PHARMACOEPIDEMIOLOGY Drug Safety 1997 Mar: 16 (3): 180-204 0114~5916/97/0003-0180/$12.50/O

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Drug-Induced Movement Disorders Felix Javier Jimenez-Jimenez,l Pedro Jose Garcia-Ruiz2 and Jose Antonio Molina3

1 Department of Neurology of Hospital Universitario 'Principe de Asturias', Alcala de Henares, Madrid, Spain

2 Department of Neurology of Fundaci6n Jimenez Diaz, Madrid, Spain 3 Department of Neurology of Hospital Universitario Doce de Octubre, Madrid, Spain

Contents Summary 1. Parkinsonism ..

1 .1 Frequency. 1.2 Implicated Drugs 1.3 Clinical Features and Prognosis. 1.4 Prevention 1.5 Therapy ... .

2. Tremor ..... . 2.1 Antipsychotics. 2.2 Calcium Antagonists . 2.3 Other Drugs ..... .

3. Chorea ......... . 3.1 Antiparkinsonian Drugs. 3.2 Anticonvulsant Drugs.

4. Dystonia .......... . 4.1 Antipsychotic Drugs . . 4.2 Orthopramides and Substituted Benzamides . 4.3 Antiparkinsonian Drugs.

5. Tardive Dyskinesia .. 6. Myoclonus. . . . . . . . . . .

6.1 Dopamine Antagonists 6.2 Antidepressant Drugs and Lithium 6.3 Antiparkinsonian Drugs. 6.4 Bismuth Salts .

7. Tics or Tourettism ...... . 8. Akathisia ........ .

8.1 Dopamine Antagonists 8.2 Antidepressant Drugs

9. Conclusion ......... .

180 181 181 181 183 183 184 184 184 184 185 185 185 186 186 186 187 187 187 188 188 188 189 189 189 189 190 190 190

Summary Parkinsonism, tremor, chorea-ballismus, dystonia, tardive dyskinesia, myoc­lonus, tics and akathisia can be induced by many drugs. The drugs that are most frequently implicated in movement disorders are antipsychotics, calcium antag­onists, orthopramides and substituted benzamides (e.g. metoclopramide, sulpir­ide, clebopride, domperidone), eNS stimulants, antidepressants, anticonvulsants, antiparkinsonian drugs and lithium. It is possible for a single drug to induce 2 or

Drug-Induced Movement Disorders 181

more types of movement disorders in the same patient. Movement disorders are not always reversible after drug withdrawal.

Drug-induced movement disorders include par­kinsonism, tremor, chorea-ballismus, dystonia, tar­dive dyskinesia, myoclonus, tics, or akathisia. Such disorders can be caused by a wide variety of drugs, with parkinsonism, tardive dyskinesia and dysto­nia being the most frequent iatrogenic movement disorders found in clinical practice. Not infre­quently, 2 or more types of drug-induced move­ment disorder coexist in the same patient. This ar­ticle focuses on the distinct types of iatrogenic movement disorders and their associations with various drugs.

1. Parkinsonism

Major signs of parkinsonism include resting tremor, cogwheel rigidity, akinesia and postural instability. Until recently, the term drug-induced parkinsonism was nearly synonymous with anti­psychotic-induced parkinsonism. However, drug­induced parkinsonism is a frequent adverse effect of numerous drugs that interfere with dopamine function in the basal ganglia,[I-4) including calcium antagonists, orthopramides and substituted benza­mides.[2,5-8) Table I summarises the drugs that have been associated with induction or aggravation of parkinsonism.

1.1 Frequency

In Spain, several studies have reported that drug-induced parkinsonism accounts for 24 to 35% of parkinsonian syndromesp,5,7,8) The prevalence of drug-induced parkinsonism in a door-to-door survey conducted in Italy was 32.7 per 100 000 individuals, in other words, approximately 8 times less than that of idiopathic Parkinson's disease.[9) Another door-to-door survey conducted in Ger­many, but restricted to individuals older than 65 years, showed a prevalence of 0.41 % for drug­induced parkinsonism and 0.71 % for Parkinson's disease.! 10)

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Table I. Drugs associated with induction or aggravation of parkinsonism

Drug Antipsychotics[l-l7]

Calcium antagonists: flunarizine, cinnarizine[7,8,18-31]

diltiazem,!32-34] verapamil,[33,35,38] amlodipine,!37] manidipine[38]

Orthopramides and substituted benzamides: metoclopramide[39-48] sulpiride,[1,7,8] clebopride[l,7,8,49-51]

cisapride,[52] domperidone,[53] veralipride!54,55]

Dopamine storage and transport inhibitors: reserpine, [56] tetrabenazine!57]

Antiemeticlantivertiginous agents: thiethylperazine!8,58,59] prochlorperazine[48]

Methyldopa[8,60,61]

Antidepressants:

Evidence

././

././

?

././

./

?

././

././

./

fluoxetine[62-69], paroxetine,!70,71] trazodone[72] ?

phenelzine[73] ?

amfebutomone (bupropion)[74] ? Lithium[75-79] ?

Diazepam[60] ?

Anticonvulsants: valproic acid (sodium valproate),[81-84] phenytoin[85] ?

Cholinergic agents bethanechol, [86] pyridostigmine!87] ?

