Odyssey - Paxil titration

[Odyssey]

I have been on Paxil for 12 years. Gradually increasing dosing to 60 mg / day. Sometimes 75 were needed to fifgt depression. Dr agreed to try a different med. I have titrated down to 0 mg of Paxil in one week while adding 20 mg of lexapro the last 4 days. Having increasing dizziness and brain zaps along w short instances of my lips tingling. I fear I am becoming non functional. Didn't work or exercise today. No depression or anxiety, just very dizzy. How long until symptoms weaken? I have a call into my doc

[Odyssey]

Correction. 10mg of lexapro not 20

[Altostrata]

Hello, Odyssey, welcome.

 

As you may have suspected, you have withdrawal symptoms from Paxil. One week is a very fast taper, and Paxil is particularly difficult for withdrawal symptoms.

 

Some people get over withdrawal symptoms in a few weeks, but for others it can take a very long time to recover from withdrawal symptoms, months or even years. The Lexapro may or may not compensate for the disappearance of the Paxil. You can have withdrawal symptoms from one SSRI even when you're on another.

 

Many doctors cross-taper -- gradually introduce the new antidepressant while decreasing the old one -- because they think it is safer.

 

SurvivingAntidepressants offers peer support for going off drugs. We can't offer advice about switching from one to another. You'll have to work out the switching strategy with your doctor.

[dalsaan]

Hi Odyssey,

 

Welcome to the forums. I moved your topic to the introduction section (rather than tapering) given that it is your first post. You can add posts to this thread to keep us updated on how

you are going. Your intro thread is where you share key info about your history, experiences and progress.

 

It is highly likely that what you are experiencing is withdrawal from your very fast taper off Paxil. All of your symptoms are classic withdrawal. You may also be experiencing some adverse reactions to the Lexapro but its impossible to seperate out what is what given you have done both at the same time.

 

We recommend that you taper off no more than 10% at a time and hold 3-4 weeks between dose reductions. There is a lot of info on tapering here tapering FAQ

 

No one can tell you how long they will last. Your symptoms indicate that your system has been thrown into shock and is not coping. Many of us have had to reinstate our medication in order to stabalize our system and then taper off more slowly. Personally, I have never been able to 'see out' the withdrawal symptoms. The longest I lasted was 3 months and my functionality/quality of life were appalling. I was on a different drug to you but we've seen this with every type of antidepressant.

 

Unfortunately Drs are frequently ignorant of withdrawal and the fact that some people need to taper very slowly. If I was you I would look at reinstating the paxil and developing a plan for what you do in the future (keeping in mind that medication can cause depressive symptoms, as can withdrawal)

 

Dalsaan

[Odyssey]

Thanks I will be talking to my specialist tomorrow. I remember having vertigo going off Effexor years ago. I suffered weight gain,diabetes, two stents while on Paxil but no depression or anxiety attacks nice trade off eh? I bike long 5 or 6 days a week and had lost a lot of weight. But feel and can't prove Paxil was a factor in my health

[xDebbiejo]

Hi odyssey

 

Welcome to the site.

 

I too am on Paxil , 16-17 years now.

I followed my docs tapering instructions, was fine for a few weeks after coming off, then all hel broke lose.

 

I had the most horrific withdrawal symptoms, couldn't cope anymore ! Luckily I found this site and reinstated following the advice and support of knowledgeable people on this site

 

I am now on 7mg and stable and will be tapering I guess for another year or so.

 

I hope you find relief soon

 

Debbie x

[Odyssey]

Thanks. I'm at 15mg and may try 7.5 in a couple of weeks. Slow is key here or your receptors freak out

[dalsaan]

Hi Odyssey

 

You're right that slow and steady wins the race. On that basis I would encourage you to rethink your next move. The most we recommend is a 10 percent drop. Given you are on 15mg, you should look at a drop to 13.5 rather than 7.5

 

Kind regards

 

Dalsaan

[areyouthere]

I have been on Paxil for 12 years. I have titrated down to 0 mg of Paxil in one week while adding 20 mg of lexapro the last 4 days. Having increasing dizziness and brain zaps along w short instances of my lips tingling. I fear I am becoming non functional. Didn't work or exercise today. No depression or anxiety, just very dizzy. How long until symptoms weaken? I have a call into my doc

 

No one can tell you how long the symptoms will last.

 

Listen to your gut feelings:

 

I fear I am becoming non functional.

