Clinical significance of glutamic acid decarboxylase antibodies in patients with epilepsy

Summary Purpose:  Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined. Methods:  We analyzed GADA with a radioimmunoassay in sera of 253 well‐characterized patients with epil...

Full description

Saved in:
Bibliographic Details
Published inEpilepsia (Copenhagen) Vol. 51; no. 5; pp. 760 - 767
Main Authors Liimatainen, Suvi, Peltola, Maria, Sabater, Lidia, Fallah, Mahdi, Kharazmi, Elham, Haapala, Anna‐Maija, Dastidar, Prasun, Knip, Mikael, Saiz, Albert, Peltola, Jukka
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.05.2010
Wiley-Blackwell
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Summary Purpose:  Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined. Methods:  We analyzed GADA with a radioimmunoassay in sera of 253 well‐characterized patients with epilepsy and 200 control subjects. The positive samples were confirmed by immunohistochemistry and western blotting (WB). Sera were screened for other autoantibodies. Results:  GADA were detected in 15 patients (5.9%) and in three control subjects (1.5%) (p = 0.026). Seven patients (2.8%) had high GADA titers [≥1,000 relative units (RUs)/ml], six of whom had temporal lobe epilepsy (TLE). All three GADA‐positive control subjects had low titers. Two of the five patients with high GADA titers and available cerebrospinal fluid (CSF) samples had intrathecal synthesis (IS) of GADA; one patient had CSF oligoclonal bands. The prevalence of increased levels of GADA tended to be higher in patients with TLE than in patients with extra‐TLE [odds ratio (OR) 1.32, 95% confidence interval (CI) 0.39–4.42; p = 0.657]. The patients with high GADA titers had significantly higher number of other autoantibodies compared to the patients with low GADA titers (p = 0.001) and the patients with normal GADA (p < 0.001). Discussion:  High GADA titers were present in a subgroup of patients; close to 90% had TLE. The immunologic profile of these patients suggests that the most probable origin of their epilepsy is autoimmune. A positive IS of GADA may be a marker of an ongoing immune response that could identify those patients in whom a trial with immunosuppressive therapy might be warranted.
AbstractList Purpose:   Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined. Methods:   We analyzed GADA with a radioimmunoassay in sera of 253 well‐characterized patients with epilepsy and 200 control subjects. The positive samples were confirmed by immunohistochemistry and western blotting (WB). Sera were screened for other autoantibodies. Results:   GADA were detected in 15 patients (5.9%) and in three control subjects (1.5%) (p = 0.026). Seven patients (2.8%) had high GADA titers [≥1,000 relative units (RUs)/ml], six of whom had temporal lobe epilepsy (TLE). All three GADA‐positive control subjects had low titers. Two of the five patients with high GADA titers and available cerebrospinal fluid (CSF) samples had intrathecal synthesis (IS) of GADA; one patient had CSF oligoclonal bands. The prevalence of increased levels of GADA tended to be higher in patients with TLE than in patients with extra‐TLE [odds ratio (OR) 1.32, 95% confidence interval (CI) 0.39–4.42; p = 0.657]. The patients with high GADA titers had significantly higher number of other autoantibodies compared to the patients with low GADA titers (p = 0.001) and the patients with normal GADA (p < 0.001). Discussion:   High GADA titers were present in a subgroup of patients; close to 90% had TLE. The immunologic profile of these patients suggests that the most probable origin of their epilepsy is autoimmune. A positive IS of GADA may be a marker of an ongoing immune response that could identify those patients in whom a trial with immunosuppressive therapy might be warranted.
SummaryPurpose:Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined.Methods:We analyzed GADA with a radioimmunoassay in sera of 253 well-characterized patients with epilepsy and 200 control subjects. The positive samples were confirmed by immunohistochemistry and western blotting (WB). Sera were screened for other autoantibodies.Results:GADA were detected in 15 patients (5.9%) and in three control subjects (1.5%) (p = 0.026). Seven patients (2.8%) had high GADA titers [ greater than or equal to 1,000 relative units (RUs)-ml], six of whom had temporal lobe epilepsy (TLE). All three GADA-positive control subjects had low titers. Two of the five patients with high GADA titers and available cerebrospinal fluid (CSF) samples had intrathecal synthesis (IS) of GADA; one patient had CSF oligoclonal bands. The prevalence of increased levels of GADA tended to be higher in patients with TLE than in patients with extra-TLE [odds ratio (OR) 1.32, 95% confidence interval (CI) 0.39-4.42; p = 0.657]. The patients with high GADA titers had significantly higher number of other autoantibodies compared to the patients with low GADA titers (p = 0.001) and the patients with normal GADA (p < 0.001).Discussion:High GADA titers were present in a subgroup of patients; close to 90% had TLE. The immunologic profile of these patients suggests that the most probable origin of their epilepsy is autoimmune. A positive IS of GADA may be a marker of an ongoing immune response that could identify those patients in whom a trial with immunosuppressive therapy might be warranted.
Summary Purpose:  Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined. Methods:  We analyzed GADA with a radioimmunoassay in sera of 253 well‐characterized patients with epilepsy and 200 control subjects. The positive samples were confirmed by immunohistochemistry and western blotting (WB). Sera were screened for other autoantibodies. Results:  GADA were detected in 15 patients (5.9%) and in three control subjects (1.5%) (p = 0.026). Seven patients (2.8%) had high GADA titers [≥1,000 relative units (RUs)/ml], six of whom had temporal lobe epilepsy (TLE). All three GADA‐positive control subjects had low titers. Two of the five patients with high GADA titers and available cerebrospinal fluid (CSF) samples had intrathecal synthesis (IS) of GADA; one patient had CSF oligoclonal bands. The prevalence of increased levels of GADA tended to be higher in patients with TLE than in patients with extra‐TLE [odds ratio (OR) 1.32, 95% confidence interval (CI) 0.39–4.42; p = 0.657]. The patients with high GADA titers had significantly higher number of other autoantibodies compared to the patients with low GADA titers (p = 0.001) and the patients with normal GADA (p < 0.001). Discussion:  High GADA titers were present in a subgroup of patients; close to 90% had TLE. The immunologic profile of these patients suggests that the most probable origin of their epilepsy is autoimmune. A positive IS of GADA may be a marker of an ongoing immune response that could identify those patients in whom a trial with immunosuppressive therapy might be warranted.
Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined.PURPOSEGlutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined.We analyzed GADA with a radioimmunoassay in sera of 253 well-characterized patients with epilepsy and 200 control subjects. The positive samples were confirmed by immunohistochemistry and western blotting (WB). Sera were screened for other autoantibodies.METHODSWe analyzed GADA with a radioimmunoassay in sera of 253 well-characterized patients with epilepsy and 200 control subjects. The positive samples were confirmed by immunohistochemistry and western blotting (WB). Sera were screened for other autoantibodies.GADA were detected in 15 patients (5.9%) and in three control subjects (1.5%) (p = 0.026). Seven patients (2.8%) had high GADA titers [>or=1,000 relative units (RUs)/ml], six of whom had temporal lobe epilepsy (TLE). All three GADA-positive control subjects had low titers. Two of the five patients with high GADA titers and available cerebrospinal fluid (CSF) samples had intrathecal synthesis (IS) of GADA; one patient had CSF oligoclonal bands. The prevalence of increased levels of GADA tended to be higher in patients with TLE than in patients with extra-TLE [odds ratio (OR) 1.32, 95% confidence interval (CI) 0.39-4.42; p = 0.657]. The patients with high GADA titers had significantly higher number of other autoantibodies compared to the patients with low GADA titers (p = 0.001) and the patients with normal GADA (p < 0.001).RESULTSGADA were detected in 15 patients (5.9%) and in three control subjects (1.5%) (p = 0.026). Seven patients (2.8%) had high GADA titers [>or=1,000 relative units (RUs)/ml], six of whom had temporal lobe epilepsy (TLE). All three GADA-positive control subjects had low titers. Two of the five patients with high GADA titers and available cerebrospinal fluid (CSF) samples had intrathecal synthesis (IS) of GADA; one patient had CSF oligoclonal bands. The prevalence of increased levels of GADA tended to be higher in patients with TLE than in patients with extra-TLE [odds ratio (OR) 1.32, 95% confidence interval (CI) 0.39-4.42; p = 0.657]. The patients with high GADA titers had significantly higher number of other autoantibodies compared to the patients with low GADA titers (p = 0.001) and the patients with normal GADA (p < 0.001).High GADA titers were present in a subgroup of patients; close to 90% had TLE. The immunologic profile of these patients suggests that the most probable origin of their epilepsy is autoimmune. A positive IS of GADA may be a marker of an ongoing immune response that could identify those patients in whom a trial with immunosuppressive therapy might be warranted.DISCUSSIONHigh GADA titers were present in a subgroup of patients; close to 90% had TLE. The immunologic profile of these patients suggests that the most probable origin of their epilepsy is autoimmune. A positive IS of GADA may be a marker of an ongoing immune response that could identify those patients in whom a trial with immunosuppressive therapy might be warranted.
Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA have not been defined. We analyzed GADA with a radioimmunoassay in sera of 253 well-characterized patients with epilepsy and 200 control subjects. The positive samples were confirmed by immunohistochemistry and western blotting (WB). Sera were screened for other autoantibodies. GADA were detected in 15 patients (5.9%) and in three control subjects (1.5%) (p = 0.026). Seven patients (2.8%) had high GADA titers [>or=1,000 relative units (RUs)/ml], six of whom had temporal lobe epilepsy (TLE). All three GADA-positive control subjects had low titers. Two of the five patients with high GADA titers and available cerebrospinal fluid (CSF) samples had intrathecal synthesis (IS) of GADA; one patient had CSF oligoclonal bands. The prevalence of increased levels of GADA tended to be higher in patients with TLE than in patients with extra-TLE [odds ratio (OR) 1.32, 95% confidence interval (CI) 0.39-4.42; p = 0.657]. The patients with high GADA titers had significantly higher number of other autoantibodies compared to the patients with low GADA titers (p = 0.001) and the patients with normal GADA (p < 0.001). High GADA titers were present in a subgroup of patients; close to 90% had TLE. The immunologic profile of these patients suggests that the most probable origin of their epilepsy is autoimmune. A positive IS of GADA may be a marker of an ongoing immune response that could identify those patients in whom a trial with immunosuppressive therapy might be warranted.
