DanceTherParkinsonV1, Istex, Corpus, bibRecord, 000229

DRUG-INDUCED MOVEMENT DISORDERS

Identifieur interne : 000229 ( Istex/Corpus ); précédent : 000228; suivant : 000230

DRUG-INDUCED MOVEMENT DISORDERS

Auteurs : Nico J. Diederich ; Christopher G. Goetz

Source :

Neurologic Clinics [ 0733-8619 ] ; 1998.

RBID : ISTEX:D2F9963190E612FDB833E7F219C66F639D75C31E

Abstract

Although known for four decades,33,105 drug-induced movement disorders are still underrecognized. Patients are thought to suffer from idiopathic Parkinson's disease (PD), when, in fact, they have drug-induced parkinsonism (DIP) often from unidentified neuroleptics given for vegetative or psychiatric symptoms. Neuroleptics, drugs that are dopamine receptor blockers (DRBs), can cause a gamut of movement disorders occurring acutely, subacutely, and chronically. The movement disorderinducing potential of new drugs is often not recognized until they have been marketed and large populations have been exposed. This article focuses on several movement disorders caused by various commonly prescribed drugs but does not include neuroleptic malignant syndrome or rare chronic stereotypies. Classic theories as well as new pathophysiologic concepts are discussed.

Url:

https://api.istex.fr/document/D2F9963190E612FDB833E7F219C66F639D75C31E/fulltext/pdf

