Neuroleptic-induced
Acute Dystonia
This
long-lasting contraction or spasm of musculature develops in conjunction with
the use of antipsychotic medication. The pathophysiological mechanism of
neuroleptic-induced acute dystonia is presently unknown. The finding that
anticholinergic medication reverses the dystonia consistently may suggest that
a hypercholinergic state is a correlate of dystonia. There is some suggestion
of a correlation with changing blood–brain levels of antipsychotic medication.
It is also possible that dystonia is re-lated to the changing ratio of dopamine
D2 to D1 receptors that accompany the normal aging process.
Abnormalities
in dopamine–acetylcholine balance have been suggested as a possible mechanism
because cholinergic antagonists and dopaminergic agonists seem to improve the
dys-tonia in many patients, in contrast to dopaminergic antagonists, which seem
to exacerbate or even cause dystonia. In contrast, some investigators have
proposed that dopaminergic excess may be the responsible factor.
Acute
dystonia is generally less common than most other ex-trapyramidal side effects
of antipsychotics. Its frequency has been reported to range from 2 to 12% of
patients taking conventional antipsychotic medication. For patients who receive
high doses of high-potency conventional agents, however, the frequency may be
as high as 50%. Incidence of acute dystonia can probably be reducedto
approximately 2% if low-dose treatment strategies are employed. Furthermore,
acute dystonia is considerably less likely to occur with atypical antipsychotic
medications (i.e., less than 5% of individuals) (American Psychiatric
Association, 2000). For example, dystonic reactions occurred in less than 5% of
patients in a study of ziprasi-done and 1% in a dose comparison study with
quetiapine.
Large doses of high-potency conventional antipsychotics appear to be the most consistent risk factor reported for acute dystonia. Other factors that also seem to predispose to dystonia are young age and male sex. A prior dystonic reaction is a good predictor of a repeated episode when the same antipsychotic at the same dose is reapplied.
Neuroleptic-induced
dystonia (sometimes referred to as a dys-tonic reaction) usually begins 12 to
36 hours after a new antipsy-chotic is started or the dosage of a preexisting
one is increased. It is unusual to see a dystonia after 2 weeks of
antipsychotic treat-ment, and probably 90% of all neuroleptic-induced dystonias
oc-cur within the first 5 days of antipsychotic treatment. Patients may report
a sense of tongue “thickness” or difficulty in swal-lowing in the 3 to 6 hours
preceding the acute dystonia.
Acute
dystonia presents as a sustained, painful muscle spasm that produces twisting,
squeezing and pulling movements of the muscle groups involved. The most common
muscle groups affected are the eyes, jaw, tongue and neck, but any muscle group
in the body can be involved. On occasion, the larynx or pharynx may be
involved, and this can result in rapid respiratory compro-mise (American
Psychiatric Association, 2000).
Neuroleptic-induced
acute dystonias are dramatic and usually easy to diagnose. There are, however,
a number of other conditions that can present similarly and need to be ruled
out. Spontaneously occurring focal or segmental dystonias may per-sist for days
to weeks independent of medication. Neurological conditions such as temporal
lobe seizures, infections, trauma, or tumors can produce symptoms similar to
the neuroleptic-induced acute dystonia. A number of medications, while
generally less common than antipsychotics, can cause dystonias (e.g.,
anticon-vulsant medications and selective serotonin reuptake inhibitors)
(American Psychiatric Association, 2000).
Neuroleptic
malignant syndrome (NMS) can produce muscle contractions that look similar to
acute dystonia but can be distinguished by generalized “lead pipe” type of
rigidity, fever, fluctuating consciousness and unstable vital signs. Catatonia
as-sociated with an affective or psychotic disorder can be difficult to
distinguish from dystonia clinically but does not respond to the administration
of anticholinergic or antihistaminic medication. Furthermore, patients with
catatonia are typically not concerned about their stiffness, whereas the
patient with dystonia are likely to be extremely distressed (American Psychiatric
Association, 2000).
On
occasion, an acute dystonic reaction may resemble tar-dive dyskinesia (TD).
This is easily clarified by administering anticholinergic medications, which
rapidly clear dystonia and do not affect (or may worsen) TD. Making a differential
diagnosis between an acute dystonia and tardive dystonia can be difficult.
Tardive dystonia (similar to TD) is a diagnosis made late in the course of
antipsychotic treatment and is generally a chronic con-dition compared with
acute dystonia, which occurs early in the course of medication treatment and
typically responds rapidly to pharmacological intervention.
neuroleptic-induced
acute dystonia typically subsides sponta-neously within hours after onset.
However, treatment should be started as soon as the dystonia is diagnosed
because the experi-ence is “intensely” distressing to the patient.
The
standard approach to treatment is the immediate administra-tion of an
anticholinergic or antihistaminic agent. In most cases, this medication may be
administered orally, intramuscularly, or intravenously. The first dose of
medication should be the equiva-lent of 2 mg of benztropine or 50 mg of
diphenhydramine. This should be repeated if the first dose does not produce a
robust response within 30 minutes. This standard approach is usually successful
in resolving the dystonia.
In the
unusual refractory case, intramuscular or intra-venous anticholinergic or
antihistaminic drugs should be used at more frequent dosing intervals, and consideration
should be given to adding an intramuscular injection of lorazepam for
ad-ditional sedation. Since even the milder dystonias respond much more quickly
to intramuscular or intravenous medication, it may therefore be worth avoiding
the use of oral medication in treating dystonia. Oral medication takes much
longer to work and is likely to result in unnecessarily prolonged distress of
the patient.
In cases
of laryngeal or pharyngeal dystonias with air-way compromise, repeated dosing
of medication should oc-cur at shorter intervals until resolution is achieved.
Arana and Rosenbaum (2000) recommended that the patient receive 4 mg of
intravenous benztropine within 10 minutes followed by 1 to 2 mg of intravenous
lorazepam. If airway compromise continues for any appreciable amount of time,
emergent support from an an-esthesiologist should be obtained and the patient
should receive general anesthesia with airway protection. Fortunately, the need
for such measures is rare.
After a
dystonia, a patient should be maintained with oral anticholinergic or
antihistaminic medication for at least 48 hours. If there is a history of
previous dystonias, the medication should be continued for 2 weeks.
Consideration should be given to decreas-ing the previous dose of the
antipsychotic or possibly switching to a low-potency neuroleptic or atypical
agent if the patient has been prescribed a conventional antipsychotic. The use
of prophylactic anticholinergic medication will be discussed later.
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