose was reduced to the previous level. These preliminary data suggest that venlafaxine may be an effective medication in the treatment of some children and adolescents with ADHD. Future double-blind controlled trials should be undertaken
Biol Psychiatry 2002 Dec 15;52(12):1166-74
:
Comparative efficacy between venlafaxine and SSRIs: a pooled
analysis of patients with depression.
Stahl SM, Entsuah R, Rudolph RL.
The Neuroscience Education Institute (SMS), Carlsbad, California, USASerotonergic and adrenergic enhancement may be synergistic and more effective
than serotonergic enhancement alone in treating depression. The dual
serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine is a dual reuptake
inhibitor that may therefore offer greater efficacy than selective serotonin
reuptake inhibitors (SSRIs).Data from eight randomized, double-blind, controlled
studies were pooled to compare efficacy in depressed patients receiving
venlafaxine/venlafaxine extended release (XR), SSRIs, or placebo for
Withdrawal reactions associated with venlafaxine.
Parker G, Blennerhassett J.
University of New South Wales, Sydney, Australia.OBJECTIVE: The aim of this paper is to describe discontinuation syndromes
associated with abrupt and tapered withdrawal fo venlafaxine, and to document
that withdrawal symptoms may occur after missing a single dose. CLINICAL
PICTURE: We report on two patients prescribed venlafaxine. One developed a broad
range of serious side effects after reaching a dose of 300 mg a day, and a severe
withdrawal syndrome (including hallucinations) during a slow taper regime. The
second had severe discontinuation symptoms during and aborting a slow taper
regime, and described withdrawal responses after missing a single dose of
venlafaxine. CONCLUSIONS: As for the short-acting selective serotonin re-uptake
inhibitors, severe discontinuation reactions may occur with venlafaxine, seemingly
marked most distinctly by headache, nausea, fatigue, dizziness and dysphoria, and
may make cessation of the drug extremely difficult. Two strategies for addressing
the concern are considered.
J Clin Psychiatry 2002 Jun;63(6):508-12
:
A randomized trial comparing paroxetine and venlafaxine in the
treatment of bipolar depressed patients taking mood stabilizers.
Vieta E, Martinez-Aran A, Goikolea JM, Torrent C, Colom F, Benabarre A,
Reinares M.
Bipolar Disorders Program, Barcelona Stanley Foundation Research Center,
IDIBAPS, Hospital Clinic, University of Barcelona, Spain.
evieta@clinic.ub.esBACKGROUND: The treatment of depressive episodes occurring in bipolar patients
taking mood stabilizers is an understudied area of research with outstanding clinical
consequences. This study was aimed to assess and compare the efficacy and safety
of 2 different antidepressant drugs, paroxetine and venlafaxine, in this indication.
METHOD: Sixty DSM-IV bipolar patients. each presenting with a major depressive
episode while receiving mood stabilizers, were randomly assigned to either
paroxetine (N = 30) or venlafaxine (N = 30) for 6 weeks in a single-blind manner.
They had to score higher than 17 on the 17-item Hamilton Rating Scale for
Depression (HAM-D-17) and have their mood stabilizer blood levels within the
therapeutic range. Efficacy was measured by the HAM-D. Reports of side effects
were collected at each visit; switch to mania or hypomania was specifically assessed
by the Young Mania Rating Scale at 5 of 7 visits. RESULTS: Significant
improvements in HAM-D scores were observed in both paroxetine- and
venlafaxine-treated patients (Wilcoxon p < .0001). There were no significant
differences in either efficacy or safety measures between the 2 drugs. By
intention-to-treat analysis, 43% (N = 13) of patients taking paroxetine and 48% (N
= 14) taking venlafaxine were considered to be responders. Only 3% (N = 1) of
patients switched to hypomania or mania in the paroxetine group, whereas 13% (N =
4) switched in the venlafaxine group. CONCLUSION: Paroxetine and venlafaxine are
both effective and safe in the treatment of depressive breakthrough episodes in
bipolar disorder. There was a suggestion of a slightly higher risk for switch to mania
or hypomania with venlafaxine.
J Affect Disord 2000 Sep;59(3):225-9
:
Venlafaxine monotherapy in women with bipolar II and unipolar
major depression.
Amsterdam JD, Garcia-Espana F.