DOI: 10.1016/S0733-8619(05)70370-4

Links to Exploration step

ISTEX:D2F9963190E612FDB833E7F219C66F639D75C31E

Le document en format XML

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<front><div type="abstract">Although known for four decades,33,105 drug-induced movement disorders are still underrecognized. Patients are thought to suffer from idiopathic Parkinson's disease (PD), when, in fact, they have drug-induced parkinsonism (DIP) often from unidentified neuroleptics given for vegetative or psychiatric symptoms. Neuroleptics, drugs that are dopamine receptor blockers (DRBs), can cause a gamut of movement disorders occurring acutely, subacutely, and chronically. The movement disorderinducing potential of new drugs is often not recognized until they have been marketed and large populations have been exposed. This article focuses on several movement disorders caused by various commonly prescribed drugs but does not include neuroleptic malignant syndrome or rare chronic stereotypies. Classic theories as well as new pathophysiologic concepts are discussed.</div>
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<note type="content">Table 1: PATHOPHYSIOLOGIC MECHANISMS IN DRUG-INDUCED PARKINSONISM</note>
<note type="content">Table 2: DRUG-INDUCED PARKINSONISM EVOLUTION</note>
<note type="content">Table 3: FREQUENT TREMOR INDUCERS</note>
<note type="content">Table 4: FREQUENTLY UNIDENTIFIED DRUGS CAUSING MOVEMENT DISORDERS</note>
<note type="content">Table 5: SEQUENTIAL TREATMENT OPTIONS FOR TARDIVE DYSKINESIAS</note>
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 <ce:floats> <ce:table id="cetable1" frame="topbot" colsep="1" rowsep="0"> <ce:label>Table 1</ce:label>
 <ce:caption> <ce:simple-para>PATHOPHYSIOLOGIC MECHANISMS IN DRUG-INDUCED PARKINSONISM</ce:simple-para>
 </ce:caption>
 <tgroup cols="2" colsep="0" rowsep="0"> <colspec colnum="1" colname="col1" colwidth="50*"></colspec>
 <colspec colnum="2" colname="col2" colwidth="50*"></colspec>
 <thead> <row rowsep="1"> <entry colname="col1" align="left"></entry>
 <entry colname="col2" align="left"><ce:bold>Drug Involved</ce:bold>
</entry>
 </row>
 </thead>
 <tbody> <row> <entry colname="col1" align="left"><ce:bold>Cellular Level</ce:bold>
</entry>
 </row>
 <row> <entry colname="col1" align="left">Mitochondrial respiratory chain dysfunction</entry>
 <entry colname="col2" align="left">Calcium channel blockers, valproic acid</entry>
 </row>
 <row> <entry colname="col1" align="left"><ce:bold>Dopamine Receptor Level</ce:bold>
</entry>
 </row>
 <row> <entry colname="col1" align="left">Presynaptic dopamine depletion</entry>
 <entry colname="col2" align="left">Reserpine, tetrabenazine</entry>
 </row>
 <row> <entry colname="col1" align="left">False transmitter</entry>
 <entry colname="col2" align="left">Methyldopa</entry>
 </row>
 <row> <entry colname="col1" align="left">D<ce:inf>2</ce:inf>
 receptor blockade</entry>
 <entry colname="col2" align="left">Dopamine receptor blockers, antiemetic agents, tetrabenazine, calcium channel blockers</entry>
 </row>
 <row> <entry colname="col1" align="left"><ce:bold>Motor Circuitry Level</ce:bold>
</entry>
 </row>
 <row> <entry colname="col1" align="left">GABAergic overactivity</entry>
 <entry colname="col2" align="left">Valproic acid</entry>
 </row>
 <row> <entry colname="col1" align="left">Cholinomimetic action</entry>
 <entry colname="col2" align="left">Tacrine, bethanechol</entry>
 </row>
 </tbody>
 </tgroup>
 </ce:table>
 <ce:table id="cetable2" frame="topbot" colsep="1" rowsep="0"> <ce:label>Table 2</ce:label>
 <ce:caption> <ce:simple-para>DRUG-INDUCED PARKINSONISM EVOLUTION</ce:simple-para>
 </ce:caption>
 <tgroup cols="1" colsep="0" rowsep="0"> <colspec colnum="1" colname="col1" colwidth="100*"></colspec>
 <tbody> <row> <entry colname="col1" align="left"><ce:italic>Stops</ce:italic>
 with arrest of the drug</entry>
 </row>
 <row> <entry colname="col1" align="center">or</entry>
 </row>
 <row> <entry colname="col1" align="left"><ce:italic>Reappears</ce:italic>
 months to years later</entry>
 </row>
 <row> <entry colname="col1" align="left"> Temporary unmasking of subclinical PD</entry>
 </row>
 <row> <entry colname="col1" align="center">or</entry>
 </row>
 <row> <entry colname="col1" align="left">Full-blown PD syndrome <ce:italic>persists</ce:italic>
</entry>
 </row>
 <row> <entry colname="col1" align="left"> Nigral PD-like damage</entry>
 </row>
 <row> <entry colname="col1">PD = Parkinson's disease.</entry>
 </row>
 </tbody>
 </tgroup>
 </ce:table>
 <ce:table id="cetable3" frame="topbot" colsep="1" rowsep="0"> <ce:label>Table 3</ce:label>
 <ce:caption> <ce:simple-para>FREQUENT TREMOR INDUCERS</ce:simple-para>
 </ce:caption>
 <tgroup cols="1" colsep="0" rowsep="0"> <colspec colnum="1" colname="col1" colwidth="100*"></colspec>
 <tbody> <row> <entry colname="col1" align="left">Essential tremorlike or exaggerated physiologic tremor</entry>
 </row>
 <row> <entry colname="col1" align="left"> Sympathomimetics</entry>
 </row>
 <row> <entry colname="col1" align="left"> Theophylline</entry>
 </row>
 <row> <entry colname="col1" align="left"> Tricyclic antidepressants</entry>
 </row>
 <row> <entry colname="col1" align="left"> Lithium</entry>
 </row>
 <row> <entry colname="col1" align="left"> Valproic acid</entry>
 </row>
 <row> <entry colname="col1" align="left"> Cyclosporin A</entry>
 </row>
 <row> <entry colname="col1" align="left"> Amiodarone</entry>
 </row>
 <row> <entry colname="col1" align="left"> Amphetamine (alcohol withdrawal, caffeine)</entry>
 </row>
 <row> <entry colname="col1" align="left">Asterixis</entry>
 </row>
 <row> <entry colname="col1" align="left"> Carbamazepine (combination therapy of lithium, clozapine, carbamazepine)</entry>
 </row>
 <row> <entry colname="col1" align="left">Cerebellar tremor</entry>
 </row>
 <row> <entry colname="col1" align="left"> Cyclosporin A (rare)</entry>
 </row>
 </tbody>
 </tgroup>
 </ce:table>
 <ce:table id="cetable4" frame="topbot" colsep="1" rowsep="0"> <ce:label>Table 4</ce:label>
 <ce:caption> <ce:simple-para>FREQUENTLY UNIDENTIFIED DRUGS CAUSING MOVEMENT DISORDERS</ce:simple-para>
 </ce:caption>
 <tgroup cols="2" colsep="0" rowsep="0"> <colspec colnum="1" colname="col1" colwidth="40*"></colspec>
 <colspec colnum="2" colname="col2" colwidth="60*"></colspec>
 <tbody> <row> <entry colname="col1" align="left">Acute dystonia</entry>
 <entry colname="col2">Cocaine, amphetamine, birth control pills</entry>
 </row>
 <row> <entry colname="col1" align="left">Parkinsonism</entry>
 <entry colname="col2">Calcium channel blockers, antiemetics</entry>
 </row>
 <row> <entry colname="col1" align="left">Tremor</entry>
 <entry colname="col2">Amiodarone</entry>
 </row>
 <row> <entry colname="col1" align="left">Tardive dyskinesia</entry>
 <entry colname="col2">Antiemetics, antivertiginous drugs</entry>
 </row>
 </tbody>
 </tgroup>
 </ce:table>
 <ce:table id="cetable5" frame="topbot" colsep="1" rowsep="0"> <ce:label>Table 5</ce:label>
 <ce:caption> <ce:simple-para>SEQUENTIAL TREATMENT OPTIONS FOR TARDIVE DYSKINESIAS</ce:simple-para>
 </ce:caption>
 <tgroup cols="1" colsep="0" rowsep="0"> <colspec colnum="1" colname="col1" colwidth="100*"></colspec>
 <tbody> <row> <entry colname="col1" align="left">Prevention</entry>
 </row>
 <row> <entry colname="col1" align="left">Withdrawal of DRB</entry>
 </row>
 <row> <entry colname="col1" align="left">Switch to another (atypical) DRB</entry>
 </row>
 <row> <entry colname="col1" align="left">Dopamine–depleting agents</entry>
 </row>
 <row> <entry colname="col1" align="left">Withdrawal of anticholinergics</entry>
