![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 18 of 18. This is the beginning of the thread.
Posted by SueG on July 13, 2000, at 17:49:02
I seem to have gained a very annoying twitch on my left lower eye-lid. It began a few weeks ago, just once or twice per day but now is happening every 5 minutes or so. Is this known to be a side effect of Prozac? It seems to have co-incided with my starting this medication. I am into my 5th week now. No other real problems with the medication besides the odd sleepless night and delayed orgasm - nothing I can't put up with at this stage. Otherwise it is doing great things for me. I am on 20mg/day.
Anyone else had any eye twitches????
Sue
Posted by Sunnely on July 13, 2000, at 23:20:29
In reply to Prozac causing eye twitch?, posted by SueG on July 13, 2000, at 17:49:02
> I seem to have gained a very annoying twitch on my left lower eye-lid. It began a few weeks ago, just once or twice per day but now is happening every 5 minutes or so. Is this known to be a side effect of Prozac? It seems to have co-incided with my starting this medication. I am into my 5th week now. No other real problems with the medication besides the odd sleepless night and delayed orgasm - nothing I can't put up with at this stage. Otherwise it is doing great things for me. I am on 20mg/day.
> Anyone else had any eye twitches????
> Sue======================
If you noticed the occurrence of eye twitching with the start of Prozac and continues to worsen while on this drug, most likely it is the main culprit. (Unless you are taking other drugs that may cause similar problem.) Not to cause undue alarm, I have a gut feeling that you are experiencing the beginning of a condition called "tardive dyskinesia" (TD). Eye twitching or tic has been reported with the SSRIs. Sometimes, it is accompanied by other involuntary facial and mouth movements. Tardive dyskinesia is one form of extrapyramidal symptoms (EPS). The other forms include dystonia (muscle rigidity), akathisia (motor restlessness), and parkinsonism (e.g., tremor).
EPS is believed to be due to the blockade of brain dopamine action. SSRIs (Prozac, Zoloft, Paxil, Luvox, Celexa) are known for their serotonin-boosting effect. Serotonin is a brain chemical which exerts some influence on the action of dopamine i.e., it is a "neuromodulator" of dopamine. Increased serotonin action leads to decreased dopamine action.
Tardive dyskinesia (TD) has been known to occur with the antipsychotics (more common with the older drugs). However, there are increasing number of anecdotal reports published in the literature of TD from the use of SSRIs (more common with Prozac). The exact cause of TD is unknown but it is believed that after long-standing blockade of the dopamine receptors, they become "supersensitive and overactive" leading to the involuntary muscle movement known as TD. This is known as the "supersensitivity of postsynaptic dopamine receptors" hypothesis. Muscle areas more commonly affected by TD are the mouth and facial muscles. Patient may develop repetitive tongue protrusion or darting, chewing, puckering, sucking movements of the lips; facial twitchings, teeth-clenching, etc. The eye muscles may be affected such as twitching, frequent blinking, and spasm/tightness called "blepharospasm." ("Blepharospasm" can be sometimes so severe that a series of injections of a drug called "Botox" have to be given in some cases to alleviate the problem.) TD can be very distressing and sometimes irreversible if not recognized and treated early.
I suggest you discuss this matter with your physician. At times lowering the dose of the medication may alleviate the problem. However, in most cases, a change in the medication may be the best approach to alleviate this potentially serious problem. To continue with the offending drug risks worsening the TD which could eventually involve the other muscle areas.
An excellent description of eye twitching (and other dyskinetic movements) caused by Prozac can be found in the book "Prozac Backlash" page 29, "Maura: A Case of Disfiguring Tics."
Posted by danf on July 14, 2000, at 1:12:40
In reply to Re: Prozac causing eye twitch?, posted by Sunnely on July 13, 2000, at 23:20:29
Sue,
How do you do ?
most of the time good information comes out here on Babble.
On occasion BS floats to the top. TD is a late effect. A twitch is rarely TD.
OK for the book. I write in a terse form, Bear or bare with me. The likelyhood that an early eyelid twitch is TD is close to an iceberg hitting Key West, particularly when the med is known for serotonin induced muscle fasics !
first it is not an eye twitch. it is an eyelid twitch. A major difference. Eyelid twitches are rare in TD. rhythmic ( wish I could spell ) repetitive movements are the rule.
To advance a theory of TD as a cause is irresponsible in this situation.
SSRIs cause muscle twitches for several weeks after starting the meds.