Author Saiz, Albert
Liimatainen, Suvi
Kharazmi, Elham
Sabater, Lidia
Peltola, Jukka
Fallah, Mahdi
Knip, Mikael
Haapala, Anna‐Maija
Dastidar, Prasun
Peltola, Maria
Author_xml – sequence: 1
  givenname: Suvi
  surname: Liimatainen
  fullname: Liimatainen, Suvi
– sequence: 2
  givenname: Maria
  surname: Peltola
  fullname: Peltola, Maria
– sequence: 3
  givenname: Lidia
  surname: Sabater
  fullname: Sabater, Lidia
– sequence: 4
  givenname: Mahdi
  surname: Fallah
  fullname: Fallah, Mahdi
– sequence: 5
  givenname: Elham
  surname: Kharazmi
  fullname: Kharazmi, Elham
– sequence: 6
  givenname: Anna‐Maija
  surname: Haapala
  fullname: Haapala, Anna‐Maija
– sequence: 7
  givenname: Prasun
  surname: Dastidar
  fullname: Dastidar, Prasun
– sequence: 8
  givenname: Mikael
  surname: Knip
  fullname: Knip, Mikael
– sequence: 9
  givenname: Albert
  surname: Saiz
  fullname: Saiz, Albert
– sequence: 10
  givenname: Jukka
  surname: Peltola
  fullname: Peltola, Jukka
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22781150$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/19817821$$D View this record in MEDLINE/PubMed
BookMark eNqNkUFvFCEYhompsdvqXzBcjKeZfsAwwEETs6napIke9OCJMAxUNiwzDrPp7r-Xcdea9GK58CU830vyPhfoLA3JIYQJ1KScq01NOJUVIa2oKYCqgTLK6_0ztHp4OEMrAMIqxSWco4ucNwAgWsFeoHOiJBGSkhX6sY4hBWsizuEuBV_GZB0ePL6Lu9lsg8XGhh73zpqpG_aHaLLDJs2hG_rgMg4Jj2YOLs0Z34f5J3ZjiG7Mh5fouTcxu1en-xJ9_3j9bf25uv3y6Wb94bayjQReib7tuk4RTxsnrbegJBe-Jcb3wgDQnlFKLTWeScGBe95IoxrRNB1zHXGEXaK3x9xxGn7tXJ71NmTrYjTJDbusRdNSpZhQ_ycZo1ICo4V8fSJ33db1epzC1kwH_be3Arw5ASaX8vxUWgv5gaNUSEI4FE4eOTsNOU_O_4sCvajUG70Y04sxvajUf1TqfVl9_2jVhrk0PaR5MiE-JeDdMeC-CDk8-WN9_fVmmdhvyz23FA
CODEN EPILAK
CitedBy_id crossref_primary_10_11648_j_iji_20241202_12
crossref_primary_10_1111_apa_14910
crossref_primary_10_1259_bjr_20170869
crossref_primary_10_1111_ene_12261
crossref_primary_10_1111_epi_14534
crossref_primary_10_1016_j_spen_2014_08_002
crossref_primary_10_1001_jamaneurol_2021_3113
crossref_primary_10_1097_MD_0000000000019601
crossref_primary_10_1097_NRL_0b013e318247b87d
crossref_primary_10_1007_s10309_020_00363_3
crossref_primary_10_1097_WCO_0b013e3283446f05
crossref_primary_10_1212_CON_0000000000001079
crossref_primary_10_1002_acn3_520
crossref_primary_10_1177_1550059418800867
crossref_primary_10_1186_s13023_018_0787_5
crossref_primary_10_1016_j_yebeh_2014_04_022
crossref_primary_10_2106_JBJS_CC_20_00378
crossref_primary_10_1007_s00125_016_3929_0
crossref_primary_10_1016_j_seizure_2018_05_004
crossref_primary_10_1007_s00115_012_3605_7
crossref_primary_10_1016_j_eplepsyres_2013_12_015
crossref_primary_10_1371_journal_pone_0241289
crossref_primary_10_3390_brainsci13101361
crossref_primary_10_1111_j_1468_1331_2011_03609_x
crossref_primary_10_3390_brainsci11030392
crossref_primary_10_1007_s00415_020_09814_3
crossref_primary_10_1212_NXI_0000000000200034
crossref_primary_10_1007_s00415_020_09807_2
crossref_primary_10_1530_EJE_12_0699
crossref_primary_10_1017_S0317167100013147
crossref_primary_10_1007_s11940_012_0212_7
crossref_primary_10_1017_S0317167100015444
crossref_primary_10_1016_j_jns_2014_08_024
crossref_primary_10_1007_s10072_011_0566_8
crossref_primary_10_1136_bcr_2024_260503
crossref_primary_10_1080_1744666X_2017_1327351
crossref_primary_10_1097_WCO_0000000000000449
crossref_primary_10_1016_j_jns_2022_120540
crossref_primary_10_3390_brainsci13020369
crossref_primary_10_1111_j_1750_3639_2012_00580_x
crossref_primary_10_1016_j_neurol_2018_07_006
crossref_primary_10_1177_1756286420952901
crossref_primary_10_1016_j_yebeh_2011_03_038
crossref_primary_10_1111_epi_13784
crossref_primary_10_1016_j_eplepsyres_2015_05_008
crossref_primary_10_1016_j_jneuroim_2013_08_001
crossref_primary_10_20515_otd_1167517
crossref_primary_10_3390_ijms21103701
crossref_primary_10_1111_cen3_12154
crossref_primary_10_1016_j_eplepsyres_2013_02_009
crossref_primary_10_1016_j_yebeh_2018_03_004
crossref_primary_10_5698_1535_7511_13_1_24
crossref_primary_10_3390_bios14110543
crossref_primary_10_5698_1535_7511_17_3_134
crossref_primary_10_1111_j_1528_1167_2011_03031_x
crossref_primary_10_1038_s41582_020_0359_x
crossref_primary_10_1177_0883073813500527
