Jump to content
Altostrata

Shelton, 2001 Steps Following Attainment of Remission: Discontinuation of Antidepressant Therapy

Recommended Posts

Altostrata

As the author admits: "Unfortunately, no drug-specific protocols for discontinuing antidepressants have been established. Prescribing information for each drug typically lacks recommendations for the rate and duration of tapering or criteria for antidepressant discontinuation. A review of the literature on these phenomena, however, shows that a slow taper is uniformly recommended. Inasmuch as antidepressant treatment generally continues for months to years, so should the taper be given adequate time to take effect. Several months may be required, depending on the dose, the pharmacologic profile of the drug, the duration of treatment, and the response of the patient.

 

"Because there has been so little research on the ideal rates for antidepressant discontinuation, published recommendation rates are often vague...."

 

As usual, no definition of "slow taper."

 

Prim Care Companion J Clin Psychiatry. 2001 Aug;3(4):168-174.

Steps Following Attainment of Remission: Discontinuation of Antidepressant Therapy.

Shelton RC.

 

Source

 

Vanderbilt University Medical Center, Nashville, Tenn.

 

Abstract at http://www.ncbi.nlm.nih.gov/pubmed/15014601 Full text here.

 

Depressive disorders require long-term treatment with antidepressants, psychotherapy, or both. The goal of antidepressant therapy is complete remission of symptoms and return to normal daily functioning. Studies have shown that achieving remission and continuing antidepressant therapy long after the acute symptoms remit can protect against the relapse or recurrence of the psychiatric episode. Many patients, however, inadvertently or intentionally skip doses of their antidepressant, and even discontinue it, if their symptoms improve or if they experience side effects. Antidepressant discontinuation may increase the risk of relapse or precipitate certain distressing symptoms such as gastrointestinal complaints, dizziness, flu-like symptoms, equilibrium disturbances, and sleep disorders. Documented with all classes of antidepressants, these reactions may emerge within a couple of days, or even hours, after the abrupt discontinuation of an antidepressant with a short half-life. These distressing responses may be mistaken for a relapse or recurrence. It is important to recognize the potential for these sequelae and educate patients about the need to take all antidepressants at the doses prescribed, warning them of the symptoms that may occur if they skip doses or stop their medication too quickly. Antidepressants should be tapered slowly over a period of days, weeks, or even months, depending on the dose, duration of treatment, and pharmacologic properties of the agent, as well as the patient's individual response. This article reviews the risks and reactions associated with discontinuation of antidepressants. It offers guidelines for distinguishing relapse and recurrence from discontinuation responses as well as for prevention and management of the antidepressant discontinuation syndrome.

Share this post


Link to post
Share on other sites
Barbarannamated

I saw that this article had been referred to in 2 places previously, but not his attention to the 6 to 9 month duration of treatemnt. Wasn't sure where to comment, so posted full text here with some highlighting. Taper rates are ridiculously short. I disagree w/his comment about differentiating relapse. Sorry if this has all been discussed previously.

 

WHEN TO DISCONTINUE ANTIDEPRESSANT THERAPY, RISKS ASSOCIATED WITH DISCONTINUING ANTIDEPRESSANT THERAPY

ANTIDEPRESSANT DISCONTINUATION: RECOMMENDATIONS FOR DOSAGE TAPERINGPREVENTION AND MANAGEMENT OF DISCONTINUATION SYMPTOMS

 

Shelton -discontinue after 6 to 9 month of treatment

 

I like the way he addresses how long to continue AD therapy:

 

Pharmacologic therapy should be continued long enough to sustain remission and avoid relapses and recurrences. Relapse refers to a return of symptoms during the time in which the original depressive episode would have been expected to last (4–9 months). Recurrence refers to a return of depression at a time beyond the expected duration of the index episode (> 9 months after remission). This means that physicians and patients alike should not be too eager to discontinue medication prematurely. An interval of 6 months has been thought to be the usual duration of antidepressant therapy. New recommendations, however, suggest that treatment should continue for up to 9 months after symptoms have resolved (continuation phase) to prevent relapse and for longer to help prevent recurrence (maintenance phase).3 Some experts maintain that antidepressant treatment should continue for 3 to 5 years and possibly for life.

Steps Following Attainment of Remission: Discontinuation of Antidepressant Therapy

Richard C. Shelton, M.D.From the Vanderbilt University Medical Center, Nashville, Tenn.

Reprint requests to: Richard C. Shelton, M.D., Vanderbilt University Medical Center, 1500 21st Avenue South, Suite 2200, Nashville, TN 37212-8646 (e-mail: richard.shelton@mcmail.vanderbilt.edu).

Received May 14, 2001; Accepted June 28, 2001.

 

Depressive disorders require long-term treatment with antidepressants, psychotherapy, or both. The goal of antidepressant therapy is complete remission of symptoms and return to normal daily functioning. Studies have shown that achieving remission and continuing antidepressant therapy long after the acute symptoms remit can protect against the relapse or recurrence of the psychiatric episode. Many patients, however, inadvertently or intentionally skip doses of their antidepressant, and even discontinue it, if their symptoms improve or if they experience side effects. Antidepressant discontinuation may increase the risk of relapse or precipitate certain distressing symptoms such as gastrointestinal complaints, dizziness, flu-like symptoms, equilibrium disturbances, and sleep disorders. Documented with all classes of antidepressants, these reactions may emerge within a couple of days, or even hours, after the abrupt discontinuation of an antidepressant with a short half-life. These distressing responses may be mistaken for a relapse or recurrence. It is important to recognize the potential for these sequelae and educate patients about the need to take all antidepressants at the doses prescribed, warning them of the symptoms that may occur if they skip doses or stop their medication too quickly. Antidepressants should be tapered slowly over a period of days, weeks, or even months, depending on the dose, duration of treatment, and pharmacologic properties of the agent, as well as the patient's individual response. This article reviews the risks and reactions associated with discontinuation of antidepressants. It offers guidelines for distinguishing relapse and recurrence from discontinuation responses as well as for prevention and management of the antidepressant discontinuation syndrome.

