Posted by Sunnely on July 14, 2000, at 22:26:56
In reply to Whoa !!! here !!!!, posted by danf on July 14, 2000, at 1:12:40
> TD is a late effect.
>Wait. Not too fast with your conclusion. In contrast to the antipsychotics, TD in association with antidepressant treatment appears to be typically rapid in onset and disappears rapidly after the offending antidepressant is removed. (Reference: Yassa R, Camille Y, Belzile L: Tardive dyskinesia in the course of antidepressant therapy: a prevalence study and review of the literature. Journal of Clinical Psychopharmacology 1987;7:243:246.)
Although it may sound a contradiction ("tardive" means late-onset), TD is not always a late-onset adverse event (i.e. only occurs after several months or years of treatment). The following illustrates an example of early-onset TD. (Reference: Spivak M, Smart M: Tardive dyskinesia from low-dose risperidone (letter). The Canadian Journal of Psychiatry 2000;45:202. This a case of a 74-year-old female who developed depression and anxiety following left knee replacement. She refused to take antidepressant but agreed to take risperidone 0.5 mg twice daily. Three weeks after, she developed features of TD including oral, truncal, and limb movements.)
Although in most cases, the symptoms of TD first show after several months or years of antipsychotic treatment, there are certain groups of patients who are at much higher risk for TD (and at earlier stage). At least, these things what are generally known about the risks of TD with antipsychotic drugs, sometimes called "major tranquilizers". They include:
1) Age - age is still the most consistent risk factor. The older the patient is, the higher the risk for TD. TD can develop in the elderly within a couple of weeks. This is the reason why, in this group of patients, it is recommended to do AIMS at much more frequent intervals than the others.
2) Gender - Women has higher risk of TD than men, although this may be limited to the geriatric age range. Postmenopausal women have a higher risk of TD than premenopausal.
3) Psychiatric Diagnoses - those with dementia (e.g., Alzheimer's disease) and other organic brain syndromes, history of brain injury, developemtally disabled or mentally retarded, and affective/mood disorders have higher risk for TD. Patients with depression and bipolar disorder have a higher risk for TD than patients with schizoprenia.
4) Dose and Duration of Antipsychotic Treatment - the higher the dose, the longer the treatment, the higher the risk for TD.
5) Early Signs of Extrapyramidal Symptoms such as acute dystonia, akathisia (motor restlessness), parkinsonism, are more likely to develop TD in the future, if treatment is continued.
6) Smokers - appears to be associated with higher risk for TD (but lower risk for Parkinson's disease).
7) Alcohol abuse - higher risk for TD than nonalcohol abusers.
8) Diabetics (on antipsychotics) appear to have higher risk for TD than nondiabetics on antipsychotics.
9) Concomitant use of drugs that have the potential to cause TD such as tricyclic antidepressants, SSRI antidepressants, metoclopramide (Reglan).
9) Unknown individual factors - possibly a genetically determined vulnerability plays an essential part. For example, one may have a genetic polymorphism (defective) for certain liver enzymes (cytochrome enzymes) responsible for the metabolism of certain psychotropics leading to much higher blood level than the "normal" population, leading to higher risk for TD.
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> To advance a theory of TD as a cause is irresponsible in this situation.I must admit I may have rushed into suggesting that this could be the beginning of TD. I was merely trying to point out that TD from SSRIs is for real and has been reported. (References: [1] Lauterbach ED, Meyer JM, Simpson GM: Clinical menifestations of dystonia and dyskinesia after SSRI administration (letter). Journal of Clinical Psychiatry 1997;58:403. [2] Budman DL, Bruun RD: Persistent dyskinesia in a patient receiving fluoxetine (letter). American Journal of Psychiatry 1991;148:1403. [3] Nielsen AS, Mors O: Choreiform dyskinesia with acute onset and protracted course following fluoxetine treatment (letter). Journal of Clinical Psychiatry 1999;60:868-869. [4] Oslin DW, Duffy K: Dyskinesia associated with fluvoxamine (letter). Journal of Clinical Psychopharmacology 1993;13:365. [5] Madhussodanan S, Brenner R: Reversible choreiform dyskinesia and extrapyramidal symptoms associated with sertraline therapy (letter). Journal of Clinical Psychopharmacology 1997;17:138-139.)
As of December 31, 1996, postmarketing surveillances indicated 383 cases of dystonia, 403 cases of akathisia, 503 cases of parkinsonism, and 120 CASES OF TARDIVE DYSKINESIA associated with the use of fluoxetine, sertraline, and paroxetine. (Reference: Leo RJ: Clinical manifestations of dystonia and dyskinesia after SSRI administration: A reply. Journal of Clinical Psychiatry 1997;58:403-404.)
Based on this action, I would not consider this an "irresponsible" behavior. Of course, TD can only be diagnosed by a face-to-face examination of the patient. Without this luxury, one's description of a movement disturbance could be interpreted in various ways. But if I were prescribed an SSRI and suddenly experience some form of involuntary movement (call it a "twitch", "tic", "jerkiness," "spasm," "shake" or what-have-you), not present in the beginning and seems to be worsening (from 2 "twitch" a day to every 5 minutes), I'd be really worried and call my doctor ASAP. Of course, one has the option to wait it out to see if the "twitch" gets better in several weeks. But personally, I'd rather be wrong (that it's not a TD) than sorry. Just my own 2 cents.
poster:Sunnely
thread:40349
URL: http://www.dr-bob.org/babble/20000708/msgs/40477.html