Depression Research Unit, Department of Psychiatry, University of Pennsylvania
Medical Center, Philadelphia, PA 19104, USA.BACKGROUND: Women with bipolar (BP) disorder have more depressive episodes
and drug-induced manic switches compared to men. Current guidelines suggest
treating BP type I and type II major depressive episode (MDE) with both a
mood-stabilizer and antidepressant. In a post hoc analysis, we examined the safety
and efficacy of venlafaxine monotherapy in women with BP II MDE. METHODS: 15
women with BP II MDE (mean+/-SD age: 37+/-12 years) were compared to 17 women
with unipolar (UP) MDE (41+/-12 years). Patients were randomized to double-blind
treatment with once versus twice daily venlafaxine up to 225 mg for 6 weeks.
Efficacy was measured using the HAM-D(21), MADRS and CGI scales. Drug-induced
manic switch episodes characterized by agitation, irritability, euphoria or mood
lability were assessed at each visit. RESULTS: No episodes of drug-induced
hypomania or rapid cycling were observed during 6 weeks of venlafaxine
monotherapy. Similar efficacy was observed in BP and UP depressed women (p=ns).
LIMITATIONS: This study was retrospective in nature and limited in patient
number. Only BP II women were included in this study, and it is possible that
efficacy and the manic switch rate might have differed if BP I women were
included. CONCLUSION: Short-term venlafaxine monotherapy may be a safe and
effective antidepressant treatment in women with BP II MDE.
J Clin Psychopharmacol 1998 Oct;18(5):414-7
:
Efficacy and safety of venlafaxine in the treatment of bipolar II
major depressive episode.
Amsterdam J.
Department of Psychiatry, University of Pennsylvania Medical Center, Philadelphia,
USA.J Clin Psychopharmacol 1998 Oct;18(5):414-7
Related Articles, Links
Efficacy and safety of venlafaxine in the treatment of bipolar II
major depressive episode.
Amsterdam J.
Department of Psychiatry, University of Pennsylvania Medical Center, Philadelphia,
USA.
Depress Anxiety 2000;12 Suppl 1:45-9
:
Antidepressant efficacy of venlafaxine
.
Golden RN, Nicholas L.
Department of Psychiatry, University of North Carolina School of Medicine, Chapel
Hill 27599-7160, USA.
rgolden@css.unc.eduVenlafaxine is a unique antidepressant medication with well documented efficacy
and safety in the acute treatment of major depressive disorder. Reports suggest
that it may also be effective in the treatment of dysthymic disorder and bipolar II
depression, but the available data for these conditions are more limited compared to
major depressive disorder. Several studies suggest that there may be a more rapid
onset of action for venlafaxine in the treatment of major depression compared to
other antidepressant pharmacotherapies, but this has not been fully established.
Venlafaxine is also effective in the important long term continuation and
maintenance phases of the treatment of depression.
Depress Anxiety 1998;7(2):73-5
:
Use of bupropion with SRIs and venlafaxine.
Spier SA.
University of Maryland School of Medicine, Baltimore 21202-2165, USA.Because of reported efficacy of combining classes of antidepressants, 25 patients
were treated with bupropion in combination with SRI's and venlafaxine. Fifteen
patients inadequately responsive to monotherapy received combination treatment;
ten patients without residual symptoms received adjunctive bupropion to treat SRI-
or venlafaxine-induced side effects. Fourteen subjects (56%) responded, 11 (44%)
did not. Twelve of 15 subjects receiving combination treatment to boost the effects
of monotherapy responded, while only 2 of 10 subjects receiving combination
treatment for side effects responded. Combination therapy was well tolerated even
by geriatric and "medically frail" patients.
Int J Neuropsychopharmacol 2002 Dec;5(4):413-4
:
Venlafaxine and reversible blepharoedema.
Reif A, Pfuhlmann B.
Department of Psychiatry, Julius-Maximilians-University of Wurzburg, Fuchsleinstr.
15, 97080 Wurzburg, Germany.The newer antidepressant venlafaxine is known to cause dilutional hyponatraemia,
but to our knowledge no reports on localized oedemas in the absence of electrolyte
disturbances are available. We present a case in which venlafaxine caused reversible
blepharoedema in an otherwise physically healthy patient. Ms. M., a 25-yr-old women,
suffered from schizoaffective disorder since being 23 years old. Upon
administration of quetiapine, she completely recovered but relapsed twice due to
medical non-compliance, resulting in the third hospitalization. Again, psychotic
symptoms cleared upon prescription of 600 mg quetiapine; further, 45 mg
mirtazapine was given. Quetiapine remained at a stable dose for 10 wk, mirtazapine
for 2 wk; no side-effects were reported by the patient or observed by her
physicians and no other medication was used. As she persistently complained about
depressed mood, loss of motivation and drive, we additionally administered 75 mg of
retarded venlafaxine in the morning. The next day, marked bilateral and symmetric
blepharoedema could be noted which did not ache on palpation, but caused
discomfort on eye movements, generally worrying Ms. M. She had no relevant past
medical history besides her psychiatric disorder, especially no occurrence of allergic
sensitivity, and had never experienced localized oedema. No other oedemas were
present, nor were other medical symptoms. Serum electrolytes were within the
normal range. Believing that venlafaxine caused lid oedema, we discontinued
venlafaxine after the second day; within 24 h, the symptom completely vanished.