crossref_primary_10_1016_j_seizure_2014_04_009
crossref_primary_10_1016_j_epag_2013_05_002
crossref_primary_10_1212_WNL_0000000000000383
crossref_primary_10_1016_j_jneuroim_2020_577189
crossref_primary_10_1016_j_jneuroim_2015_11_012
crossref_primary_10_1016_j_pediatrneurol_2012_06_013
crossref_primary_10_1002_epi4_12395
crossref_primary_10_1016_j_ejpn_2012_11_003
crossref_primary_10_1111_pcn_12543
crossref_primary_10_3389_fncel_2023_1129907
crossref_primary_10_1007_s13311_019_00750_3
crossref_primary_10_1016_j_autrev_2015_01_002
crossref_primary_10_1016_j_eplepsyres_2017_06_008
crossref_primary_10_1007_s00415_024_12210_w
crossref_primary_10_1136_bcr_2020_237913
crossref_primary_10_1016_j_yebeh_2018_01_021
crossref_primary_10_4103_nsn_nsn_226_21
crossref_primary_10_1111_j_1468_1331_2011_03641_x
crossref_primary_10_1159_000369058
crossref_primary_10_1136_jnnp_2020_325275
crossref_primary_10_1007_s11892_015_0588_3
crossref_primary_10_1007_s00415_015_8002_2
crossref_primary_10_1038_s41598_017_06294_w
crossref_primary_10_1007_s13760_017_0796_5
crossref_primary_10_3389_fneur_2023_1211812
crossref_primary_10_1016_j_jneuroim_2019_577063
crossref_primary_10_1016_j_jns_2019_06_021
crossref_primary_10_1177_1535759720949238
crossref_primary_10_1007_s00115_011_3257_z
crossref_primary_10_1016_j_eplepsyres_2011_02_003
crossref_primary_10_1016_j_seizure_2020_05_008
crossref_primary_10_1007_s11910_013_0348_1
crossref_primary_10_1016_j_jneuroim_2020_577324
crossref_primary_10_1155_2020_8454532
crossref_primary_10_1016_j_yebeh_2012_08_008
crossref_primary_10_3389_fncel_2016_00130
crossref_primary_10_1016_j_eplepsyres_2012_06_002
crossref_primary_10_1080_00207454_2017_1389928
crossref_primary_10_1111_epi_12127
crossref_primary_10_2217_bmm_13_142
crossref_primary_10_1093_brain_awac404
crossref_primary_10_1111_epi_12528
Cites_doi 10.1111/j.1468-1331.2004.00933.x
10.1053/seiz.2002.0593
10.1212/01.wnl.0000187129.66353.13
10.1073/pnas.94.25.14060
10.1111/j.1468-1331.2008.02373.x
10.1126/science.8036512
10.1212/WNL.49.4.1026
10.1002/ana.410440209
10.1080/08916930701619565
10.1056/NEJM200002033420503
10.1007/s001250051067
10.1007/s102380300013
10.1111/j.1528-1157.1996.tb00527.x
10.1016/j.jneuroim.2008.05.015
10.1136/jnnp.2006.089268
10.1136/jnnp.41.5.458
10.1212/WNL.55.1.46
10.1016/S0920-1211(00)00180-7
10.1080/17402520400001736
10.1001/archneur.58.2.225
10.1038/nm0296-148
10.2169/internalmedicine.44.1174
10.1212/01.WNL.0000106821.83436.59
10.1002/ana.21123
10.1002/ana.410360419
10.1111/j.1528-1157.1989.tb05316.x
10.1212/WNL.57.5.780
10.1084/jem.178.6.2097
10.1016/S0165-5728(02)00261-8
10.1586/14737175.8.7.1141
10.1093/brain/awn183
10.1111/j.1528-1167.2007.01500.x
10.1056/NEJM198804213181602
10.1542/peds.109.3.e50
10.1016/j.eplepsyres.2006.06.003
10.1056/NEJM199005313222202
10.1111/j.1528-1157.1997.tb01226.x
10.1038/347151a0
10.1016/S0140-6736(05)79192-3
10.7326/0003-4819-131-7-199910050-00008
ContentType Journal Article
Copyright Wiley Periodicals, Inc. © 2009 International League Against Epilepsy
2015 INIST-CNRS
Copyright_xml – notice: Wiley Periodicals, Inc. © 2009 International League Against Epilepsy
– notice: 2015 INIST-CNRS
DBID AAYXX
CITATION
IQODW
CGR
CUY
CVF
ECM
EIF
NPM
7X8
7TK
DOI 10.1111/j.1528-1167.2009.02325.x
DatabaseName CrossRef
Pascal-Francis
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
Neurosciences Abstracts
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
Neurosciences Abstracts
DatabaseTitleList CrossRef
Neurosciences Abstracts

MEDLINE - Academic
MEDLINE
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1528-1167
EndPage 767
ExternalDocumentID 19817821
22781150
10_1111_j_1528_1167_2009_02325_x
EPI2325
Genre article
Research Support, Non-U.S. Gov't
Journal Article
Comparative Study
GroupedDBID ---
.3N
.55
.GA
.GJ
.Y3
05W
0R~
10A
1OB
1OC
24P
29G
2WC
31~
33P
36B
3SF
4.4
50Y
50Z
51W
51X
52M
52N
52O
52P
52R
52S
52T
52U
52V
52W
52X
53G
5GY
5HH
5LA
5RE
5VS
66C
702
7PT
8-0
8-1
8-3
8-4
8-5
8UM
930
A01
A03
AAESR
AAEVG
AAGKA
AAHHS
AAHQN
AAIPD
AAMNL
AANHP
AANLZ
AAONW
AASGY
AAXRX
AAYCA
AAZKR
ABCQN
ABCUV
ABEML
ABIVO
ABJNI
ABLJU
ABPVW
ABQWH
ABXGK
ACAHQ
ACBWZ
ACCFJ
ACCZN
ACGFO
ACGFS
ACGOF
ACMXC
ACPOU
ACPRK
ACRPL
ACSCC
ACXBN
ACXQS
ACYXJ
ADBBV
ADBTR
ADEOM
ADIZJ
ADKYN
ADMGS
ADNMO
ADOZA
ADXAS
ADZMN
ADZOD
AEEZP
AEIGN
AEIMD
AENEX
AEQDE
AEUQT
AEUYR
AFBPY
AFEBI
AFFPM
AFGKR
AFPWT
AFWVQ
AFZJQ
AHBTC
AHEFC
AI.
