Increased cerebrospinal fluid levels of neurofilament protein in progressive supranuclear palsy and multiple-system atrophy compared with Parkinson's disease.
Identifieur interne : 004514 ( PubMed/Curation ); précédent : 004513; suivant : 004515Increased cerebrospinal fluid levels of neurofilament protein in progressive supranuclear palsy and multiple-system atrophy compared with Parkinson's disease.
Auteurs : B. Holmberg [Suède] ; L. Rosengren ; J E Karlsson ; B. JohnelsSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1998.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Analysis of Variance, Biological Markers, Case-Control Studies, Cross-Sectional Studies, Diagnosis, Differential, Disease Progression, Enzyme-Linked Immunosorbent Assay, Female, Follow-Up Studies, Glial Fibrillary Acidic Protein (cerebrospinal fluid), Humans, Male, Middle Aged, Multiple System Atrophy (cerebrospinal fluid), Multiple System Atrophy (diagnosis), Neurofilament Proteins (cerebrospinal fluid), Parkinson Disease (cerebrospinal fluid), Parkinson Disease (diagnosis), Prognosis, Sensitivity and Specificity, Statistics, Nonparametric, Supranuclear Palsy, Progressive (cerebrospinal fluid), Supranuclear Palsy, Progressive (diagnosis).
- MESH :
- chemical , cerebrospinal fluid : Glial Fibrillary Acidic Protein, Neurofilament Proteins.
- chemical : Biological Markers.
- cerebrospinal fluid : Multiple System Atrophy, Parkinson Disease, Supranuclear Palsy, Progressive.
- diagnosis : Multiple System Atrophy, Parkinson Disease, Supranuclear Palsy, Progressive.
- Adult, Aged, Aged, 80 and over, Analysis of Variance, Case-Control Studies, Cross-Sectional Studies, Diagnosis, Differential, Disease Progression, Enzyme-Linked Immunosorbent Assay, Female, Follow-Up Studies, Humans, Male, Middle Aged, Prognosis, Sensitivity and Specificity, Statistics, Nonparametric.
Abstract
More reliable tools are needed for the differentiation of Parkinson's disease (PD) from other parkinsonian disorders. The neurofilament protein (NFL) and the glial fibrillary acidic protein (GFAP) are main structural proteins of axons and fibrillary astroglial cells. By using enzyme-linked immunosorbent assays, these proteins were quantified in the cerebrospinal fluid (CSF) of 49 patients referred to the Department of Neurology for diagnostic consideration or treatment of parkinsonism of different etiologies. All patients were first diagnostically evaluated by strict clinical criteria. The procedure included a neurologic and neuro-ophthalmologic examination as well as computed tomography or magnetic resonance imaging. These were performed independently and in advance of the CSF analysis. A total of 19 patients were diagnosed as having PD, 12 had progressive supranuclear palsy (PSP), and 10 had multiple-system atrophy (MSA). Eight were diagnosed as having other diseases, such as arteriosclerotic parkinsonism and undefined parkinsonian syndromes. The content of NFL was significantly higher both in the PSP group (p < 0.001) and in the MSA group (p < 0.0001) compared with the PD group. The high values of NFL indicate an ongoing neuronal degeneration affecting mainly the axonal compartment in the PSP and MSA groups, whereas there was no difference in glial involvement as measured by GFAP in the PD, PSP, and MSA groups. There was a relation between high CSF levels of NFL in the various patient groups and the occurrence of pyramidal symptoms (p < 0.001), possibly reflecting the axonal damage to the corticospinal tract. Furthermore, mortality at 24-month follow up was associated with high NFL levels (p < 0.01). We conclude that analysis of NFL in CSF may become useful in the differential diagnosis of parkinsonian syndromes.
