SEROXAT AND OTHER SSRIs

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Posts Tagged ‘Paxil’

SSRI Comparison Facts

Posted by shutah on February 14, 2011

Comparison of Selective Serotonin Reuptake Inhibitors (SSRIs)

Efficacy and effectiveness

Clinical trials comparing one SSRI with another indicate that drugs in this class are equally efficacious. Each antidepressant produces approximately a 60% overall response rate (ie, at least a 50% reduction in symptoms as a result of treatment). However, some differences in the SSRIs efficacy exist.

Escitalopram may be superior in efficacy compared with other SSRIs in the treatment of major depressive disorder2. Also escitalopram has better efficacy in the treatment of severe depression than citalopram4.  A major consideration with escitalopram is that it is not yet available in lower-cost generic form. The drug is still under patent. In 2006 Forest Laboratories was granted an 828 day (2 years and 3 months) extension on its patent for escitalopram31. This pushed the patent expiry from December 7, 2009 to March 14, 2012.

Paroxetine, fluoxetine, and sertraline are similar in effectiveness for major depression and depression with high levels of anxiety3,5.

Paroxetine is the only SSRI indicated for all five anxiety disorders in addition to major depressive disorder.

Fluoxetine has a slower onset of antidepressants effect than other SSRIs4. Also, fluoxetine appears to be somewhat less effective, than other drugs in this class24,25.

Sertraline may have a slightly higher rate of response than fluoxetine and paroxetine26. Sertraline has advantages over paroxetine in the treatment of panic disorder27.

Interesting and important fact is that SSRI antidepressants are not interchangeable. Persons who discontinue one SSRI for lack of tolerability or response can be effectively treated with another19.

Discontinuation symptoms (withdrawal)

SSRIs aren’t considered addictive.  YET !! However, stopping treatment abruptly or missing several doses can cause withdrawal-like symptoms, including nausea, headache, dizziness, lethargy and flu-like symptoms. This is sometimes called discontinuation syndrome.

All antidepressants do not have the same type or severity of withdrawal symptoms. Discontinuation syndrome is more common with the SSRIs with shorter half lives and inactive metabolites, such as paroxetine, sertraline, and fluvoxamine. The incidence of discontinuation syndrome is highest with paroxetine followed by fluvoxamine and sertraline. Citalopram and fluoxetine have a lower occurrence of withdrawal symptoms10.

Abrupt interruption of antidepressant therapy for 5-8 days was associated with the emergence of new somatic and psychological symptoms in patients treated with paroxetine and to a lesser degree sertraline, with few symptoms seen with fluoxetine12.

Pregnancy category

All SSRIs (except paroxetine) are classified as pregnancy Category C, meaning that they may not be safe for use during pregnancy.

Paroxetine (Paxil, Paxil CR) is pregnancy Category D medication. Paroxetine may cause heart defects or serious, life-threatening lung problems in newborn babies whose mothers take the medication during pregnancy.

Pharmacology

Selective serotonin reuptake inhibitors differ in their potency and selectivity in inhibiting serotonin reuptake and there may be important effects on other transporters and receptors, indicating that they are not as selective as their manufacturers suggest. It has been proposed, for example, that fluoxetine’s effects on 5-HT2C receptors may underlie a propensity to cause agitation; paroxetine’s affinity for muscarinic receptors causes its increased tendency to produce discontinuation effects; sertraline’s affinity for the dopamine transporter results in a greater efficacy in severe depression; and sertraline’s and fluvoxamine’s affinity for sigma1 opioid receptors is responsible for their efficacy in psychotic depression (Goodnick & Goldstein, 1998a).

Half-life

The half-life of a drug is the time required to achieve steady-state plasma concentrations (i.e., to metabolize half the dose and lower blood concentrations by 50%). Half-life can be used to estimate how long it will take to clear a drug from the body after treatment is discontinued.

Fluoxetine is unique because of its long half-life and the long half-life of its active metabolite norfluoxetine. Fluoxetine has a half-life of 2-4 days and its active metabolite, norfluoxetine, has a half-life of 4-16 days.