 

Major depression is a chronic condition with a naturally fluctuating course. Eventually, symptoms recur in half or more of patients.1,2 Numerous classes of antidepressant agents can successfully reduce depressive symptoms within several weeks, but this early improvement represents an acute response to treatment rather than a true remission.The goal of antidepressant therapy is not just to reduce or eliminate the acute symptoms but also to achieve full remission—i.e., the complete relief of symptoms and the restoration of social and occupational functioning—and to maintain remission for as long as possible.2–4 Studies have shown that long-term use of antidepressants can protect against relapse (an early return or worsening of symptoms) and recurrence (later episodes occurring after remission) of depressive symptoms.4–6 Evidence also shows that recurrences are more common and develop earlier in patients who continue to experience residual symptoms than in patients who have achieved full remission.7,8 Discontinuation of antidepressant treatment too soon after an initial acute response may, therefore, increase the risk of relapse or recurrence.3,4Antidepressant discontinuation at any stage of treatment can cause a variety of somatic and psychological reactions, especially if the withdrawal is abrupt. Although first identified 30 years ago with tricyclic antidepressants (TCAs), these symptoms are not unique to TCAs, having now been documented with all classes of antidepressants, including monoamine oxidase inhibitors (MAOIs), the serotonin reuptake inhibitors (SRIs) and selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and atypical agents (e.g., trazodone).4,9 Discontinuation symptoms are often associated with rapid withdrawal, but they have been reported with gradual dose tapering and even after 1 or 2 skipped doses.This review examines current recommendations for long-term maintenance therapy with antidepressants as well as the timing and rate of discontinuation. It also outlines the symptoms associated with discontinuation of antidepressants, their possible mechanisms, and recommendations for preventing or managing the antidepressant discontinuation syndrome. Other Sections▼

 

At some point in the treatment of mood disorders, the question of when to stop antidepressant treatment arises. Patients or physicians may opt to stop treatment after a symptomatic response is seen, after remission is achieved, after remission and functional improvements have been maintained for a reasonable amount of time, or when intolerable side effects occur or appear to outweigh the benefits of the drug.Since true remission, rather than partial symptomatic response, is the therapeutic goal, it is essential to determine if remission has occurred before stopping treatment. The severity of depression and the response to antidepressant therapy are assessed with a number of tools. The Hamilton Rating Scale for Depression (HAM-D) and the Clinical Global Impressions-Severity and -Improvement scales (CGI-S and CGI-I, respectively) are commonly used. Generally, a 50% reduction in the baseline HAM-D score and a CGI-I score of 1 (very much improved) or 2 (much improved) are considered to represent a good response to antidepressant treatment. However, these criteria may document symptomatic improvement but not necessarily remission. Minor symptoms may remain, increasing the risk of recurrence.3 More stringent criteria have been proposed that distinguish true remission from acute symptomatic response or a placebo response. These new remission criteria require a HAM-D score of ≤ 7 (considered a return to normal functioning) and a CGI-I score of 1. The Sheehan Disability Scale may be used to assess improvements in function, with a score of ≤ 1 (mild disability) indicating a complete return to normal functioning in family, social, and work situations.3 The Psychiatric Status Rating Scale may be used to evaluate recovery. Scores on this scale range from 1 (usual self, normal, no symptoms) to 6 (meets criteria for prominent symptoms or severe functional impairment). These and similar scales can be used in clinical practice to determine the return of normal functioning. The principle is that clinicians need to evaluate motivation and performance just as they would any other symptoms, such as sleep disturbance.Pharmacologic therapy should be continued long enough to sustain remission and avoid relapses and recurrences. Relapse refers to a return of symptoms during the time in which the original depressive episode would have been expected to last (4–9 months). Recurrence refers to a return of depression at a time beyond the expected duration of the index episode (> 9 months after remission). This means that physicians and patients alike should not be too eager to discontinue medication prematurely. An interval of 6 months has been thought to be the usual duration of antidepressant therapy. New recommendations, however, suggest that treatment should continue for up to 9 months after symptoms have resolved (continuation phase) to prevent relapse and for longer to help prevent recurrence (maintenance phase).3 Some experts maintain that antidepressant treatment should continue for 3 to 5 years and possibly for life.1Like all drugs, antidepressants may cause a variety of side effects that in some cases are severe enough to necessitate a quick discontinuation and a switch to another medication.1 Side effects, or the fear of side effects, may prompt patients to delay filling their antidepressant prescription or stop taking it as soon as their depressive symptoms begin to abate. Many patients take their antidepressant for 14 weeks or less.10 The effects of antidepressant treatment, however, may not be fully evident for 6 to 8 weeks, and long-term treatment is needed to ensure complete recovery and to prevent recurrence. Nevertheless, patients who are experiencing adverse reactions may be apt to discontinue their antidepressant prematurely, never achieving full remission and increasing their risk of relapse or of discontinuation reactions.

 

The major risks after discontinuing an antidepressant include relapse or recurrence and discontinuation symptoms. These are quite distinct phenomena, with different causes and management implications.

Relapse or Recurrence

Long-term antidepressant treatment can prolong remission and protect against recurrence.1,4–6 Discontinuing antidepressant treatment is associated with a shorter time to relapse and an increased incidence of recurrence.1,10 One factor that appears to increase the risk of relapse is the persistence of residual symptoms.7,8 In one 10-year follow-up of patients with major depressive disorder, those with residual symptoms had a recurrence 5 times sooner than did those who had achieved asymptomatic status; the asymptomatic patients experienced fewer relapses and longer symptom-free intervals.2 Other factors predicting risk of relapse include a history of chronic depression11 and a history of multiple prior episodes.12 In a study of 141 patients diagnosed with major depressive disorder, those patients with 3 or more prior episodes had significantly shorter intervals from recovery to relapse than did patients having fewer than 3 prior depressive episodes.12Age also is a predictive factor for recurrence: patients who had their first episode at an older age tend to relapse sooner than younger patients.1,12,13 Another factor that increases the likelihood of recurrence is the concurrent presence of substance abuse or comorbid anxiety disorder.11 A depressive relapse is more likely in the first weeks and months after recovery, with the risk declining with time.11,12 Continuing treatment is, therefore, especially crucial immediately after the acute resolution of symptoms.

 

Discontinuation SymptomsDiscontinuing antidepressant medications can precipitate a variety of somatic and psychological reactions in patients. These reactions, often termed antidepressant withdrawal or discontinuation syndrome, have been noted with all classes of antidepressant agents including TCAs, MAOIs, SRIs, SSRIs, and SNRIs. Since antidepressants are not addictive agents and do not directly evoke the brain reward systems, the term “discontinuation” is preferred over “withdrawal” when describing these symptoms. Although discontinuation symptoms are most often associated with the abrupt discontinuation of an antidepressant, they have been reported during gradual tapering and intermittent noncompliance as well.Other risk factors associated with discontinuation reactions were reviewed by Lejoyeux and colleagues.14 These include the use of concurrent long-term medications such as antihypertensives, anticonvulsants, and antihistamines. Antidepressant treatment lasting 2 months or more and, in some reports, young age were also factors.14Table 1 lists some of the symptoms associated with the discontinuation of TCAs and SRIs.15,16 Although much of the evidence for the discontinuation syndrome comes from case reports, controlled clinical trials involving the abrupt switch from active antidepressant to placebo also have documented the occurrence of these reactions.17 Table 1.

