eMedicine Specialties > Psychiatry > Psychosomatic
Dystonia, Tardive: Treatment & Medication
Updated: Aug 31, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
The treatment of patients with tardive dystonia is difficult. Refractoriness to treatment is a substantial clinical concern. Several pharmacologic and other somatic interventions have been tried with variable results. The treatment of this condition is probably more difficult and frustrating than for any other movement disorder.
- The clinical pharmacology of tardive dystonia differs from that of classic tardive dyskinesia. Both respond to dopamine-depleting drugs and dopamine antagonists, but tardive dyskinesia does not respond to anticholinergics and may worsen with therapy with these agents.
- The first therapeutic step after the diagnosis of tardive dystonia induced by neuroleptics or other drugs is to taper and then discontinue the causative drugs. Many times, a severe psychiatric illness makes this impossible, but carefully reconsidering the indications for dopamine antagonists in a given patient and considering alternate therapy are imperative. No study mentioned declares how quickly the neuroleptic must be withdrawn, but the recommendation is to attempt a progressive dose reduction.
- A comprehensive approach to patients with tardive dystonia includes patient education and supportive care. Physical therapy and well-fitted braces are designed primarily to improve posture and to prevent contractures. Although braces are tolerated poorly, particularly by children, they may be used in some cases as a substitute for sensory input. For example, in some patients with cervical dystonia, neck and head braces seem to provide sensory input by touching certain portions of the head or neck in a fashion similar to the patient's own sensory trick, thus enabling the patient to maintain a desirable head position.
- In an attempt to help patients with writer's cramp, various hand devices have been developed to enable them to use their hands more effectively and comfortably. Some patients find various muscle relaxation techniques and sensory feedback therapy useful adjuncts to medical or surgical management.
Surgical Care
- The surgical approach for patients with tardive dystonia is indicated in those who do not respond to medical treatment and continue having severe disabling dystonic forms. The most successful surgeries are stereotactic thalamotomy and selective denervation for cervical dystonia.
- Thalamotomy helps most for upper limb dystonia, offers (at most) a mild benefit for dystonia of the lower extremities, and has virtually no effect on cervical or truncal dystonia. Thalamotomy should be considered in patients with hemidystonia or generalized dystonia who, at least, are moderately disabled and in whom medical therapies have failed.
- Selective denervation for cervical dystonia is both safe and effective in carefully selected patients. Good results are obtained in patients with a stereotyped pattern of head deviation, such as pure rotation, lateral tilt, or retrocollis, who have a limited number of involved muscles and significant improvement with botulinum toxin therapy.
- The role of pallidotomy and deep brain stimulation in the treatment of the dystonic abnormal movements is currently under investigation.
- Small studies by Trottenberg et al and Zhang et al have reported some success in deep brain stimulation of the globus pallidus interna and bilateral subthalamic nuclei.18,19
- Gruber et al assessed the long-term effects, including motor function, quality of life, and mood, of bilateral globus pallidus internus deep brain stimulation on patients with tardive dystonia and concluded it is a safe and effective long-term treatment. Patients were assessed 3 times using established movement disorder and neuropsychological scales. Results showed significant improvement in quality of life regarding physical components and affective state. They also noted that cognitive functions remained unchanged, and no permanent adverse effects occurred.20
Activity
Physical activity depends on the grade of disability caused by the dystonic movements. In most patients, physical and occupational therapy encourage activity and help make life more comfortable and actions more effective.
Medication
Tardive dystonia may improve or, rarely, may resolve, after discontinuation of neuroleptics; however, the condition is often permanent. Treatment with medications includes antidopaminergics, anticholinergics, atypical antipsychotics, benzodiazepines, baclofen, anticonvulsants, or local botulinum toxin injections.
Acetylcholine receptor inhibitors
The most promising development for treating tardive dystonia and all other forms of dystonia has been botulinum toxin type A (BTTA). BTTA produces neuromuscular blockade by inhibiting the calcium ion–mediated release of acetylcholine at the motor nerve terminals. This results in diminished endplate potential and subsequent flaccid paralysis of the affected muscles. The paralysis persists until new nerve terminals form, usually within 2-3 months.