In comparison, citalopram, escitalopram, paroxetine, and sertraline have shorter half-lives in the range of 20-35 hours, and steady-state concentrations (and therapeutic effect) are reached much more rapidly. The long half-life of fluoxetine may blunt the effects of missed doses or treatment discontinuation and makes it easier to discontinue than any of the other SSRIs. On the other hand, fluoxetine requires a much longer washout period than the other SSRIs (several weeks), particularly when switching to monoamine oxidase inhibitors (MAOIs) or TCA.

Antidepressants with relatively short half-lives are desirable for people with multiple comorbidities and complex, multiple-drug regimens because they allow for once-daily dosing. A short half-life enables physicians to switch more rapidly and safely to an alternative antidepressant if treatment fails or if unfavorable drug reactions occur.

Paroxetine and fluvoxamine are more quickly cleared from the body than the other SSRIs.

The possible slower onset of antidepressant action of fluoxetine may be owing to a longer time taken to achieve therapeutic plasma concentrations. In situations where the speed of onset of therapeutic effect is particularly important, such as in severe depression, fluoxetine may not be the SSRI of choice. Patients in whom the long half-life may have advantages (and therefore for whom fluoxetine should be considered) include those who are poorly compliant and those in whom administration less frequent than daily is contemplated.

Sertraline exhibits a sex- and age-dependent half-life. In men, the half-life is approximately 30% shorter (22.4 hr) than in females or the elderly (32.1-36.7 hr).