 </row>
 <row> <entry colname="col1" align="left">Vitamin E</entry>
 </row>
 <row> <entry colname="col1" align="left">Levodopa</entry>
 </row>
 <row> <entry colname="col1" align="left">Benzodiazepines</entry>
 </row>
 <row> <entry colname="col1" align="left">Botulinum toxin</entry>
 </row>
 <row> <entry colname="col1" align="left">Increase of DRB</entry>
 </row>
 <row> <entry colname="col1" align="left">DRB = Dopamine receptor blocker.</entry>
 </row>
 </tbody>
 </tgroup>
 </ce:table>
 </ce:floats>
 <head> <ce:article-footnote> <ce:note-para><ce:italic>Address reprint requests to</ce:italic>
 Nico J. Diederich, M.D., Department of Neuroscience, Centre Hospitalier de, Luxembourg, 4, rue Barble, L-1210 Luxembourg (Europe)</ce:note-para>
 <ce:note-para>This work was supported by grants from the Foundations Leir and Think, Luxembourg, and the United Parkinson Foundation, Chicago, IL.</ce:note-para>
 </ce:article-footnote>
 <ce:title>DRUG-INDUCED MOVEMENT DISORDERS</ce:title>
 <ce:author-group> <ce:author> <ce:given-name>Nico J.</ce:given-name>
 <ce:surname>Diederich</ce:surname>
 <ce:degrees>MD</ce:degrees>
<ce:cross-ref refid="aff1"><ce:sup>a</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff2"><ce:sup>b</ce:sup>
</ce:cross-ref>
 </ce:author>
 <ce:author> <ce:given-name>Christopher G.</ce:given-name>
 <ce:surname>Goetz</ce:surname>
 <ce:degrees>MD</ce:degrees>
<ce:cross-ref refid="aff1"><ce:sup>a</ce:sup>
</ce:cross-ref>
 </ce:author>
 <ce:affiliation id="aff1"> <ce:label>a</ce:label>
 <ce:textfn>Department of Neurological Sciences, Rush–Presbyterian–St. Luke's Medical Center (NJD, CGG), Chicago, Illinois</ce:textfn>
 </ce:affiliation>
 <ce:affiliation id="aff2"> <ce:label>b</ce:label>
 <ce:textfn>Department of Neurosciences, (NJD) Centre Hospitalier de Luxembourg, Luxembourg</ce:textfn>
 </ce:affiliation>
 </ce:author-group>
 <ce:abstract> <ce:abstract-sec> <ce:simple-para>Although known for four decades,<ce:cross-refs refid="bib33 bib105"><ce:sup>33,105</ce:sup>
</ce:cross-refs>
 drug-induced movement disorders are still underrecognized. Patients are thought to suffer from idiopathic Parkinson's disease (PD), when, in fact, they have drug-induced parkinsonism (DIP) often from unidentified neuroleptics given for vegetative or psychiatric symptoms. Neuroleptics, drugs that are dopamine receptor blockers (DRBs), can cause a gamut of movement disorders occurring acutely, subacutely, and chronically. The movement disorder–inducing potential of new drugs is often not recognized until they have been marketed and large populations have been exposed. This article focuses on several movement disorders caused by various commonly prescribed drugs but does not include neuroleptic malignant syndrome or rare chronic stereotypies. Classic theories as well as new pathophysiologic concepts are discussed.</ce:simple-para>
 </ce:abstract-sec>
 </ce:abstract>
 </head>
 <body> <ce:sections> <ce:section id="cesec1"> <ce:section-title>ACUTE SYNDROMES</ce:section-title>
 <ce:para>Acute dyskinesias compose a wide variety of phenomena but are mostly dystonic. They are often caused by DRBs. These dramatic but treatable conditions, however, can also be due to birth control pills, numerous illicit street drugs, central stimulants, and antiepileptic medications. Although the induced abnormal movements are not pathognomonic, a few characteristic syndromes can orient the clinician searching for the responsible drug.</ce:para>
 <ce:section id="cesec2"> <ce:section-title>Dystonia</ce:section-title>
 <ce:para>Drug-induced acute dystonia (AD) mostly affects face and neck, as suggested by the <ce:italic>three Os: oculogyric crisis, oromandibular dystonia, and opisthotonos.</ce:italic>
<ce:cross-ref refid="bib88"><ce:sup>88</ce:sup>
</ce:cross-ref>
 Blepharospasmus, trismus, and respiratory stridor as well as trunk and extremity dystonia are other frightening and painful manifestations. Because of their often bizarre appearance, ADs can easily be mistaken for a hysterical conversion.<ce:cross-ref refid="bib111"><ce:sup>111</ce:sup>
</ce:cross-ref>
 There may be spontaneous resolution, and the syndrome is directly abated by parenteral use of benztropine or diphenhydramine. Often the injection has to be repeated, and patients should take oral anticholinergics for at least a few days, after the causative drug is discontinued. Apomorphine and benzodiazepines are less potent alternative drugs.</ce:para>
 <ce:para>Compared with DIP and tardive dyskinesia (TD) (see later), ADs are less frequent movement disorders, associated with DRBs, affecting 2% to 3% of the exposed patients.<ce:cross-ref refid="bib5"><ce:sup>5</ce:sup>
</ce:cross-ref>
 Any DRB can cause AD, and young adults have the highest potential. The onset is abrupt, and 90% of AD occur within the first 5 days of exposure. The incidence may be reduced with prophylactic use of anticholinergic drugs. Dopaminergic antagonists given for gastrointestinal problems and vertigo or as antinausea medication in cancer treatment, such as <ce:italic>sulpiride, domperidone, metoclopramide</ce:italic>
 and <ce:italic>prochlorperazine</ce:italic>
, are often unidentified causes. Drugs with affinity to different subtypes of the serotoninergic 5-hydroxytryptamine (5-HT) receptor have been described as well, including <ce:italic>buspirone</ce:italic>
, an anxiolytic, binding to 5-HT<ce:inf>1A</ce:inf>
, and sumatriptan, an antimigraine drug with agonistic properties for the receptors of the subclass 5-HT<ce:inf>1-like</ce:inf>
 and 5-HT <ce:inf>1B/D</ce:inf>
.<ce:cross-refs refid="bib12 bib66"><ce:sup>12,66</ce:sup>
</ce:cross-refs>
 In latter case, the syndrome may be a dystonia or an acute akathisia and can occur minutes after the intake of sumatriptan.<ce:cross-ref refid="bib66"><ce:sup>66</ce:sup>
</ce:cross-ref>
</ce:para>
 <ce:para>Two contradictory hypotheses propose that ADs are either due to a relative <ce:italic>dopaminergic understimulation</ce:italic>
 or <ce:italic>overstimulation</ce:italic>
, although both accept acute dopaminergic D<ce:inf>2</ce:inf>
 blockade as the primary event and the reaction to be especially brisk in young adults. The first hypothesis can easily explain why ADs can be treated by dopamine agonists, such as apomorphine or anticholinergics. The second hypothesis argues that the acute dopaminergic blockade causes an overcompensatory increase in dopamine synthesis in the nigrostriatal system or blocks the presynaptic dopaminergic autoreceptors, thus causing a secondary acceleration of dopamine turnover. This could explain why ADs resemble treatment-induced dyskinesias in PD.</ce:para>
 </ce:section>
 <ce:section id="cesec3"> <ce:section-title>Choreoathetosis</ce:section-title>
 <ce:para>Movements in choreoathetosis predominate in the extremities and may vary largely in complexity and temporal expression from one patient to another. They clear on drug withdrawal, and specific antidote treatment is not needed. Multiple causative drugs have been described in case reports, and it may be hard to identify the responsible drug in the individual patient, especially with polytherapy. Considering the wide use of some of the incriminated drugs, such as birth control pills and antiepileptics, and the contrasting rarity of the induced abnormal movements, <ce:italic>individual susceptibility</ce:italic>
 for these side effects may be due to preexisting basal ganglia abnormalities, such as prior Sydenham chorea or anoxic encephalopathy.</ce:para>
 <ce:para>Such specific vulnerability has been well established for <ce:italic>contraceptive</ce:italic>