Other agents: amiodarone,[88-91] procaine,[92] pethidine ? (meperidine),193,94] amphotericin B,[95,96] cefaloridine,[97] naproxen,[98] ethanol,[99] oral contraceptives, [1 DD] indeloxazine, [1 01,102] captopril,[103] cytarabine[104]

Symbols: ././ = well documented or frequent; ./ = relatively well documented or relatively frequent; ? = not well documented or anecdotal reports_

1 ,2 Implicated Drugs

1.2. 1 Antlpsychotlcs Parkinsonism has been a well known adverse

effect of antipsychotic drugs since their introduc­tion for the treatment of patients with psychiatric illnesses.! 11,12) Development of parkinsonism is not infrequent in antipsychotic users, especially in older individuals.[13-17) In our series of patients

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with drug-induced parkinsonism, based on patients who were referred to a Movement Disorders Unit, 'typical' antipsychotic drugs were implicated in 27.6% of those with parkinsonism.[8] Psychiatrists do not usually refer patients with mild parkinsonism to neurological clinics and, in addition, iatrogenic parkinsonism is not always recognised.[105,106] These 2 reasons may explain the relatively low fre­quency. In a lO-year series at a regional pharmaco­vigilance centre in France, antipsychotics were the offending drug in 39% of 53 patients with drug­induced parkinsonism.l6]

Antipsychotics act as dopamine receptor antag­onists. The development of drug-induced parkin­sonism is usually dose-dependent for each drug, and seems to be related to the blockade of dopa­mine D2 receptors, and with the degree of D2 re­ceptor occupancy in the striatum.l 107] Halogenated and piperazine phenothiazines, and butyrophen­ones, are the antipsychotics with the greatest like­lihood of producing this complication.l12,15, 108, 109] The phenothiazine derivatives thiethylperazine[8,58,59] and prochlorperazine,[46] which are used for the treatment of vertigo, may also induce parkinson­ism.

Although comparisons of absolute prevalence levels for parkinsonism and other movement disor­ders are difficult to make, the risk of developing these movement disorders with the newer 'atypical' antipsychotics (risperidone, remoxipride, clozapine) seems to be lower than that of the 'typical' ones.[lIO-1l71 This is probably linked with a lower affinity for D2 receptors: risperidone binds to sero­tonin (5-hydroxytryptamine; 5-HThA receptors with 20 times greater affinity than it binds to D2 receptors; remoxipride binds selectively, but weakly, to D2 receptors; and clozapine preferentially binds to D4 receptors.[l17]

Early age at onset of schizophrenia,[118] high ventricle: brain ratio,l1l8,119] and severity of negative symptoms of schizophrenia[l19,120] seem to be related to an increased risk and severity of antipsychotic­induced parkinsonism.

In a number of patients, the onset or aggravation of parkinsonian signs has occurred following anti-

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Jimenez-Jimenez et al.

psychotic withdrawaI.lI21,122] Melamed et al,l 1221 suggested that the antipsychotic may precipitate degeneration of vulnerable nigrostriatal neurons by generating cytotoxic free radicals or accelerating neuronal firing rates. Besides the blockade of do­pamine receptors, antipsychotics inhibit complex I of the mitochondrial electron-transport chain in vitro, and patients with antipsychotic-induced par­kinsonism showed decreased complex I activity in platelets.[123] This is a potentially interesting find­ing, since it is known that complex I activity is reduced in the substantia nigra of patients with Parkinson's disease.[124,125]

1.2.2 Calcium Antagonists Since the original description of cinnarizine­

induced parkinsonism by Marti-Masso et al. in 1985,[18] many authors have indicated that calcium antagonists, mainly cinnarizine and flunarizine, are a frequent cause of drug-induced parkinsonism, at least in Europe and South America,[7,8,19-30] where their use is common; cinnarizine was used by 5 to 7% of the elderly Spanish popUlation in 1985.[31] Cinnarizine and flunarizine, taken alone or with other drugs, were the most frequently reported causes of drug-induced parkinsonism in several Spanish series.l5,7,81 Other calcium antagonists have been associated with induction or aggravation of parkinsonism in anecdotal reports (table I).

Calcium antagonists were implicated in 58.1 % of cases of drug-induced parkinsonism in our own series,[8] and were the offending drug in 30% of cases of drug-induced parkinsonism in a lO-year series at a regional pharmacovigilance centre in France.l6] Old age and a family history of essential tremor seem to predispose to calcium antagonist­induced drug-induced parkinsonism.[29,30,126]

Garcia-Ruiz et al,l127] described an experimen­tal model of parkinsonism induced by cinnarizine in aged monkeys. Cinnarizine produced a persist­ent reduction of homo vanillic acid and 5-hydroxy­indoleacetic acid (5-HIAA) levels in the CSF. The authors suggested that this effect is the result of a predominant presynaptic effect of cinnarizine on dopaminergic and serotonergic neurons - resulting

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Drug-Induced Movement Disorders

in inhibition of synthesis or release of their respec­tive neurotransmitters - or a possible toxic effect.l127]

Several in vitro studies have shown that calcium antagonists decrease the synthesisl128] and re­leaseI129-13I] of dopamine from the striatum, inhibit [3H]spiperone binding to postsynaptic D2 recep­tors in the striatum,I13I,132] and reduce the levels of catecholamines and [3H] dopamine uptake, with­out neurotoxicity in dopamine-rich neuroblastoma cells.1133] The binding of metabolites offlunarizine and cinnarizine to striatal D2 receptors is higher than that of the parent drug,l134] In addition, like antipsychotics (section 1.2.1), flunarizine and cinnarizine inhibit mitochondrial complex 1,1135]

1.2.3 Orthopramides and Substituted Benzamides Several orthopramides and substituted benza­

mides can induce or aggravate parkinsonism (table I). Like antipsychotics, these drugs block striatal D2 receptors.