DOI: 10.1002/mds.870130116
PubMed: 9452329
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Increased cerebrospinal fluid levels of neurofilament protein in progressive supranuclear palsy and multiple-system atrophy compared with Parkinson's disease.</title><author><name sortKey="Holmberg, B" sort="Holmberg, B" uniqKey="Holmberg B" first="B" last="Holmberg">B. Holmberg</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Clinical Neuroscience, Department of Neurology, University of Göteborg, Sahlgren's Hospital, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Institute of Clinical Neuroscience, Department of Neurology, University of Göteborg, Sahlgren's Hospital</wicri:regionArea></affiliation></author><author><name sortKey="Rosengren, L" sort="Rosengren, L" uniqKey="Rosengren L" first="L" last="Rosengren">L. Rosengren</name></author><author><name sortKey="Karlsson, J E" sort="Karlsson, J E" uniqKey="Karlsson J" first="J E" last="Karlsson">J E Karlsson</name></author><author><name sortKey="Johnels, B" sort="Johnels, B" uniqKey="Johnels B" first="B" last="Johnels">B. Johnels</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9452329</idno><idno type="pmid">9452329</idno><idno type="doi">10.1002/mds.870130116</idno><idno type="wicri:Area/PubMed/Corpus">004514</idno><idno type="wicri:Area/PubMed/Curation">004514</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Increased cerebrospinal fluid levels of neurofilament protein in progressive supranuclear palsy and multiple-system atrophy compared with Parkinson's disease.</title><author><name sortKey="Holmberg, B" sort="Holmberg, B" uniqKey="Holmberg B" first="B" last="Holmberg">B. Holmberg</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Clinical Neuroscience, Department of Neurology, University of Göteborg, Sahlgren's Hospital, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Institute of Clinical Neuroscience, Department of Neurology, University of Göteborg, Sahlgren's Hospital</wicri:regionArea></affiliation></author><author><name sortKey="Rosengren, L" sort="Rosengren, L" uniqKey="Rosengren L" first="L" last="Rosengren">L. Rosengren</name></author><author><name sortKey="Karlsson, J E" sort="Karlsson, J E" uniqKey="Karlsson J" first="J E" last="Karlsson">J E Karlsson</name></author><author><name sortKey="Johnels, B" sort="Johnels, B" uniqKey="Johnels B" first="B" last="Johnels">B. Johnels</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Analysis of Variance</term><term>Biological Markers</term><term>Case-Control Studies</term><term>Cross-Sectional Studies</term><term>Diagnosis, Differential</term><term>Disease Progression</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Female</term><term>Follow-Up Studies</term><term>Glial Fibrillary Acidic Protein (cerebrospinal fluid)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Multiple System Atrophy (cerebrospinal fluid)</term><term>Multiple System Atrophy (diagnosis)</term><term>Neurofilament Proteins (cerebrospinal fluid)</term><term>Parkinson Disease (cerebrospinal fluid)</term><term>Parkinson Disease (diagnosis)</term><term>Prognosis</term><term>Sensitivity and Specificity</term><term>Statistics, Nonparametric</term><term>Supranuclear Palsy, Progressive (cerebrospinal fluid)</term><term>Supranuclear Palsy, Progressive (diagnosis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="cerebrospinal fluid" xml:lang="en"><term>Glial Fibrillary Acidic Protein</term><term>Neurofilament Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Biological Markers</term></keywords><keywords scheme="MESH" qualifier="cerebrospinal fluid" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinson Disease</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinson Disease</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Analysis of Variance</term><term>Case-Control Studies</term><term>Cross-Sectional Studies</term><term>Diagnosis, Differential</term><term>Disease Progression</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Prognosis</term><term>Sensitivity and Specificity</term><term>Statistics, Nonparametric</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">More reliable tools are needed for the differentiation of Parkinson's disease (PD) from other parkinsonian disorders. The neurofilament protein (NFL) and the glial fibrillary acidic protein (GFAP) are main structural proteins of axons and fibrillary astroglial cells. By using enzyme-linked immunosorbent assays, these proteins were quantified in the cerebrospinal