AIACR
AIAGR
AITYG
AIURR
AIWBW
AJBDE
ALAGY
ALMA_UNASSIGNED_HOLDINGS
ALUQN
ALVPJ
AMBMR
AMYDB
ASPBG
ATUGU
AVWKF
AZBYB
AZFZN
AZVAB
BAFTC
BAWUL
BDRZF
BFHJK
BHBCM
BMXJE
BROTX
BRXPI
BY8
C45
CAG
COF
CS3
D-6
D-7
D-E
D-F
DCZOG
DIK
DPXWK
DR2
DRFUL
DRMAN
DRSTM
DU5
E3Z
EBS
EJD
EMOBN
ESX
EX3
F00
F01
F04
F5P
FEDTE
FIJ
FUBAC
FYBCS
G-S
G.N
GODZA
H.X
HF~
HGLYW
HVGLF
HZI
HZ~
IHE
IPNFZ
IX1
J0M
K48
KBYEO
LATKE
LC2
LC3
LEEKS
LH4
LITHE
LOXES
LP6
LP7
LUTES
LW6
LYRES
MEWTI
MK4
MRFUL
MRMAN
MRSTM
MSFUL
MSMAN
MSSTM
MXFUL
MXMAN
MXSTM
N04
N05
N9A
NF~
O66
O9-
OHT
OIG
OK1
OVD
P2P
P2W
P2X
P2Z
P4B
P4D
PALCI
Q.N
Q11
QB0
R.K
RIWAO
RJQFR
ROL
RX1
SAMSI
SUPJJ
TEORI
TR2
UB1
V8K
V9Y
VH1
W8V
W99
WBKPD
WHWMO
WIH
WIJ
WIK
WIN
WOHZO
WOW
WQJ
WRC
WUP
WVDHM
WXI
WXSBR
X7M
XG1
YFH
YOC
YUY
ZGI
ZXP
ZZTAW
~IA
~WT
AAFWJ
AAYXX
AEYWJ
AGHNM
AGQPQ
AGYGG
CITATION
AAMMB
AEFGJ
AGXDD
AIDQK
AIDYY
IQODW
CGR
CUY
CVF
ECM
EIF
NPM
7X8
7TK
ID FETCH-LOGICAL-c4805-7d6bbb91f24e8cfc09857f61afd7a002d3222c2af387505f548a94744b3eb1e13
IEDL.DBID DR2
ISSN 0013-9580
1528-1167
IngestDate Thu Jul 10 22:12:37 EDT 2025
Fri Jul 11 00:08:50 EDT 2025
Mon Jul 21 05:36:26 EDT 2025
Mon Jul 21 09:14:07 EDT 2025
Thu Apr 24 23:05:23 EDT 2025
Tue Jul 01 03:56:16 EDT 2025
Wed Jan 22 16:12:49 EST 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 5
Keywords Human
Glutamic acid
Nervous system diseases
Aminoacid
Central nervous system disease
Complex partial epilepsy
Temporal lobe epilepsy
Polyendocrinopathy
Glutamic acid decarboxylase antibody
Cerebral disorder
Immune system
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
CC BY 4.0
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c4805-7d6bbb91f24e8cfc09857f61afd7a002d3222c2af387505f548a94744b3eb1e13
Notes ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
OpenAccessLink https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/j.1528-1167.2009.02325.x
PMID 19817821
PQID 733288032
PQPubID 23479
PageCount 9
ParticipantIDs proquest_miscellaneous_746299379
proquest_miscellaneous_733288032
pubmed_primary_19817821
pascalfrancis_primary_22781150
crossref_primary_10_1111_j_1528_1167_2009_02325_x
crossref_citationtrail_10_1111_j_1528_1167_2009_02325_x
wiley_primary_10_1111_j_1528_1167_2009_02325_x_EPI2325
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate May 2010
PublicationDateYYYYMMDD 2010-05-01
PublicationDate_xml – month: 05
  year: 2010
  text: May 2010
PublicationDecade 2010
PublicationPlace Oxford, UK
PublicationPlace_xml – name: Oxford, UK
– name: Malden, MA
– name: United States
PublicationTitle Epilepsia (Copenhagen)
PublicationTitleAlternate Epilepsia
PublicationYear 2010
Publisher Blackwell Publishing Ltd
Wiley-Blackwell
Publisher_xml – name: Blackwell Publishing Ltd
– name: Wiley-Blackwell
References 2006; 71
1990; 347
2004; 62
2002; 131
2000; 42
2002; 11
2008; 8
2008; 13
2005; 65
1997; 49
1998; 41
1990; 322
1996; 37
2007; 78
2005; 44
1998; 44
1989; 30
2004; 11
1994; 265
1997; 94
1978; 41
2000; 55
2008; 49
1999; 131
2003; 3
1994; 36
1997; 38
2007; 61
2000; 342
2008; 41
2002; 109
2001; 57
1996; 2
1988; 318
2001; 58
2008; 131
2009; 16
2005; 12
1993; 178
1998; 8
e_1_2_6_32_1
e_1_2_6_10_1
e_1_2_6_31_1
e_1_2_6_30_1
e_1_2_6_19_1
e_1_2_6_13_1
e_1_2_6_36_1
e_1_2_6_14_1
e_1_2_6_35_1
e_1_2_6_11_1
e_1_2_6_34_1
e_1_2_6_12_1
e_1_2_6_33_1
e_1_2_6_17_1
e_1_2_6_18_1
e_1_2_6_39_1
e_1_2_6_15_1
e_1_2_6_38_1
e_1_2_6_16_1
e_1_2_6_37_1
e_1_2_6_21_1
e_1_2_6_20_1
e_1_2_6_41_1
e_1_2_6_40_1
e_1_2_6_9_1
e_1_2_6_8_1
e_1_2_6_5_1
e_1_2_6_4_1
e_1_2_6_7_1
e_1_2_6_6_1
e_1_2_6_25_1
e_1_2_6_24_1
e_1_2_6_3_1
e_1_2_6_23_1
e_1_2_6_2_1
e_1_2_6_22_1
e_1_2_6_29_1
e_1_2_6_28_1
e_1_2_6_27_1
e_1_2_6_26_1
References_xml – volume: 57
  start-page: 780
  year: 2001
  end-page: 784
  article-title: Stiff‐person syndrome. Quantification, specificity, and intrathecal synthesis of GAD65 antibodies
  publication-title: Neurology
– volume: 42
  start-page: 191
  year: 2000
  end-page: 195
  article-title: Glutamic acid decarboxylase autoantibodies in controlled and uncontrolled epilepsy: a pilot study
  publication-title: Epilepsy Res
– volume: 131
  start-page: 2553
  year: 2008
  end-page: 2563
  article-title: Spectrum of neurological syndromes associated with glutamic acid decarboxylase antibodies: diagnostic clues for this association
  publication-title: Brain
– volume: 347
  start-page: 151
  year: 1990
  end-page: 156
  article-title: Identification of the 64K autoantigen in insulin‐dependent diabetes as the GABA‐synthesizing enzyme glutamic acid decarboxylase
  publication-title: Nature
– volume: 41
  start-page: 458
  year: 1978
  end-page: 462
  article-title: Stiff‐man syndrome associated with nocturnal myoclonus and epilepsy
  publication-title: J Neurol Neurosurg Psychiatry
– volume: 342
  start-page: 314
  year: 2000
  end-page: 319
  article-title: Early identification of refractory epilepsy
  publication-title: N Engl J Med
– volume: 41
  start-page: 1293
  year: 1998
  end-page: 1297
  article-title: Autoantibodies associated with Type I diabetes mellitus persist after diagnosis in children
  publication-title: Diabetologia
– volume: 322
  start-page: 1555
  year: 1990
  end-page: 1560
  article-title: Autoantibodies to GABA‐ergic neurons and pancreatic beta cells in stiff‐man syndrome
  publication-title: N Engl J Med
– volume: 49
  start-page: 914
  year: 2008
  end-page: 920
  article-title: Cyclophosphamide for anti‐GAD antibody‐positive refractory status epilepticus
  publication-title: Epilepsia
– volume: 11
  start-page: 77
  year: 2002
  end-page: 84
  article-title: Refractory epilepsy: a progressive, intractable but preventable condition?
