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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 16 of 16. This is the beginning of the thread.
Posted by steve on February 26, 2001, at 1:01:13
Hi,
Does anyone know if tardive dystonia is a permanent condition, in the sense that
it comes and goes, or is it a constant state.TIA
Posted by willow on February 26, 2001, at 8:08:27
In reply to Tardive Dystonia Question (Cam W?), posted by steve on February 26, 2001, at 1:01:13
"Does anyone know if tardive dystonia is a permanent condition, in the sense that
it comes and goes, or is it a constant state."Hi,
My father has severe td caused by his meds. It isn't constant in the sense of every minute of the 24 hour day. Stress and anxiety make it worse. If you are concerned about it seek out a doctor who is familar with it. From my understanding it is easier to treat if caught early, perhaps even reversible.Willow
Posted by judy1 on February 26, 2001, at 11:26:10
In reply to Tardive Dystonia Question (Cam W?), posted by steve on February 26, 2001, at 1:01:13
Is this a question for yourself? Are you taking anti-psychotics? When I was on an older AP (Mellaril), I had some symptoms of TD, but like Willow said, if caught early it can be reversible. With the newer atypicals, I can have problems at higher doses- but none at lower. I also take frequent drug holidays with AP's, but I do not have a chronic psychotic condition. I hope this helps a little- Judy
Posted by danf on February 26, 2001, at 14:15:05
In reply to Tardive Dystonia Question (Cam W?), posted by steve on February 26, 2001, at 1:01:13
& then of course is it TD or EPS ?
one can have both or either...
EPS responds to meds... TD does not very well.
Posted by Cam W. on February 26, 2001, at 15:07:08
In reply to Tardive Dystonia Question (Cam W?), posted by steve on February 26, 2001, at 1:01:13
Steve - Tardive dystonia (I have never heard of) differs from tardive dyskinesia (TD) in that while both appear late in the development of the disorder (tardive), dystonia refers to prolonged muscle contractions that may cause twisting repetitive movements or abnormal posture. Dystonic movements may be in the form of rhythmic jerks. The condition may progress in childhood, but progression is rare in adults. In children the legs are usually the first affected. The cause of dystonias could be from head traumas, strokes, brain tumors, toxic levels of manganeses or carbon disulfide, wasp stings or the side effects of some drugs used to treat parkinsonism or some antipsychotics.
Removal of the offending drug or treatment of the condition with anticholinergics, levodopa, localized botulanum toxin (for focal dystonias) have been used to reverse the dystonias.
I have never heard of "tardive dystonia" but, as I have said before diagnosis and disease states are really out of the realm of my expertise. I really am only an expert in psychopharmaceuticals.
OTOH - "Tardive dyskinesia" is a condition of slow, rhythmical, automatic stereotyped movements, either generalized or in a single muscle group. These occur as an undesired effect of therapy with certain psychotropic drugs (esp. the traditional antipsychotics like phenothiazines).
"Tardive dyskinesia" is usually (mostly) irreversible, or at least very hard to treat, but I don't know about "tardive dystonia" as I have never heard of it. Dystonias, in general, are easier to treat than tardive dyskinesia (but, like I say, I don't know about "tardive dystonia"). I'm not saying that this disorder doesn't exist; I am saying that it is out of my area of expertise and the information I have given is out of a medical dictionary.
Sorry that I cannot be of more help - Cam
> Hi,
>
> Does anyone know if tardive dystonia is a permanent condition, in the sense that
> it comes and goes, or is it a constant state.
>
> TIA
Posted by willow on February 26, 2001, at 22:24:40
In reply to Re: Tardive Dystonia Question (Cam W?) » steve, posted by Cam W. on February 26, 2001, at 15:07:08
"Tardive dyskinesia" is a condition of slow, rhythmical, automatic stereotyped movements, either generalized or in a single muscle group. These occur as an undesired effect of therapy with certain psychotropic drugs (esp. the traditional antipsychotics like phenothiazines)."
What is foot in mouth disease? (My poor attempt at a joke. :) I saw the tardive and made an assumption, oops.I had asked before about the quick jerks caused by effexor. I believe it was Noa who explained that it could be myclonic (sp) or something. They are infrequent during the day and not bothersome, but during sleep a different story. Baclofen helps with this. I'm assuming again that this has no relation to the TD? Just looking for a second assumption.
Twitching Willow
Posted by danf on February 27, 2001, at 6:39:36
In reply to What is ... (Cam W?), posted by willow on February 26, 2001, at 22:24:40
I'm assuming again that this has no relation to the TD? Just looking for a second assumption.
>
> Twitching WillowNo the muscle twitches of effexor, are not the same. Meds which 'classically' cause TD & EPS are the major tranqs. There is some debate if the SSRIs & effexor cause them ? is is very uncommon if it occurs.