References
  • Celexa Prescribing Information Celexa.com, Forest Pharmaceuticals, Inc.
  • Lexapro Prescribing Information Lexapro.com, Forest Pharmaceuticals, Inc.
  • Paxil Prescribing Information – Paxil.com, GlaxoSmithKline
  • Prozac Prescribing Information Prozac.com, Eli Lilly and Company
  • Zoloft Prescribing Information – Zoloft.com, Pfizer Inc.
  • 1. Side-effect profile of fluoxetine in comparison with other SSRIs, tricyclic and newer antidepressants: a meta-analysis of clinical trial data. Pharmacopsychiatry. 2005 Mar;38(2):69-77 MedLine
  • 2. Efficacy of escitalopram in the treatment of major depressive disorder compared with conventional selective serotonin reuptake inhibitors and venlafaxine XR: a meta-analysis. J Psychiatry Neurosci. 2006 Mar;31(2):122-31. MedLine
  • 3. Similar effectiveness of paroxetine, fluoxetine, and sertraline in primary care: a randomized trial. JAMA. 2001 Dec 19;286(23):2947-55
  • 4. Escitalopram is more effective than citalopram for the treatment of severe major depressive disorder Encephale. 2004 Mar-Apr;30(2):158-66. MedLine
  • 5. Fluoxetine versus sertraline and paroxetine in major depression: tolerability and efficacy in anxious depression. J Affect Disord. 2000 Aug;59(2):119-26.
  • 6. Labbate LA. Sex and serotonin reuptake inhibitor antidepressants. Psychiatr Ann. 1999;29:571–9.
  • 7. Meijer WE, Heerdink ER, van Eijk JT, Leufkens HG. Adverse events in users of sertraline: results from an observational study in psychiatric practice in The Netherlands. Pharmacoepidemiol Drug Saf. 2002;11:655–62. PubMed
  • 8. Fava M. Weight gain and antidepressants. J Clin Psychiatry. 2000;61(Suppl.):37–41. PubMed
  • 9. Fergunson JM. SSRI antidepressant medications: adverse effects and tolerability. Primary Care Companion. J Clin Pschiatry. 2001;3:22–7.
  • 10. Schatzberg AF, Haddad P, Kaplan EM, Lejoyeux M, Rosenbaum JF, Young AH, Zajecka J. Serotonin reuptake inhibitor discontinuation syndrome: a hypothetical definition. Discontinuation Consensus panel. J Clin Psychiatry. 1997;58
  • 11. Westenberg HG, Sandner C. Tolerability and safety of fluvoxamine and other antidepressants. Int J Clin Pract. 2006 Apr;60(4):482-91. PubMed
  • 12. Rosenbaum JF, Fava M, Hoog SL, Ascroft RC, Krebs WB. Selective serotonin reuptake inhibitor discontinuation syndrome: a randomized clinical trial. Biol Psychiatry. 1998 Jul 15;44(2):77-87. PubMed
  • 14. Ian M. Anderson and J. Guy Edwards. Guidelines for choice of selective serotonin reuptake inhibitor in depressive illness Advances in Psychiatric Treatment (2001) 7: 170-180
  • 15. Fava M, Judge R, Hoog SL, Nilsson ME, Koke SC. Fluoxetine versus sertraline and paroxetine in major depressive disorder: changes in weight with long-term treatment. J Clin Psychiatry. 2000 Nov;61(11):863-7.PubMed
  • 16. Montejo-Gonzalez AL, Llorca G, Izquierdo JA, Ledesma A, Bousono M, Calcedo A, Carrasco JL, Ciudad J, Daniel E, De la Gandara J, Derecho J, Franco M, Gomez MJ, Macias JA, Martin T, Perez V, Sanchez JM, Sanchez S, Vicens E. SSRI-induced sexual dysfunction: fluoxetine, paroxetine, sertraline, and fluvoxamine in a prospective, multicenter, and descriptive clinical study of 344 patients. J Sex Marital Ther. 1997 Fall;23(3):176-94.PubMed
  • 17. Maina G, Albert U, Salvi V, Bogetto F. Weight gain during long-term treatment of obsessive-compulsive disorder: a prospective comparison between serotonin reuptake inhibitors. J Clin Psychiatry. 2004 Oct;65(10):1365-71.PubMed
  • 18. Bymaster FP, Zhang W, Carter PA, Shaw J, Chernet E, Phebus L, Wong DT, Perry KW. Fluoxetine, but not other selective serotonin uptake inhibitors, increases norepinephrine and dopamine extracellular levels in prefrontal cortex. Psychopharmacology (Berl). 2002 Apr;160(4):353-61.
  • 19. Nurnberg HG, Thompson PM, Hensley PL. Antidepressant medication change in a clinical treatment setting: a comparison of the effectiveness of selective serotonin reuptake inhibitors. J Clin Psychiatry. 1999 Sep;60(9):574-9.
  • 20. Stahl SM. Not so selective serotonin reuptake inhibitors. J Clin Psychiatry 1998;59:343-4. Psychiatrist
  • 21. Owens JM, Knight DL, Nemeroff CB. Second generation SSRIS: human monoamine transporter binding profile of escitalopram and R-fluoxetine. Encephale. 2002 Jul-Aug;28(4):350-5. PubMed
  • 22. Bolden-Watson C, Richelson E. Blockade by newly-developed antidepressants of biogenic amine uptake into rat brain synaptosomes. Life Sci. 1993;52(12):1023-9. PubMed
  • 23. Edwards JG, Anderson I. Systematic review and guide to selection of selective serotonin reuptake inhibitors. Drugs. 1999 Apr;57(4):507-33. PubMed
  • 24. Geretsegger C, Bo”hmer F, Ludwig M. Paroxetine in the elderly depressed patient: randomized comparison with fluoxetine of efficacy, cognitive and behavioural effects. Int Clin Psychopharmacol. 1994 Spring;9(1):25-9. PubMed
  • 25. Flament MF, Lane RM, Zhu R, Ying Z. Predictors of an acute antidepressant response to fluoxetine and sertraline. PubMed
  • 26. Clinical Pharmacology of SSRI’s. How SSRIs as a Group Are Similar.Sheldon H. Preskorn, M.D.
  • 27. Bandelow B, Behnke K, Lenoir S, Hendriks GJ, Alkin T, Goebel C, Clary CM. Sertraline versus paroxetine in the treatment of panic disorder: an acute, double-blind noninferiority comparison. J Clin Psychiatry. 2004 Mar;65(3):405-13 PubMed
  • 28. Montejo AL, Llorca G, Izquierdo JA, Rico-Villademoros F. Incidence of sexual dysfunction associated with antidepressant agents: a prospective multicenter study of 1022 outpatients. Spanish Working Group for the Study of Psychotropic-Related Sexual Dysfunction. J Clin Psychiatry. 2001;62 Suppl 3:10-21. PubMed
  • 29. Winokur A, Lexon N, Allen K, and et al. Sertraline administered for 8 weeks to depressed patients did not alter sleep architecture: a preliminary report. New Research Program and Abstracts of the 147th Annual Meeting of the American Psychiatric Association; May 24, 1994
  • 30. Cipriani A, Furukawa TA, Salanti G, Geddes JR, Higgins JP, Churchill R, Watanabe N, Nakagawa A, Omori IM, McGuire H, Tansella M, Barbui C. Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis. Lancet. 2009 Feb 28;373(9665):746-58.
  • 31. “Forest Laboratories Receives Patent Term Extension for Lexapro” Press release