1.2.4 Dopamine Storage and Transport Inhibitors Methyldopa has been reported to induce parkin­

sonism in individual patients.18,60,61] Drug-induced parkinsonism is a well known adverse effect of drugs that interfere with the intraneuronal storage of dopamine, such as reserpinel56] and tetrabena­zine.l57] Tetrabenazine also may also block post­synaptic dopamine receptors.

1 .3 Clinical Features and Prognosis

The clinical manifestations of drug-induced parkinsonism are often indistinguishable from those of idiopathic Parkinson's disease, although drug-induced parkinsonism more frequently causes postural tremor and bilateral symptoms,I136] and often coexists with tardive dyskinesia, tardive dys­tonia and/or akathisia,l8,15,19,21,28,137-139]

It has been traditionally assumed that drug­induced parkinsonism was reversible; however, in many patients with parkinsonism-induced by anti­psychoticsl12l ,138,139] or other antidopaminergic drugs, such as flunarizine or cinnarizine,18,25,29,121] the parkinsonian symptoms and signs do not com­pletely disappear, despite withdrawal of the of­fending drug. The persistence of parkinsonian

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183

symptoms might reflect the fact that the patients have subclinical idiopathic parkinsonism, a condi­tion that was unmasked by the offending drug. On the other hand, this could also represent the onset of Parkinson's disease in the patients while they were taking the drug, and a direct toxic effect on the dopaminergic system cannot be ruled out.

1 .4 Prevention

The best prevention of drug-induced parkinson­ism (and other drug-induced movement disorders) is to avoid the inappropriate use of drugs that are capable of inducing these adverse effects. The pro­longed and, in many cases, unnecessary use of cinna­rizine or flunarizine in elderly patients in Spainl31] resulted in a high frequency of parkinsonism in­duced by these drugs.l5,7,8,18,25,29,30] In our own

drug-induced parkinsonism series, many patients were taking drugs to treat 'vertigo' or 'dyspepsia' for months or even years;18] also, there was fre­quent use of the antipsychotic drug flupenthixol, a thioxanthene that is marketed in combination with a benzodiazepine, with a trade name that could lead general physicians to suppose that he or she is pre­scribing an anxiolytic drug.

The choice and dosage of antipsychotic drugs in the treatment of patients with psychiatric disorders are crucial. It seems reasonable that the dosage of antipsychotic should be kept to the minimum re­quired to achieve and maintain a therapeutic re­sponse, and that those antipsychotics (risperidone, remoxipride and clozapine) with a lower risk of inducing drug-induced parkinsonism (or other movement disorders) should be preferred.

The use of adjunctive anticholinergic drugs to prevent the development of parkinsonism is con­troversial. A consensus statement by the World Health Organization did not recommend the use of these compounds because of their adverse effects, the potentially increased risk of developing tardive dyskinesia, and the fact that many patients taking antipsychotic therapy do not develop drug-induced parkinsonism. I 140,141]

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1.5 Therapy

The first therapeutic measure for patients with drug-induced parkinsonism should be the discon­tinuation of the offending drug, whenever possible. In those patients with persistent parkinsonian signs, especially elderly individuals with presumed sub­clinical idiopathic parkinsonism that has been un­masked by the offending drug, management should be similar to that of Parkinson's disease.

In psychiatric patients with antipsychotic­induced parkinsonism, the first approach should be to reduce the antipsychotic dosage or switch to an­other antipsychotic with a lower incidence of this adverse effect. If these measures are ineffective, it may be necessary to consider pharmacological treatment, including anticholinergics[l40,141] or amantadine.[140] Levodopa or direct dopamine ag­onists could increase psychotic symptomsY09] and are not useful in many patients.[142]

2. Tremor

Tremor is defined as a rhythmic oscillation of a body part, produced by either alternating or synch­ronous contractions of reciprocally innervated an­tagonistic muscles. Tremor is a common adverse effect of a wide variety of drugs (table II).

Although drugs that induce parkinsonism can produce a typical parkinsonian resting tremor, more characteristically, drug-induced tremors are pos­tural. [I 64] Antipsychotic drugs produce a low­frequency postural tremor, anticonvulsant drugs and lithium produce a high-frequency low-amplitude tremor, while other drugs may enhance physiolog­ical tremor.

2.1 Antipsychotics

Miller and Jankovic[15] reported that 2% of pa­tients with antipsychotic-induced movement disor­ders have postural tremor. Stacy and JankoviC[143] described 5 patients with a predominantly postural tremor ('tardive tremor') that had a frequency range of 3 to 5Hz (a type oftremor that is usually accom­panied by other tardive movement disorders). Moreover, tremor recordings in psychiatric pa-

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Jimenez-Jimenez et al.