Common Discontinuation Symptoms With Tricyclic Antidepressants and Serotonin Reuptake Inhibitorsa

 

It is especially important to recognize the symptoms of discontinuation and distinguish them from relapse and recurrence because a misdiagnosis may lead to unnecessary tests, useless treatments, and increased costs.18Gastrointestinal complaints are common, with patients frequently suffering from nausea, vomiting, abdominal pain and distention, and diarrhea.19,20 General somatic symptoms (e.g., sweating, lethargy, headaches, and a flu-like syndrome of chills, aches, and headaches), affective symptoms (e.g., anxiety, low mood), and sleep disorders (e.g., insomnia, vivid dreaming) are characteristic. Dizziness, balance problems, and sensory disturbances are also widely recognized with SSRI discontinuation.16,19,20 Mania or hypomania, movement disorders such as parkinsonism and akathisia, and cardiac arrhythmias also have been reported with antidepressant cessation but are not as common as the mood, somatic, and sleep problems.9,14,16,24The symptoms of discontinuation, although usually mild and transient, can range widely in severity.15 Although the true incidence of discontinuation phenomena has not been established, these symptoms are believed to be common but not universal.22 Some patients may be genetically or temperamentally more susceptible to these responses, while other patients may be better able to tolerate them.23Class-Specific Symptoms

Discontinuation symptoms differ among the antidepressant classes and even among the individual drugs within each class owing to the different mechanisms of action and the pharmacologic properties of the individual drugs.TCAs.

TCA discontinuation reactions have been reported within hours of even 1 missed dose of imipramine.15 Typical responses to TCA discontinuation include abdominal pain, anorexia, nausea, vomiting, diarrhea, chills, fatigue, and weakness.14 The symptoms of TCA discontinuation, believed to be related in part to an adaptive hypersensitivity of muscarinic cholinergic receptors, are called cholinergic rebound or cholinergic overdrive. Long-term administration of TCAs blocks muscarinic cholinergic receptors in the human caudate,14,24 leading to a compensatory increase in the number of postsynaptic muscarinic receptors (up-regulation) and thus a supersensitivity to muscarinic agonists. Stopping the TCA unmasks this supersensitivity and may also disrupt the cholinergic-dopaminergic balance, contributing to the signs of parkinsonism and other balance disturbances that may occur with TCA discontinuation.14 Similar to SSRIs, most SRIs and TCAs can produce discontinuation symptoms.

 

MAOIs.

Discontinuation of MAOIs may cause severe and serious adverse events, including various types of cognitive impairment, aggression, catatonia, insomnia, irritability, paranoid delusions, depressed mood, and hallucinations (Table 2).14 These drugs down-regulate α2-adrenergic and dopaminergic receptors and possibly affect cholinergic receptors as well. MAOI withdrawal may stimulate the excessive release of both dopamine and norepinephrine via the removal of agonist activity on catecholamine receptors. Therefore, the symptoms can resemble those of amphetamine withdrawal.14,25,26 In 1 report, reducing the dose of tranylcypromine precipitated depressive episodes that were said to be worse than the depression for which the 5 patients were being treated; discontinuation also caused cognitive disturbances.27 Table 2.

Symptoms Reported After MAOI Discontinuationa

 

SRIs and SSRIs.

The SRIs and SSRIs block serotonin reuptake, increasing the amount of synaptic serotonin; this increase in available serotonin leads to a compensatory decrease in the number of some postsynaptic serotonin receptors (down-regulation).17 When the SSRI is discontinued abruptly, reuptake is reestablished (and possibly enhanced transiently), lowering the amount of available serotonin within the synapse. The resulting reduced concentration of available serotonin, plus the receptor down-regulation, causes clinical signs of serotonin deficiency. Since serotonin interacts with numerous other neurotransmitter systems, its deficiency has the potential to disrupt many other neuronal functions.SSRI discontinuation symptoms are similar to those of the TCAs, with dizziness, gastrointestinal symptoms, and sleep disorders common. Anecdotal reports have included complaints of “electric shock–like” sensations, flashes, and “withdrawal buzz.”15,17,18,23–26,28–32 The type and severity of the symptoms correlate with the relative affinities of the agents for the serotonin reuptake sites and with secondary effects on other neurotransmitters; with SRIs that also affect cholinergic systems, the symptoms possibly correlate with cholinergic rebound.Sudden discontinuation is a particular problem with agents that have a relatively short half-life, which include the SSRI paroxetine and the SNRI venlafaxine. With these types of drug, the symptoms can last up to 2 weeks.29 A randomized clinical trial reported that in the 5 to 8 days after discontinuation of an SSRI, symptoms were most common with paroxetine—the most potent SSRI and one with a short half-life—and least common with fluoxetine—an SSRI with a lower serotonin reuptake affinity and a longer half-life.31 Reactions to sertraline were mild and infrequent. However, this trial was designed to simulate intermittent noncompliance and did not attempt to document late-emerging effects that might occur with a drug with a long half-life, such as fluoxetine. There have been reports of symptoms starting 25 days after fluoxetine withdrawal with some persisting as long as 56 days.29 Late reactions to fluoxetine cessation may be reported less often because trials do not follow patients long enough after withdrawal to observe them. Further, the symptoms may be mild and patients may not attribute general symptoms such as flu-like complaints, dizziness, or sleep disturbances to a drug they had stopped taking weeks earlier.29In addition to its effects on serotonin reuptake, paroxetine affects muscarinic receptors, and its withdrawal could contribute to symptoms of cholinergic rebound, a mechanism usually not attributed to other SSRIs.23 One case report of a patient discontinuing low-dose paroxetine (10 to 20 mg/day) noted symptoms that were very disabling initially and lasted longer than the 5 to 15 days mentioned in the prescribing information. The responses included agitation, anorexia, nausea and diarrhea, vertigo and dizziness, paresthesia, and a shaking chill.30 Sertraline, which like paroxetine is associated with a higher occurrence of discontinuation reactions, is the only SSRI that strongly blocks dopamine reuptake as well as serotonin-reuptake sites.23 Further, discontinuation symptoms with sertraline, although usually mild, may be related to its effect on both dopamine and serotonin reuptake.SNRIs.