Published: May 05, 2007
Last updated: August, 2009

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Nurses Drug Handbook 2010

Posted by shutah on January 28, 2011

Pages 775 and 777

Take a look at this, read it, digest it and then tell me this medication does anyone any good whatsoever!!

Nurses Drug Handbook 2010

 

 

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When secret settlements are taken to their illogical extreme

Posted by shutah on January 26, 2011

from The Moral Compass of the American Lawyer
by Richard Zitrin & Carol M. Langford

This story is not about Prozac, which from the weight of evidence appears to be a relatively safe drug. Rather, this is a tale of what happens when secret settlements are taken to their illogical extreme — in this case, a “sham” trial in which the plaintiffs and their lawyers were paid to pull their punches so the defendant could get a favorable verdict.

It started in September 1989, when Joseph Wesbecker armed himself with an AK-47, walked into the Louisville printing plant where he had worked, and started shooting. He killed eight people, wounded twelve more, and finished matters by blowing his own brains out. One month before, Wesbecker had begun taking Prozac. The lawyers for the shooting victims soon focused on the drug as the cause for Wesbecker’s extraordinary violence, and they targeted Eli Lilly, Prozac’s manufacturer, as the “deep pocket.”

The Fentress case, named for one of Wesbecker’s victims, was the first of 160 cases pending against Prozac to go to trial in the autumn of 1994. By then, Prozac had become the aspirin of anti-depressants — the wonder drug everyone was talking about and millions were using. Prozac represented almost one-third of all Lilly sales in 1994 — $1.7 billion. A great deal was at stake: If Lilly lost, other plaintiffs waiting in the wings would gain strength and resolve. But a verdict for the drug company might make those other plaintiffs reconsider.

Throughout the case, plaintiffs’ attorneys pushed Judge John Potter to allow evidence about another Lilly product, the anti-inflammatory drug Oraflex, which had been taken off the market in 1982 as too dangerous. In 1985, Lilly had pled guilty to 25 criminal counts of failing to report adverse reactions to Oraflex, including four deaths, to the Food & Drug Administration. Central to the plaintiffs’s claims was that Lilly had done the same thing with Prozac. Potter refused to allow the evidence, saying it was marginally relevant at best, and would prejudice the jury more than it would prove anything.

But when Lilly executives testified that the company had an excellent reputation for reporting problem incidents — what they euphemistically called “adverse events” — plaintiffs’ counsel immediately renewed their request to bring in the Oraflex evidence. Potter agreed, noting that “Lilly has injected the issue into the trial.” Potter’s ruling set off a flurry of activity around his courtroom. The lawyers jointly asked for a recess, and then asked to adjourn for a day.

By mid-afternoon, a strong scent of settlement was in the air. But when Judge Potter reconvened the case the following afternoon, he was surprised by what he heard. Chief plaintiffs’ counsel Paul Smith announced that the plaintiffs would rest without presenting the Oraflex evidence unless the trial went to its second phase, which would address the amount of the financial award. That stage would occur only if the jury decided in the first phase that Lilly was liable. If the jury found Lilly not liable, the case would be over, and the Oraflex evidence would never be heard.

The plaintiffs’ high-risk strategy puzzled Judge Potter; they could lose their whole case without presenting their best evidence. Potter asked the lawyers whether they had reached a settlement. He was told unequivocally that they had not. While the jury was deliberating, a juror came forward and told Judge Potter that she had overheard settlement negotiations going on in the hallway. She repeated this in chambers with the lawyers present and was then excused. Potter turned to the lawyers and said, “Does anybody have anything they want to say?” A moment later, he asked again, “Does anybody have the slightest clue?” “No,” said Smith. “I can’t imagine,” said one of the defense lawyers.