J Clin Psychopharmacol 2003 Feb;23(1):27-30
:
A Prospective Trial of Bupropion SR Augmentation of Partial and
Non-Responders to Serotonergic Antidepressants.:
DeBattista C, Solvason HB, Poirier J, Kendrick E, Schatzberg AF.Many patients fail to achieve an adequate response to a given antidepressant trial.
The best-studied augmentation agents, lithium and thyroid supplementation are less
commonly used. Augmenting antidepressants with bupropion has become an
increasingly common strategy in the treatment of resistant depression. Several case
reports and 2 open label studies suggest efficacy of this strategy. The purpose of
this study is to further examine the utility of bupropion sustained release (SR)
augmentation in patients with inadequate response to selective serotonin reuptake
inhibitors. Patients who met DSM-IV criteria for major depression and had failed to
achieve adequate response to an SSRI were considered for this study. Eligible
patients were required to have a score of 16 on the 24-item Hamilton Depression
Rating Scale (HDRS). Patients were treated openly for 6 weeks with bupropion SR
added to their existing antidepressant. The dose range of bupropion was 150 to 300
mg per day. At each visit, patients were assessed using the Beck Depression
Inventory (BDI), the Hamilton Depression Ratings Scale (HDRS), and the Clinical
Global Impression (CGI). Twenty-eight patients (12 men, 16 women) entered the
study. Twenty-five patients completed the six-week trial. With respect to the
clinical benefit of bupropion SR augmentation, 15 out of 28, or 54% of patients,
were classified as responders, showing a decrease in their HDRS or BDI scores of
50% or more between baseline and Week 6. This prospective, open-label trial
supports the use of bupropion SR in the augmentation of SSRIs and venlafaxine.
Placebo controlled trials should be completed to further evaluate the efficacy of
this strategy.
J Clin Psychiatry 2000 Apr;61(4):276-81
:
Antidepressant-induced sexual dysfunction during treatment with
moclobemide, paroxetine, sertraline, and venlafaxine.
Kennedy SH, Eisfeld BS, Dickens SE, Bacchiochi JR, Bagby RM.
Department of Psychiatry, University of Toronto, Centre for Addiction and Mental
Health, Ontario, Canada. sidney_kennedy@camh.netBACKGROUND: Recent reports suggest that adverse effects on sexual function
occur in up to 50% of patients who are treated with selective serotonin reuptake
inhibitor (SSRI) antidepressants. Previously cited low rates were more likely a
function of underreporting than underoccurrence. There is less evidence about
rates of dysfunction with serotonin-norepinephrine reuptake inhibitor (SNRI) and
reversible inhibitor of monoamine oxidase A (RIMA) antidepressants. The purpose
of this report is to evaluate disturbances in sexual drive/desire and arousal/orgasm
in 107 patients who met criteria for major depressive disorder and received
treatment with either moclobemide, paroxetine, sertraline, or venlafaxine.
METHOD: All consenting eligible patients who met DSM-IV criteria for major
depressive disorder completed the Sexual Functioning Questionnaire, version 1
(SFQ) and were assessed using the 17-item Hamilton Rating Scale for Depression
(HAM-D) prior to and after 8 or 14 weeks of antidepressant therapy. Analyses were
carried out to examine the effect of gender, drug type, pretreatment level of
sexual dysfunction, and drug response on reported sexual dysfunction. RESULTS:
Compared with women, men experienced a significantly greater level of drug-related
impairment in drive/desire (p < .05), whereas there were no statistically significant
differences in levels of arousal/orgasm impairment between men and women. The
reported impairment in drive/desire items for men ranged from 38% to 50% and
from 26% to 32% for women. No differences were found across the 4
antidepressants in men, whereas in women, rates of dysfunction were generally
higher with sertraline and paroxetine, but only significantly so in comparison with
moclobemide on some measures (p < .03). Rates of sexual dysfunction with
venlafaxine tended to fall between those of SSRIs and the RIMA agent. An
unexpected relationship was found between favorable drug response and a
decreased level of drug-induced sexual dysfunction. CONCLUSION:
Antidepressant-induced sexual dysfunction occurs in approximately 30% to 70% of
patients who are treated with sertraline or paroxetine. Lower rates are reported
with moclobemide and venlafaxine. Clinicians should evaluate the various aspects of
sexual dysfunction before and during antidepressant therapy.