5HTP & dextromethorphan will cause myoclonic twitches as will SSRIs & effexor & [b]anxiety[/b]. They are caused by an excitable myo-neural junction or excitable /irritable muscle membrane.beta blockers do not block the twitches.
the effect can be countered in many by magnesium & vit E supplements.
These are 2 very different med side effects.
twitchy Dan
Posted by willow on February 27, 2001, at 13:37:20
In reply to Re: What is ... (Cam W?), posted by danf on February 27, 2001, at 6:39:36
"the effect can be countered in many by magnesium & vit E supplements."
Are these supplements for the effexor side effects or TD? My father is on vitamin E for the TD. I find the low dose of baclofen at night helps, but I still feel a mild jump though I don't think I physically move when I take the baclofen.
If you find the supplements work what dosage do you take of them and can you take them when you take the effexor?
Willow
Posted by danf on February 27, 2001, at 14:53:00
In reply to Re: What is ... (Danf?), posted by willow on February 27, 2001, at 13:37:20
> "the effect can be countered in many by magnesium & vit E supplements."
>
> Are these supplements for the effexor side effects or TD?They are for muscle twitches... both vit E & Mg have a stabilizing on excitable membranes ( different mechanisms )
vit E, a couple of jelcaps /day
Mg 250 mg 2x /day ( 500 mg /day total
with both start at lowest dose & see how they work ? it takes about a week for full effect
Mg may cause loose BMs & vit E pimples.
There are no adverse interactions or problems with absorption, etc
Posted by SLS on February 27, 2001, at 19:28:52
In reply to Re: Tardive Dystonia Question (Cam W?) » steve, posted by Cam W. on February 26, 2001, at 15:07:08
> I have never heard of "tardive dystonia" but, as I have said before diagnosis and disease states are really out of the realm of my expertise. I really am only an expert in psychopharmaceuticals.I have seen the term "tardive dystonia" used in medical literature.
Can you give a more detailed description of what is "stereotyped" behavior or stereotypy?
Thanks.
- Scott
---------------------------------------------------------: Schizophr Bull 1999;25(4):741-8 Related Articles, Books, LinkOut
Tardive dystonia.van Harten PN, Kahn RS
Psychiatric Center Zon & Schild, Amersfoort, The Netherlands. zonenschild.a-opl@wxs.nl
This paper provides an overview of the phenomenology, epidemiology, and treatment of tardive dystonia. Tardive dystonia is one of the extrapyramidal syndromes that starts after long-term use of dopamine receptor antagonists. The diagnosis is based on the presence of chronic dystonia, defined as a syndrome of sustained muscle contractions, frequently causing twisting and repetitive movements or abnormal postures. Furthermore, dystonia must develop either during or within 3 months of a course of antipsychotic treatment, and other causes such as Wilson's disease, acute dystonia, or a conversion reaction must be ruled out. Tardive dystonia occurs in about 3 percent of patients on long-term antipsychotic treatment. Some probable risk factors for tardive dystonia are younger age, male, and the presence of tardive dyskinesia. The treatment of tardive dystonia starts with an evaluation of the need for using the causative drug. If antipsychotics must be continued, a switch to an atypical antipsychotic, particularly clozapine, may be helpful. If the dystonia is relatively localized, botulinum toxin is an effective but not well-known treatment possibility. If tardive dystonia is more extensive, either dopamine-depleting drugs or high dosages of anticholinergics can be tried.
Publication Types:
Review
Review, tutorialPMID: 10667744
Posted by Sunnely on February 27, 2001, at 19:41:35
In reply to Tardive Dystonia Question (Cam W?), posted by steve on February 26, 2001, at 1:01:13
Steve,
The term "tardive dystonia," (TDt) in the context of antipsychotic use was used by Burke et al. in 1982 to describe the dystonia in patients receiving dopamine antagonists (antipsychotics), who had no other known cause of dystonia. Their descriptions of patients with TDt included "arms often forcibly extend at the elbow; the trunk may be in form of back arching with excess lordosis, flexion, or lateral leaning." TDt may make walking and even eating difficult.
TDt is a form of tardive dyskinesia (TD) characterized by sustained or slow involuntary twisting movements of the face, neck, trunk, or limbs, has been described. This condition may co-exist with TD. TDt occurs much later than acute dystonic reactions. On the other hand, TDt occurs after a shorter exposure time to antipsychotics than tardive dyskinesia (TD). The patient may have history of acute dystonia and later develops similar but prolonged muscle spasms, torsion movements. TDt is more difficult to treat than TD; many patients with TDt continue to have disabling symptoms despite therapies.