Table II. Drugs associated with induction or aggravation of postural tremor

Drug Antipsychotics[143-147J Lithium[76.146.149]

Anticonvulsant drugs[l50] Tricyclic antidepressants[151.152]

~-Adrenergic agonists[l53] Theophylline[l54] Levodopa[l54]

Amphetamines[l54] Thyroxine[154]

Antihyperglycaemic drugs[154] Caffeine[l54]

Corticosteroids[l54]

Calcium antagonists: flunarizine, cinnarizine[30]

Amiodarone[l54]

Anticonvulsants: phenytoin,1155] zonisamide,[156]lamotrigine[157J

Selective serotonin reuptake inhibitors[l56-160]

Histamine Hl antagonists[161]

Pentavalent antimonials[l62]

Evidence

.1.1 ,/,/

,/,/

,/,/

,/,/

,/,/

.1.1 ,/,/

,/,/

,/,/

,/,/

,/,/

,/

,/

? ?

?

? Cocaine[163] ?

Symbols: ,/,/ = well documented or not infrequent; ,/ = relatively well documented or relatively frequent; ? = not well documented or anecdotal reports.

tients treated with antipsychotics have shown that many of these patients had postural tremor of low frequency.[145] There have been reports of single cases of tongue tremor[l44] and rubral like trem­or[146] in patients exposed to antipsychotics. Finally, antipsychotics can induce postural tremor in all 4 limbs of guinea-pigs)l47]

2.2 Calcium Antagonists

Postural tremor seems to be a frequent clinical feature of calcium antagonist-induced parkinson­ism. In our experience, this type of parkinsonism improves after withdrawal of the offending drug, but a coarse mixed tremor persists for many months, despite disappearance of parkinsonism. [30] We suggest that this persistent tremor is the equiv­alent of the antipsychotic-induced 'tardive tremor' reported by Stacy and Jankovic (section 2.1))143] A

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Drug-Induced Movement Disorders

case of tongue tremor has been reported in a patient treated with flunarizine.[145]

2.3 Other Drugs

Tremor is a common problem in patients taking lithiump6] Studies show a wide range of incidences of lithium-induced tremor - from 4 to 65% - as a result of differences in defining and reporting this adverse effect.[l48] Tremor often decreases as dura­tion of lithium therapy increases.[l49]

Postural tremor appears in 20 to 25% of patients treated with valproic acid (sodium valproate),[145] and more infrequently, in patients treated with other anticonvulsant drugs (table II).

3. Chorea

Chorea refers to irregular, unpredictable, brief, jerky movements that flit from one part of the body to another in a random sequence. Table III summa­rises the drugs that can induce chorea. The chore­iform movements induced by dopamine antago­nists are part of the spectrum of tardive dyskinesia, and are discussed in section 5.

3.1 Antiparkinsonian Drugs

Choreiform dyskinesias are a well known ad­verse effect of levodopa,[165-171] dopamine ago­nists[l72-176] and, less frequently, of anticholinergic drugS[l85-188] and amantadineP26] Choreiform dys­kinesias associated with levodopa therapy in pa­tients with Parkinson's disease usually follow 2 patterns: 'peak-dose' and 'diphasic' (at the onset and the end of the beneficial effect).

3.1.1 Peak-Dose Dyskineslas Peak-dose dyskinesias can improve after reduc­

tion of the levodopa dosage, but this measure re­sults in increased parkinsonismP45.246] The redis­tribution of the total dose of levodopa to more frequent and lower individual doses, together with the addition of a dopamine agonist, or a change to a liquid formulation of levodopa, should be useful for the treatment of this pattern of dyskinesiasP47]

When the patient is treated simultaneously with anticholinergics, reduction of dosage or withdrawal

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185

of these drugs should contribute to improvement of the dyskinesias. Recently, improvement of dys­kinesias has been reported with the addition of clozapine,[248] buspirone,[249.250] and fluoxetine}251] In contrast, cholinergic agents[252.253] and drugs that are active at y-aminobutyric acid (GAB A) sites[254.255] do not improve dyskinesias, and the lat­ter can aggravate parkinsonism.l256]

Isoniazid can improve dyskinesias, but also ag­gravates parkinsonian signs.l257] Improvement of levodopa-induced dyskinesias is one of the most im­portant benefits of posteroventral pallidotomy. [258-260]

3.1.2 Diphasic Dysklnesias Diphasic dyskinesias, which can be choreiform

or dystonic, are present at the beginning and at the end of the levodopa response cycle, coinciding

Table III. Drugs associated with induction of chorea

Drugs

Dopamine antagonists (including antipsychotics)

Dopamine agonists: levodopa,[165-171] direct dopamine agonists]172-176]

eNS stimulants:

Evidence ,/,/

,/,/

amphetamines,[177-180] pemoline.]181] ,/,/ methylphenidate, [182] cocaine, [163.183] xanthines]184]

Anticholinergics]185-188] ,/

H1 antihistamines]189] ,/

H2 antihistamines[190] ,/ Oral contraceptives[191-201] ,/

Anticonvulsants: phenytoin[202-209] ,/

phenobarbital (phenobarbitone),[202] ? carbamazepine,[210,211] ethosuximide,[212] valproic acid (sodium valproate),[213] felbamate,[214] gabapentin[215]

Withdrawal of diazepam + pentobarbital[216] ?