BTTA is effective in treating focal dystonias, including blepharospasm, oromandibular dystonia, spasmodic torticollis, spasmodic dysphonia (especially the adductor form), and some cases of focal limb dystonia. Injections are well tolerated. Systemic complications are not evident, although single-fiber electromyelogram studies show mild distant effects. Following administration, the onset of effect is apparent within a few days. Peak effects are evident within the first few weeks and wear off over 2-4 months.
Typical adverse effects are excessive weakness with inadvertent IM injection (eg, ptosis with eyelid injection, dysphagia in spasmodic torticollis). Treatment with large or frequent doses may prompt the development of antibodies to the toxin and may correlate with loss of the original benefit. Development of less antigenic forms of type A toxin or use of other botulinum toxin strains (ie, strains B or F) may overcome this problem. Patients should be advised that botulinum toxin is not curative but offers nonimmediate temporary improvement.
Botulinum toxin type A (BOTOX®)
Neurotoxins produced by Clostridium botulinum exert paralytic effects at the neuromuscular junction by inhibiting the release of acetylcholine, thus, inhibiting impulse transmission in neuromuscular tissue. Has become a mainstay of therapy for focal and segmental dystonia, including tardive dystonia.
Adult
Be aware of differences in relative potencies of the United Kingdom and North American botulinum A toxin preparations (4:1 conversion ratio of Dysport to BOTOX®); considerable variation of injection techniques, number of injection/muscle, doses, combinations of muscle injected, and use of tool to identify overactive muscles; 5-100 U depending on muscle affected; not to exceed 300-400 U/treatment session
Pediatric
Not established
Aminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Avoid in pregnancy or breastfeeding; do not exceed recommended dosages and frequencies of administration; lethal dose unknown (estimated at 3000 U); extent of reversible denervation is dependent on dose and volume of injection; proper selection of most involved muscles is the most important determinant of response; presence of antibodies to BTTA may reduce effects of therapy (may benefit from injections with other serotypes, including type B, C, and F); minimize immunoresistance by using smallest possible dose; extend interval between treatment as long as possible, with at least 3 mo between injections, and avoid using booster injections
Long-term effects may include changes in muscle fiber size, EMG abnormalities, gall bladder attack, urinary incontinence, brachial plexopathy, and generalized botulismlike syndrome; caution in patients with preexisting neuromuscular disorders
Anticholinergic agents
Anticholinergic therapy (eg, trihexyphenidyl, ethopropazine) has been used. Kang et al reported a 38% response to trihexyphenidyl alone and 44% when combined with other medications.3 Effective doses were 10-32 mg/d. Severe adverse effects (eg, drowsiness, confusion, hallucinosis, memory difficulties) occurred at 60-100 mg/d. Ethopropazine showed 27% improvement when administered alone and 42% as adjuvant therapy. Doses were 100-450 mg/d. Adverse effects included confusion, forgetfulness, GI problems, dizziness, blurry vision, dry mouth, urinary retention, lethargy, palpitations, and sleep disturbances. Diphenhydramine, an anticholinergic with H1 antagonist properties, also has antidystonic effects.
Trihexyphenidyl (Artane)
Central inhibitor of parasympathetic nervous system, resulting in diminished muscle spasms. Often DOC for young person with generalized, multifocal, or segmental dystonia, especially with lower extremities and trunk involvement.
Adult
1-2 mg/d PO initially; titrate upward by 2 mg/d q5-10d divided tid as tolerated; not to exceed 40 mg/d
Pediatric
Not established
Amantadine and anticholinergic coadministration may increase adverse anticholinergic effects, which disappear when dose is reduced; drugs with anticholinergic activity (eg, H2 antagonists, TCAs) used together can lead to anticholinergic toxicity; pharmacologic/therapeutic actions of phenothiazines and other antipsychotics may be reduced by concurrent administration of anticholinergics
Documented hypersensitivity; glaucoma; peptic ulcers; pyloric or duodenal obstruction; stenosing prostatic hypertrophy or bladder neck obstructions; achalasia; toxic megacolon
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Middle-aged and older adults intolerant of high doses; children, adolescents, and young adults have a high threshold for adverse effects with slow dosage escalation; caution in patients with tachycardia, cardiac hypotension, prostatic hypertrophy, arrhythmias, hypertension, or any tendency toward urinary retention, liver or kidney disorders, and obstructive disease of GI or GU tract; if dry mouth is severe and impairs swallowing or speaking or if loss of appetite and weight occurs, reduce dosage or discontinue medication temporarily
Ethopropazine (Parsitan)
Not available in United States. Phenothiazine derivative that has antimuscarinic and antiparkinsonian activity. Demonstrates poor oral bioavailability.