 

 

You have a long(er) history than many with these powerful drugs and so the good is that your gut feeling has a better chance of being correct. Listen to it. The bad is that You have a long(er) history than most with these powerful drugs so MAY be more sensitive to changes......

 

Hi Odyssey

 

You're right that slow and steady wins the race. On that basis I would encourage you to rethink your next move. The most we recommend is a 10 percent drop. Given you are on 15mg, you should look at a drop to 13.5 rather than 7.5

 

Kind regards

 

Dalsaan

 

I am all over in favor with Dalsaan with this. For two reasons.... your nervous system has already been upset by the attempted switch

BTW..... a very gentle reminder to reconsider your attitude toward your doc knowing the perfect path for you to take. Re read what you have written.... it explains itself! and 2) 10 % is the maximum amount suggested here. Some, even at being stable to begin with, are much more sensitive and need to go even slower.

 

I would recommend doing whatever you think you need to do to get stable as soon as you can ( I don't know what to tell you there...I truly am sorry) and then wait for at least a month after you are stable for a month before you even begin another change.... and then a very, very small one.

 

PS. You can and maybe should just read what I have to say and let it in one ear and out the other as I am just beginning. But I have been just beginning at a snail's pace since August 16th and have had to adjust my normally very linear way of thinking. I have learned that there are cornerstones of truth to getting off of these drugs ( don't ask me what they are... that is for the staff here) but we all have to very carefully craft our own milestones and equally as slowly reach for them as they may have to change.

 

SIDE NOTE THREAD JACK......

 

I think Surviving Antidepressants should be written as a fantasy book. It could make millions of dollars. I think it should be called The Habbit ( not Hobbit) and considering the infancy of understanding of this Habbit it could certainly eveolve into a Trilogy and perhaps even become a movie. Since this is Odyssey's post I think The Odyssey of the Habbit should be the name of the first book.

 

Get better Odyssey.....this stuff is no joke. Be careful in your decisions and keep listening to your gut feelings. That would be the Yoda of your mind. sorry.... couldn't help that.

[Altostrata]

Very good joke, areyouthere!

 

I agree with dalsaan, Odyssey. Your system is likely sensitized by your earlier cold turkey, as that's what the cold switch amounted to.

 

Are you off Lexapro now? How did you go off? Did reinstating Paxil relieve your symptoms?

[Odyssey]

I am converting to lexapro so I know I do not fit the format of this site. FYI I have been on 10 mg lexapro since rotating down to 15 mg Paxil. O Paxil was a disaster and 15 took away my dizziness and vertigo. I have no more sexual side effects since reducing Paxil. My goal is 10 mg lexapro and 0 Paxil. Why stay on a ssri? Anxiety attacks and mild depression are non existent for me vs no ssri's at all. Plus lexapro seems sexual side effect neutral. Hopefully weight loss or neutral weight effects will result

[Altostrata]

If someone told you Lexapro has no sexual side effects, you were misinformed. It has the same risk of sexual side effects as other SSRIs.

 

Still, you may react differently to it, so who knows.

[Odyssey]

The Product insert is more promising for lexapro. I have seen the difference. We shall see. I rely on my docs clinical experience. She's a straight shooter and avidly warns me

[Altostrata]

Yes, when Lexapro was first advertised, that was one of the selling points.

 

It turned out to be a lie, as usual.

 

http://www.scientifica.com/2012/965908/

Scientifica Volume 2012 (2012), Article ID 965908, 6 pages

http://dx.doi.org/10.6064/2012/965908

Review Article

Relabeling the Medications We Call Antidepressants

David Antonuccio1,2 and David Healy3

 

Sexual side effects caused by antidepressant medications appear to be a bigger problem than first thought in the original clinical trials. Premarket trials estimated that 2–16% of patients taking SSRIs and SNRIs experienced sexual dysfunction [32]. Montejo et al. [33] examined outpatients (610 women and 412 men) with previously normal sexual function who were being treated with antidepressants from April 1995 to February 2000. All patients were interviewed with the Psychotropic Sexual Dysfunction Questionnaire. Sexual dysfunction was reported by 62% of the men and 57% of the women. Women reported more severe symptoms. Dysfunctions included decreased libido, delayed orgasm, inability to have an orgasm, or decreased arousal. The SSRIs and venlafaxine resulted in the highest rates of dysfunction. Comparable rates of sexual dysfunction have been found in a more recent study [34]. There is even evidence that some patients may experience genital anesthesia or pleasureless orgasm, a problem that for some patients may persist even after the medication is discontinued [32].