Antidepressants: tricyclic antidepressants,[217-219] fluoxetine[220] ?

Lithium[221-225] ?

Other drugs: amantadine,[226] anabolic steroids,[227] ? methadone,[228] baclofen,[229] benzodiazepines,[230] methyldopa, [231,232] digoxin, [233.234] diazoxide,l235] gold salts,1236-238] cyproheptadine,1239] cyclosporin,[240] sulfasalazine,[241] aciclovir,[242] propofol[243.244]

Symbols: ,/,/ = well documented or frequent; ,/ = relatively well documented or relatively frequent; ? = not well documented or anecdotal reports_

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with the rise and fall of plasma levodopa concen­trationsP61,262] The management ofthis pattern of dyskinesias is very difficult. The best measure is to administer more frequent doses of levodopa, in an attempt to overlap the end-of-dose period with the beginning of the levodopa response cycle, and the addition of a dopamine agonist.[246,247,262] Admin-istration of subcutaneous apomorphine at the be­ginning of the levodopa response cycle decreases the duration, but not the intensity of the dyskine­siasP63,264]

3.2 Anticonvulsant Drugs

Patients who are treated with anticonvulsant drugs, usually at toxic concentrations, can develop chorea. The anticonvulsant drug that has most fre­quently been associated with chorea is pheny­toin,[202-209] although this adverse effect has been also reported with phenobarbital (phenobarbi­tone), [202] carbamazepine, [210,211] ethosuximide, [212] valproic acid,[213] felbamate[214] and gabapen­tin,[215] and after withdrawal of combined therapy with pentobarbital and diazepamPl6]

4. Dystonia

Dystonia is a syndrome dominated by sustained muscle contractions, frequently causing twisting and repetitive movements or abnormal postures. Acute and tardive (or chronic) dystonia can be in­duced by the drugs that are listed in table IV.

4.1 Antipsychotic Drugs

Antipsychotic drugs can induce acute and, less frequently, tardive dystonia. First reported by Burke et al. in 1982,[265] tardive dystonia usually develops within 6 years of starting antipsychotic treat­ment, [266] although it can appear after a short period of exposure. Miller and lankovicf l5] reported that 24% of patients with antipsychotic-induced move­ment disorders have dystonia. The frequency of de­velopment of antipsychotic-induced acute and tar­dive dystonia has been reported to range from 5.3 to 66.7%,[267-271] and 0.4 to 21 %,[272-276] respec-

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Jimenez-Jimenez et al.

tively. These wide ranges result from the various diagnostic criteria that are used.

Butyrophenones, and halogenated and pipera­zine phenothiazines, are the antipsychotics with the greatest likelihood of producing these compli­cations, but the newer 'atypical' antipsychotics, such as risperidone and clozapine, are not devoid of this adverse effect.[117,339-345] The phenothiazine thi­

ethylperazine, which is used for the therapy of ver­tigo,[298,346,347] and the butyrophenone droperidol,

used in epidural anaesthesia,[348] can also induce dystonia.

Table IV. Drugs associated with induction of acute and/or tardive dystonia

Drug Evidence Antipsychotic drugs[lS.265.276] ,/,/

Orthopramides and substituted benzamides: metoclopramide[45-47,2n] ,/,/

su]piride,[278-28l] tiapride,[279] cisapride,[282] ? domperidone, [283,284] vera]ipride[28S]

Dopamine agonists: ]evodopa[170,17l ,286-289] ,/ ,/

Direct dopamine agonists[290] ,/

Antidepressants: selective serotonin reuptake inhibitors[291-301] ,/

tricyclic antidepressants,[302.303] monoamine oxidase inhibitors[304,30S]

Anticonvu]sants:

?

carbamazepine,[306-308] phenytoin[309] ,/

phenobarbital (phenobarbitone)[310] ?

Anticholinergics[311] ?

Anxiolytics: buspirone,[293.300,3l2] diazepam,[3l3] ? bromazepam,[314] midazolam[31S]

CNS stimulants: amphetamines,[3l6.3l7] methylphenidate,[3l8] ? cocaine (and cocaine withdrawal)[163.319-323]

anti migraine drugs ergotamine,[324,32S] sumatriptan[326] ?

Calcium antagonists: cinnarizine,[8.28] flunarizine,[8.28] nifedipine[327] ?

Histamine antagonists (H1 and H2)[328-332] ?

Other drugs: a-Methylparatyrosine,[333] tetrabenazine,[S7] ? bethanechol chloride,[334] flecainide,[33S] chloroquine,[338] etoposide,[337] alfentanil[338]

Symbols: ,/,/ = well documented or frequent; ,/ = relatively well documented or relatively frequent; ? = not well documented or anecdotal reports.