Clinical Features of TDt:
TDt has been estimated to occur in 2% of patients treated long-term with antipsychotics. The onset of TDt tends to be gradual after months or more commonly years of treatment with dopamine antagonists (antipsychotics). The median years of exposure is 5 years, although an atypical onset after only a few weeks or even days of exposure has been described. TDt uniformly affects various age groups with a mean age of 39 years. TDt in males appear to develop at an earlier age; men - 34 years, women - 44 years. TDt usually begins in the face or neck (67%), less common to begin in one of the arms (11%) but never been observed to begin as focal dystonia of the foot.
In retrospective studies of patients with TDt, the condition usually begins in one location and then spreads. Following an early period of progression, TDt then stabilizes, whether or not the patient is continued on antipsychotics, and it does not spread further or worsen in severity. It tends to be a chronic condition. Fifteen percent of TDt are focal (localized in a region of the body), 72% develop to several regions, and 13% develop into a generalized dystonia. Focal TDt tends to involve the head muscles, either the neck, upper face, or lower face. Those with generalized TDt tend to be younger than those with focal TDt. At the maximum severity of TDt, 80% involve the neck (50% with retrocollis, head arched backward), 35% involve the trunk (mostly back-arching), 42% involve the arms (e.g., sustained extension of the elbow, especially when walking). The legs are affected infrequently.
Meige's syndrome associated with antipsychotic use is a form of TDt. This is characterized by blepharospasm (uncontrollable eyelid spasms) and oromandibular dystonia (mouth, jaw rigidity).
Diagnostic criteria for TDt:
1. Presence of dystonia (sustained, involuntary muscle spasm, frequently causing twisting and repetitive movements or abnormal postures) for more than 1 month.
2. If other involuntary movements (such as dyskinesia, akathisia) are additional present, the dystonia is the most prominent disturbance.
3. The dystonia develops during or within 3 months of discontinuation of treatment with dopamine antagonists.
4. No other neurologic signs to suggest one of the many known causes of secondary dystonia (e.g., Wilson's disease must be ruled out by a blood ceruloplasmin [copper] level and a slit-lamp examination for Keyser-Fleischer rings.)
5. A negative family history of dystonia.
Treatment of TDt:
1. Primary treatment is to discontinue the antipsychotic.
2. Pharmacologic treatment tried (mostly ineffective): a) choline agonists (choline, deanol), b) anticholinergics, c) dopamine agonists (e.g., amphetamine, L-dopa), d) dopamine antagonists (antipsychotic themselves), e) monoamine depleters (e.g., tetrabenazine, reserpine), f) benzodiazepines (clonazepam, alprazolam), g) others (baclofen, dantrolene).
3. There have been reports of TDt improving with Botolinum Toxin A (Botox A) injections. The toxin blocks the release of acetylcholine from motor end plates producing paralysis. It is generally well tolerated.
4. Clozapine - anecdotal reports alleviating symptoms of TDt and/or TD.
Future of TDt:
With the advent of newer generation of antipsychotics with absent/minimal extrapyramidal symptoms and less propensity to cause TD, it is anticipated that rate of occurence of TD/TDt should diminished. Probably not completely eliminated, as I believe I read somewhere of a case of Meige syndrome induced by risperidone (Risperdal).
=================================================
> Hi,
>
> Does anyone know if tardive dystonia is a permanent condition, in the sense that
> it comes and goes, or is it a constant state.
>
> TIA
Posted by Cam W. on February 27, 2001, at 19:47:26
In reply to Re: Tardive Dystonia Question (Cam W?) » Cam W., posted by SLS on February 27, 2001, at 19:28:52
Scott - As you know, I am the drug guy and for the dystonia/dyskinesia answer, I paraphrased it out of a dictionary. Further to this:
stereotypy - the persistent inappropriate mechanical repetition of actions, body postures, or speech patterns, usually occurring with a lack of variation in thought processes or ideas. It is often seen in patients with schizophrenia.
Like I say, if it is out of my realm of knowledge, you get the book answer. Sorry Scott - Cam
P.S. None of the 3 medical dictionaries that I have, nor the 2 dictionary websites I have bookmarked, include tardive dystonia in them.
> I have seen the term "tardive dystonia" used in medical literature.
>
> Can you give a more detailed description of what is "stereotyped" behavior or stereotypy?
>
Posted by dj on February 27, 2001, at 20:41:19
In reply to Re: Tardive Dystonia Question (Cam W?) » SLS, posted by Cam W. on February 27, 2001, at 19:47:26
> stereotypy - the persistent inappropriate mechanical repetition of actions, body postures, or speech patterns, usually occurring with a lack of variation in thought processes or ideas. It is >often seen in patients with schizophrenia.