The therapeutic effectiveness of the SNRI venlafaxine is related to its dual inhibition of serotonin and norepinephrine reuptake. These actions stimulate a down-regulation of serotonergic and adrenergic receptors. Venlafaxine also weakly inhibits dopamine reuptake but has no significant affinity for muscarinic, histaminergic, or adrenergic receptors. Considering its relative lack of affinity for muscarinic cholinergic receptors, discontinuation symptoms associated with venlafaxine are probably not attributed to a cholinergic rebound phenomenon.33A decrease in venlafaxine dose over 4 days to 2 weeks in a small sample of patients caused a flu-like syndrome with muscle pain, headaches, nausea, and dizziness.34 Eight patients in an open-label study reported discontinuation symptoms of rebound anxiety, vertigo, headache, nausea, tachycardia, tinnitus, and akathisia starting about 12 hours after discontinuing venlafaxine. For most patients, the dose was reduced gradually over 7 to 14 days, and the symptoms peaked in severity 4 days after the complete discontinuation before gradually dissipating.28Distinguishing Discontinuation Syndrome From Relapse and Recurrence

The nature of the symptoms and the time course of their emergence can help in distinguishing discontinuation syndrome from relapse or recurrence. Discontinuation reactions may be physical as well as psychological, and they are usually not attributable to other causes. A distinctive symptom of discontinuation is dizziness, which is not characteristic of relapse and can often therefore be used in making the differentiation.35 Although discontinuation responses are generally mild, they can be severe, interfering with home, work, and daily activities such as driving. If symptoms of discontinuation emerge, they can be reversed by restarting the original antidepressant or a similar medication, which should then be slowly tapered to minimize the recurrence of the symptoms. Symptoms of relapse or remission are not so readily reversed.The time course of the appearance of the symptoms also gives a clue as to their origin. Discontinuation-emergent reactions occur after abrupt discontinuation of the antidepressant or frequently missed doses, although they may occur as the dose is being reduced.32 The symptoms emerge within a couple of days—sometimes hours—of discontinuation and gradually remit over a few days to 2 weeks. In contrast, relapse or recurrence typically takes 2 or 3 weeks or longer after the medication is discontinued to emerge, and these events are heralded by worsening depression, insomnia, and psychomotor symptoms.18Owing to their antidepressant and anxiolytic properties, newer antidepressant drugs such as the SSRIs and SNRIs also are being widely prescribed for anxiety disorders. The SSRIs have demonstrated efficacy for several anxiety disorders, including obsessive-compulsive disorder, panic disorder, generalized anxiety disorder (GAD), and social anxiety disorder.36 Venlafaxine XR (extended release) and paroxetine are the only antidepressants to receive U.S. Food and Drug Administration (FDA) approval for the treatment of GAD. The antidepressant and anxiolytic efficacy of these drugs can be attributed to their serotonin reuptake properties, which relate to their propensity for discontinuation effects. The relative contribution of the noradrenergic action of venlafaxine XR to its anxiolytic effect is unclear.37,38 It is not known whether discontinuing these medications among patients with anxiety disorders will result in the same somatic and psychological reactions as seen in patients with depression. Further research is needed. Other Sections▼

Abstract

 

Unfortunately, no drug-specific protocols for discontinuing antidepressants have been established. Prescribing information for each drug typically lacks recommendations for the rate and duration of tapering or criteria for antidepressant discontinuation. A review of the literature on these phenomena, however, shows that a slow taper is uniformly recommended.14,15,18 Inasmuch as antidepressant treatment generally continues for months to years, so should the taper be accorded adequate time to take effect. Several months may be required, depending on the dose, the pharmacologic profile of the drug, the duration of treatment, and the response of the patient.15Because there has been little research on the ideal rates for antidepressant discontinuation, published recommendations for taper rates are often vague.39 Consequently, the magnitude and speed of the dose reduction are often left to clinical judgment. Some specific recommendations have been reported (Table 3).14,18,25,40 For example, MAOI dosages should not usually be reduced by more than 10% per week, and patients should be monitored carefully. TCAs should be reduced with great care over at least 2 to 3 months; if symptoms occur, the dose should be increased and the taper started again at a slower rate. With TCAs, it may be advisable to slow the taper even more near the end of the discontinuation phase.14 Table 3.

 

Gradual Taper Rates for Antidepressantsa

Since the therapeutic dosage levels of individual SSRIs vary so widely, their taper rate varies as well; however, gradual tapering also is recommended for this group of agents. A long half-life itself may provide a form of self-tapering but is not an absolute protection against discontinuation symptoms. For venlafaxine, even a taper regimen lasting 7 to 14 days induced symptoms of discontinuation in several patients in 1 of the clinical trials. The investigators therefore recommended that the drug be reduced over a minimum of 2 to 4 weeks (the prescribing information recommends a 2-week tapering for any patient treated for more than 1 week).28 Recently, the British National Formulary recommended a 4-week gradual dose reduction for any antidepressant prescribed for 2 months or more.19 The final step in the dosage taper may be lower than the minimum therapeutic or the initial treatment dose.

 

Prevention is the best strategy for avoiding or minimizing discontinuation symptoms. Since some cases of discontinuation syndrome are due to missed doses or premature discontinuation by the patient, the first management goal is patient education. At the initiation of treatment, patients need to understand the chronic nature and fluctuating course of their symptoms and know that their symptoms will probably regress slowly over time. They should not consider symptom improvement as a cure, nor should they interpret the persistence of minor symptoms as a sign that treatment is ineffective. The goal of remission should be emphasized during patient encounters, and the need to continue treatment for months or even years should be explained thoroughly. As their symptoms remit and they begin to feel better, patients may wonder why they should continue taking their medication, especially if they are experiencing adverse reactions to the antidepressant. They may pressure their physicians into considering discontinuation of the drug. Since premature discontinuation can lead to both relapse and discontinuation reactions, the physician should ensure that patients understand that they must continue to take their medication, in the doses prescribed, for as long as necessary to achieve a true remission and avoid or delay recurrence. Antidepressant “vacations” should be discouraged, especially with antidepressants that have a short half-life, as even brief interruptions in therapy may precipitate an episode of discontinuation reactions.16 Patients suffering from discontinuation symptoms may attribute them to a direct side effect of the antidepressant and resist restarting the medication.Physicians must consider the possibility of noncompliance when they encounter symptoms that might be related to antidepressant discontinuation. Asking patients if they have missed any doses may help avoid unnecessary tests and treatments as well as help initiate a discussion of the risks associated with stopping medication prematurely. Knowing the nature and duration of symptoms, plus obtaining information about noncompliance, can help differentiate discontinuation reactions from side effects and recurrences.

 

Discontinuation symptoms occur even with a careful and gradual taper. They can be managed with several options. For mild symptoms, education and reassurance may be adequate.18 Symptoms can be reversed by restoring the antidepressant (or starting a similar antidepressant) and starting the taper again, reducing the dose in smaller increments during longer intervals. If restarting the antidepressant is not feasible for safety or tolerability reasons, other agents may be used to relieve the symptoms. Anticholinergic agents (e.g., benztropine, trihexyphenidyl) will improve the gastrointestinal symptoms, anxiety, sleep problems, and somatic reactions associated with the discontinuation of anticholinergic drugs such as the TCAs.Anxiety can be managed with a benzodiazepine and dizziness relieved with motion sickness agents (e.g., meclizine, dimenhydrinate). Propranolol can be used for akathisia, benzodiazepines for dyskinesia, and anticholinergic agents or antihistamines for dystonia, should these more serious reactions occur.