Adult
50 mg PO qd/bid initially; gradually increase prn
Usual maintenance: 100-400 mg/d PO
Pediatric
Not established
Additive effect with drugs prolonging QT interval (eg, dofetilide, sotalol, gatifloxacin, pimozide); may increase meperidine effects; additive effect with other anticholinergic agents; increases risk of tramadol CNS toxicity
Documented hypersensitivity; glaucoma; prostatic hypertrophy
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause CNS depression; long-term therapy may exacerbate extrapyramidal symptoms; caution in elderly patients
Dopamine-depleting agents
The most effective medications are those that deplete catecholamines (eg, reserpine, tetrabenazine). A study by Kang et al in 1988 showed a 63% response to at least one of these drugs.3 Effective doses of reserpine were 2-9 mg/d. Significant adverse effects were parkinsonism, dizziness, lethargy, depression, headache, GI upset, and hallucination. Effective doses of tetrabenazine were 12.5-250 mg/d. Most patients required >100 mg/d. Adverse effects included parkinsonism, depression, lethargy, euphoria, hallucinations, confusion, dizziness, vomiting, and unilateral leg tremor. Tetrabenazine (not available in United States) has minimal risk of tardive dyskinesia, which is an advantage compared to other antidopaminergic drugs.
Tetrabenazine (Nitoman)
Not available in United States. Presynaptic dopamine antagonist with minimal risk of tardive dystonia.
Adult
12.5 mg PO bid/tid initially; titrate upward by 12.5 mg/d q3-5d until maximal tolerated and effective dose achieved; not to exceed 200 mg/d
Pediatric
Not established
Do not use within 14 d of MAOIs
Documented hypersensitivity; clinical depression; MAOIs within 14 d
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Common adverse effects include fatigue, sedation, impotence, depression, and anxiety; parkinsonism occurs in up to 25%; less frequent adverse effects include postural hypotension, insomnia, akathisia, confusion, irritability, dizziness, dysphagia, paranoia, and hallucinations; adverse effects usually respond to dose reduction; rarely causes acute dystonic reactions or oculogyric crisis; may aggravate tardive dyskinesia
Benzodiazepines
Bind to a specific benzodiazepine receptor on GABA receptor complex, thereby increasing GABA affinity for its receptor. Also increases the frequency of chlorine channel opening in response to GABA binding. GABA receptors are chlorine channels that mediate postsynaptic inhibition, resulting in postsynaptic neuron hyperpolarization. Final result is a sedative-hypnotic effect. Benzodiazepines may provide additional benefit. Clonazepam is effective for blepharospasm and myoclonic dystonia.
Clonazepam (Klonopin)
Long-acting benzodiazepine that increases presynaptic GABA inhibition and reduces monosynaptic and polysynaptic reflexes. Has multiple indications, including suppression of myoclonic, akinetic, or petit mal seizure activity and focal or generalized dystonias (eg, tardive dystonia).
Adult
0.5-1 mg PO hs initially; may titrate upward to 3 mg/d PO divided bid as tolerated
Pediatric
Not established
Concomitant use of valproic acid and clonazepam may produce absence status; phenytoin, carbamazepine, rifampin, and barbiturates may reduce effects; coadministration of CNS depressants increases toxicity; coadministration of valproic acid may produce absence status; ketoconazole, ritonavir, and cimetidine decrease clearance, resulting in enhanced effects and toxicity
Documented hypersensitivity; severe liver disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Measure blood cell counts and LFTs periodically during long-term treatment; adjust dose in severe hepatic dysfunction; caution in chronic respiratory disease or impaired renal function; withdrawal symptoms may result from abrupt discontinuation
Diazepam (Valium)
Demonstrates clinical efficacy for athetosis and spasticity. Improvement is attributed to general relaxation. Used at night to suppress spasms that disrupt sleep.