J Clin Psychopharmacol 2003 Feb;23(1):21-6
:
Single-blind Comparison of Venlafaxine and Nortriptyline in
Elderly Major Depression.
Gasto C, Navarro V, Marcos T, Portella MJ, Torra M, Rodamilans M.The objective of this single-blind study was to compare the efficacy and safety of
venlafaxine extended-release and nortriptyline in elderly patients with moderate to
severe major depression. In- and out-patients (N=68) with unipolar major depression
were randomized to receive 6-month treatment with either nortriptyline or
venlafaxine. Outcomes of the two groups were compared using measures including
the Hamilton Depression Rating Scale (HDRS) and the Newcastle Scale. Side
effects were assessed with the UKU side-effect rating scale. Of the 34
venlafaxine-treated patients, 22 were remitters, 7 were nonremitters, and 5
dropped out. The intent-to-treat remission rate was 71% (22 of 31). Of the 34 who
received nortriptyline, 21 were remitters, 7 were nonremitters, and 6 dropped out.
The intent-to-treat remission rate was 70% (21 of 30). These results suggest that
the remission rate with a therapeutic plasma level of nortriptyline is similar to the
remission rate with a standard dose of venlafaxine in this group of elderly major
depressed patients. No significant differences were observed between dropout
rates in the two groups, but autonomic side-effects were significantly more
frequent for nortriptyline than for venlafaxine. These results confirm the efficacy
and safety of venlafaxine extended-release for treating elderly major depression.
Am J Physiol Gastrointest Liver Physiol 2003
Jan;284(1):G130-7
:
Selective effects of serotonergic psychoactive agents on
gastrointestinal functions in health.
Chial HJ, Camilleri M, Burton D, Thomforde G, Olden KW, Stephens D.
Clinical Enteric Neuroscience Translational and Epidemiological Research Program,
Mayo Clinic, Rochester, Minnesota 55905, USA.This study evaluated the effects of serotonergic psychoactive agents on
gastrointestinal functions in healthy human subjects. Participants received one of
four regimens in a randomized, double-blind manner: buspirone, a 5-HT(1A) receptor
agonist (10 mg twice daily); paroxetine, a selective serotonin reuptake inhibitor (20
mg daily); venlafaxine-XR, a selective serotonin and norepinephrine reuptake
inhibitor (75 mg daily); or placebo for 11 days. Physiological testing performed on
days 8-11 included scintigraphic assessment of gastrointestinal and colonic transit,
the nutrient drink test, and assessment of the postprandial change in gastric volume.
Fifty-one healthy adults (40 females, 11 males) participated in this study. No
effects on gastric emptying or colonic transit were identified with any agent. Small
bowel transit of a solid meal was accelerated by paroxetine. Buspirone decreased
postprandial aggregate symptom and nausea scores. Venlafaxine-XR increased the
postprandial change in gastric volume. Buspirone, paroxetine, and venlafaxine-XR
affect upper gastrointestinal functions in healthy humans. These data support the
need for clinical and physiological studies of these agents in functional
gastrointestinal disorders.
Am J Psychiatry 2003 Jan;160(1):64-75
:
The neural substrates of affective processing in depressed
patients treated with venlafaxine.
Davidson RJ, Irwin W, Anderle MJ, Kalin NH.OBJECTIVE: The purpose of this study was to use functional magnetic resonance
imaging (fMRI) to probe the neural circuitry associated with reactivity to negative
and positive affective stimuli in patients with major depressive disorder before
treatment and after 2 and 8 weeks of treatment with venlafaxine. Relations
between baseline neural activation and response to treatment were also evaluated.