  publication-title: Seizure
– volume: 131
  start-page: 179
  year: 2002
  end-page: 185
  article-title: Antibodies against GluR3 peptides are not specific for Rasmussen’s encephalitis but are also present in epilepsy patients with severe, early onset disease and intractable seizures
  publication-title: J Neuroimmunol
– volume: 178
  start-page: 2097
  year: 1993
  end-page: 2106
  article-title: Identification of a dominant epitope of glutamic acid decarboxylase (GAD‐65) recognized by autoantibodies in stiff‐man syndrome
  publication-title: J Exp Med
– volume: 49
  start-page: 1026
  year: 1997
  end-page: 1030
  article-title: Autoantibodies to glutamic acid decarboxylase in three patients with cerebellar ataxia, late‐onset insulin‐dependent diabetes mellitus, and polyendocrine autoimmunity
  publication-title: Neurology
– volume: 78
  start-page: 187
  year: 2007
  end-page: 189
  article-title: Epilepsy and cerebellar ataxia associated with anti‐glutamic acid decarboxylase antibodies
  publication-title: J Neurol Neurosurg Psychiatry
– volume: 36
  start-page: 665
  year: 1994
  end-page: 667
  article-title: Autoantibodies to glutamic acid decarboxylase in palatal myoclonus and epilepsy
  publication-title: Ann Neurol
– volume: 265
  start-page: 648
  year: 1994
  end-page: 651
  article-title: Autoantibodies to glutamate receptor GluR3 in Rasmussen’s encephalitis
  publication-title: Science
– volume: 12
  start-page: 294
  year: 2005
  end-page: 299
  article-title: Antigenic differences between neurological and diabetic patients with anti‐glutamic acid decarboxylase antibodies
  publication-title: Eur J Neurol
– volume: 44
  start-page: 1174
  year: 2005
  end-page: 1177
  article-title: Type 1 diabetes mellitus and drug‐resistant epilepsy: presence of high titer of anti‐glutamic acid decarboxylase autoantibodies in serum and cerebrospinal fluid
  publication-title: Intern Med
– volume: 65
  start-page: 1730
  year: 2005
  end-page: 1736
  article-title: Serum antibodies in epilepsy and seizure‐associated disorders
  publication-title: Neurology
– volume: 58
  start-page: 225
  year: 2001
  end-page: 230
  article-title: Cerebellar ataxia with anti‐glutamic acid decarboxylase antibodies: study of 14 patients
  publication-title: Arch Neurol
– volume: 8
  start-page: 457
  year: 1998
  article-title: Temporal‐lobe epilepsy associated with glutamic‐acid‐decarboxylase autoantibodies
  publication-title: Lancet
– volume: 13
  start-page: 155
  year: 2008
  end-page: 159
  article-title: Non‐paraneoplastic limbic encephalitis associated with anti‐glutamic acid decarboxylase antibodies
  publication-title: J Neuroimmunol
– volume: 8
  start-page: 1141
  year: 2008
  end-page: 1160
  article-title: Autoantibodies to glutamate receptors can damage the brain in epilepsy, systemic lupus erythematosus and encephalitis
  publication-title: Expert Rev Neurother
– volume: 94
  start-page: 14060
  year: 1997
  end-page: 14065
  article-title: Epilepsy in mice deficient in the 65‐kDa isoform of glutamic acid decarboxylase
  publication-title: Proc Natl Acad Sci U S A
– volume: 71
  start-page: 135
  year: 2006
  end-page: 141
  article-title: Antibodies to voltage‐gated potassium and calcium channels in epilepsy
  publication-title: Epilepsy Res
– volume: 30
  start-page: 389
  year: 1989
  end-page: 399
  article-title: Proposal for revised classification of epilepsies and epileptic syndromes
  publication-title: Epilepsia
– volume: 41
  start-page: 66
  year: 2008
  end-page: 73
  article-title: Increased spontaneous activity of a network of hippocampal neurons in culture caused by suppression of inhibitory potentials mediated by anti‐gad antibodies
  publication-title: Autoimmunity
– volume: 62
  start-page: 517
  year: 2004
  end-page: 518
  article-title: Antiphospholipid and glutamic acid decarboxylase antibodies in patients with focal epilepsy
  publication-title: Neurology
– volume: 318
  start-page: 1012
  year: 1988
  end-page: 1020
  article-title: Autoantibodies to glutamic acid decarboxylase in a patient with stiff‐man syndrome, epilepsy, and type I diabetes mellitus
  publication-title: N Engl J Med
– volume: 131
  start-page: 522
  year: 1999
  end-page: 530
  article-title: The stiff‐person syndrome: an autoimmune disorder affecting neurotransmission of gamma‐aminobutyric acid
  publication-title: Ann Intern Med
– volume: 2
  start-page: 148
  year: 1996
  end-page: 153
  article-title: The clinical significance of an autoimmune response against glutamic acid decarboxylase
  publication-title: Nat Med
– volume: 3
  start-page: 32
  year: 2003
  end-page: 36
  article-title: Anticardiolipin, glutamic acid decarboxylase, and antinuclear antibodies in epileptic patients
  publication-title: Clin Exp Med
– volume: 109
  start-page: E50
  year: 2002
  article-title: Type 1 diabetes mellitus and epilepsia partialis continua in a 6‐year‐old boy with elevated anti‐GAD65 antibodies
  publication-title: Pediatrics
– volume: 55
  start-page: 46
  year: 2000
  end-page: 50
  article-title: Autoantibodies to glutamic acid decarboxylase in patients with therapy‐resistant epilepsy
  publication-title: Neurology
– volume: 61
  start-page: 544
  year: 2007
  end-page: 551
  article-title: Effects of anti‐glutamic acid decarboxylase antibodies associated with neurological diseases
  publication-title: Ann Neurol
– volume: 38
  start-page: 1255
  year: 1997
  end-page: 1256
  article-title: Recommendations for neuroimaging of patients with epilepsy
  publication-title: Epilepsia
– volume: 11
  start-page: 241
  year: 2004
  end-page: 252
  article-title: Autoimmune epilepsy: some epilepsy patients harbor autoantibodies to glutamate receptors and dsDNA on both sides of the blood‐brain barrier, which may kill neurons and decrease in brain fluids after hemispherotomy
  publication-title: Clin Dev Immunol
– volume: 37
  start-page: 922
  year: 1996
  end-page: 926
  article-title: Cryptogenic partial epilepsies with anti‐GM1 antibodies: a new form of immune‐mediated epilepsy?