Sounds like it may be similar to obsessive-compulsive patterning when referring to "thought processes or ideas"...???? And depression can also involve getting 'stuck' in a negative frame of reference...and negative actions and re-actions...Sunnely's reference, above, refers to TD &/or TD? as a reaction to antipsychotics which are used for bipolar treatment, I believe. Have any such reactions been noticed with SSRI's or other AD's, that any one knows of? One thing that put me off Paxil or Zoloft (one or the other) besides the other negative effects I experienced on it (deep, annoying yawns, etc - dullness of mood tone) and coming off (flu-like symptoms, electric buzz) was attempting to go back on one of them (Zoloft I think) and noticing some odd involuntary twitching which seems to be some of what is referred to above (so much jargon : ( ).
I just came back from a visit with the chiro. He was helping me loosen up some areas of fibrosis (his term for stuck, stiff atrophied areas of musculature) which I've have found bothersome over the past couple of years, in particular, - partly as a result of being hunched over a computer too much, bad postural habits and not enough consistent stretching, exercies and re-adjusting...
I've noticed when I'm really down that I can become almost catatonic at times, deep lethargy, poor reactivity, haphazard activity, not inflating my upper chest/lungs sufficiently, etc.-deep apathy and dire inactivity. A former pdoc. of mine, who's now running a Pscyh. dept. in an easern-Cdn. medical school (Dalhousie) once told me that ADs have some sort of tightening or firming approach on muscles grown flacid because of the biochemical processes of depression (never mind the inactivity contributing to this notably as well). Anyone know anything about these effects?
Sante!
dj
Posted by willow on February 27, 2001, at 22:49:08
In reply to Re: What is ... (Danf?), posted by danf on February 27, 2001, at 14:53:00
> > "the effect can be countered in many by magnesium & vit E supplements."
> >
> > Are these supplements for the effexor side effects or TD?
>
> They are for muscle twitches... both vit E & Mg have a stabilizing on excitable membranes ( different mechanisms )
>
> vit E, a couple of jelcaps /day
>
> Mg 250 mg 2x /day ( 500 mg /day total
>
> with both start at lowest dose & see how they work ? it takes about a week for full effect
>
> Mg may cause loose BMs & vit E pimples.
>
> There are no adverse interactions or problems with absorption, etc
Posted by SLS on February 28, 2001, at 6:34:31
In reply to Re: Tardive Dystonia Question (Cam W?) » SLS, posted by Cam W. on February 27, 2001, at 19:47:26
Dear Sunnely and Cam,
Thanks for addressing the questions regarding tardive dyskinetic syndromes.
Regarding Risperdal (risperidone), it is my impression that this drug lies somewhere between clozapine and the typical antipsychotics (Haldol) with regard to EPS and tardive dyskinesia. Whenever I browse Medline for antipsychotic related material, Risperdal pops up most often as the "atypical" that produces these conditions. There seems to be many more anecdotal reports for Risperdal. This is probably due, in part, to Risperdal being around longer than Zyprexa (olanzapine) and Seroquel (quetiapine). However, this trend also makes itself evident in controlled studies investigating other APs. In addition, of the atypicals, Risperdal is the one known to significantly produce increased secretion of prolactin in a way similar to the older drugs.
Does Risperdal possess the highest binding affinity for DA D2 receptors of the atypicals?
I like Risperdal and think it is an amazing drug for many people.
How would you guys rate the risk of EPS and TD for different dosages of Risperdal?
0.5mg
1.0mg
2.0mg
6.0mg
12.0mg
Thanks.- Scott
Posted by Cam W. on February 28, 2001, at 10:51:30
In reply to Re: Tardive Dystonia Question (Cam W?), posted by SLS on February 28, 2001, at 6:34:31
Scott - Risperdal probably causes more EPS than Clozaril and Zyprexa because when it was first marketed the doses recommended were in the 8mg to 12mg range. Subsequently, through clinical experience it was found that doses above 6mg/day greatly increased the incidence of EPS and that doses above 6mg/day are seldom more efficacious than those below this dosage (ie more is not necessarily better).
The reason that Risperdal causes more EPS than Zyprexa or Clozaril is that over 6mg/day Risperdal is saturating D2 receptors, making act more like a typical antipsychotic. When kept below 6mg/day (in most people) the incidence of EPS in comparable to low to mid-range doses of Zyprexa (7.5mg to 10mg/day).
Recent research has found that low doses of Risperdal (0.5mg - 1mg/day) are often enough for a therapeutic effect. Janssen really shot themselves in the foot when they came out with their original dosing guidelines. Risperdal is an effective drug when kept to lower doses, but the bad publicity in the past has really restricted it's use (unnecessarily).
Prolactin increases are also seen with Risperdal, but they are generally asymptomatic. I am not sure if they are dose related, but I do know that you do not see as many symptomatic cases (ie amenorrhea, galactorrhea, etc) at doses under 6mg/day.
Hope this helps - Cam
This is the end of the thread.
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