Gastrointestinal complaints, dizziness, flu-like symptoms, sleep disorders, balance and sensory disorders, affective symptoms, and other reactions have been seen with the discontinuation of all classes of antidepressants. Antidepressant discontinuation symptoms typically emerge within a few days of drug discontinuation. Although sometimes very distressing, the symptoms are rarely serious and will dissipate within about 2 weeks. Reactions to MAOI withdrawal, however, may be more severe. Discontinuation symptoms can best be prevented or minimized by allowing neural adaptation to the loss of the drug to occur gradually, with careful and deliberate drug tapers over a few weeks to a few months. Specific discontinuation protocols for some of the new antidepressants such as venlafaxine may be found in the prescribing information published in the Physicians' Desk Reference.40

However, until data from systematic controlled studies are available, the case report literature offers some insight and suggestions, however vague, on the management and prevention of discontinuation symptoms.More controlled studies on this common phenomenon are needed. For now, physicians must remind patients who suffer from depressive and anxiety disorders that the goal of antidepressant therapy is remission and that definite and immediate risks are associated with abruptly stopping antidepressant therapy, even for brief periods, or prematurely discontinuing treatment. Therefore, it is important for psychiatrists and primary care physicians to question patients about emerging discontinuation symptoms to ensure optimal management of treatment discontinuation and to prevent the emergence of additional discontinuation symptoms.Drug names: benztropine (Cogentin and others), fluvoxamine (Luvox), fluoxetine (Prozac and others), meclizine (Antivert, Bonine, and others), paroxetine (Paxil), phenelzine (Nardil), propranolol (Inderal and others), sertraline (Zoloft), tranylcypromine (Parnate), trazodone (Desyrel and others), trihexyphenidyl (Artane and others), venlafaxine (Effexor).

FootnotesSupported by an unrestricted educational grant from Wyeth-Ayerst Laboratories, Philadelphia, Pa.

Dr. Shelton has received grant/research support from Eli Lilly, Glaxo, Janssen, Pfizer, Roehn-Polenc-Rorer, Sanofi, SmithKline Beecham, Wyeth-Ayerst, Zeneca, and Abbott; is a paid consultant for Pfizer and Janssen; and serves on the speakers bureau for Bristol-Meyers Squibb, Eli Lilly, Janssen, Pfizer, SmithKline Beecham, Solvay, Wyeth-Ayerst, and Abbott. Other Sections▼

AbstractWHEN TO DISCONTINUE ANTIDEPRESSANT THERAPYRISKS ASSOCIATED WITH DISCONTINUING ANTIDEPRESSANT THERAPYANTIDEPRESSANT DISCONTINUATION: RECOMMENDATIONS FOR DOSAGE TAPERINGPREVENTION AND MANAGEMENT OF DISCONTINUATION SYMPTOMSCONCLUSIONREFERENCESREFERENCES1.Keller MB, Lavori PW, Mueller TI, et al. Time to recovery, chronicity, and levels of psychopathology in major depression: a 5-year prospective follow-up of 431 subjects. Arch Gen Psychiatry. 1992;49:809–816. [PubMed]

Share this post


Link to post
Share on other sites
Altostrata

Could it be any more confusing? No wonder most doctors just give up and keep their patients on drugs forever.

Share this post


Link to post
Share on other sites
Barbarannamated

Could it be any more confusing? No wonder most doctors just give up and keep their patients on drugs forever.

 

This is definitely confusing. It has some nuggets that I haven't seen published before. Most of the citations are pre-2000 and then research *appeared* to be drop off. This was published in Primary Care Companion, but not in any Psych journals. ?? And funded by Wyeth.

I think he's using a 'meta-analysis' to say as much as he can and be published. It comes across as though he's throwing everything at the wall to see what sticks. He doesn't have evidence in the form of RCTs, but is planting alot of seeds 'for future research'. He says alot of what David Healy has said online but not been able to publish (that I can find). I've been critical of ones who seem to know, but haven't published. But realized it's not their choice in what gets published. They can submit, but control is with the journals. even ones not supported by advertising. And he's at Vanderbilt who may exert more control. IRBs can be brutal.

 

In reading his other areas of research and publications (including lay articles not in favor of ADs), he seems to be trying to fly under the radar while still get some info out and encourage more research. Playing the political game, so to speak. JAMA article - AD Effects and Depression Severity (Jan. 6, 2010). Link to come.

 

Shelton - Antidepressant Effects and Depression Severity

Share this post


Link to post
Share on other sites
Barbarannamated

It is definitely not a how-to manual on tapering. The first part of the title is the key part: that remission can be attained and therapy is not 'for life' as many patients are told.

 

I especially like where he says that DC symptoms occur in patients 'after 4 months of therapy'.

He is screaming "read between the lines!"

Share this post


Link to post
Share on other sites
Altostrata

He did that for a while. He popped up here and there in news articles warning about the dangers of Paxil withdrawal. Some of us thought he might have a guilty conscience.

 

You are absolutely right the journal article tune changed after 2000. That's when a huge Paxil lawsuit was settled for the plaintiffs. As a result, the FDA put the withdrawal warning on Paxil (December 2001) and other antidepressants.

 

Clearly, this was not good for business. We can surmise from Shelton's publications that after that, his charge from pharma sponsors was more clear. And what to make of his partnership with Schatzberg as Schatzberg was being disciplined for conflict of interest?

 

You've got the scent, Bar. Good hunting.

Share this post


Link to post
Share on other sites
Barbarannamated

What's the saying?

Keep your friends close and ...

Share this post


Link to post
Share on other sites
btdt

He did that for a while. He popped up here and there in news articles warning about the dangers of Paxil withdrawal. Some of us thought he might have a guilty conscience.

 

You are absolutely right the journal article tune changed after 2000. That's when a huge Paxil lawsuit was settled for the plaintiffs. As a result, the FDA put the withdrawal warning on Paxil (December 2001) and other antidepressants.

 

Clearly, this was not good for business. We can surmise from Shelton's publications that after that, his charge from pharma sponsors was more clear. And what to make of his partnership with Schatzberg as Schatzberg was being disciplined for conflict of interest?

 

You've got the scent, Bar. Good hunting.

Settled or started it is difficult to find anything out about this withdrawal case... I have looked all the info If I can find it disappears off the web ... found this tho.. says it was started in 2000 not settled... always confusion.  When I talk to people hurt by not knowing there is a withdrawal syndrome from Effexor I can't find info to reference the case.  I know you will say that folks who took the drug after the warning went on in 2000 can't sue but believe me myself and many others were on these drugs including effexor way before 2000...still no lawyer I talk to is interested... 

