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Re: Tardive Dystonia Question (Cam W?) » steve

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


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