fluid (CSF) of 49 patients referred to the Department of Neurology for diagnostic consideration or treatment of parkinsonism of different etiologies. All patients were first diagnostically evaluated by strict clinical criteria. The procedure included a neurologic and neuro-ophthalmologic examination as well as computed tomography or magnetic resonance imaging. These were performed independently and in advance of the CSF analysis. A total of 19 patients were diagnosed as having PD, 12 had progressive supranuclear palsy (PSP), and 10 had multiple-system atrophy (MSA). Eight were diagnosed as having other diseases, such as arteriosclerotic parkinsonism and undefined parkinsonian syndromes. The content of NFL was significantly higher both in the PSP group (p < 0.001) and in the MSA group (p < 0.0001) compared with the PD group. The high values of NFL indicate an ongoing neuronal degeneration affecting mainly the axonal compartment in the PSP and MSA groups, whereas there was no difference in glial involvement as measured by GFAP in the PD, PSP, and MSA groups. There was a relation between high CSF levels of NFL in the various patient groups and the occurrence of pyramidal symptoms (p < 0.001), possibly reflecting the axonal damage to the corticospinal tract. Furthermore, mortality at 24-month follow up was associated with high NFL levels (p < 0.01). We conclude that analysis of NFL in CSF may become useful in the differential diagnosis of parkinsonian syndromes.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9452329</PMID><DateCreated><Year>1998</Year><Month>03</Month><Day>26</Day></DateCreated><DateCompleted><Year>1998</Year><Month>03</Month><Day>26</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>13</Volume><Issue>1</Issue><PubDate><Year>1998</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Increased cerebrospinal fluid levels of neurofilament protein in progressive supranuclear palsy and multiple-system atrophy compared with Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>70-7</MedlinePgn></Pagination><Abstract><AbstractText>More reliable tools are needed for the differentiation of Parkinson's disease (PD) from other parkinsonian disorders. The neurofilament protein (NFL) and the glial fibrillary acidic protein (GFAP) are main structural proteins of axons and fibrillary astroglial cells. By using enzyme-linked immunosorbent assays, these proteins were quantified in the cerebrospinal fluid (CSF) of 49 patients referred to the Department of Neurology for diagnostic consideration or treatment of parkinsonism of different etiologies. All patients were first diagnostically evaluated by strict clinical criteria. The procedure included a neurologic and neuro-ophthalmologic examination as well as computed tomography or magnetic resonance imaging. These were performed independently and in advance of the CSF analysis. A total of 19 patients were diagnosed as having PD, 12 had progressive supranuclear palsy (PSP), and 10 had multiple-system atrophy (MSA). Eight were diagnosed as having other diseases, such as arteriosclerotic parkinsonism and undefined parkinsonian syndromes. The content of NFL was significantly higher both in the PSP group (p < 0.001) and in the MSA group (p < 0.0001) compared with the PD group. The high values of NFL indicate an ongoing neuronal degeneration affecting mainly the axonal compartment in the PSP and MSA groups, whereas there was no difference in glial involvement as measured by GFAP in the PD, PSP, and MSA groups. There was a relation between high CSF levels of NFL in the various patient groups and the occurrence of pyramidal symptoms (p < 0.001), possibly reflecting the axonal damage to the corticospinal tract. Furthermore, mortality at 24-month follow up was associated with high NFL levels (p < 0.01). We conclude that analysis of NFL in CSF may become useful in the differential diagnosis of parkinsonian syndromes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Holmberg</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Institute of Clinical Neuroscience, Department of Neurology, University of Göteborg, Sahlgren's Hospital, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rosengren</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Karlsson</LastName><ForeName>J E</ForeName><Initials>JE</Initials></Author><Author ValidYN="Y"><LastName>Johnels</LastName><ForeName>B</ForeName><Initials>B</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. 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