Damn, I know it well. Have had twitches in almost every part of the body ( not eyelid yet ).What makes a difference in where the twitches occur ? If one has any kind of panic or anxiety induced twitches, that pattern is amplified when starting SSRIs. The strange thing is that it is not the same for the different meds. the patterns are usually like the anxiety patterns (key is LIKE, not exact same as ). so usually the same body area is affected. I get left leg, in the calf, with some above the knee in the quads. Not arm, not face, not right leg, etc.
A personal observation, based on prozac, celexa & zoloft. I have a bitch of startup symptoms, with zoloft being the worst , so far, bordering on psychosis induction ( and don't ever plan on zoloft again, by the way )
Anyway ..... muscle twitches are induced by hyper sensitivity of the muscle & /or neuro muscular junction. they usually go away after a few weeks. Magnesium helps in decreasing them. If there is either a local or general warm /hot skin feeling at about the same time, best thing to do is decrease the med dose & then increase it slowly over time ( this is usually serotonin induced).
This will give the body time to adapt to the higher serotonin levels.
If you have a question about this you can do your own self experiment ( which has danger !!!!!!!!!! ). yes, I have done it !!!!
Take a reduced dose of med until the twitches stop or greatly reduce & then add a dose of 5HTP ( 25mg ), If the Sx recurr after the 5HTTP it is serotonin induced.
I do not recommend this !!! Because you can cause a serotonin toxic syndrome.
Any way., the evidence points to SSRI serotonin induced med related startup side effects & not TD.
Posted by noa on July 14, 2000, at 7:23:39
In reply to Whoa !!! here !!!!, posted by danf on July 14, 2000, at 1:12:40
I would agree that it is not likely to be TD. First of all, my understanding is that TD is not common in Prozac. Second, my understanding is that TD comes as a result of ongoing, longterm use of certain meds at high doses.
I have had muscle twitching as a reaction to paxil and effexor, though only when at rest, like when lying in bed before sleep. It is helped by taking another antidepressant, Serzone, which is sedating, and counters the activating aspects of effexor.
It could be an INITIAL effect, meaning it will fade with time. If it doesn't, I would consider trying a different medication, or try lowering the dose and adding another AD, one less activating than PRozac.
Posted by Angela5 on July 14, 2000, at 12:06:57
In reply to Re: Whoa !!! here !!!!, posted by noa on July 14, 2000, at 7:23:39
The other issue here is that you mentioned sleepless nights. This eyelid twitch is likely to improve greatly as your sleep schedule straightens out.
Posted by Dr. Bob on July 14, 2000, at 22:25:20
In reply to Whoa !!! here !!!!, posted by danf on July 14, 2000, at 1:12:40
> On occasion BS floats to the top.
> To advance a theory of TD as a cause is irresponsible in this situation.
Please feel free to express opposing points of view, but please also try to be sensitive to the feelings of others. Thanks,
Bob
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.
==================================================
>
> 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.
Posted by SLS on July 15, 2000, at 11:36:21
In reply to Re: Whoa !!! here !!!!, posted by Sunnely on July 14, 2000, at 22:26:56
Dear Sunnely,
Thank you for posting such a comprehensive, organized, and well documented review regarding TD.
I recently bumped into one study that's statistics indicated that it was not age that was the associative factor, but rather the number of years on the medication. They concluded that it was the elderly population that have been taking neuroleptics the longest.
Your wording of #1 implies otherwise. However, I wonder what the rate is at which this elderly population have cycled on and off neuroleptics, perhaps with the waxing and waning of their illness or for having taken "drug holidays". Employing drug holidays had been the standard practice years ago, but we now know that this actually increases the risk of developing TD many fold.
Are blood-levels of neuroleptics ever used clinically?
- Scott
> 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.
>
Posted by Sunnely on July 15, 2000, at 17:16:26
In reply to Re: Risks of developing TD » Sunnely, posted by SLS on July 15, 2000, at 11:36:21
> Thank you for posting such a comprehensive, organized, and well documented review regarding TD.
Thanks for those kind words.
--------------------------------------------------> I recently bumped into one study that's statistics indicated that it was not age that was the associative factor, but rather the number of years on the medication. They concluded that it was the elderly population that have been taking neuroleptics the longest.
As I have mentioned in my previous post, both age and duration of neuroleptic treatment are considered among the risk factors for TD. (Reference: Tardive Dyskinesia: A Task Force Report of the American Psychiatric Association. American Pwsychiatric Association Press, Washington, DC, 1992.)The study you bumped into is correct but does not paint the whole picture. FYI, the usual onset of schizophrenia is at late teens to 20s. (Earlier onset with males than females.) If these people start receiving neuroleptics at this age range, in 40 to 50 years they would be considered elderly and therefore high risk for TD (elderly with 40-50 years exposure to neuroleptics). However, if you compare the risk of TD on a person in his/her 20s receiving neuroleptic for the first time and an individual in his/her 60s receiving neuroleptic for the first time, the chance of TD developing and at much earlier stage is much higher in the latter.