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Drug-Induced Movement Disorders

Risk factors for the development of acute and tard­ive dystonia in patients receiving antipsychotic treat­ment include younger age,l240,245,246,265,270,27 1,349-352] male gender, [271,349,353] severity of schizophrenia, [271] and the presence of negative symptoms of schizo­phrenia at baseline.l271 ] Although some authors have reported that patients with mania were more likely to develop antipsychotic-induced dystonia than those with schizophrenia,[267,269] others have found no such differences.[267] Concomitant treat­ment with anticholinergics seems to prevent the development of dystonia. [270]

4.2 Orthopramides and Substituted Benzamides

Several orthopramides and substituted benz a­rnides, such as sulpiride,[278-281] tiapride,[279] meto­cloprarnide,[45,47,277] cisapride,[282] domperidone,[283,284]

and veralipride, a drug used in the treatment of postmenopausal symptoms, can induce tardive dystonia. [285]

4.3 Antiparkinsonian Drugs

Dystonia can be induced by levodopa,[170,171,286-289] anticholinergic agents[311] and dopamine agonists.[290] Dystonias associated with levodopa therapy can follow 3 patterns: 'early morning', 'peak-dose' and 'off-period' dystonias. The therapy of peak-dose dystonia is similar to that previously described for peak-dose choreiform dyskinesias (section 3.1).

Off-period dystonias usually affect the toes or legs, and less frequently, the face and neck.[260,289] They are usually painful, are asscciated with low plasma levodopa concentrations and coincide with the 'off' periods of motor fluctuationsP60]

In certain patients, painful dystonia of the lower extremities is a particular problem on waking in the morning (early morning dystonia). Early morning dystonia can be avoided by administering a dose of sustained-release carbidopa/levodopa or a long­acting dopamine agonist at bedtime, or a dose of standard carbidopa/levodopa in the early morning or on waking.[246] Subcutaneous apomorphine,[354] oral lithium,[355,356] baclofen,[356] anticholiner­gics[356] or benzodiazepines, or (if dystonia is sus-

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tained) botulinum toxin injections,[356] can be use­ful alternatives.

5. Tardive Dyskinesia

The term 'tardive dyskinesia' is used to describe all persistent, occasionally reversible, abnormal in­voluntary movements caused by prolonged expo­sure to anti psychotics or other dopamine antago­nists. The most common form of tardive dyskinesia presents as orofacial stereotypy ('buccolinguo­masticatory syndrome'), at times associated with choreatic movements of the extremities and trunkJ357] In this section, we will review the data regarding this common form of tardive dyskinesia. Other tardive syndromes such as tremor (section 2), dystonia (section 4), myoclonus (section 6) and akathisia (section 8) are described elsewhere in this review.

Tardive dyskinesia was first described by Faur­bye et al. in 1964.[358] It usually develops after a minimum of 1 to 2 years of antipsychotic therapy. Tardive dyskinesia accounted for 14% of patients with drug-induced movement disorders in a French study at a regional pharmacovigilance centre[359] and 63% of such patients referred to a Movement Disorders Unit in the US.[15]

The prevalence of tardi ve dyskinesia is reported to range from 3.7% and 60%, depending on demo­graphic factors, inclusion criteria, and study de­signP76,360-384] Studies in Asiatic countries have shown low prevalence ratesP76,369,370]

The newer atypical anti psychotics risperidone, remoxipride, and clozapine, are associated with a lower incidence of tardive dyskinesia than typical anti psychotics, but are not devoid of this adverse effect. [114, 117,342,385-390] The anti vertiginous pheno-

thiazine thiethylperazine can also induce tardive dyskinesia.l59] Besides antipsychotics, other drugs can induce tardive dyskinesia (table V).

Proposed risk factors for tardive dyskinesia in­clude: • advanced age[36I,362,368,382,384,435-437] • female gender[365,369,380,437-439]

• prolonged duration of exposure to antipsychot­ics[362,363,365,381]

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188

• high antipsychotic dosage, and use of 'depot' antipsychotics and high potency antipsychot­iCS[361,384,439]

• presence of subtle movement disorders before initiation of antipsychotic therapy[380,384,440]

• diabetes mellitus[380,440-442] • 'organic' brain dysfunction[369,380,443] and brain

atrophy [444]

• affective disorders,[365,380,436] especially in pa­tients taking concomitant lithium therapy[445]

• negative schizophrenic symptoms[446] and a poor prognosis of schizophrenia[363]

• family history of mental illness[372] and • alcohol abuse/dependence)384,447]

There is debate over whether early or late onset psychosis is a risk factor for tardive dyskinesia.[448] The concomitant use of anticholinergic drugs does not seem to increase the risk of tardive dyskine­sia. [368.449]

Preventive measures against tardive dyskinesia are similar to those for drug-induced parkinsonism (section 1.4). Drugs that have been used or pro-

Table V. Drugs associated with the development of tardive dyskinesia

Drugs Evidence

Antipsychotic drugs

Orthopramides and substituted benzamides: metoclopramideI42,4S-47,391-401] ,(,(

clebopride,[SO,Sl] su[piride,[403,404J veralipride[40SJ ?

Calcium antagonists: flunarizine, cinnarizine[19,21 ,28,402J ,(

Antidepressants:

cyclic antidepressants[406-414J ,(

fluoxetine,[41S] paroxetine,[416] fluvoxamine[417,418] ? Lithium[419-421]

Anxiolytics: buspirone,[312,422-42S] lorazepam[426,427]

Anticholinergics:

carbamazepine, [420J mesuximide (methsuximide )[428J

Anticholinergic agents[429,430]

Other drugs:

?