Adult
5 mg PO hs initially; may increase to 10 mg PO hs prn; initiate daytime therapy at 2 mg PO bid; may titrate upward as tolerated to 60 mg/d PO divided q4-6h
Initial dose: 1.5 mg PO divided tid
Maintenance dose: Increase initial dose by 0.5-1 mg q3d to a dose of 0.05-0.2 mg/kg in divided doses; not to exceed 20 mg/d
Pediatric
<6 months: Not recommended
>6 months: 0.12-0.8 mg/kg/d PO divided q4-6h
CYP450 inducers (eg, phenytoin, carbamazepine, rifampin, barbiturates) may reduce effects; coadministration of phenothiazines, barbiturates, alcohols, or other CNS depressants may increase CNS toxicity
Documented hypersensitivity; severe liver disease
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Wide margin of safety, but potential for overdose; signs of intoxication are somnolence progressing to coma (may require flumazenil as antidote); physiologic addiction may occur; do not decrease dose rapidly or abruptly discontinue following prolonged use; may worsen symptoms of suicidal ideation or intention in severe depression; caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)
Gamma-aminobutyric acid inhibitors
Structural analog of GABA that inhibits both monosynaptic and polysynaptic reflexes at the spinal level. Decreases excitatory neurotransmitter release from primary afferent terminals. Several studies have shown reduction in spasticity and sudden painful spasms. Anxiolytic effect may contribute to antispasticity action. Used IT for severe spasticity.
Baclofen (Lioresal)
Used successfully in oromandibular and cranial dystonias. Studies support baclofen IT in severe cervical and truncal dystonias.
Adult
5 mg PO tid initially, followed by gradual increase of 5 mg/d q4-7d to therapeutic level (0.08-0.4 mcg/mL); not to exceed 80 mg/d divided qid (occasionally up to 150 mg/d)
Alternatively, 50-100 mcg IT; give doses >50 mcg in 25-mcg increments 24 h apart
Pediatric
<2 years: Not recommended
>2 years: 2.5-5 mg/d PO divided tid initially, followed by gradual titration as tolerated; not to exceed 30 mg/d (2-8 y) to 60 mg/d (>8 y)
Coadministration with imipramine, amitriptyline, or clomipramine may produce short-term memory loss
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Increases incidence of omphaloceles (ventral hernias) in rat fetuses and unossified phalangeal nuclei of forelimbs and hand limbs in rabbit fetuses; no studies in pregnant women; use in pregnancy only if benefit clearly justifies potential risk to fetus; excretion in human milk unknown; abrupt withdrawal may produce autonomic dysreflexia, hallucinations, or seizures; must be gradually tapered prior to discontinuation; caution in renal dysfunction (decrease dose); may cause sedation
Atypical antipsychotics (serotonin dopamine receptor antagonists)
Atypical antipsychotics (eg, clozapine, risperidone, olanzapine) bind to dopamine D2 receptors and may improve tardive dystonia when lower doses are used. Recent trials have shown that they not only may cause or aggravate tardive dystonia but ultimately may prove to be highly useful therapeutic agents to treat dystonias. Long-term safety is not fully established for this indication.
Clozapine (Clozaril)
Binds to dopamine D2-receptor with 20 times lower affinity than for serotonin-2 receptor.
Adult
12.5 mg/d PO initially; slowly increase by 12.5 mg q4-7d until therapeutic effect achieved; effective dose for psychosis is 300-450 mg/d, and tardive dystonia dose is much less; for psychosis, not to exceed 900 mg/d
Pediatric
Not established
Coadministration with drugs likely to cause agranulocytosis or otherwise suppress bone marrow function; epinephrine and phenytoin may decrease effects; TCAs, neuroleptics, CNS depressants, guanabenz, and anticholinergics may increase risk for adverse effects
Documented hypersensitivity; WBC count <3500 cells/µL before or during therapy; comatose states; uncontrolled epilepsy
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Measure baseline WBC count before initial dose and weekly for 6 mo; then, administer q2wk; may cause orthostatic hypotension, drowsiness, sedation, dizziness, vertigo, constipation, salivation, and weight gain and may increase risk for hyperlipidemia and diabetes mellitus
Olanzapine (Zyprexa)
May inhibit serotonin, muscarinic, and dopamine effects.