 

"Paxil Withdrawal Case Settled in California

 

A California lawsuit against Glaxo SmithKline (GSK) charged the drug company with failing to warn the public about the dangers of Paxil withdrawal.  Glaxo SmithKline (GSK), the manufacturer of the antidepressant Paxil, resolved the suit in January 2002.  The results of the resolution, including any settlement by defendant Glaxo SmithKline, were not announced.  The outcome was described as a resolution rather than a settlement. 

 

Psychiatrist Peter Breggin, M.D. was the plaintiff's medical expert and worked closely with the attorneys in formulating the suit.  According to Dr. Breggin, there is published and clinical evidence that all of the SSRIs can cause serious withdrawal reactions.  Paxil, because of its intense impact and short duration of action, causes the most severe withdrawal reactions. 

 

Paxil is an antidepressant of the SSRI class that also includes Prozac, Zoloft, Celexa and Luvox.  The suit charged that Paxil causes serious withdrawal problems of many kinds, resulting in a widespread societal problem when many individuals find themselves unable to stop taking the drug. 

 

The Paxil withdrawal suit was brought in San Jose, California on August 19, 2000 as a "Complaint for Injunctive Relief Under Business and Professions Code" (Nguyen & Farber, plaintiffs vs. SmithKline Beecham Corporation, Case No: CV791998). 

 

Legal brief for the resolved Paxil withdrawal suit

 

GSK Updates the Paxil Label

 

In December, in an event that may have been in part motivated by the Paxil withdrawal suit, GSK finally updated its label for Paxil with a specific mention of the danger of Paxil withdrawal reactions. One of the attorneys who filed the suit, Don Farber of San Rafael, California, told Dr. Breggin that it is highly likely that the suit influenced both the drug company and the FDA to strengthen the label in regard to Paxil withdrawal effects.  Farber and his colleague Vince Nguyen voluntarily dismissed the suit when the new label was issued on December 14, 2001. 

The revised label uses the industry-favored term "discontinuation" instead of withdrawal.  Discontinuation is a euphemism for withdrawal that is used to circumvent the negative connotations associated with addiction, dependency and withdrawal syndrome.  By using the term discontinuation instead of withdrawal, the drug company obscures the potential severity of these symptoms and their tendency to force patients to continue taking the drug. 

The updated label can be found on the company website (www.GSK.com under Products). 

In the Precautions section of the new label, GSK cites clinical trial data confirming the existence of several withdrawal symptoms, including abnormal dreams, paresthesia [abnormal sensations], and dizziness.  According to the label, since the marketing of Paxil, other withdrawal symptoms have been reported in association with the discontinuation of the drug.  These post-marketing reports include "dizziness, sensory disturbances (e.g., paresthesias such as electric shock sensations), agitation, anxiety, nausea and sweating."  However, the company claims that the reactions reported since the start of marketing "may have no causal relationship to the drug" and are "generally self-limiting."

Dr. Breggin stressed the importance of the "anxiety" and "agitation" mentioned in the label as reported in association with Paxil withdrawal.  He observed that anxiety and agitation can contribute to aggressive, violent or suicidal behavior.  Aggressive behavior is especially likely to result when a drug causes or increases agitation and anxiety in individuals already suffering from psychiatric disorders such as anxiety, depression, panic, stress, and obsessions or compulsions.  Dr. Breggin also stated that there is a growing body of clinical and research literature demonstrating irritability and aggression during withdrawal from Paxil.  However, the updated label makes no mention of any danger of aggressive, violent or suicidal behavior during Paxil withdrawal. 

Dr. Breggin was gratified to see the company update its label to specifically mention withdrawal reactions.  However, he described the updated label as grossly inadequate in regard to the range, intensity and persistence of Paxil withdrawal reactions, including the danger of aggressive, violent, or suicidal behavior, and an overall worsening of the patient's mental condition.

 

Longstanding Concerns About SSRI Withdrawal Effects

Dr. Breggin was among the first to warn about the dangers of SSRI withdrawal in his book Talking Back to Prozac(with Ginger Breggin, St. Martin's Press, 1994) and in two more recent books, Brain-Disabling Treatments in Psychiatry (Springer Publishing Company, 1997, revised 2008) and The Antidepressant Fact Book (Perseus Books, 2001).  Dr. Breggin and co-author David Cohen, Ph.D. also discuss the overall problem of drug withdrawal in Your Drug May Be Your Problem: How and Why to Stop Taking Psychiatric Medications (Perseus Books, 1999, revised 2007). These books should be consulted for documentation and further discussion of the issues surrounding the SSRI antidepressants such as Paxil, Prozac, Zoloft, Celexa and Luvox.

Dr. Breggin is currently a medical expert in other cases related to Paxil withdrawal. In a criminal case, a young man physically assaulted a female friend while he was undergoing withdrawal from Paxil.  The young man had no previous history of violence.  The assault was extremely out of character.

Dr. Breggin is also actively involved in treating patients who have experienced serious difficulty withdrawing from Paxil and other SSRI antidepressants. Headaches, nausea, dizziness, painful internal sensations, and various manifestations of emotional distress can make it difficult to withdraw from these medications.  Some patients experience very lengthy withdrawal periods lasting several months or more. 

 

Direct Toxic Effects Caused by SSRIs

In 1994 Dr. Breggin developed and provided the scientific basis for a large series of combined product liability cases alleging violence and suicide caused by Prozac.  The court combined the cases in order to facilitate the discovery process.  It facilitated one organized effort for evaluating secret materials obtained from the company.  In his role as the medical expert for the combined cases, Dr. Breggin reviewed internal documents from Eli Lilly & Company, the manufacturer of Prozac, and also interviewed FDA officials, examined FDA materials, and reviewed and analyzed the scientific literature.  In a more recent suit product liability suit against Eli Lilly & Company, Dr. Breggin once again had the opportunity to examine internal documents, this time at the corporate headquarters.  As far as Dr. Breggin is aware, all of the individual Prozac product liability suits in which he has agreed to be an expert have been settled or remain active. 

 

Background Science

SSRI's including Prozac, Paxil, Zoloft, Luvox and Celexa block the removal of serotonin from the synapse or space between neurons.  Other antidepressants, such as Effexor, can also block this reuptake of serotonin causing similar effects.  These drugs can cause suicide, violence and other criminal acts through several mechanisms, including the following: 

 

(1) SSRI-induced mania, sometimes (but not always) with psychotic features, such as hallucinations or delusions.  During drug-induced mania, the individual can make elaborate plans, including robberies or embezzlement.  However, the plans are often outlandish and doomed to failure due to obviously poor judgment.  Drug-induced mania can cause many expressions of disinhibited or out-of-control behavior, including sexual acting out, road rage, buying sprees and shoplifting.  Drug-induced mania, even when seemingly not intense, can ruin marriages and destroy careers. 