The risk of TD remains fairly stable through ages 20 to 40, then rises considerably. TD is 3 times higher in people over age 40 than under 40. Postmenopausal women have a higher risk for TD than premenopausals. (The female hormones may have some protective factor.) This risk continues to rise until about age 70 when the risk of TD in women becomes similar to that seen in men.
The bottom line here is, the older a person is when he/she first receives neuroleptic, the more likely he/she is to develop TD early in treatment. Not only does TD occur earlier in the elderly, it is more severe and persistent in this age population.
--------------------------------------------------> Employing drug holidays had been the standard practice years ago, but we now know that this actually increases the risk of developing TD many fold.
Exactly. There were 2 types of maintenance treatment strategies with neuroleptic: 1) Continuous "low-dose" neuroleptic treatment, and 2) Intermittent or "targeted" neuroleptic treatment strategy. With the first strategy, neuroleptic is administered continuously but at doses that are lower than those conventionally used used to treat psychotic symptoms. With the second strategy, patients require neuroleptic medication ONLY during time of symptom exacerbation. One of the drawbacks found with the intermittent treatment strategy is that, there appears to be a correlation between the number of on/off cycles of medication and incidence, severity, and persistence of TD. Needless to say, the second treatment strategy was subsequently abandoned.
--------------------------------------------------> Are blood-levels of neuroleptics ever used clinically?
Yes, but not routinely. For many drugs, determining blood levels are not available or reliable. As much as 100-fold variation in blood levels among patients receiving the same dose of neuroleptics have been recorded. For others, blood levels have little relationship to clinical effects. Some drugs have several metabolites that just complicate the picture.There are at least 2 neuroleptics, I am aware of wherein determining blood levels are beneficial: haloperidol and clozapine. It was suggested that there is a curvilinear (inverted "U" shape or bell-shape) relationship between the blood level of haloperidol and clinical response. (Sometimes this is called "therapeutic window.") The late Dr. Van Putten suggested a haloperidol blood level range of 5-12 ng/ml although some consider an optimal range of 4 to 25 ng/ml. What this curve means is that, anything below and above the suggested blood level range leads to poor response. Higher levels lead to loss of antipsychotic effect but continued rise in side effects. Of course, this is not etched in stone. In some patients, their psychosis only remit with higher blood levels. (Reference: Clinical Use of Neuroleptic Plasma Levels by Marder SR, Davis JM, and Janicak PG. American Psychiatric Press, Inc., Washington, DC, 1993.)
Clozapine is another drug where blood level determinination is considered beneficial. Clozapine experts like Perry PJ and others, recommend a "therapeutic" blood level of at least 350 ng/ml. Again, this is not etched in stone. A number of patients on Clozaril do well with blood levels less than 350. Another occasion where clozapine blood level is beneficial is in situation where you would like to avoid a serious side effect. Patients with clozapine blood levels higher than 1000 ng/ml are at high risk for seizures. Rising clozapine blood level can happen when another drug that inhibits the metabolism of clozapine is added. For example, Luvox is a marked inhibitor of CYP1A2 (main metabolic pathway of clozapine).
Determining blood levels of a neuroleptic is helpful in the following situations:
1) Distinguishing between side effects and psychosis.
2) Drug-drug interactions.
3) Suspected noncompliance.
4) When toxicity is suspected.
5) In elderly or medical ill, monitor side effects.
6) To document the level of a therapeutic dose for an individual patient, especially those requiring unusually high or low doses (may be helpful in legal cases).
7) To expedite rapid treatment of suicidal or homicidal patients.
8) Help define the dose-response relationship.
9) Provide objective data when there is paucity of hard information.
10) Determine if there has been an adequate trial.
11) Determine if the patient responded to the active drug or had a placebo response.
12) Determine if the benefit outweighs the potential for adverse effects.
13) Minimize cost. (a) Noncompliance and subtherapeutic blood levels ----> delay remission of schizophrenic condition ----> prolongs hospital stay or additional outpatient visits. (b) Identifying excessive blood levels ----> avoids toxicity ----> avoids unnecessary or prolonged hospitalization (and additional laboratory work up).