-induced chorea because the women often have a past history of Sydenham chorea, rheumatic fever, or cyanotic congenital heart disease.<ce:cross-ref refid="bib78"><ce:sup>78</ce:sup>
</ce:cross-ref>
 The syndrome can be a generalized chorea or a hemichorea and develop acutely or subacutely.<ce:cross-refs refid="bib63 bib78"><ce:sup>63,78</ce:sup>
</ce:cross-refs>
 From animal experiments, it is known that female hormones enhance postsynaptic dopaminergic sensitivity.<ce:cross-ref refid="bib79"><ce:sup>79</ce:sup>
</ce:cross-ref>
 <ce:italic>Cocaine</ce:italic>
 is an underestimated cause or triggering factor of benign hyperkinetic movement disorders. By binding to presynaptic dopaminergic transporter sites, cocaine blocks dopamine reuptake, thus potentiating dopaminergic neurotransmission. It may also influence postsynaptic receptor sensitivity. Choreoathetosis, dystonic reactions, stereotypies, and tics may thus be caused or exacerbated. Although these symptoms are known by drug users as <ce:italic>crack dance</ce:italic>
, they are seldom reported to physicians.<ce:cross-refs refid="bib20 bib25"><ce:sup>20,25</ce:sup>
</ce:cross-refs>
 Choreoathetotic movements and less frequently tremor, asterixis, and myoclonus have also been reported from the use of <ce:italic>phenytoin.</ce:italic>
<ce:cross-ref refid="bib43"><ce:sup>43</ce:sup>
</ce:cross-ref>
 Static encephalopathy seems to be a predisposing factor. Underlying focal structural lesions may explain why there may be only focal dystonia.<ce:cross-ref refid="bib99"><ce:sup>99</ce:sup>
</ce:cross-ref>
 Case studies have also documented chorea for <ce:italic>carbamazepine, felbamate,</ce:italic>
 and <ce:italic>gabapentin.</ce:italic>
<ce:cross-refs refid="bib15 bib52 bib57"><ce:sup>15,52,57</ce:sup>
</ce:cross-refs>
 Mild or moderate <ce:italic>lithium</ce:italic>
 intoxication, with peak levels varying between 1.2 and 5.7 mEq/L, can cause chorea and myoclonus. Besides potentiation of do paminergic transmission, direct alteration of a second messenger has been discussed as a possible cause.<ce:cross-ref refid="bib89"><ce:sup>89</ce:sup>
</ce:cross-ref>
</ce:para>
 </ce:section>
 <ce:section id="cesec4"> <ce:section-title>Akathisia</ce:section-title>
 <ce:para>Akathisia is a daytime restlessness that leads to an inability to keep the legs still and is often confused with agitation and hyperactivity.<ce:cross-refs refid="bib23 bib95"><ce:sup>23,95</ce:sup>
</ce:cross-refs>
 Nevertheless, it is increasingly recognized as an acute side effect of most DRBs, with prevalence estimates of 20% to 30% of exposed subjects.<ce:cross-ref refid="bib94"><ce:sup>94</ce:sup>
</ce:cross-ref>
 It is less frequent when atypical antipsychotics are used.<ce:cross-ref refid="bib60"><ce:sup>60</ce:sup>
</ce:cross-ref>
 Case reports also document akathisia with the use of selective serotonin reuptake inhibitors (SSRI).<ce:cross-refs refid="bib6 bib61"><ce:sup>6,61</ce:sup>
</ce:cross-refs>
 If treatment is necessary, it includes withdrawal of the offending drug or, if this is not feasible, -blockers, anticholinergics, and benzodiazepines.<ce:cross-ref refid="bib10"><ce:sup>10</ce:sup>
</ce:cross-ref>
</ce:para>
 </ce:section>
 <ce:section id="cesec5"> <ce:section-title>Tics</ce:section-title>
 <ce:para>Drug-induced tics are indistinguishable from those seen in Gilles de la Tourette syndrome and are due to drugs that enhance dopaminergic transmission. The phenomenon is well known for <ce:italic>methylphenidate</ce:italic>
 (Ritalin), <ce:italic>pemoline</ce:italic>
 (Cylert), and amphetamine products, used for abating attention deficit disorder or hyperactivity in children.<ce:cross-ref refid="bib28"><ce:sup>28</ce:sup>
</ce:cross-ref>
 <ce:italic>Sertraline</ce:italic>
, an SSRI antidepressant with potent dopamine reuptake inhibition as well, can provoke acute tic aggravation,<ce:cross-ref refid="bib44"><ce:sup>44</ce:sup>
</ce:cross-ref>
 and tics also range in the panoply of movement disorders exacerbated by cocaine (see later).<ce:cross-ref refid="bib86"><ce:sup>86</ce:sup>
</ce:cross-ref>
 Because tics are not universally exacerbated by central stimulants, undefined predisposing factors may also be important to this drug effect.</ce:para>
 </ce:section>
 </ce:section>
 <ce:section id="cesec6"> <ce:section-title>SUBACUTE SYNDROMES</ce:section-title>
 <ce:section id="cesec7"> <ce:section-title>Drug-Induced Parkinsonism</ce:section-title>
 <ce:para>In 1954, Steck<ce:cross-ref refid="bib103"><ce:sup>103</ce:sup>
</ce:cross-ref>
 first described extrapyramidal signs resembling postencephalitic PD in patients taking chlorpromazine. This observation was confirmed by Gäde and Heinrich in 1955.<ce:cross-ref refid="bib33"><ce:sup>33</ce:sup>
</ce:cross-ref>
 Early authors were convinced that extrapyramidal signs were a reliable indicator of the neuroleptic antipsychotic potency of these medications and thus implicitly connected with efficacy.</ce:para>
 <ce:section id="cesec8"> <ce:section-title>Epidemiology</ce:section-title>
 <ce:para>DIP, related to DRBs, occurs in fewer than half of the treated patients, although prevalence studies of parkinsonism give a wide range of 5% to 90% of treated patients, depending on neuroleptic potency, dose, population examined, and measurements applied. In patients at risk for DIP, the syndrome develops within 1 month in 50% to 70% of the patients and within 3 months in 90% of the patients. When DIP, akathisia, and dyskinesia were considered together, 39% of patients were affected in a collective of 3775 patients.<ce:cross-ref refid="bib5"><ce:sup>5</ce:sup>
</ce:cross-ref>
 In one study of patients primarily referred to a general neurology service for parkinsonism, a detailed drug history revealed that 24% had DIP.<ce:cross-ref refid="bib71"><ce:sup>71</ce:sup>
</ce:cross-ref>
 It is difficult to predict which patients are maximally at risk for DIP and what is the maximal time of onset. Higher prevalence has been described for elderly and female patients. Low-frequency tremor, without other signs sufficient to diagnose parkinsonism, has been discussed as an early sign,<ce:cross-ref refid="bib3"><ce:sup>3</ce:sup>
</ce:cross-ref>
 and when routine examination with the Simpson scale is applied, minor extrapyramidal signs can be identified as early as the fourth day of the neuroleptic treatment in elderly patients.<ce:cross-ref refid="bib106"><ce:sup>106</ce:sup>
</ce:cross-ref>
 Onset, however, is generally considered subacute, occurring after several days or weeks of drug exposure. DIP can occur in the context of long-term drug treatment, when the dose of DRB is increased. For this reason, TD (see later), usually occurring months or years after antipsychotic drug use, can exist concomitantly with DIP in instances in which the DRB dose is increased for control of psychosis.</ce:para>
 </ce:section>
 <ce:section id="cesec9"> <ce:section-title>Phenomenology</ce:section-title>
 <ce:para>Clinical phenomenology of DIP is indistinguishable from PD. Early reports claimed that DIP is more symmetric, has predominant bradykinetic features, and often lacks tremor. No unique syndrome is identified, however, and asymmetric and tremor-dominant DIP patients are well described. One sign that may be more frequent in DIP is a low-frequency, high-amplitude jaw tremor, termed <ce:italic>rabbit syndrome.</ce:italic>
</ce:para>
 </ce:section>
 <ce:section id="cesec10"> <ce:section-title>Pathophysiology</ce:section-title>