....

If we do not call these medications antidepressants, what are some alternative labels that may better fit the existing data? The effect sizes for many of the “side effects” are larger than the antidepressant effect sizes. Using labels like antiaphrodisiac medications, agitation enhancers, insomnia inducers, suicidality inducers, mania stimulators, or gas busters obviously would not offer the same marketing appeal. Though tongue in cheek, we consider these possible labels to be more accurate than the commonly used label of “antidepressant.” It could be argued that the outcomes with the largest effect sizes should be offered as the primary label for a medication....

 

http://www.ncbi.nlm.nih.gov/pubmed/17627739

J Sex Med. 2007 Jul;4(4 Pt 1):917-29.

Changes in sexual functioning associated with duloxetine, escitalopram, and placebo in the treatment of patients with major depressive disorder.

Clayton A, Kornstein S, Prakash A, Mallinckrodt C, Wohlreich M.

 

Source

Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA, USA.

 

Abstract

 

INTRODUCTION:

Depression and antidepressant therapy have been associated with sexual dysfunction in short-term and point-prevalence trials.

 

AIM:

This report describes effects of duloxetine and escitalopram on sexual functioning during acute and long-term treatment of major depressive disorder (MDD).

 

METHODS:

In this 8-month, double-blind, placebo-controlled study, adult outpatients with Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV)-defined MDD were randomized to duloxetine 60 mg/day (N = 273; 173 female), escitalopram 10 mg/day (N = 274; 186 female), or placebo (N = 137; 87 female). After the first 8 weeks of treatment, dose increases were permitted to optimize treatment.

 

MAIN OUTCOME MEASURE:

The 14-item Changes in Sexual Functioning Questionnaire (CSFQ) was used to assess sexual functioning.

 

RESULTS:

Of the 114 patients who did not meet total CSFQ score criteria for global sexual dysfunction at baseline (duloxetine, N = 51; escitalopram, N = 39; placebo, N = 24), the incidence of treatment-emergent sexual dysfunction was significantly higher for escitalopram compared with placebo at 4 and 8 weeks, and significantly higher compared with duloxetine at 4 weeks. At 8 weeks, the incidence of treatment-emergent sexual dysfunction was 17/51 (33.3%) for duloxetine-treated patients; 19/39 (48.7%) for escitalopram-treated patients; and 4/24 (16.7%) for placebo-treated patients (P = 0.01 escitalopram vs. placebo; P = 0.13 duloxetine vs. placebo). After 12 weeks, no significant differences were observed between active drugs. At 8 months, the incidence of treatment-emergent sexual dysfunction was 33.3% for duloxetine, 43.6% for escitalopram, and 25.0% for placebo. Regardless of treatment, patients who achieved remission of MDD showed improvement in global sexual functioning, whereas worsening was observed for patients who did not achieve remission (P < 0.001). Discontinuation rates for sexual side effects did not differ between duloxetine (N = 2) and escitalopram (N = 7) (P = 0.07).

 

CONCLUSIONS:

Short-term treatment demonstrated a higher incidence of treatment-emergent sexual dysfunction with escitalopram compared with duloxetine and placebo. After 12 weeks, there were no statistically significant differences between drugs; however, MDD outcome (regardless of treatment) had a significant impact on improvement in global sexual functioning.

 

________________

http://www.ncbi.nlm.nih.gov/pubmed/22392456

Pharmacotherapy. 2012 Mar;32(3):234-43. doi: 10.1002/j.1875-9114.2011.01020.x.

Distressing adverse events after antidepressant switch in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial: influence of adverse events during initial treatment with citalopram on development of subsequent adverse events with an alternative antidepressant.

Katz AJ, Dusetzina SB, Farley JF, Ellis AR, Gaynes BN, Castillo WC, Stürmer T, Hansen RA.

 

Source

Division of Pharmaceutical Outcomes and Policy, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA. aj_katz@unc.edu

 

Abstract

 

STUDY OBJECTIVE:

To determine whether distressing adverse events (DAEs) experienced during initial antidepressant treatment are associated with subsequent DAEs after switching to a second antidepressant.

 

DESIGN:

Secondary analysis of data from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial.

 

SETTING:

Primary care and psychiatric care facilities.

 

PATIENTS:

A total of 727 outpatients aged 18-75 years with nonpsychotic major depressive disorder who failed first-step therapy with citalopram and were switched to second-step monotherapy with an alternative antidepressant.