Posted by SueG on July 15, 2000, at 17:21:36
In reply to Whoa !!! here !!!!, posted by danf on July 14, 2000, at 1:12:40
Thanks to all who replied to my post. Because i am only in the early stages of medication and it is helping my depression immensely, I am reluctant at this stage to alter my dose. However, in a few weeks i may try to lower it by taking it every second day and see what happens. I have tried Paxil before but this gives me anorgasmia. At least with Prozac its manageable.
I have not noticed any other involuntary body movements apart from this twitch. I do, however, bite my lips and mouth quite a bit now (anxiety I suppose.) I have always done this but seems to be happening more frequently.
My sleeping over this weekend was pretty bad. I try to use a natural sedative (Valerian) but this is rarely enough. I use temazepam otherwise. I still wake up early, my mind really active. This is not a completely bad thing though. I need activation, as my depression caused major apathy so it is refreshing to be able to get out of bed at 6am and feel "awake"! It is annoying though, that my sleep is so broken. I am hoping it will settle down.
Once again, thanks to your replies.
> Sue,
>
> How do you do ?
>
> most of the time good information comes out here on Babble.
>
> On occasion BS floats to the top. TD is a late effect. A twitch is rarely TD.
>
> OK for the book. I write in a terse form, Bear or bare with me. The likelyhood that an early eyelid twitch is TD is close to an iceberg hitting Key West, particularly when the med is known for serotonin induced muscle fasics !
>
> first it is not an eye twitch. it is an eyelid twitch. A major difference. Eyelid twitches are rare in TD. rhythmic ( wish I could spell ) repetitive movements are the rule.
>
> To advance a theory of TD as a cause is irresponsible in this situation.
>
> SSRIs cause muscle twitches for several weeks after starting the meds.
> Damn, I know it well. Have had twitches in almost every part of the body ( not eyelid yet ).
>
> What makes a difference in where the twitches occur ? If one has any kind of panic or anxiety induced twitches, that pattern is amplified when starting SSRIs. The strange thing is that it is not the same for the different meds. the patterns are usually like the anxiety patterns (key is LIKE, not exact same as ). so usually the same body area is affected. I get left leg, in the calf, with some above the knee in the quads. Not arm, not face, not right leg, etc.
>
> A personal observation, based on prozac, celexa & zoloft. I have a bitch of startup symptoms, with zoloft being the worst , so far, bordering on psychosis induction ( and don't ever plan on zoloft again, by the way )
>
> Anyway ..... muscle twitches are induced by hyper sensitivity of the muscle & /or neuro muscular junction. they usually go away after a few weeks. Magnesium helps in decreasing them. If there is either a local or general warm /hot skin feeling at about the same time, best thing to do is decrease the med dose & then increase it slowly over time ( this is usually serotonin induced).
>
> This will give the body time to adapt to the higher serotonin levels.
>
> If you have a question about this you can do your own self experiment ( which has danger !!!!!!!!!! ). yes, I have done it !!!!
>
> Take a reduced dose of med until the twitches stop or greatly reduce & then add a dose of 5HTP ( 25mg ), If the Sx recurr after the 5HTTP it is serotonin induced.
>
> I do not recommend this !!! Because you can cause a serotonin toxic syndrome.
>
> Any way., the evidence points to SSRI serotonin induced med related startup side effects & not TD.
Posted by danf on July 15, 2000, at 17:24:09
In reply to Re: Risks of developing TD » Sunnely, posted by SLS on July 15, 2000, at 11:36:21
civil... yes, I was uncivil
I am sorry for any offense.
atypical TD following any SSRI use is not likely to follow any typical AP stastics. the jury is out !
What is missing here is the anxiety quotient of the person.
If this is anxiety, panic, depression under Tx & other anxiety induced physical body Sx have happened in the past, then this is likely med / anxiety related.
The old zebra /horse analogy comes to mind. If one hears hoof beats, don't look for a zebra. look for the most reasonable thing first. This does not mean there is never a zebra, just that it is usually a horse.
Zebra lovers with a penchant for words can convince us it is a zebra based on the cadence of the hoof beats, the phase of the moon, et al.
A look at the animal is much better for identity.
atypical TD from a non AP drug is possible ! It should not be high on the list of reasonable causes. TD would be a major cause to discontinue the med ASAP !!!!!
Posted by Dr. Bob on July 15, 2000, at 23:06:49
In reply to RE: TD civility, posted by danf on July 15, 2000, at 17:24:09
> civil... yes, I was uncivil
>
> I am sorry for any offense.Thanks for apologizing. It seemed clear that you meant well, but still I thought I needed to say something. OK, back to business...