All of the features of mania are not required in order to meet the diagnosis of Antidepressant-Induced Mood Disorder with Manic Features.  If the individual's mood is  "elevated, euphoric, or irritable," the necessary criteria are met. 

 

(2) SSRI-induced depression or worsening of depression.  In a seemingly paradoxical effect, antidepressants can cause or worsen depression.  In controlled clinical trials for Prozac that were conducted by the manufacturer, Eli Lilly and Company, depressed patients taking Prozac attempted suicide more frequently than depressed patients taking placebo (sugar pill) or older antidepressants. 

 

(3) SSRI-induced severe anxiety and agitation, especially in a patient already suffering from depression with anxiety and agitation; 

 

(4) SSRI-induced obsessions and compulsions that motivate violence toward oneself or others. 

 

(5) SSRI-induced akathisia, an internal sensation of agitation or discomfort that drives a person to move about, and also to lose impulse control.  During akathisia, the inner experience of agitation includes many unusual physical feelings, such as electricity in the head or body. The person suffering from akathisia typically feels compelled to move the feet when sitting, to stand, or to pace.  Akathisia is known to increase the risk of suicide and violence.

 

Severe Adverse Effects After One or Two Doses

Dr. Breggin stated that physicians and patients are not aware that many severe adverse drug effects can surface after the first or second dose of any SSRI antidepressant.  Because the "therapeutic effect" of any antidepressant usually takes several weeks or more to develop, some doctors fail to realize that toxic effects can develop beginning with the first dose.  These doctors are not likely to warn patients and their families about adverse events occurring after one or two doses.  Furthermore, these doctors may discount the patient's report when these early reactions occur.  They may urge the patient to continue taking the drug so that the patient ends up developing an unnecessarily severe reaction. 

Dr. Breggin is a medical expert in cases in which SSRI antidepressants, including Prozac, Paxil, Zoloft, Celexa and Luvox, have caused suicidal and violent behavior in individuals while taking the drug rather than during withdrawal.  In some cases, it can be difficult to determine if the adverse drug effect is caused by direct drug toxicity, by drug withdrawal, or by both. 

Dr. Breggin is also involved in a variety of other suits relating to harmful effects of the SSRIs.  This website contains additional relevant materials, including >discussions of other lawsuits, and details about how the SSRI antidepressants can cause mania, psychosis, depression, violence, and suicide."

 

http://breggin.com/index.php?option=com_content&task=view&id=76

putting it here in case it disappears too... 

would like to know is this the case that settled in 2000 if anybody knows???

 

Brief filed in Paxil withdrawal suit

Share this post


Link to post
Share on other sites
btdt

 

He did that for a while. He popped up here and there in news articles warning about the dangers of Paxil withdrawal. Some of us thought he might have a guilty conscience.

 

You are absolutely right the journal article tune changed after 2000. That's when a huge Paxil lawsuit was settled for the plaintiffs. As a result, the FDA put the withdrawal warning on Paxil (December 2001) and other antidepressants.

 

Clearly, this was not good for business. We can surmise from Shelton's publications that after that, his charge from pharma sponsors was more clear. And what to make of his partnership with Schatzberg as Schatzberg was being disciplined for conflict of interest?

 

You've got the scent, Bar. Good hunting.

Settled or started it is difficult to find anything out about this withdrawal case... I have looked all the info If I can find it disappears off the web ... found this tho.. says it was started in 2000 not settled... always confusion.  When I talk to people hurt by not knowing there is a withdrawal syndrome from Effexor I can't find info to reference the case.  I know you will say that folks who took the drug after the warning went on in 2000 can't sue but believe me myself and many others were on these drugs including effexor way before 2000...still no lawyer I talk to is interested... 

 

"Paxil Withdrawal Case Settled in California

 

A California lawsuit against Glaxo SmithKline (GSK) charged the drug company with failing to warn the public about the dangers of Paxil withdrawal.  Glaxo SmithKline (GSK), the manufacturer of the antidepressant Paxil, resolved the suit in January 2002.  The results of the resolution, including any settlement by defendant Glaxo SmithKline, were not announced.  The outcome was described as a resolution rather than a settlement. 

 

Psychiatrist Peter Breggin, M.D. was the plaintiff's medical expert and worked closely with the attorneys in formulating the suit.  According to Dr. Breggin, there is published and clinical evidence that all of the SSRIs can cause serious withdrawal reactions.  Paxil, because of its intense impact and short duration of action, causes the most severe withdrawal reactions. 

 

Paxil is an antidepressant of the SSRI class that also includes Prozac, Zoloft, Celexa and Luvox.  The suit charged that Paxil causes serious withdrawal problems of many kinds, resulting in a widespread societal problem when many individuals find themselves unable to stop taking the drug. 

 

The Paxil withdrawal suit was brought in San Jose, California on August 19, 2000 as a "Complaint for Injunctive Relief Under Business and Professions Code" (Nguyen & Farber, plaintiffs vs. SmithKline Beecham Corporation, Case No: CV791998). 

 

Legal brief for the resolved Paxil withdrawal suit

 

GSK Updates the Paxil Label

 

In December, in an event that may have been in part motivated by the Paxil withdrawal suit, GSK finally updated its label for Paxil with a specific mention of the danger of Paxil withdrawal reactions. One of the attorneys who filed the suit, Don Farber of San Rafael, California, told Dr. Breggin that it is highly likely that the suit influenced both the drug company and the FDA to strengthen the label in regard to Paxil withdrawal effects.  Farber and his colleague Vince Nguyen voluntarily dismissed the suit when the new label was issued on December 14, 2001. 

The revised label uses the industry-favored term "discontinuation" instead of withdrawal.  Discontinuation is a euphemism for withdrawal that is used to circumvent the negative connotations associated with addiction, dependency and withdrawal syndrome.  By using the term discontinuation instead of withdrawal, the drug company obscures the potential severity of these symptoms and their tendency to force patients to continue taking the drug. 

The updated label can be found on the company website (www.GSK.com under Products). 

In the Precautions section of the new label, GSK cites clinical trial data confirming the existence of several withdrawal symptoms, including abnormal dreams, paresthesia [abnormal sensations], and dizziness.  According to the label, since the marketing of Paxil, other withdrawal symptoms have been reported in association with the discontinuation of the drug.  These post-marketing reports include "dizziness, sensory disturbances (e.g., paresthesias such as electric shock sensations), agitation, anxiety, nausea and sweating."  However, the company claims that the reactions reported since the start of marketing "may have no causal relationship to the drug" and are "generally self-limiting."