In other chambers meetings, lawyers from both sides emphasized their plans for Phase Two of the trial — the money, or “damages” phase — and the possibility of settlement discussions if the plaintiffs won Phase One. All this would be unnecessary, of course, if the case actually had been settled already. On December 12, only three court days after Potter’s ruling allowing the Oraflex evidence, the jury returned a verdict for Lilly.

In January 1995, Judge Potter formally entered his order in Fentress v. Eli Lilly, dismissing the case after verdict by jury. As soon as the verdict was in, Lilly and its lawyers trumpeted their victory across the country. “We were able, finally,” said one of Lilly’s lead attorneys, “to get people head to head in a courtroom and say ‘Put up or shut up.’ … [T]his is a complete vindication of the medicine.”

Had John Potter not been the judge, the Fentress case might have ended there. He asked himself why any lawyer would fight so hard over the key Oraflex evidence and then not present it in the most important part of the case.

Despite what the lawyers had told him, Potter suspected that some kind of deal had been made. But he decided to be patient. He waited to see whether the plaintiffs filed a notice of their intent to appeal, a routine matter after losing a case. When they didn’t, Potter called in the lawyers from both sides. They continued to deny that a settlement had been reached. Although Potter was more suspicious than ever, he had no power to do anything, except as to his own order of dismissal. So in April 1995, stating “it is more likely than not that the case was settled,” Potter filed an unusual document: his own motion to change his post-trial order from a dismissal after verdict to “dismissed as settled.” He set a hearing for May.

Quickly, the lawyers on both sides joined forces to file an objection with Kentucky’s appeals court to prevent Judge Potter’s hearing anything about what they considered a closed case. Paul Smith stated flatly that “there was no secret settlement…. This was a hard fought case.” Potter, meanwhile, now needed a lawyer himself. After Potter’s changed order had become public, Richard Hay, then President of the Kentucky Academy of Trial Attorneys, told reporters that if money had been traded for evidence, the trial was “a sham,” like “taking a dive in a boxing match.”

Potter read Hay’s comments, called him, and asked how outraged Hay was about the case. “Enough to represent you,” Hay replied. Together, Hay and Potter filed a brief that emphasized a “public silence [that] has been bought and paid for,” robbing millions who “want the truth.”

In June 1995, the appeals court ruled against Potter, saying he no longer had jurisdiction over the case. Potter appealed to the Kentucky Supreme Court. Before the fall Supreme Court hearing, lawyers for both sides finally acknowledged that they had indeed settled all money issues and had agreed to go through only the first phase of the trial no matter what the result. Still, they refused to disclose specifics.

Meanwhile, in Indianapolis, Lilly’s hometown, Paul Smith suddenly withdrew as lead counsel in a series of consolidated Prozac cases in federal court. He wouldn’t say whether he had settled his Indianapolis cases as part of the Fentress settlement, and the judge refused to ask. In their appeal to the Supreme Court, Potter and Hay de-emphasized the importance of public disclosure, and focused instead on the lawyers’ failure to be candid with the judge.

On May 23, 1996, the Kentucky Supreme Court decided the case of Hon. John W. Potter v. Eli Lilly unanimously in Judge Potter’s favor, citing the lawyers’ “serious lack of candor” and evidence of bad faith, abuse of process, even fraud. Although the court said that “the only result” of exposing the secret Fentress agreement “is that the truth will be revealed,” the decision was less a victory for open settlements, and more a demand that the judge be included in the secret.

Judge Potter, though, still saw the larger issue. Armed with Supreme Court authority to conduct an investigation and hold a hearing, Potter asked Deputy State Attorney General Ann Sheadel to investigate, giving her the power to subpoena documents and question witnesses under oath. Sheadel’s March 1997 report uncovered new twists to the story. A complex agreement did exist between Lilly and the plaintiffs, one so secret that it was never fully reduced to writing. All Sheadel could find was a written summary of the verbal agreement. No lawyer would admit preparing it, and no plaintiff was allowed to have it.

In exchange for the plaintiffs agreeing not to present the evidence of Lilly’s criminal conduct with Oraflex, Lilly had agreed to pay all plaintiffs, win or lose. Part of the agreement was that all of chief plaintiffs’ counsel Smith’s Prozac cases, including those in Indianapolis, were settled, and half his overall expenses paid by Lilly.