METHOD: Patients with major depressive disorder (N=12) and healthy comparison
subjects (N=5) were scanned on three occasions, during which trials of alternating
blocks of affective and neutral pictorial visual stimuli were presented. Symptoms
were evaluated at each testing occasion, and both groups completed self-report
measures of mood. Statistical parametric mapping was used to examine the fMRI
data with a focus on the group-by-time interactions. RESULTS: Patients showed a
significant reduction in depressive symptoms with treatment. Group-by-time
interactions in response to the negative versus neutral stimuli were found in the left
insular cortex and the left anterior cingulate. At baseline, both groups showed
bilateral activation in the visual cortices, lateral prefrontal cortex, and amygdala in
response to the negative versus neutral stimuli, with patients showing greater
activation in the visual cortex and less activation in the left lateral prefrontal
cortex. Patients with greater relative anterior cingulate activation at baseline in
response to the negative versus neutral stimuli showed the most robust treatment
response. CONCLUSIONS: The findings underscore the importance of the neural
circuitry activated by negative affect in depression and indicate that components
of this circuitry can be changed within 2 weeks of treatment with antidepressant
medication.
Int Clin Psychopharmacol 2003 Jan;18(1):29-33
:
Effect of a pharmacological intervention on quality of life in
patients with obsessive-compulsive disorder.
Tenney NH, Denys DA, Van Megen HJ, Glas G, Westenberg
HG.
Department of Psychiatry, University Medical Centre, Utrecht.Patients with obsessive-compulsive disorder (OCD) not only suffer from
obsessive-compulsive symptoms, but also the disorder is associated with aberrant
social functioning and a diminished quality of life (QoL). Although studies
concerning the effect of treatment interventions on symptoms are common, studies
with regard to the effect of treatment interventions on QoL are scarce. We
examined the effect of a pharmacological intervention on QoL in 150 patients with
OCD. Furthermore, we studied whether two different drugs, venlafaxine and
paroxetine, differed in their effect on QoL. Finally, we examined whether any found
improvement in QoL was related to improvement in symptoms and/or the baseline
self-directedness score, which is one of the character dimensions of the
psychobiological model of Cloninger. We demonstrated that QoL, as assessed with
the Lancashire Quality of Life Profile, improved following pharmacological
intervention, for which paroxetine and venlafaxine appeared to be equally effective.
Furthermore, neither improvement in symptoms, nor baseline self-directedness, was
associated with the improvement in QoL.
J Clin Psychopharmacol 2002 Dec;22(6):561-7
:
Effectiveness of venlafaxine, extended release formulation, in
the short-term and long-term treatment of generalized anxiety
disorder: results of a survival analysis.
Montgomery SA, Mahe V, Haudiquet V, Hackett D.
Imperial College School of Medicine, London, United Kingdom.
SAM@montgomery.demon.co.ukA survival analysis of data from two placebo-controlled, randomized, long-term
(6-month) studies was used to examine the effectiveness of venlafaxine, extended
release (XR) formulation, in patients with generalized anxiety disorder (GAD).
Patients in a placebo-controlled, flexible-dose study received 75 to 225 mg/day
venlafaxine XR, while patients in a placebo-controlled, fixed-dose study received
once-daily venlafaxine XR doses of 37.5 mg, 75 mg, or 150 mg. The survival analysis
was based on the clinician's decision to discontinue treatment in a
placebo-controlled study and incorporated data from all patients who were
randomized. In each study, placebo-treated patients discontinued treatment due to
lack of efficacy more frequently and earlier than those receiving venlafaxine XR (p
< 0.001, log-rank test). A dose-response relationship was apparent, with the lowest
rate of withdrawal seen at the highest venlafaxine XR dose. Survival curves for
discontinuations due to adverse events did not differ significantly in either study.
These results were consistent with the conventional intent-to-treat efficacy
assessments of changes in anxiety severity, highlighting the superiority of
venlafaxine XR over placebo in the long-term treatment of GAD. Overall, these
results demonstrate the clinical effectiveness of venlafaxine XR in the short-term
and long-term treatment of GAD.
J Clin Psychiatry 2002 Nov;63(11):1004-9
:
Venlafaxine versus clomipramine in the treatment of
obsessive-compulsive disorder: a preliminary single-blind,
12-week, controlled study.
Albert U, Aguglia E, Maina G, Bogetto F.
Anxiety and Mood Disorders Unit, Department of Neurosciences, University of
Turin, Italy.BACKGROUND: The objective of this study was to investigate, in a single-blind
manner over a period of 12 weeks, the efficacy and tolerability of venlafaxine
versus clomipramine in the treatment of obsessive-compulsive disorder (OCD).