  publication-title: Epilepsia
– volume: 44
  start-page: 194
  year: 1998
  end-page: 201
  article-title: Inhibition of gamma‐aminobutyric acid synthesis by glutamic acid decarboxylase autoantibodies in stiff‐man syndrome
  publication-title: Ann Neurol
– volume: 16
  start-page: 134
  year: 2009
  end-page: 141
  article-title: The high prevalence of antiphospholipid antibodies in refractory focal epilepsy is related to recurrent seizures
  publication-title: Eur J Neurol
– ident: e_1_2_6_38_1
  doi: 10.1111/j.1468-1331.2004.00933.x
– ident: e_1_2_6_17_1
  doi: 10.1053/seiz.2002.0593
– ident: e_1_2_6_26_1
  doi: 10.1212/01.wnl.0000187129.66353.13
– ident: e_1_2_6_14_1
  doi: 10.1073/pnas.94.25.14060
– ident: e_1_2_6_20_1
  doi: 10.1111/j.1468-1331.2008.02373.x
– ident: e_1_2_6_30_1
  doi: 10.1126/science.8036512
– ident: e_1_2_6_31_1
  doi: 10.1212/WNL.49.4.1026
– ident: e_1_2_6_8_1
  doi: 10.1002/ana.410440209
– ident: e_1_2_6_39_1
  doi: 10.1080/08916930701619565
– ident: e_1_2_6_15_1
  doi: 10.1056/NEJM200002033420503
– ident: e_1_2_6_33_1
  doi: 10.1007/s001250051067
– ident: e_1_2_6_37_1
  doi: 10.1007/s102380300013
– ident: e_1_2_6_3_1
  doi: 10.1111/j.1528-1157.1996.tb00527.x
– ident: e_1_2_6_25_1
  doi: 10.1016/j.jneuroim.2008.05.015
– ident: e_1_2_6_40_1
  doi: 10.1136/jnnp.2006.089268
– ident: e_1_2_6_24_1
  doi: 10.1136/jnnp.41.5.458
– ident: e_1_2_6_29_1
  doi: 10.1212/WNL.55.1.46
– ident: e_1_2_6_16_1
  doi: 10.1016/S0920-1211(00)00180-7
– ident: e_1_2_6_10_1
  doi: 10.1080/17402520400001736
– ident: e_1_2_6_12_1
  doi: 10.1001/archneur.58.2.225
– ident: e_1_2_6_9_1
  doi: 10.1038/nm0296-148
– ident: e_1_2_6_41_1
  doi: 10.2169/internalmedicine.44.1174
– ident: e_1_2_6_34_1
  doi: 10.1212/01.WNL.0000106821.83436.59
– ident: e_1_2_6_23_1
  doi: 10.1002/ana.21123
– ident: e_1_2_6_27_1
  doi: 10.1002/ana.410360419
– ident: e_1_2_6_5_1
  doi: 10.1111/j.1528-1157.1989.tb05316.x
– ident: e_1_2_6_7_1
  doi: 10.1212/WNL.57.5.780
– ident: e_1_2_6_4_1
  doi: 10.1084/jem.178.6.2097
– ident: e_1_2_6_22_1
  doi: 10.1016/S0165-5728(02)00261-8
– ident: e_1_2_6_18_1
  doi: 10.1586/14737175.8.7.1141
– ident: e_1_2_6_32_1
  doi: 10.1093/brain/awn183
– ident: e_1_2_6_13_1
  doi: 10.1111/j.1528-1167.2007.01500.x
– ident: e_1_2_6_35_1
  doi: 10.1056/NEJM198804213181602
– ident: e_1_2_6_28_1
  doi: 10.1542/peds.109.3.e50
– ident: e_1_2_6_21_1
  doi: 10.1016/j.eplepsyres.2006.06.003
– ident: e_1_2_6_36_1
  doi: 10.1056/NEJM199005313222202
– ident: e_1_2_6_6_1
  doi: 10.1111/j.1528-1157.1997.tb01226.x
– ident: e_1_2_6_2_1
  doi: 10.1038/347151a0
– ident: e_1_2_6_11_1
  doi: 10.1016/S0140-6736(05)79192-3
– ident: e_1_2_6_19_1
  doi: 10.7326/0003-4819-131-7-199910050-00008
SSID ssj0007673
Score 2.3573234
Snippet Summary Purpose:  Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy...
Purpose:   Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated...
Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy associated with GADA...
SummaryPurpose:Glutamic acid decarboxylase antibodies (GADAs) have been detected in patients with epilepsy, but the clinical determinants of epilepsy...