 

MEASUREMENTS AND MAIN RESULTS:

In the STAR*D trial, patient-reported DAEs were entered into the Patient-Rated Inventory of Side Effects (PRISE). In this secondary analysis, data from PRISE were used to determine the incidence of DAEs during first-step treatment with citalopram and second-step treatment with sustained-release bupropion, sertraline, or extended-release venlafaxine. Regression models were used to compare the risk of adverse events during second-step treatment between those who reported similar adverse events during first-step treatment and those who did not, while controlling for potential confounders. Of the 727 patients analyzed, DAEs were reported by 514 patients (70.7%) during first-step treatment and 626 (86.1%) during second-step treatment; no significant differences were observed among the three second-step treatment groups. Overall, patients reporting DAEs during first-step treatment were more likely to report DAEs during second-step treatment (risk ratio [RR] 1.11, 95% confidence interval [CI] 1.03-1.20). After controlling for confounders, patients were significantly more likely to report DAEs specific to a body function or organ system, such as those involving the genitourinary system (RR 3.39, 95% CI 2.41-4.78) or sexual functioning (RR 2.75, 95% CI 2.29-3.29), if the patients had reported similar events during initial treatment.

 

CONCLUSION:

Patients who experienced DAEs with initial antidepressant treatment were likely to report similar adverse events after switching to an alternative antidepressant, even when subsequent treatment is from a different class of antidepressants.

 

________________

http://www.ncbi.nlm.nih.gov/pubmed/22299185

Second-Generation Antidepressants in the Pharmacologic Treatment of Adult Depression: An Update of the 2007 Comparative Effectiveness Review [internet].

 

Editors

 

Gartlehner G, Hansen RA, Morgan LC, Thaler K, Lux LJ, Van Noord M, Mager U, Gaynes BN, Thieda P, Strobelberger M, Lloyd S, Reichenpfader U, Lohr KN.

 

Source

Rockville (MD): Agency for Healthcare Research and Quality (US); 2011 Dec. Report No.: 12-EHC012-EF.

AHRQ Comparative Effectiveness Reviews.

 

Excerpt

 

BACKGROUND:

Depressive disorders such as major depressive disorder (MDD), dysthymia, and subsyndromal depression may be serious disabling illnesses. MDD affects more than 16 percent of adults at some point during their lifetimes. Second-generation antidepressants dominate the medical management of depressive disorders. These drugs include selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), and other drugs with related mechanisms of action that selectively target neurotransmitters.

 

OBJECTIVES:

The objective of this report was to compare the benefits and harms of bupropion, citalopram, desvenlafaxine, duloxetine, escitalopram, fluoxetine, fluvoxamine, mirtazapine, nefazodone, paroxetine, sertraline, trazodone, and venlafaxine for the treatment of depressive disorders, including variations of effects in patients with accompanying symptoms and patient subgroups.

 

DATA SOURCES:

We updated a comparative effectiveness review published in 2007 by the Agency for Healthcare Research and Quality searching PubMed, Embase, The Cochrane Library, and International Pharmaceutical Abstracts up to January 2011.

 

REVIEW METHODS:

Two people independently reviewed the literature, abstracted data, and rated the risk of bias. If data were sufficient, we conducted meta-analyses of head-to-head trials of the relative benefit of response to treatment. In addition, we conducted mixed treatment comparisons to derive indirect estimates of the comparative efficacy among all second-generation antidepressants.

 

RESULTS:

From a total of 3,722 citations, we identified 248 studies of good or fair quality. Overall, no substantial differences in efficacy could be detected among second-generation antidepressants for the treatment of acute-phase MDD. Statistically significant differences in response rates between some drugs are small and likely not clinically relevant. No differences in efficacy were apparent in patients with accompanying symptoms or in subgroups based on age, sex, ethnicity, or comorbidities, although evidence within these subpopulations was limited. Differences exist in the incidence of specific adverse events and the onset of action. Venlafaxine leads to higher rates of nausea and vomiting, sertraline to higher rates of diarrhea, and mirtazapine to higher rates of weight gain than comparator drugs. Bupropion causes lower rates of sexual dysfunction than other antidepressants. The evidence is insufficient to draw conclusions about the comparative efficacy and effectiveness for the treatment of dysthymia and subsyndromal depression.

 

CONCLUSIONS:

Our findings indicate that the existing evidence does not warrant the choice of one second-generation antidepressant over another based on greater efficacy and effectiveness. Differences with respect to onset of action and adverse events may be taken into consideration for the choice of a medication.