 <ce:para>As a phenomenon, parkinsonism is caused by underactivity of the dopaminergic pathway, traveling from the substantia nigra to the striatum (caudate nucleus and putamen). In PD, cells in the substantia nigra degenerate, whereas DIP is caused by reversible alterations involving the same system, either presynaptically or postsynaptically. Although the antipsychiatric action of the DRBs relates to dopaminergic <ce:italic>mesolimbic</ce:italic>
 receptor blockade, inadvertent <ce:italic>nigrostriatal</ce:italic>
 receptor antagonism accounts for parkinsonism. A presynaptic dopamine depletion is caused by antihypertensive drugs of the reserpine type. Methyldopa is posited to act as a false transmitter, being transformed into methyldopamine, which is inactive and acts competitively with dopamine. Other drugs causing DIP alter other neurotransmitters that normally function in conjunction with dopamine. Overwhelming GABAergic activity may account for DIP related to valproic acid. Mitochondrial respiratory chain dysfunction, along with dopamine receptor blockade, may cause DIP associated with calcium channel blockers <ce:cross-ref refid="cetable1">(Table 1)</ce:cross-ref>
<ce:float-anchor refid="cetable1"></ce:float-anchor>
.</ce:para>
 <ce:para>Varying individual susceptibility to DIP suggests that affected patients may already suffer from <ce:italic>subclinical PD, temporarily unmasked</ce:italic>
 by pharmaceutical manipulation <ce:cross-ref refid="cetable2">(Table 2).</ce:cross-ref>
<ce:float-anchor refid="cetable2"></ce:float-anchor>
 These patients may be sensitive to a large variety of drugs, even at low dosages. One explanation for the observed higher incidence of DIP in elderly patients could thus relate to drug-related interference with age-dependent loss of dopaminergic cells. Although most patients recover after withdrawal from the incriminated drug, some develop idiopathic PD a few years later.<ce:cross-ref refid="bib41"><ce:sup>41</ce:sup>
</ce:cross-ref>
 In a subgroup of other patients, the parkinsonian signs even persist directly after withdrawal. Imaging by <ce:sup>18F</ce:sup>
 fluorodopa positron-emission tomography shows that the radioactive dopa uptake in these patients is reduced, whereas it generally normalizes in patients recovering after withdrawal.<ce:cross-ref refid="bib18"><ce:sup>18</ce:sup>
</ce:cross-ref>
 High-field magnetic resonance imaging also detects putaminal hypointensities in some young patients.<ce:cross-ref refid="bib11"><ce:sup>11</ce:sup>
</ce:cross-ref>
</ce:para>
 </ce:section>
 <ce:section id="cesec11"> <ce:section-title>Drugs Involved</ce:section-title>
 <ce:para>Most studies describe DIP after use of DRB. All types of DRB are involved, especially the <ce:italic>piperazine</ce:italic>
 class of phenothiazines and <ce:italic>butyrophenones.</ce:italic>
 The risk is smaller with molindone, thioridazine, and risperidone.<ce:cross-ref refid="bib7"><ce:sup>7</ce:sup>
</ce:cross-ref>
 Except for rare instances, clozapine induces DIP only at a daily dosage above 250 mg. The calcium entry blockers <ce:italic>flunarizine</ce:italic>
 and <ce:italic>cinnarizine</ce:italic>
, are piperazine derivatives resembling the neuroleptic trifluoperazine. They are used to treat vertigo, tinnitus, and cognitive disorders, especially in the elderly. Similar to neuroleptics, they partially block the D<ce:inf>2</ce:inf>
 receptor bindings. This is visualized by single-photon emission computed tomography by a reduced (s)–(–)–2–hydroxy–3–iode–6–methoxy–N– [(l–ethyl–2–pyrrolidonyl) methyl] benzamide (IBZM) uptake.<ce:cross-ref refid="bib13"><ce:sup>13</ce:sup>
</ce:cross-ref>
 Mitochondrial respiratory chain dysfunction may occur as well. Several studies, especially from Mediterranean and South American countries, have documented numerous cases of DIP, appearing with a mean exposure of 4 ± 4 years.<ce:cross-ref refid="bib39"><ce:sup>39</ce:sup>
</ce:cross-ref>
 After withdrawal of the drug, symptoms disappeared in two studies<ce:cross-refs refid="bib70 bib73"><ce:sup>70,73</ce:sup>
</ce:cross-refs>
 but persisted in 33% to 100% in two other studies with follow-up periods of 18 months and 7 years.<ce:cross-refs refid="bib36 bib79"><ce:sup>36,79</ce:sup>
</ce:cross-refs>
 Elderly patients seem especially prone to this side effect, and there is debate if family history of essential tremor may be an additional risk factor.<ce:cross-ref refid="bib39"><ce:sup>39</ce:sup>
</ce:cross-ref>
 Careful epidemiologic data are missing, but large numbers of patients take these drugs. In 1985, 5% to 7% of people over age 60 were treated with cinnarizine in Spain. Other calcium entry blockers, such as nifedipine and verapamil, have only occasionally been associated with involuntary movement disorders, such as myoclonic dystonia and akathisia,<ce:cross-refs refid="bib45 bib72"><ce:sup>45,72</ce:sup>
</ce:cross-refs>
 and unmasking of PD is exceptional.<ce:cross-ref refid="bib34"><ce:sup>34</ce:sup>
</ce:cross-ref>
</ce:para>
 <ce:para>The SSRI <ce:italic>fluoxetine</ce:italic>
 and, to a lesser extent, <ce:italic>paroxetine</ce:italic>
 and <ce:italic>fluvoxamine</ce:italic>
 have been reported to induce or exacerbate parkinsonian syndromes.<ce:cross-refs refid="bib51 bib100 bib104"><ce:sup>51,100,104</ce:sup>
</ce:cross-refs>
 In two studies, no other drugs were involved,<ce:cross-refs refid="bib100 bib104"><ce:sup>100,104</ce:sup>
</ce:cross-refs>
 whereas two case reports discuss putative interactions with cimetidine, which may inhibit hepatic P-450 cytochrome enzymes,<ce:cross-ref refid="bib61"><ce:sup>61</ce:sup>
</ce:cross-ref>
 or with selegiline, provoking DIP in the context of a <ce:italic>serotonin syndrome.</ce:italic>
<ce:cross-ref refid="bib35"><ce:sup>35</ce:sup>
</ce:cross-ref>
 The actual relationship of fluoxetine with DIP remains controversial, however, because no association was found in two other studies,<ce:cross-refs refid="bib19 bib75"><ce:sup>19,75</ce:sup>
</ce:cross-refs>
 and fluoxetine is widely used in clinical practice.</ce:para>
 <ce:para>A study in epileptic patients treated with <ce:italic>valproic acid</ce:italic>
 over 12 months demonstrated an insidious onset of parkinsonian features in 32 out of 37 patients. Almost all improved after discontinuation of the drug. The syndrome was often associated with cognitive and hearing impairment, and it was speculated that this may be due to overwhelming GABAergic activity and mitochondrial respiratory chain dysfunction.<ce:cross-ref refid="bib4"><ce:sup>4</ce:sup>
</ce:cross-ref>
</ce:para>
 <ce:para><ce:italic>Numerous other drugs</ce:italic>
 have been reported in case studies as causing or exacerbating preexisting parkinsonism. In most reports, the association is based on observation of clinical improvement after withdrawal, and only a few have data on rechallenging trials. The drugs are difficult to classify. Antidopaminergic drugs with presumably only peripheral activity are one group and include <ce:italic>veralipride, cisapride</ce:italic>
, and <ce:italic>clebopride</ce:italic>
.<ce:cross-refs refid="bib32 bib50 bib77 bib98"><ce:sup>32,50,77,98</ce:sup>
</ce:cross-refs>
 The presynaptic dopamine depletors <ce:italic>reserpine</ce:italic>
 and <ce:italic>tetrabenazine</ce:italic>
, used in the treatment of hyperkinetic movement disorders, can cause DIP in less than a third of patients.<ce:cross-ref refid="bib48"><ce:sup>48</ce:sup>
</ce:cross-ref>
 Transient parkinsonism has also been seen as a side effect of meperidine.<ce:cross-ref refid="bib82"><ce:sup>82</ce:sup>
</ce:cross-ref>