METHOD: Patients with a DSM-IV diagnosis of OCD and a Yale-Brown Obsessive
Compulsive Scale (YBOCS) score >/= 16 were randomly assigned to receive
venlafaxine, 225 to 350 mg/day (26 patients), or clomipramine, 150 to 225 mg/day
(47 patients), for 12 weeks, with dosage adjustments according to tolerability and
response to treatment. All patients were medication-free from at least 2 months
prior to study enrollment. Efficacy measures were the YBOCS and the Clinical Global
Impressions scale (CGI), which were completed at baseline and every 4 weeks.We
defined responders as patients who had an improvement from baseline in YBOCS
score of >/= 35% and a CGI score
Int Clin Psychopharmacol 2002 Nov;17(6):273-80
:
Two items on the Hamilton Depression rating scale are effective
predictors of remission: comparison of selective serotonin
reuptake inhibitors with the combined serotonin/norepinephrine
reuptake inhibitor, venlafaxine.
Silverstone PH, Entsuah R, Hackett D.
Department of Psychiatry, University of Alberta, Edmonton, Alberta, Canada.Recent studies have shown that the use of subscales derived from the Hamilton
Depression (HAM-D) rating scale are just as reliable and enhance sensitivity for
detecting response and remission after antidepressant treatment. The purpose of
the present study was to determine if the responses on two items of the HAM-D
scale, Depressed Mood (item 1) and Psychic Anxiety (item 10), were predictive of
remission of depression in placebo-controlled studies following treatment with
venlafaxine or selective serotonin reuptake inhibitors (SSRIs). Data from eight
active- and placebo-controlled studies consisting of 2027 subjects who met the
DSM-III-R/-IV criteria for major depressive disorder were analysed. Three
treatment groups were compared: venlafaxine (n =843), SSRI (either fluoxetine,
paroxetine or fluvoxamine, n=743) and placebo (n=441). Treatment duration was 6-8
weeks. Patients who scored zero on the depressed mood and the psychic anxiety
items of the HAM-D17 scale were designated as responders. These two scores were
also combined to create an Absence of Depressive and Anxious Mood (ADAM) score.
Between-group rate comparisons in outcome measures were carried out using
Fisher's exact test and logistic regression models. Venlafaxine treatment improved
depressed mood, psychic anxiety and ADAM scores after 2 weeks with greater
efficacy than treatment with SSRIs or placebo. ADAM scores could also predict the
odds ratio of a patient achieving a clinical remission (defined as total HAM-D17
score
Hum Psychopharmacol 2002 Oct;17(7):335-9
:
Safety and efficacy of high dose of venlafaxine XL in treatment
resistant major depression.
Mbaya P.
Laureate House, Wythenshawe Hospital, Southmoor Road, Wythenshawe,
Manchester, M23 9LT, UK.
nichola.coleman@smuht.nwest.nhs.ukAIM: The aim of the study was to look at efficacy and the safety profile of high
dose (450-600 mg) venlafaxine XL in five patients with treatment resistant major
depressive illness. METHODS: Five patients with treatment resistant depression
were treated with high dose venlafaxine XL. Efficacy was evaluated using the
Montgomery-Asberg depression rating scale (MADRS), the 21-item Hamilton rating
scale for depression (HAM-D-21) and the clinical global impressions (CGI) scale.
Level of functioning was evaluated by social adaptation self-evaluation scale
(SASS). Body weight, supine pulse and blood pressure were recorded. RESULTS: The
response rate was based on a 50% decrease in MADRS and HAM-D scores between
weeks 1 and 24. There was a more than 50% decrease in MADRS scores in 3 of 5
patients and 4 of 5 patients in HAM-D scores. There was a trend to improvement of
SASS scores in three of the study patients and in two of them the mean scores
were within the normal range. Supine pulse and blood pressure remained stable in
four patients, except in one patient where there was a slight increase although the
final reading at week 24 was normal. Weight was relatively stable in all three
patients where it was recorded, but in one patient there was a slight increase which
may have been due to an atypical neuroleptic the patient was taking at the time.
CONCLUSION: High dose venlafaxine was safe, well tolerated and effective in this
small number of severe treatment resistant patients with major depression and it
also improved social functioning.
SNRI
J Affect Disord 2002 Oct;72(1):21-31
:
A randomised, double-blind comparison of milnacipran and
imipramine in the treatment of depression.
Van Amerongen AP, Ferrey G, Tournoux A.