Bob
Posted by MB on July 17, 2000, at 11:11:34
In reply to Re: Whoa !!! here !!!!, posted by noa on July 14, 2000, at 7:23:39
Tardive = "Late in Treatment"
Dyskinesia = "Ill/Bad Movement"By definition, TD could not happen
early in Treatment. It would simply
be dyskinesia, or a movement disorder.
I *have* found prozac to exacerbate
tics in my eye muscles, but these are
not involuntary, just seemingly irresistable
at times.>Second, my understanding is that TD comes as a result of ongoing, longterm use of certain meds at high doses.
Posted by afatchic on July 17, 2000, at 19:17:25
In reply to RE: TD civility, posted by danf on July 15, 2000, at 17:24:09
I took prozac for several years. It worked fantastic as an AD. I quit last year when I finally made the connection with prozac and the mystery of my vanishing sex drive. The last three months I was on the medication, I developed a very annoying twitch in my right eye that steadily got worse. I remember thinking that it couldn't be the prozac because I'd been taking it for many years without this side-effect(ignorance is not always bliss). I quit taking prozac and the twitch went away. And if anyone is interested, the sex drive came back 8-)
> civil... yes, I was uncivil
>
> I am sorry for any offense.
>
> atypical TD following any SSRI use is not likely to follow any typical AP stastics. the jury is out !
>
> What is missing here is the anxiety quotient of the person.
>
> If this is anxiety, panic, depression under Tx & other anxiety induced physical body Sx have happened in the past, then this is likely med / anxiety related.
>
> The old zebra /horse analogy comes to mind. If one hears hoof beats, don't look for a zebra. look for the most reasonable thing first. This does not mean there is never a zebra, just that it is usually a horse.
>
> Zebra lovers with a penchant for words can convince us it is a zebra based on the cadence of the hoof beats, the phase of the moon, et al.
>
> A look at the animal is much better for identity.
>
> atypical TD from a non AP drug is possible ! It should not be high on the list of reasonable causes. TD would be a major cause to discontinue the med ASAP !!!!!
Posted by Alison27 on February 2, 2001, at 11:12:29
In reply to Re: Prozac causing eye twitch?, posted by Sunnely on July 13, 2000, at 23:20:29
Hi - I have read your comments with interest. I am 30 yr old English lady and have developed a twitch in my left upper eye lid around the central eyelashes. It had not occured to me that it could be to do with an anti-depressant. I am on Zyban, to stop smoking.. which has worked. It is however, a mild anti-depressant. Could the messages about Prozac and this link to another similar medicine mean there is an association between seratonin releasing medecines and a twitching eye?
Posted by SLS on February 2, 2001, at 15:55:13
In reply to Zyban and eye twitch, posted by Alison27 on February 2, 2001, at 11:12:29
Hi Alison.
As you know, Zyban is another name for the same drugs Wellbutrin and bupropion, commonly used as antidepressants. It is not a Prozac-type drug. Twitching and tics, although uncommon, are reported side effects. Bupropion has been known to make tic disorders worse. I don't know if these side effects are dependant on dosage, so I can't say whether lowering the dosage would help. Maybe the side effect will dissipate with time.
Good luck.
- Scott
> Hi - I have read your comments with interest. I am 30 yr old English lady and have developed a twitch in my left upper eye lid around the central eyelashes. It had not occured to me that it could be to do with an anti-depressant. I am on Zyban, to stop smoking.. which has worked. It is however, a mild anti-depressant. Could the messages about Prozac and this link to another similar medicine mean there is an association between seratonin releasing medecines and a twitching eye?
Posted by DianeD on February 9, 2001, at 12:40:25
In reply to Zyban and eye twitch, posted by Alison27 on February 2, 2001, at 11:12:29
When ever I take Wellbutrin SR (just 150mg) now I get a twitch under my left eye. I stopped taking it because of that. I take nothing else.
Posted by janeraab on June 30, 2001, at 17:05:55
In reply to Wellbutrin and eye twitch, posted by DianeD on February 9, 2001, at 12:40:25
> When ever I take Wellbutrin SR (just 150mg) now I get a twitch under my left eye. I stopped taking it because of that. I take nothing else.
I have had my lower lips twitch only as I am about to go to sleep. I have taken Wellbutrin for about 5 years and took Nardil for about 11 years before that. This lower lip twitching started sometime when I was on Nardil. It has not changed; it's not gotten better or worse. I don't know what to make of it. It only happens when I am about to fall asleep. It doesn't really seem the same as what everyone is talking about. But it is something that concerns me that I have not gotten any info about from any doctor or any source I have looked at. Does anybody have any ideas about it?
This is the end of the thread.
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