 1–Methyl–4–phenyl–1,2,3,6–tetrahydropyridine (MPTP), a meperidine derivative, can cause severe parkinsonism by its active metabolite MPP+, and MPTP–parkinsonism is the most widely accepted animal model of PD. Unmasking PD has been associated with the use of the cholinomimetics <ce:italic>tacrine</ce:italic>
 and <ce:italic>bethanechol</ce:italic>
, which may alter the balance between the cholinergic and the dopaminergic striatal systems.<ce:cross-refs refid="bib31 bib83"><ce:sup>31,83</ce:sup>
</ce:cross-refs>
 Other case studies claim an association with the use of amiodarone,<ce:cross-ref refid="bib26"><ce:sup>26</ce:sup>
</ce:cross-ref>
 <ce:italic>lovastatin,</ce:italic>
<ce:cross-ref refid="bib76"><ce:sup>76</ce:sup>
</ce:cross-ref>
 and <ce:italic>lithium.</ce:italic>
<ce:cross-ref refid="bib46"><ce:sup>46</ce:sup>
</ce:cross-ref>
</ce:para>
 </ce:section>
 </ce:section>
 <ce:section id="cesec12"> <ce:section-title>Tremor</ce:section-title>
 <ce:para>Tremor is an easily recognizable movement disorder, which can be subacutely induced by numerous drugs and clears on drug withdrawal. It is usually a low–amplitude and high–frequency postural tremor, indistinguishable from essential tremor. Well–known causative agents are sympathomimetics, tricyclic antidepressants, theophylline, and lithium. Up to 25% of patients on long–term valproate therapy with a daily dose greater than 750 mg suffer from a postural or action–induced tremor.<ce:cross-ref refid="bib55"><ce:sup>55</ce:sup>
</ce:cross-ref>
 Drug withdrawal leads to a resolution of the movement disorder. If the causative medication is necessary, patients may benefit from propranolol or other –adrenergic antagonists.<ce:cross-ref refid="bib56"><ce:sup>56</ce:sup>
</ce:cross-ref>
 Exaggerated physiologic tremor is a frequent, initial side effect from cylosporin A (up to 39% of patients), but both prevalence and severity diminish with time.<ce:cross-ref refid="bib53"><ce:sup>53</ce:sup>
</ce:cross-ref>
 Cerebellar tremor, characterized by a coarse shaking with superimposed dyssynergia and an end point exacerbation of shaking, may also occur, but in these cases an ongoing encephalopathic process is suggested.<ce:cross-ref refid="bib114"><ce:sup>114</ce:sup>
</ce:cross-ref>
 Postural tremor is frequent (43% to 59%) in patients treated with amiodarone and can be associated with ataxia and peripheral polyneuropathy.<ce:cross-refs refid="bib21 bib85"><ce:sup>21,85</ce:sup>
</ce:cross-refs>
 Asterixis, a form of myoclonus, and large–amplitude <ce:italic>flapping</ce:italic>
 tremor can be induced notably by carbamazepine and several psychoactive drugs, especially clozapine and lithium<ce:cross-ref refid="bib93"><ce:sup>93</ce:sup>
</ce:cross-ref>
 <ce:cross-ref refid="cetable3">(Table 3</ce:cross-ref>
<ce:float-anchor refid="cetable3"></ce:float-anchor>
 and <ce:cross-ref refid="cetable4">4</ce:cross-ref>
<ce:float-anchor refid="cetable4"></ce:float-anchor>
).</ce:para>
 </ce:section>
 </ce:section>
 <ce:section id="cesec13"> <ce:section-title>CHRONIC SYNDROMES</ce:section-title>
 <ce:section id="cesec14"> <ce:section-title>Levodopa–Induced Dyskinesias in Parkinson's Disease</ce:section-title>
 <ce:para>In PD, levodopa–induced choreic or dystonic dyskinesias occur when patients are treated long–term. They are often asymmetric, affecting the most affected side of the disease. The duration may be only minutes, and diurnal variation is a cardinal clue because the signs appear more often when the serum level of the antiparkinsonian medication is at its most efficient level (<ce:italic>peak dose</ce:italic>
 dyskinesia) and less often when the therapeutic effect starts or vanishes (<ce:italic>end dose</ce:italic>
 or <ce:italic>biphasic</ce:italic>
 dys kinesia). Any antiparkinsonian drug, given on a long–term basis, can cause levo dopa–induced dyskinesias in the late phase of PD. High dosage standard formulation of levodopa, with rapid enteric absorption, is at highest risk, whereas slow–release formulas and the different dopaminergic agonists may be less prone. Numerous therapeutic manipulations have been proposed to influence these phenomena: spreading of the daily dose to numerous intakes, change to dopamine agonists, <ce:italic>add–on</ce:italic>
 treatment with selegiline or clozapine, and even neurosurgical techniques (pallidotomy, various techniques of deep brain stimulation).</ce:para>
 <ce:para>Levodopa–induced dyskinesia is thought to be due in part to <ce:italic>hypersensitivity of striatal dopamine neurons</ce:italic>
 caused by the prolonged denervation together with reduced presynaptic <ce:italic>buffer</ce:italic>
 capacities (reduced storage capacities).<ce:cross-ref refid="bib1"><ce:sup>1</ce:sup>
</ce:cross-ref>
 Thus, exogenous levodopa is metabolized to dopamine but cannot be adequately stored so that it floods the hypersensitive postsynaptic receptors and induces hyperkinesia. The pathophysiology of these complex movements is discussed in a number of sources.<ce:cross-refs refid="bib70 bib81 bib108"><ce:sup>70,81,108</ce:sup>
</ce:cross-refs>
</ce:para>
 </ce:section>
 <ce:section id="cesec15"> <ce:section-title>Tardive Dyskinesias</ce:section-title>
 <ce:section id="cesec16"> <ce:section-title>Risk Factors and Epidemiology</ce:section-title>
 <ce:para>Curious chronic movements and mannerisms were observed in schizophrenic patients long before the neuroleptic era and were described as athetoid ataxia f. ex. by Kraepelin.<ce:cross-ref refid="bib69"><ce:sup>69</ce:sup>
</ce:cross-ref>
 The widespread use of DRBs, however, has led to a far more frequent occurrence of persisting and disabling abnormal movements in schizophrenic patients, called TD. TD is defined as a movement disorder specifically related to chronic (>.3 months) exposure to DRB agents. Terms such as <ce:italic>spontaneous TD</ce:italic>
 have no sense and should be abandoned. Except for rare instances, rest tremor is not included as a TD symptom because it is due to subacute DIP. Ongoing epidemiologic research has identified certain risk factors, including old age, female gender, and duration and dosage of DRB exposure, whereas the risk contribution of other factors still remains controversial: type of DRB, role of concomitant antiparkinsonian medication, psychiatric diagnosis, organic brain dysfunction, alcohol dependence, diabetes, and concomitant administration of hepatic enzyme inhibitors.<ce:cross-refs refid="bib8 bib38 bib87"><ce:sup>8,38,87</ce:sup>
</ce:cross-refs>
</ce:para>
 <ce:para>The prevalence rates show large variations (between 0.5% and 65%), probably reflecting differences in patient samples and diagnostic criteria.<ce:cross-ref refid="bib69"><ce:sup>69</ce:sup>
</ce:cross-ref>
 A meta–analysis of 56 surveys has calculated an average prevalence of 20%.<ce:cross-ref refid="bib54"><ce:sup>54</ce:sup>
</ce:cross-ref>
 <ce:italic>Advanced age</ce:italic>
 is seen as a major risk factor for TD, independently from the <ce:italic>cumulative DRB dosage</ce:italic>
. In a sample of chronic psychiatric inpatients, studied over 10 years, prevalence of TD was 3.7% in 1982 and 12.7% in 1992, even though cumulative DRB dose was not significantly different between those with or without TD.<ce:cross-refs refid="bib74 bib102"><ce:sup>74,102</ce:sup>
</ce:cross-refs>
 Among the high–risk group of geropsychiatric inpatients, the risk of <ce:italic>treatment duration</ce:italic>
 is also clearly documented: 29% of the patients with 3 to 12 months of DRB treatment and 41% of the patients with more than 10 years of DRB treatment develop TD.<ce:cross-ref refid="bib105"><ce:sup>105</ce:sup>
</ce:cross-ref>