Centre Medico-Psychologique Secteur VI, Centre Hospitalier Intercommunal Poissy
St-Germain-En-Laye, 20, Rue Armagis, 78105 Cedex, St-Germain-En-Laye, France.This multicentre, double-blind, randomised trial in 109 patients compared the
efficacy and tolerance of the novel selective serotonin and noradrenaline reuptake
inhibitor (SNRI) antidepressant milnacipran (50 mg twice daily, n=53) with the
established tricyclic agent imipramine (75 mg twice daily, n=56) over a period of 6
weeks, in patients with major depression (Montgomery-Asberg depression rating
score (MADRS) > or =25). Initiation of antidepressant medication was conducted
during a 2-week period of hospitalisation, after a 3- to 7-day washout period.
Concomitant psychiatric medication was limited to lorazepam, cyamemazine, chloral
hydrate and long-term uncomplicated lithium therapy. Assessment for efficacy using
the MADRS and Hamilton rating scales of depression, a visual analogue scale and
global evaluation revealed both agents to be highly effective (P=0.0001) in this
group of patients. Milnacipran was found to be of similar efficacy to imipramine.
Tolerance, assessed by physiological and biochemical examinations with routine
inventory and spontaneous report of adverse events, revealed a clear advantage for
milnacipran. The incidence of anticholinergic events with milnacipran was about half
that with imipramine and the overall incidence of adverse events by either reporting
method was markedly lower with milnacipran than with imipramine. Furthermore, the
patient drop-out rate with imipramine was double that experienced with milnacipran.
Milnacipran appears to possess equal antidepressant efficacy to imipramine but with
markedly superior tolerance. Therefore, milnacipran constitutes an important new
treatment option in major depression.
Therapie 2002 Jul-Aug;57(4):385-96
:
[Mechanism of action of antidepressants and therapeutic
perspectives]
[Article in French]
Bourin M, David DJ, Jolliet P, Gardier A.
Laboratoire de Neuropharmacologie Upres EAD MENRT, Institut de signalisation et
d'innovation therapeutique (IFR75), Faculte de Pharmacie, Universite Paris-Sud,
Chatenay-Malabry, France.
mbourin@sante.univ-nantes.frDepression is an incapacitating disease which needs appropriate treatment. This
article reviews the pharmacology of antidepressant drugs and the future
perspectives of treating mood disorders such as depression. The foremost theory
for explaining the biological basis of depression has been the monoamine hypothesis.
Depression is due to a deficiency in one or other biogenic monoamines (serotonin,
5-HT; noradrenaline, NA; dopamine, DA). Antidepressant drugs are therefore
classified according to their ability to improve monoaminergic transmission. Since
this first theory, other explanations based on abnormal function of monoamine
receptors or associated with impaired signalling pathways have been suggested.
Notable progress has been accomplished in the treatment of major depressive
disorders with new compounds recently discovered (selective serotonin reuptake
inhibitors: SSRI; serotonin noradrenaline reuptake inhibitors: SNRI). Behavioural,
electrophysiological and microdialysis studies have shown that serotonin (5-HT)
receptors, mainly 5-HT1A, 5-HT1B and 5-HT2C sub-types, exert a key role in
modulating antidepressant activity. Indirect activation of neurotransmitter
receptors by antidepressants may also lead, via increases in endogenous levels of
serotonin in synapses in specific brain regions, to activation of various G proteins
coupled to a receptor, signal of transduction, transcription factors and
neurotrophic factors such as brain-derived neurotrophic factor (BDNF). Thus,
depression may be considered as a transduction mechanism anomaly. This hypothesis
needs to be clarified by molecular biology. Although antidepressants have improved
the therapeutic potential compared to tricyclics (TCA) in terms of reduced side
effects, a number of problems still occur with these drugs. Clinical effects are not
always observed until after this time has elapsed (4-6 weeks) and a substantial
proportion of depressed patients show only partial or no response to
antidepressants. Knowledge of the existence of links between neurotransmitter
systems and the discovery of the most specific target, 5-HT receptors, should lead
to improvements in antidepressant therapy. Developing drugs using innovative
mechanisms such as directly acting on 5-HT receptors (5-HT1A agonists or 5-HT2
antagonists), would appear to be useful in the treatment of depression. The use of
antidepressants in anxiety disorders such as obsessional compulsive disorders and
even generalised anxiety, highlights the distinction between antidepressants and
classic anxiolytics such as benzodiazepines, or even buspirone.
Phys Med Rehabil Clin N Am 2002 Aug;13(3):545-65
:
Diagnostic selective nerve root blocks: indications and usefulness.
Huston CW, Slipman CW.