Judge Potter set a hearing to take sworn testimony on March 27, 1997. The hearing never happened.

On March 24, in a surprise move, attorneys for Lilly and the plaintiffs presented Judge Potter with a new stipulation and order in Fentress showing that the case was dismissed “as settled,” exactly what Potter had insisted on two years before. The judge signed the order. Three days later, Lilly’s attorney went before the appeals court to argue that any further proceedings were now moot. He also claimed that Potter had violated judicial ethics and was on a “vendetta” against Lilly. Potter recused himself, saying “the spotlight should be on what … is under the log, not the person trying to roll it over.”

The judge had succeeded in uncovering the collusive settlement. But of the approximately 160 active Prozac cases in December 1994, less than half remained.

Inexplicably, Fentress had received almost no attention in the national media, and the Kentucky court of appeal closed any further hearings to the public. Plaintiffs’ attorney Paul Smith was still practicing law in Dallas.

And the only thing that anyone ever learned about the amount of the settlement was the comment of a Louisville lawyer who represented one of the Fentress plaintiffs in a divorce. The amount, he said, was “tremendous.”

Adopted from pages 193-201 of The Moral Compass of the American Lawyer: Truth, Justice, Power, and Greed, © 1999, Richard Zitrin rzitrin@usfca.edu & Carol M. Langford langford@usfca.edu. All rights reserved.
This critically acclaimed book, about how the legal system allows lawyers to define “ethics” as what they can get away with rather than how they should behave, is written by two noted legal ethics professors who write frequently about ethics and morality in the legal profession.

 

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Could fish oil help lower your antidepressant dose?

Posted by shutah on January 26, 2011

Although the jury’s not out yet, there’s mounting evidence that the omega-3 fatty acids in fish oil can help some patients with depression.

Here’s a short article about a recent study on fish oil combined with low doses of two different kinds of antidepressants, Prozac and Remeron. The results suggest that some patients who struggle with side effects from antidepressants might be able to lower their dose and stay in remission from depression by adding fish oil. An important caveat — the study was done in rats, so the findings are preliminary.  Read more here.

 

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Potential SSRI/SNRI Withdrawal Symptoms

Posted by shutah on January 26, 2011

The SSRI/SNRI symptoms are originally from this website on Effexor withdrawal.

ANTIDEPRESSANT WITHDRAWAL SYMPTOMS. (SSRI/SNRI)

1. Crying spells
2. Worsened mood
3. Low energy (fatigue, lethargy, malaise)
4. Trouble concentrating
5. Insomnia or trouble sleeping
6. Change in appetite
7. Suicidal thoughts
8. Suicide attempts
9. Anxious, nervous, tense
10. Panic attacks (racing heart, breathless)
11. Chest pain
12. Trembling, jittery,or shaking
13. Irritability
14. Agitation (restlessness, hyperactivity)
15. Impulsivity
16. Aggressiveness
17. Self-harm
18. Homicidal thoughts or urges
19. Confusion or cognitive difficulties
20. Memory problems or forgetfulness
21. Elevated mood (feeling high)
22. Mood swings
23. Manic-like reactions
24. Auditory hallucinations
25. Visual hallucinations
26. Feeling detached or unreal
27. Excessive or intense dreaming
28. Nightmares
29. Flu-like aches and pains
30. Fever
31. Sweats
32. Chills
33. Runny nose
34. Sore eyes
35. Nausea
36. Vomiting
37. Diarrhea
38. Abdominal pain or cramps
39. Stomach bloating
40. Disequilibrium
41. Spinning, swaying, lightheaded
42. Hung over or waterlogged feeling
43. Unsteady gait, poor coordination
44. Motion sickness
45. Headache
46. Tremor
47. Numbness, burning, or tingling
48. Electric zap-like sensations in the brain
49. Electric shock-like sensations in the body
50. Abnormal visual sensations
51. Ringing or other noises in the ears
52. Abnormal smells or tastes
53. Drooling or excessive saliva
54. Slurred speech
55. Blurred vision
56. Muscle cramps, stiffness, twitches
57. Feeling of restless legs
58. Uncontrollable twitching of mouth



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