 In another study of 39,187 patients, 26.6% of the women and 21.6% of the men were affected.<ce:cross-ref refid="bib117"><ce:sup>117</ce:sup>
</ce:cross-ref>
 These rates have to be compared with the rates of spontaneous dyskinesias in elderly people, estimated between 5% and 10%.<ce:cross-refs refid="bib54 bib113"><ce:sup>54,113</ce:sup>
</ce:cross-refs>
 With this restriction in mind, a reasonable overall estimation for TD is 15% of patients treated long–term. Furthermore the differential diagnosis of spontaneous movement disorders associated with certain subtypes of schizophrenia remains extremely difficult.<ce:cross-ref refid="bib30"><ce:sup>30</ce:sup>
</ce:cross-ref>
</ce:para>
 </ce:section>
 <ce:section id="cesec17"> <ce:section-title>Phenomenology</ce:section-title>
 <ce:para>TD has several clinical subtypes, and prevalence varies largely according to the respective form. Although more patients have mixed forms, they are categorized according to their predominant movement disorder. <ce:italic>Orobuccolinguomasticatory syndrome</ce:italic>
, or orofacial dyskinesia, is the most frequent subtype, representing 40% of patients from one study of psychiatric inpatients.<ce:cross-ref refid="bib112"><ce:sup>112</ce:sup>
</ce:cross-ref>
 It is characterized by stereotyped movements of tongue twisting and protusion and facial grimaces. <ce:italic>Tardive akathisia</ce:italic>
 accounted for 13% of the patients, and the more recent delineated <ce:italic>tardive dystonia</ce:italic>
.<ce:cross-ref refid="bib17"><ce:sup>17</ce:sup>
</ce:cross-ref>
 was also seen in 13% of the patients in this group.<ce:cross-ref refid="bib112"><ce:sup>112</ce:sup>
</ce:cross-ref>
 The risk profile for tardive dystonia seems to be different from other forms of TD because mostly young patients are affected.<ce:cross-ref refid="bib90"><ce:sup>90</ce:sup>
</ce:cross-ref>
 Finally, tardive forms of tics, myoclonus, and tremor have been described.<ce:cross-ref refid="bib47"><ce:sup>47</ce:sup>
</ce:cross-ref>
</ce:para>
 </ce:section>
 <ce:section id="cesec18"> <ce:section-title>Pathophysiology</ce:section-title>
 <ce:para>The pathophysiology of TD is partly understood, and the oldest theory, although imperfect, remains the most eloquent. This model posits that the striatal dopamine receptors, blocked chronically by DRBs, develop a <ce:italic>supersensitivity</ce:italic>
 to dopamine so that amounts of dopamine normally too small to induce dyskinesias in a patient are now able to do so. It is possible that the concomitant use of anticholinergics even increases the probability of TD as the balance between dopamine and acetylcholine is brought down to a lower level.<ce:cross-refs refid="bib37 bib58"><ce:sup>37,58</ce:sup>
</ce:cross-refs>
 This theory, however, cannot explain why patients often remain dyskinetic after the DRBs are withdrawn long–term. It has been suggested that the blockade of a subgroup of dopamine receptors leads to a long–term unspecific lowering of the threshold for dyskinesias.<ce:cross-ref refid="bib37"><ce:sup>37</ce:sup>
</ce:cross-ref>
 The role of –aminobutyric acid (<ce:italic>GABA</ce:italic>
) has been argued because DRBs may decrease the activity in a subgroup of GABAergic neurons, originating from the striatum. Finally, neuroleptics inhibit complex I of the electron transport chain, which may contribute to movement disorders, as mentioned already for DIP.<ce:cross-ref refid="bib16"><ce:sup>16</ce:sup>
</ce:cross-ref>
 All these hypotheses have in common that TD is precipitated by long–term DRB treatment but that it may require that affected patients show some underlying substrate potential for development.</ce:para>
 <ce:para>Topographic or functional imaging techniques of patients with TD show in creased glucose metabolism in the globus pallidus.<ce:cross-ref refid="bib84"><ce:sup>84</ce:sup>
</ce:cross-ref>
 It remains unclear, however, if the local D<ce:inf>2</ce:inf>
 receptor density and binding affinity is increased or within normal limits.<ce:cross-refs refid="bib2 bib92"><ce:sup>2,92</ce:sup>
</ce:cross-refs>
 Early reports have indicated a trend for larger lateral ventricles on computed tomography or prominent T2 changes on magnetic resonance imaging, but these findings have not been confirmed in other studies. There is no difference in the volume of the basal ganglia in schizophrenic patients with or without TD.<ce:cross-refs refid="bib14 bib27"><ce:sup>14,27</ce:sup>
</ce:cross-refs>
</ce:para>
 </ce:section>
 <ce:section id="cesec19"> <ce:section-title>Drugs Involved</ce:section-title>
 <ce:para>Low–potency and high–potency traditional DRBs can cause TD. Presumptions that fluphenazine decanoate is a more frequent inducer and that thioridazine is of lower risk for producing TD have not been rigorously tested.<ce:cross-ref refid="bib59"><ce:sup>59</ce:sup>
</ce:cross-ref>
 New or atypical DRBs, however, appear to carry less risk, and no convincing cases of TD have been reported with clozapine.<ce:cross-ref refid="bib64"><ce:sup>64</ce:sup>
</ce:cross-ref>
 The widely used antiemetic agent metoclopramide is a potent D<ce:inf>2</ce:inf>
 antagonist and can also produce TD, especially in elderly patients.<ce:cross-refs refid="bib96 bib115"><ce:sup>96,115</ce:sup>
</ce:cross-refs>
 Isolated cases of TD have been reported with the use of antihistaminic decongestants, fluoxetine, and tricyclic antidepressants with dopamine receptor blocking properties, specifically amoxapine.<ce:cross-refs refid="bib9 bib29 bib111"><ce:sup>9,29,111</ce:sup>
</ce:cross-refs>
 Some of these patients were on a multidrug therapy, however, thus making the identification of a specific drug risk profile difficult.</ce:para>
 </ce:section>
 <ce:section id="cesec20"> <ce:section-title>Treatment and Prognosis</ce:section-title>
 <ce:section id="cesec21"> <ce:section-title>Prevention still remains the best treatment.</ce:section-title>
 <ce:para>Primary prevention should reserve DRBs only for patients in strict need of them. Although cumulative dose of DRB has not been confirmed to be a specific risk factor, secondary prevention generally involves giving the smallest dosage for the shortest period of time. Frequent assessments with attention to the early emergence of abnormal movements may alert the treating physician to intervene as soon as possible. Treatment of TD itself is multifaceted and depends largely on the individual needs of the patient <ce:cross-ref refid="cetable5">(Table 5)</ce:cross-ref>
<ce:float-anchor refid="cetable5"></ce:float-anchor>
. It should consider two strategies: first, treating the psychiatric disease and, second, treating the TD. If possible, the causative agent should be reduced or stopped. Many psychiatric patients, however, cannot tolerate discontinuation of DRB treatment because of exacerbation of their psychiatric condition. In some cases, the involuntary movements may even become increased with withdrawal of medication, presumably because of the unveiling of the receptor hypersensitivity (<ce:italic>withdrawal</ce:italic>
 or <ce:italic>covert dyskinesia</ce:italic>
).<ce:cross-ref refid="bib59"><ce:sup>59</ce:sup>
</ce:cross-ref>
 Although noticeable improvement occurs in most patients, complete and persistent resolution is seen only in 2% of them after complete discontinuation of the DRB.<ce:cross-ref refid="bib40"><ce:sup>40</ce:sup>
</ce:cross-ref>
 The switch to atypical DRBs, such as clozapine, risperidone, and sulpiride, has been proposed as a dopaminergic desensitization technique and may be helpful in up to 40% of patients, as suggested by uncontrolled studies and case histories.<ce:cross-refs refid="bib64 bib91 bib97 bib108"><ce:sup>64,91,97,108</ce:sup>