?

?

?

pethidine (meperidine),1431] pemoline,1432] ? histamine Hl antagonists,[433] clembuterol1434]

Symbols: ,( ,( = well documented or frequent; ,( = relatively well documented or relatively frequent; ? = not well documented or anecdotal reports_

© Adis International Limited. All rights reserved,

Jimenez-Jimenez et al.

posed for use in the treatment of patients with tar­dive dyskinesia, such as antidopaminergics, choli­nomimetics, GABA agonists, calcium antagonists, buspirone, clozapine and tocopherol, have been ex­tensively reviewed by Cavallaro and Smeraldi.[450]

6. Myoclonus

Myoclonus is defined as a sudden, brief, shock­like involuntary movement caused by active mus­cular contractions.l45 ]] Asterixis, which results from brief pauses in muscular activity causing pos­turallapses, may be regarded as a form of 'negative myoclonus' .[451] Drugs that may induce myoclonus are listed in table VI.

6,1 Dopamine Antagonists

Several types of dopamine-blocking agents, such as antipsychotics[452-457] (including the atypical antipsychotic clozapine)[496,541-544] and metoclo­pramide[277,545] have been reported to induce my­oclonus.

Tominaga et aI,[455] described 'tardive myoclo­nus' as persistent postural myoclonus resulting from a late complication of antipsychotic treat­ment. Later on, the same group reported that 38% of patients taking long term antipsychotic therapy developed postural myoclonus, which was more frequent in male patients. In addition, patients with myoclonus had been given significantly higher doses of antipsychotics than those without myoc­lonus.[456] Little and Jankovic reported tardive my­oclonus within 5 months of antipsychotic with­drawal.[457]

6.2 Antidepressant Drugs and Lithium

Cyclic antidepressant drugs, alone or in combi­nation with lithium, can induce reversible action myoclonus, even when used at nontoxic dos­ages.l452,453,458-469] Garvey et aI,[462] reported that

30% of patients treated with cyclic antidepressants developed myoclonus, although in only 9% was this adverse effect clinically significant. Myoclo­nus may be associated with electroencephalo­graphic abnormalities[461] and with enlarged corti-

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Drug-Induced Movement Disorders

cal somatosensory evoked potentials,[467] although such abnormalities were not found by other re­searchers in a single-patient study.[465]

Other drugs that can also induce myoclonus are selective serotonin reuptake inhibitors (SSRIs),[470-474] monoamine oxidase inhibitors (MAOIs)[471,475-477] and lithium.[464,496-499]

6.3 Antiparkinsonian Drugs

Myoclonus[478,479] and asterixis[480] can occur as a

adverse effect of long term levodopa therapy; it usu­ally involves the legs or trunk, and occurs at night. In rare instances, bromocriptine can induce myo­clonus.[516]

6.4 Bismuth Salts

Abuse of bismuth can induce a toxic encepha­lopathy with myoclonus.l481-491] Although this en­cephalopathy improves after drug withdrawal, a 10% rate of mortality and/or tardive psychic dis­abilities has been reported.l482] Neurochemical findings include increased CSF 5-HIAAlevels.[485] The metal chelator dimercaprol increases the renal clearance and improves the clinical signs of bismuth induced encephalopathy.l483,484,487]

7. Tics or Tourettism

Tics are recurrent, involuntary, repetitive, rapid, purposeless movements affecting various muscle groups (most often in the face or the head) or pro­ducing vocalisations. Since the original descrip­tion by Klawans et al. in 1978,[546] there have been a number of additional reports of tics or tourettism after exposure to antipsychotic drugs,[547-561] in­cluding the atypical antipsychotic clozapine.l562] In addition, tardive tourettism has been induced in animal models after prolonged antipsychotic expo­sure.l563]

There have been published anecdotal reports of induction of tics by drugs other than antipsychot­ics, including: CNS stimulants, such as cocaine,[163.564-566] or amphetamines, methylphenidate or pemo­line, which are used for the treatment of attention deficit hyperactivity disorder;[557,567-5721 opiate ther-

© Adls Internofionol Umlted. All rights reserved.

189

Table VI. Drugs that can induce myoclonus

Drug Evidence Antipsychotics[452-457]

Antidepressants: cyclic antidepressantsI452,453,45B-469]

selective serotonin reuptake inhibitors,[470-474] monoamine oxidase inhibitors[471,475-477]

Levodopa[478-480]

Bismuth salts[481-491]

Anticanvulsants:[492-495]

.1.1

.1.1

.1.1

valproic acid (sodium valproate), carbamazepine, .!.! phenytoin

Lithium[464,496.499] .!

Morphine or its derivatives, administered .! intravenously or intrathecallyl500-510]

Antineoplastic drugs[511.515] .!

Bromocriptine[516] ?

Anxiolytics: buspirone,[472,517] lorazepam,[518] midazolam[519] ?

