This is indistinguishable clinically from idiopathic
torsion dystonia except that it has a higher incidence of retrocollis and opisthotonic posturing. Tardive dystonia is often disabling and unfortunately has a lower rate of
remission than tardive stereotypy. It is always important to remember Wilson's disease can initially present as a psychiatric disorder acquiring neuroleptics that later becomes associated with dystonia.
Tardive dystonia differs from tardive stereotypy in
that it affects the young and old in an equal distribution and there's no increase ratio of female to male. In the younger age group males do appear to be affected more often than females. The onset of tardive
dystonia can occur as early as 3 weeks and 20% of patients are affected within the first year of exposure to the neuroleptic. Prevalence rates run from 2-20% of those chronically exposed to neuroleptics.
The overall remission rate is in the range of 10-20%,
which is much lower than tardive stereotypy. Remission can occur as late as five years after stopping the neuroleptic. Most patients progress for the first few months to a year and then stabilize.
The pharmacological substrates for tardive dystonia is
different than that in tardive stereotypy as anticholinergics often benefit these patients (45%). When tardive stereotypy is associated with tardive dystonia the use of anticholinergics can exacerbate the
stereotypies. Often it does not. The physician has to make a decision as to which of the movement disorders is more disabling and treat accordingly.
Treatment of Tardive Dystonia
As with tardive stereotypy prevention has to be
stressed. The first approach
in treatment is to remove the offending neuroleptic if possible or choose a lower potency neuroleptic. If troublesome dystonia persists then the most effective treatments are the dopamine depleters (Reserpine and Tetrabenazine) which have been reported to improve over 60% of patients. Anticholinergics improve the dystonia in 45% of patients. Some use anticholinergics in the young and dopamine depleters in older patients because of age related side effects. Other drugs that have had some success include clonazepam and Baclophen. For focal dystonias botulinum toxin is an excellent option. If all treatments fail then one has no choice but to resume the Dopamine antagonist in increasing doses. In this situation you're committing the patient to lifelong neuroleptic therapy.
Focal Bbotulinum toxin injection can provide useful
symptomatic treatment for patients with relatively localized tardive dystonia unresponsive to other treatment.
True tardive chorea is extremely rare and most cases
of "Rhythmic Chorea" would now be classified as stereotypy. These chorea-like movements are more patterned, rhythmical, and coordinated than typical chorea and the location is often different.
Tardive Tics or Tardive Tourettism
The occurrence of tardive tics is rare but there are
reports of neuroleptic induced motor and vocal tics as well as other behavioral symptoms. Often patients with this presentation have had preexisting brain damage. As this
syndrome is rare, consensus on treatment is unavailable. The guidelines as above, stopping the neuroleptic and considering dopamine depleters would likely be the main steps in management.
Tardive myoclonus has been rarely described and typically is a postural myoclonus when it occurs. Clonazepam is an effective treatment.
Tardive tremor has recently been described. As this is
typically a postural tremor but occasionally a rest tremor co-exists. Tetrabenazine was an effective treatment.
This is a late and persistent complication of
neuroleptic treatment and is similar to acute akathisia. The motor phenomenon resembles and can be termed tardive stereotypy. The pharmacology of tardive vs. acute akathisia is
clearly different, with tardive akathisia often behaving like tardive stereotypy. In one study it was found 34% of tardive akathisia occurred within one year and two-thirds of these patients had persistent tardive dyskinesia at a mean follow-up of 4.2 years. A female to male ratio of 2:1 has been reported. Leg, and or trunk movements are the most common.
The easiest and most effective treatment is to
increase the neuroleptic, but it seems judicious to try to discontinue the neuroleptic if at all possible as a first line of treatment. The next choice would be a dopamine-depleting agent such as
tetrabenazine. A trial of clonazepam, or an anticholinergic may be helpful. Unlike acute akathisia, opiates or beta-blockers are ineffective.