Dr. Breggin stressed the importance of the "anxiety" and "agitation" mentioned in the label as reported in association with Paxil withdrawal.  He observed that anxiety and agitation can contribute to aggressive, violent or suicidal behavior.  Aggressive behavior is especially likely to result when a drug causes or increases agitation and anxiety in individuals already suffering from psychiatric disorders such as anxiety, depression, panic, stress, and obsessions or compulsions.  Dr. Breggin also stated that there is a growing body of clinical and research literature demonstrating irritability and aggression during withdrawal from Paxil.  However, the updated label makes no mention of any danger of aggressive, violent or suicidal behavior during Paxil withdrawal. 

Dr. Breggin was gratified to see the company update its label to specifically mention withdrawal reactions.  However, he described the updated label as grossly inadequate in regard to the range, intensity and persistence of Paxil withdrawal reactions, including the danger of aggressive, violent, or suicidal behavior, and an overall worsening of the patient's mental condition.

 

Longstanding Concerns About SSRI Withdrawal Effects

Dr. Breggin was among the first to warn about the dangers of SSRI withdrawal in his book Talking Back to Prozac(with Ginger Breggin, St. Martin's Press, 1994) and in two more recent books, Brain-Disabling Treatments in Psychiatry (Springer Publishing Company, 1997, revised 2008) and The Antidepressant Fact Book (Perseus Books, 2001).  Dr. Breggin and co-author David Cohen, Ph.D. also discuss the overall problem of drug withdrawal in Your Drug May Be Your Problem: How and Why to Stop Taking Psychiatric Medications (Perseus Books, 1999, revised 2007). These books should be consulted for documentation and further discussion of the issues surrounding the SSRI antidepressants such as Paxil, Prozac, Zoloft, Celexa and Luvox.

Dr. Breggin is currently a medical expert in other cases related to Paxil withdrawal. In a criminal case, a young man physically assaulted a female friend while he was undergoing withdrawal from Paxil.  The young man had no previous history of violence.  The assault was extremely out of character.

Dr. Breggin is also actively involved in treating patients who have experienced serious difficulty withdrawing from Paxil and other SSRI antidepressants. Headaches, nausea, dizziness, painful internal sensations, and various manifestations of emotional distress can make it difficult to withdraw from these medications.  Some patients experience very lengthy withdrawal periods lasting several months or more. 

 

Direct Toxic Effects Caused by SSRIs

In 1994 Dr. Breggin developed and provided the scientific basis for a large series of combined product liability cases alleging violence and suicide caused by Prozac.  The court combined the cases in order to facilitate the discovery process.  It facilitated one organized effort for evaluating secret materials obtained from the company.  In his role as the medical expert for the combined cases, Dr. Breggin reviewed internal documents from Eli Lilly & Company, the manufacturer of Prozac, and also interviewed FDA officials, examined FDA materials, and reviewed and analyzed the scientific literature.  In a more recent suit product liability suit against Eli Lilly & Company, Dr. Breggin once again had the opportunity to examine internal documents, this time at the corporate headquarters.  As far as Dr. Breggin is aware, all of the individual Prozac product liability suits in which he has agreed to be an expert have been settled or remain active. 

 

Background Science

SSRI's including Prozac, Paxil, Zoloft, Luvox and Celexa block the removal of serotonin from the synapse or space between neurons.  Other antidepressants, such as Effexor, can also block this reuptake of serotonin causing similar effects.  These drugs can cause suicide, violence and other criminal acts through several mechanisms, including the following: 

 

Severe Adverse Effects After One or Two Doses(1) SSRI-induced mania, sometimes (but not always) with psychotic features, such as hallucinations or delusions.  During drug-induced mania, the individual can make elaborate plans, including robberies or embezzlement.  However, the plans are often outlandish and doomed to failure due to obviously poor judgment.  Drug-induced mania can cause many expressions of disinhibited or out-of-control behavior, including sexual acting out, road rage, buying sprees and shoplifting.  Drug-induced mania, even when seemingly not intense, can ruin marriages and destroy careers. 

All of the features of mania are not required in order to meet the diagnosis of Antidepressant-Induced Mood Disorder with Manic Features.  If the individual's mood is  "elevated, euphoric, or irritable," the necessary criteria are met. 

 

(2) SSRI-induced depression or worsening of depression.  In a seemingly paradoxical effect, antidepressants can cause or worsen depression.  In controlled clinical trials for Prozac that were conducted by the manufacturer, Eli Lilly and Company, depressed patients taking Prozac attempted suicide more frequently than depressed patients taking placebo (sugar pill) or older antidepressants. 

 

(3) SSRI-induced severe anxiety and agitation, especially in a patient already suffering from depression with anxiety and agitation; 

 

(4) SSRI-induced obsessions and compulsions that motivate violence toward oneself or others. 

 

(5) SSRI-induced akathisia, an internal sensation of agitation or discomfort that drives a person to move about, and also to lose impulse control.  During akathisia, the inner experience of agitation includes many unusual physical feelings, such as electricity in the head or body. The person suffering from akathisia typically feels compelled to move the feet when sitting, to stand, or to pace.  Akathisia is known to increase the risk of suicide and violence.

 

Dr. Breggin stated that physicians and patients are not aware that many severe adverse drug effects can surface after the first or second dose of any SSRI antidepressant.  Because the "therapeutic effect" of any antidepressant usually takes several weeks or more to develop, some doctors fail to realize that toxic effects can develop beginning with the first dose.  These doctors are not likely to warn patients and their families about adverse events occurring after one or two doses.  Furthermore, these doctors may discount the patient's report when these early reactions occur.  They may urge the patient to continue taking the drug so that the patient ends up developing an unnecessarily severe reaction. 

Dr. Breggin is a medical expert in cases in which SSRI antidepressants, including Prozac, Paxil, Zoloft, Celexa and Luvox, have caused suicidal and violent behavior in individuals while taking the drug rather than during withdrawal.  In some cases, it can be difficult to determine if the adverse drug effect is caused by direct drug toxicity, by drug withdrawal, or by both. 

Dr. Breggin is also involved in a variety of other suits relating to harmful effects of the SSRIs.  This website contains additional relevant materials, including >discussions of other lawsuits, and details about how the SSRI antidepressants can cause mania, psychosis, depression, violence, and suicide."

 

http://breggin.com/index.php?option=com_content&task=view&id=76

putting it here in case it disappears too... 

would like to know is this the case that settled in 2000 if anybody knows???

 

Brief filed in Paxil withdrawal suit

 

Maybe the only people who know about this had a claim with the lawsuit and now a gag order on not allowed to talk about it.. wonder what would happen if the gag orders did not exist and people could learn the real truth... would we be a lot further ahead as a world or just have a few people with less money... 

 

nobody could guess when we are not sure what they are forced to keep quiet about was it part science... ?  other things??? we may never know.

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

×