Neuroleptic‐induced Parkinsonism: Clinicopathological study
Identifieur interne : 000630 ( Main/Exploration ); précédent : 000629; suivant : 000631Neuroleptic‐induced Parkinsonism: Clinicopathological study
Auteurs : Umar A. Shuaib ; Ali H. Rajput ; Christopher A. Robinson ; Alex RajputSource :
- Movement Disorders [ 0885-3185 ] ; 2015.
English descriptors
- KwdEn :
- Aged, Antipsychotic Agents (adverse effects), Antipsychotic Agents (therapeutic use), Dopamine Agents (adverse effects), Dopamine Agents (therapeutic use), Humans, Levodopa (adverse effects), Levodopa (therapeutic use), Lewy Bodies (pathology), Male, Middle Aged, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (pathology), Substantia Nigra (pathology).
- MESH :
- chemical , adverse effects : Antipsychotic Agents, Dopamine Agents, Levodopa.
- chemical , therapeutic use : Antipsychotic Agents, Dopamine Agents, Levodopa.
- chemically induced : Parkinson Disease, Secondary.
- pathology : Lewy Bodies, Parkinson Disease, Secondary, Substantia Nigra.
- Aged, Humans, Male, Middle Aged.
Abstract
Drug‐induced parkinsonism is a well‐known complication of several different drugs—the most common being neuroleptic‐induced parkinsonism. However, very few autopsies have been reported in such cases.
Patients assessed at Movement Disorders Clinic Saskatchewan are offered brain autopsy. Detailed clinical records are kept.
Brains were obtained from 7 drug‐induced parkinsonism patients with parkinsonian symptom onset coinciding with use of drugs known to produce parkinsonism. Six were on antipsychotics and 1 was on metoclopramide. Three cases were treated with levodopa for parkinsonism. In two cases, parkinsonian features reversed after stopping the offending agent. Both had autopsy evidence of preclinical PD. In 4 of the remaining 5, dopamine‐blocking drugs were continued until death. In 4 of those 5, brain histology revealed no cause for the parkinsonism, but 1 had mild SN neuronal loss without Lewy bodies.
This study shows that reversal of parkinsonism after discontinuing offending drugs does not indicate absence of underlying pathology. Neuroleptics can unmask preclinical PD in patients with insufficient SN damage for the disease to manifest clinically. Though the mechanism of sustained parkinsonian features after discontinuing neuroleptics remains to be established, it is unlikely that dopamine receptor block leads to retrograde SN neuronal degeneration. Furthermore,
Url:
DOI: 10.1002/mds.26467
PubMed: 26660063
PubMed Central: 5064745
Affiliations:
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Shuaib</name><affiliation><nlm:aff id="mds26467-aff-0001"></nlm:aff></affiliation></author><author><name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H." last="Rajput">Ali H. Rajput</name><affiliation><nlm:aff id="mds26467-aff-0002"></nlm:aff></affiliation></author><author><name sortKey="Robinson, Christopher A" sort="Robinson, Christopher A" uniqKey="Robinson C" first="Christopher A." last="Robinson">Christopher A. Robinson</name><affiliation><nlm:aff id="mds26467-aff-0003"></nlm:aff></affiliation></author><author><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><affiliation><nlm:aff id="mds26467-aff-0002"></nlm:aff></affiliation></author></analytic><series><title level="j">Movement Disorders</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antipsychotic Agents (adverse effects)</term><term>Antipsychotic Agents (therapeutic use)</term><term>Dopamine Agents (adverse effects)</term><term>Dopamine Agents (therapeutic use)</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Levodopa (therapeutic use)</term><term>Lewy Bodies (pathology)</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Substantia Nigra (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antipsychotic Agents</term><term>Dopamine Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antipsychotic Agents</term><term>Dopamine Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lewy Bodies</term><term>Parkinson Disease, Secondary</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>ABSTRACT</title><sec id="mds26467-sec-0001"><title>Background</title><p>Drug‐induced parkinsonism is a well‐known complication of several different drugs—the most common being neuroleptic‐induced parkinsonism. However, very few autopsies have been reported in such cases.</p></sec><sec id="mds26467-sec-0002"><title>Methods</title><p>Patients assessed at Movement Disorders Clinic Saskatchewan are offered brain autopsy. Detailed clinical records are kept.</p></sec><sec id="mds26467-sec-0003"><title>Results</title><p>Brains were obtained from 7 drug‐induced parkinsonism patients with parkinsonian symptom onset coinciding with use of drugs known to produce parkinsonism. Six were on antipsychotics and 1 was on metoclopramide. Three cases were treated with levodopa for parkinsonism. In two cases, parkinsonian features reversed after stopping the offending agent. Both had autopsy evidence of preclinical PD. In 4 of the remaining 5, dopamine‐blocking drugs were continued until death. In 4 of those 5, brain histology revealed no cause for the parkinsonism, but 1 had mild SN neuronal loss without Lewy bodies.</p></sec><sec id="mds26467-sec-0004"><title>Conclusion</title><p>This study shows that reversal of parkinsonism after discontinuing offending drugs does not indicate absence of underlying pathology. Neuroleptics can unmask preclinical PD in patients with insufficient SN damage for the disease to manifest clinically. Though the mechanism of sustained parkinsonian features after discontinuing neuroleptics remains to be established, it is unlikely that dopamine receptor block leads to retrograde SN neuronal degeneration. Furthermore, <sc>l</sc>‐dopa does not appear to be toxic to SN. © 2015 International Parkinson and Movement Disorder Society</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Lang, Ae" uniqKey="Lang A">AE Lang</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Factor, Sa" uniqKey="Factor S">SA Factor</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Factor, Sa" uniqKey="Factor S">SA Factor</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Fahn, S" uniqKey="Fahn S">S Fahn</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Marsden, Cd" uniqKey="Marsden C">CD Marsden</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Mcdowell, Fh" uniqKey="Mcdowell F">FH McDowell</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Factor, Sa" uniqKey="Factor S">SA Factor</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H." last="Rajput">Ali H. Rajput</name><name sortKey="Robinson, Christopher A" sort="Robinson, Christopher A" uniqKey="Robinson C" first="Christopher A." last="Robinson">Christopher A. Robinson</name><name sortKey="Shuaib, Umar A" sort="Shuaib, Umar A" uniqKey="Shuaib U" first="Umar A." last="Shuaib">Umar A. Shuaib</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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