Orthopedic Clinic, Phoenix, AZ, USA
. cwhuston@aol.comDiagnostic SNRIs are a useful tool in the diagnosis of radicular pain in atypical
presentations. Diagnostic SNRI is indicated in the following circumstances: (1) for
atypical extremity pain; (2) when imaging studies and clinical presentation do not
correlate; (3) when electromyography and MRI are not corroborative or are
equivocal; (4) for anomalous innervations, such [figure: see text] as conjoint nerve
roots or furcal nerves [71]; (5) for failed back surgery syndrome with atypical
extremity pain; and (6) for transitional vertebrae. Patients should have
demonstrated a failure to improve with less invasive treatment. In these patients, a
diagnostic SNRI may localize the pain to a specific spinal nerve. It must be
emphasized that the diagnostic SNRI only determines if pain is emanating from a
specific nerve root or spinal nerve. A diagnostic SNRI does not determine what has
caused the nerve root or spinal nerve pain, nor does it provide prognostic
information. The etiology of the nerve root pain, mechanism of injury, underlying
anatomy, duration of symptoms, comorbidities, patient desire, physician skill, and a
host of other factors determine the appropriate treatment and prognosis.
Depress Anxiety 2002;16(1):4-13
:
Achieving remission with venlafaxine and fluoxetine in major
depression: its relationship to anxiety symptoms.
Davidson JR, Meoni P, Haudiquet V, Cantillon M, Hackett D.
Department of Psychology Behavioral Sciences, Anxiety and Traumatic Stress
Program, Duke University Medicine Center, Durham, North Carolina 27710, USA.
tolme@acpub.duke.eduVenlafaxine, a serotonin and norepinephrine reuptake inhibitor (SNRI), produces
significantly higher remission rates in depressed patients than do the selective
serotonin reuptake inhibitors (SSRIs). In this analysis of pooled data, we explored
the relationship between differences in treatment efficacy, early improvement of
symptoms, and severity of baseline anxiety in depressed patients treated with
either venlafaxine or fluoxetine. A pooled analysis was performed on data from
1,454 outpatients with major depression from five double-blind, randomized studies
comparing the 6-week efficacy of venlafaxine (542 patients) with fluoxetine (555
patients). The Hamilton rating scale for depression (HAM-D) total and item scores
were analyzed at different treatment times up to 6 weeks. Venlafaxine and
fluoxetine both produced statistically significant higher response and remission
rates compared with placebo starting from week 2 for response and weeks 3 to 4
for remission. Venlafaxine was statistically significantly superior to fluoxetine from
week 3 until week 6 in respect of response rate, and from week 2 until week 6 for
remission rate. After 1 week of treatment, greater improvement in individual
symptoms was observed in the depressed mood, suicide, and psychic anxiety items of
the HAM-D scale for both venlafaxine- and fluoxetine-treated patients compared
with placebo. Improvement in psychic anxiety was statistically significantly greater
with venlafaxine than with fluoxetine. The presence of baseline psychic anxiety
correlated significantly to treatment outcome when analyzing the remission rates.
In depressed patients with moderate anxiety (HAM-D psychic anxiety score < or =
2), venlafaxine statistically significantly increased remission rates compared with
placebo from week 4 until week 6, while a significant effect of fluoxetine on
remission rates was observed starting at week 6. Remission rates in the severely
anxious depressed patients (score > 2) were statistically significantly higher with
venlafaxine than placebo starting from week 3 until the end of the study period, but
no difference could be observed between fluoxetine and placebo. Baseline severity
of psychic anxiety had a significant impact on remission rates after treatment of
patients diagnosed with depression. Venlafaxine's superior remission rates in the
more severely anxious patients and its ability to improve psychic anxiety as early as
week 1 compared with fluoxetine suggest that venlafaxine's early efficacy on
anxiety symptoms may be the basis for its superior efficacy in depression. Copyright
2002 Wiley-Liss, Inc.
Meridia (Sibutramine) 15 mg 30 $103.13
Meridia (Sibutramine) 10 mg 30 $79.75
Sibutramine (Meridia) 10 mg 30 $79.75
Sibutramine (Meridia) 15 mg 30 $103.13
meridia-sibutramine
Int J Obes Relat Metab Disord 2001 Dec;25 Suppl 4:S8-11
:
How does sibutramine work?
Lean ME.
Department of Human Nutrition, University of Glasgow, Glasgow Royal Infirmary,
UK.
lean@clinmed.gla.ac.uk