Cardiovascular drugs: propafenone,[520.522] flecainide,[523] diltiazem,[524] ? nifedipine,[525] buflomedil[526]

Antibacterials: cefmetazole,[527] penicillin,[528-531] pefloxacin,[532] ? isoniazid[533]

Other drugs: veratramine,[534] propofol,[535,536] ? physostigmine,[537] norpethidine,[538] pseudoephedrine,[539] tryptophan[540]

Symbols: .!.! = well documented or frequent; .! = relatively well documented or relatively frequent; ? = not well documented or anecdotal reports,

apy,[5731 opiate withdrawal[5741 and withdrawal of opiate antagonist therapy;[5751 anticonvulsants, such as carbamazepine or phenobarbital;[576-5791 clonazepam;[580] and the SSRI fluoxetine.l581,5821 Levodopa was reported to exacerbate tics in a pa­tient with coexistent Gilles de la Tourette syn­drome and Parkinson's disease.[5831 The present au­thors have observed a patient with Parkinson's disease who developed motor and vocal tics during a treatment with trihexyphenidyl; the tics disap­peared after withdrawal of this drug (unpublished observation).

8. Akathisia

Akathisia is a subjective sensation of restless­ness, often associated with an inability to keep still

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190

or with unpleasant subjective promptings to moveJ584] Akathisia may be confused with a sim­ilar disorder described as 'restless legs syndrome' , which is characterised by sensory symptoms lo­cated mainly in the calves, primarily at rest, and associated with restlessness in the legs that leads to irresistible urge to move themJ584] Drugs that have been associated with induction of akathisia are summarised in table VII.

8.1 Dopamine Antagonists

Acute and tardive akathisia are well known ad­verse effects of antipsychotic therapy. The preva­lence of akathisia among antipsychotic-treated pa­tients ranges from 8 to 76%, the wide variation reflecting different criteria for definition, and vari­ations in the type and dosage of antipsychotic drugs.[l6,585-590] Akathisia accounted for 7% of drug-induced movement disorders in a Movement Disorders Unit.115] The newer atypical antipsychot­ics, risperidone, remoxipride and clozapine, seem to have a lower risk of inducing akathisia than typ­ical antipsychotics.11l6,1l7,591-596] Epidural droperidol can also induce akathisiaJ597,598]

The potential risk factors for antipsychotic­induced akathisia are not well established, although they are likely to include dosage, rate of dosage in­crements and potency of the antipsychoticJ588,589] The role of old age, female gender, negative symp­toms or cognitive dysfunction associated with schizophrenia, and a diagnosis of affective disorder are not well known.1590] The suggestion by a num­ber of investigatorsI638-64I] that decreased serum iron levels and percentage of saturation were re­lated to the risk of antipsychotic-induced akathisia has not been confirmed by others.1590,642,643]

Antiemetics with dopamine-blocking action (mainly metoclopramide) are also associated with the in­duction of akathisia.£38,4o,403,609-615]

8.2 Antidepressant Drugs

Akathisia can be induced by tricyclic antide­pressants,1151,621-623] MAOIs such as phenelzinel624] and moclobemide,1625] and (more frequently) by serotonergic agents, including fluoxetine,I66,605-6l2]

© Adis Intematlonal Limited. All rights reserved.

Jimenez-Jimenez et al.

Table VII. Drugs associated with induction of akathisia

Drug Evidence Antipsychotics[117.585.5981 .1.1 Metoc[opramide[45,47,400,599-6041 .1.1

Dopamine storage and transport inhibitors:

a-methyltyrosine, reserpine, tetrabenazine[584] .1.1 Levodopa and dopamine agonists[584] .I

Antidepressants:

selective serotonin reuptake inhibitors, [66,298,605-620] tricyclic antidepressants[151,621-623]

phene[zine,[624] moc[obemide[625]

Calcium antagonists: f[unarizine, cinnarizine[19,21,27,28,626,627]

Lithium[628,629]

Anxio[ytics: buspirone,[517.630] midazolam,[631-633] iorazepam[634]

Anticonvu[sants: phenytoin,[635] va[proic acid (sodium va[proate )[6361

Methysergide[637]

Pethidine (meperidine)[625]

?

.I ?

?

?

?

?

Symbols: .1.1 = well documented or frequent; .I = relatively well documented or relatively frequent; ? = not well documented or anecdotal reports.

sertraline,[298,613-617] paroxetine,[618,619] and venla­

faxine.l603,620] However, akathisia associated with serotonergic drugs is a controversial subject, and some authors consider that this may be a variant of the 'serotonin syndrome' J520,525]

9. Conclusion

Many distinct types of drugs can induce move­ment disorders. The most frequent types of drug­induced movement disorders are parkinsonism (24 to 35% of cases of parkinsonism in Spain are induced or unmasked by drugs), tardive dyskinesia and dys­tonia. The drugs that are more frequently involved include antipsychotics, calcium antagonists, ortho­prarnides and substituted benzarnides, eNS stimu­lants, antidepressants, anticonvulsants, antiparkin­sonian drugs and lithium. More than one type of movement disorder can coexist in the same patient. Many of these movement disorders improve after withdrawal of the offending drug.

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Drug-Induced Movement Disorders

Acknowledgements

This work was supported in part by grant FIS 95/0269.

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Correspondence and reprints: Dr Felix Javier Jimenez­Jimenez, C/ Corregidor Jose de Pasamonte 24, 3° D, E-28030 Madrid, Spain.

Drug Safely 1997 Mar: 16 (3)