</ce:cross-refs>
 The Canadian multicenter study has established a statistically significant antidyskinetic effect with risperidone at a daily dosage of 6 mg/day.<ce:cross-ref refid="bib22"><ce:sup>22</ce:sup>
</ce:cross-ref>
 Double–blind, controlled studies, however, are lacking. The dopamine depletors reserpine and tetrabenazine have shown dramatic improvement in some patients; however, reserpine often has dosage–limiting hypotensive and depressive side effects, and the availability of tetrabenazine is limited.<ce:cross-ref refid="bib48"><ce:sup>48</ce:sup>
</ce:cross-ref>
 The discontinuation of anticholinergics is another empirically based recommendation<ce:cross-ref refid="bib116"><ce:sup>116</ce:sup>
</ce:cross-ref>
 for orofacial dyskinesias; anticholinergics are helpful for the treatment of tardive dystonia. Therefore, in assessing the role of acetylcholine, the predominant phenomenology of the TD should be assessed in each patient. The antioxidant vitamin E has been claimed to show a significant reduction of TD in patients who suffer from the syndrome less than 5 years.<ce:cross-refs refid="bib24 bib65"><ce:sup>24,65</ce:sup>
</ce:cross-refs>
 Another theoretical way of down–regulating the dopamine supersensitivity is the use of levodopa, thus causing a temporary increase of dopamine levels.<ce:cross-refs refid="bib42 bib101"><ce:sup>42,101</ce:sup>
</ce:cross-refs>
 This approach, however, is not feasible in most schizophrenic patients, and clinical results remain controversial.<ce:cross-refs refid="bib67 bib101"><ce:sup>67,101</ce:sup>
</ce:cross-refs>
 Use of different benzodiazepines and of botulinum toxin has also been claimed to be efficient, especially in dystonic patients.<ce:cross-ref refid="bib110"><ce:sup>110</ce:sup>
</ce:cross-ref>
</ce:para>
 <ce:para>Practically speaking, the continuation of the neuroleptic treatment, even at a higher dosage, appears to be the most frequently used approach to treat TD, as concluded by the review of 285 treatment studies.<ce:cross-ref refid="bib49"><ce:sup>49</ce:sup>
</ce:cross-ref>
 Although this strategy is treatment with the actual pathogenic agent, it has been argued that continuation of therapy eventually produces a long–term <ce:italic>down–regulation</ce:italic>
 or <ce:italic>desensitization</ce:italic>
 of the dopaminergic receptors. This treatment is extremely controversial, especially in a medicolegal environment. Because TD can be life–threatening, however, causing extreme respiratory alkalosis from diaphragmatic chorea or severe and painful dystonic opisthotonic posturing, reintroducing or increasing DRBs in these extreme cases is justified and without controversy.</ce:para>
 </ce:section>
 </ce:section>
 </ce:section>
 </ce:section>
 <ce:section id="cesec22"> <ce:section-title>FUTURE RESEARCH PERSPECTIVES</ce:section-title>
 <ce:para>Drug–induced movement disorders have primarily been studied in case reports, and good epidemiologic data are missing. Prospective, multicenter studies are thus needed to elucidate further the individual susceptibility for a given syndrome. At the present time, the premorbid condition of the dopaminergic transmission seems to be pivotal for most drug–induced movements. Enhanced dopaminergic sensitivity may underlie choreatic syndromes, whereas a subclinical loss of nigral cells may predispose to DIP. Mechanisms of age–dependent reactivity to exogenous drugs should be another research target because young and old people may respond differently to the same drugs. In the case of DRBs, young people may <ce:italic>overshoot</ce:italic>
 with acute dyskinesias, whereas the dopaminergic system in elderly patients may respond more slowly, giving rise to the subacute and chronic dyskinesias.</ce:para>
 </ce:section>
 </ce:sections>
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<mods version="3.6"><titleInfo><title>DRUG-INDUCED MOVEMENT DISORDERS</title>
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<titleInfo type="alternative" contentType="CDATA"><title>DRUG-INDUCED MOVEMENT DISORDERS</title>
</titleInfo>
<name type="personal"><namePart type="given">Nico J.</namePart>
<namePart type="family">Diederich</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurological Sciences, RushPresbyterianSt. Luke's Medical Center (NJD, CGG), Chicago, Illinois</affiliation>
<affiliation>Department of Neurosciences, (NJD) Centre Hospitalier de Luxembourg, Luxembourg</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Christopher G.</namePart>
<namePart type="family">Goetz</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Department of Neurological Sciences, RushPresbyterianSt. Luke's Medical Center (NJD, CGG), Chicago, Illinois</affiliation>
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<originInfo><publisher>ELSEVIER</publisher>
<dateIssued encoding="w3cdtf">1998</dateIssued>
<copyrightDate encoding="w3cdtf">1998</copyrightDate>
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<language><languageTerm type="code" authority="iso639-2b">eng</languageTerm>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
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<abstract>Although known for four decades,33,105 drug-induced movement disorders are still underrecognized. Patients are thought to suffer from idiopathic Parkinson's disease (PD), when, in fact, they have drug-induced parkinsonism (DIP) often from unidentified neuroleptics given for vegetative or psychiatric symptoms. Neuroleptics, drugs that are dopamine receptor blockers (DRBs), can cause a gamut of movement disorders occurring acutely, subacutely, and chronically. The movement disorderinducing potential of new drugs is often not recognized until they have been marketed and large populations have been exposed. This article focuses on several movement disorders caused by various commonly prescribed drugs but does not include neuroleptic malignant syndrome or rare chronic stereotypies. Classic theories as well as new pathophysiologic concepts are discussed.</abstract>
<note>Address reprint requests to Nico J. Diederich, M.D., Department of Neuroscience, Centre Hospitalier de, Luxembourg, 4, rue Barble, L-1210 Luxembourg (Europe)</note>
<note>This work was supported by grants from the Foundations Leir and Think, Luxembourg, and the United Parkinson Foundation, Chicago, IL.</note>
<note type="content">Table 1: PATHOPHYSIOLOGIC MECHANISMS IN DRUG-INDUCED PARKINSONISM</note>
<note type="content">Table 2: DRUG-INDUCED PARKINSONISM EVOLUTION</note>
<note type="content">Table 3: FREQUENT TREMOR INDUCERS</note>
<note type="content">Table 4: FREQUENTLY UNIDENTIFIED DRUGS CAUSING MOVEMENT DISORDERS</note>
<note type="content">Table 5: SEQUENTIAL TREATMENT OPTIONS FOR TARDIVE DYSKINESIAS</note>
<relatedItem type="host"><titleInfo><title>Neurologic Clinics</title>
</titleInfo>
<titleInfo type="abbreviated"><title>NCL</title>
</titleInfo>
<genre type="journal">journal</genre>
<originInfo><dateIssued encoding="w3cdtf">19980201</dateIssued>
</originInfo>
<identifier type="ISSN">0733-8619</identifier>
<identifier type="PII">S0733-8619(05)X7025-6</identifier>
<part><date>19980201</date>
<detail type="volume"><number>16</number>
<caption>vol.</caption>
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	Danse-thérapie et Parkinson
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Danse-thérapie et Parkinson

DRUG-INDUCED MOVEMENT DISORDERS

DRUG-INDUCED MOVEMENT DISORDERS

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