Adult
5 mg PO qd; increase to 10 mg qd within 5-7 d; adjust by 5 mg/d at 1-wk interval; not to exceed 20 mg/d
Pediatric
Not established
CYP1A2 inhibitors (eg, fluvoxamine) may increase effects; antihypertensives may increase risk of hypotension and orthostatic hypotension; CYP inducers (eg, levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin cigarette smoking) may decrease the effects
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, and dehydration; may cause weight gain and increase risk for hyperlipidemia and diabetes mellitus
Risperidone (Risperdal)
Binds to dopamine D2-receptor with 20 times lower affinity than for serotonin-2 receptor.
Adult
Start with 1 mg PO bid and slowly increase to optimum range of 4-8 mg/d; doses >10 mg/d do not appear to offer additional benefit
Pediatric
Not established
Carbamazepine may decrease serum levels; may inhibit effects of levodopa
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause extrapyramidal reactions (especially >6 mg/d), hypotension/orthostasis, tachycardia, arrhythmias, amenorrhea, galactorrhea, sexual dysfunction, GI toxicity, and cholestatic jaundice
Anticonvulsants
Used to manage severe muscle spasms and to provide sedation in patients with dystonia. Kinesigenic paroxysmal dystonia may be controlled with anticonvulsants (eg, carbamazepine, phenytoin). The nonkinesigenic forms of paroxysmal dystonia are less responsive to pharmacologic therapy, although clonazepam and acetazolamide may be beneficial.
Carbamazepine (Tegretol)
May reduce polysynaptic responses and block posttetanic potentiation.
Adult
200 mg PO bid initially; increase by 200 mg/d qwk to effect; not to exceed 2.4 g/d
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Because induces its own metabolism; its half-life declines over 1 mo from 36 h to 10-20 h, so adjust dose accordingly; serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not administer within 14 d of MAOIs; cimetidine may increase toxicity, especially within first 4 wk of therapy; may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels)
Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within last 14 d
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Cross-sensitivity with TCAs; obtain CBC counts, LFTs, and serum iron level prior to treatment, during the first 2 mo, and yearly thereafter; monitor low-normal or below-normal WBC counts and neutrophil counts q2wk for the first 3 mo, and individualize monitoring based on previous results; discontinue if WBC count <3000/µL or neutrophils <1000/µL; recommend target blood levels of 4-8 mcg/mL in patients with head injury; caution with increased intraocular pressure; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; other adverse effects include Stevens-Johnson syndrome, hepatitis, nausea, ataxia, and pancreatitis
Phenytoin (Dilantin)
Primary site of action is motor cortex. Promotes sodium efflux from neurons. Stabilizes threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient, including reduction of posttetanic potentiation at synapses.
Adult
Loading dose: 15-20 mg/kg PO/IV once or divided doses followed by 100-150 mg/dose at 30-min intervals
Initial dose: 100 mg (125 mg susp) PO/IV tid
Maintenance dosage: 300-400 mg/d PO/IV divided tid, or qd/bid if using ER; increase to 600 mg/d (625 mg/d susp) may be necessary; not to exceed 1500 mg/d
Rate of infusion not to exceed 50 mg/min to avoid hypotension and arrhythmias
Pediatric
Not established
Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase toxicity
Effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate
May decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid
Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Measure CBC count and urinalyses when therapy is initiated and monthly for several months to monitor for blood dyscrasias; discontinue use if a skin rash appears, and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood glucose); discontinue use if hepatic dysfunction occurs
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References
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Further Reading
Keywords
tardive dystonia, muscle contractions, dyskinesia, repetitive movement, abnormal posture, muscle twitch, twitching, involuntary movement, writer's cramp, blepharospasm, geste antagonistique, abnormal muscle spasm, anti-psychotic drug treatment, antipsychotic drug treatment, anti-psychotics, antipsychotics, neuroleptic-induced tardive dyskinesia, dystonic movement, focal striatal lesion, dystonic posture, Westphal phenomenon, neuroleptics, neuroleptic agents, neuroleptic drugs, torticollis, oromandibular dystonia, dystonic adductor dysphonia, focal dystonia, segmental cranial dystonia, segmental axial dystonia, segmental brachial dystonia, segmental crural dystonia, multifocal dystonia, generalized dystonia, hemidystonia, hemi-dystonia, stereotactic thalamotomy, thalamotomy, selective denervation