SourceID proquest
pubmed
pascalfrancis
crossref
wiley
SourceType Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 760
SubjectTerms Adolescent
Adult
Age Distribution
Aged
Anticonvulsants. Antiepileptics. Antiparkinson agents
Autoantibodies - blood
Autoantibodies - cerebrospinal fluid
Autoantibodies - immunology
Autoimmune Diseases - blood
Autoimmune Diseases - diagnosis
Autoimmune Diseases - immunology
Biological and medical sciences
Blotting, Western
Epilepsy - blood
Epilepsy - cerebrospinal fluid
Epilepsy - immunology
Epilepsy, Temporal Lobe - blood
Epilepsy, Temporal Lobe - immunology
Female
Genetic Markers
Glutamate Decarboxylase - blood
Glutamate Decarboxylase - immunology
Glutamic acid decarboxylase antibody
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Humans
Immune system
Immunohistochemistry
Male
Medical sciences
Middle Aged
Nervous system (semeiology, syndromes)
Neurology
Neuropharmacology
Pharmacology. Drug treatments
Polyendocrinopathies, Autoimmune - diagnosis
Polyendocrinopathies, Autoimmune - immunology
Polyendocrinopathy
Radioimmunoassay
Temporal lobe epilepsy
Title Clinical significance of glutamic acid decarboxylase antibodies in patients with epilepsy
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1528-1167.2009.02325.x
https://www.ncbi.nlm.nih.gov/pubmed/19817821
https://www.proquest.com/docview/733288032
https://www.proquest.com/docview/746299379
Volume 51
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3da9RAEF-kDyKI39rUWvbB1xzZzWY_HqW0tEJFxEJ9CvspR2vuaO5A_eudSfauRooU8SGQh0yY3Z3Z-c3O7Awhb7VOYGh4LHVyqRTemdJ6zUolwZzHBh90FM8-yJNz8f6iucj5T3gXZqwPsT1wQ80Y9mtUcOv6qZI3HDwgJlUuOwngoJkhnsTULcRHn24qSSmZg82sLk2jq2lSz60_mliqh0vbw6SlsdvFbXB0im4H83T8mFxuBjZmpVzO1is38z__qPn4f0b-hDzKKJa-G8XuKbkXu2fk_lmO0z8nX3K50SuK-SGYjYTCRReJfgVJt9_mnlo_DzREb68dsAwYPlJY5LlbYFojnXc0V3ztKR4V07gEVpf9jxfk_Pjo8-FJmZs4lF7oqilVkM45wxIXUfvkK6MblSSzKSgL23HAUI_nNtXgOVVNAg_KGqGEcDWYkcjql2SnW3Rxl1BTOW9ZCCLFBChPOm5EDFIm7gJPui6I2ixY63OFc2y0cdX-5unAzLU4c9h_07TDzLXfC8K2lMuxyscdaA4mMrElxMvFiLMLQjdC0oLOYiDGdnGx7ltV1xz2zZr_5RMhOUJHU5BXo3zdMGY0A1zHCiIHKbkzx-3Rx1N82_tXwtfkwSZ5omL7ZGd1vY5vAJOt3MGgbb8A_Gwmsg
linkProvider Wiley-Blackwell
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3daxQxEA9SQQXxW7t-1Dz4uscmm80mj6ItV-0VkRbqU0iyiRyee0fvDqp_vTO7uasrRYr4sLAPmyWZzGR-k0x-Q8gbpSI4Gh5yFV3MhXc6t16xvJbgzkOFDwaKk2M5PhUfzqqzVA4I78L0_BDbDTe0jG69RgPHDemhlVccQiAm68Q7CeigGgGgvIkFvpFI__3nSy6pWqbjZlbmulLFMK3nyj8NfNXdhV2C2GJf7-IqQDrEt52DOrhPZpuh9Xkp30brlRv5n3-wPv6nsT8g9xKQpW97zXtIboT2Ebk1SUf1j8mXxDg6o5gigglJqF90HulXUHb7feqp9dOGNsHbcwd9BhgfKMzz1M0xs5FOW5pIX5cUd4tpWEBfF8sfT8jpwf7Ju3Ge6jjkXqiiyutGOuc0i1wE5aMvtKrqKJmNTW1hRW7wtMdzG0sInooqQhBltaiFcCV4ksDKp2Snnbdhl1BdOG9Z04gYIgA96bgWoZEyctfwqMqM1JsZMz6RnGOtjZn5LdgByRmUHJbg1KaTnLnICNu2XPREH9doszdQim1DvF-MUDsjdKMlBswWz2JsG-brpanLksPSWfK_fCIkR_SoM_KsV7DLjmnFANqxjMhOTa7dY7P_6RDfnv9rw9fk9vhkcmSODo8_viB3NrkUBXtJdlbn6_AKINrK7XWm9wtshCrO
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1La9wwEBYlhVAofT_cR6pDr14sWdbjWJosSduEUBpIT0bPsCT1muwutP31nbG9m7qEEkoPBh88RhrNaL7RjGYIeat1AkPDY66TS7nwzuTWa5YrCeY8Vvigo3h4JPdPxIfT6nTIf8K7MH19iM2BG2pGt1-jgrchjZW84uABMamGspMADqoJ4MnbQhYG2zjsfr4qJaXkEG1mZW4qXYyzeq7908hU3W3tAriW-nYX1-HRMbzt7NP0Pjlfz6xPSzmfrJZu4n_-UfTx_0z9Abk3wFj6rpe7h-RWbB6R7cMhUP-YfB3qjV5QTBDBdCSULjpP9AxE3X6beWr9LNAQvb10MGQA8ZHCKs_cHPMa6ayhQ8nXBcWzYhpbGGq7-PGEnEz3vrzfz4cuDrkXuqhyFaRzzrDERdQ--cLoSiXJbArKwn4cMNbjuU0luE5FlcCFskYoIVwJdiSy8inZauZNfE6oKZy3LASRYgKYJx03IgYpE3eBJ11mRK0XrPZDiXPstHFR_-bqAOdq5Bw24DR1x7n6e0bYhrLty3zcgGZnJBMbQrxdjEA7I3QtJDUoLUZibBPnq0WtypLDxlnyv3wiJEfsaDLyrJevq4EZzQDYsYzITkpuPOJ67_gA3178K-Ebsn28O60_HRx9fEnurBMpCvaKbC0vV_E14LOl2-kU7xe2sil9
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Clinical+significance+of+glutamic+acid+decarboxylase+antibodies+in+patients+with+epilepsy&rft.jtitle=Epilepsia+%28Copenhagen%29&rft.au=Liimatainen%2C+Suvi&rft.au=Peltola%2C+Maria&rft.au=Sabater%2C+Lidia&rft.au=Fallah%2C+Mahdi&rft.date=2010-05-01&rft.issn=0013-9580&rft.eissn=1528-1167&rft.volume=51&rft.issue=5&rft.spage=760&rft.epage=767&rft_id=info:doi/10.1111%2Fj.1528-1167.2009.02325.x&rft.externalDBID=n%2Fa&rft.externalDocID=10_1111_j_1528_1167_2009_02325_x
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0013-9580&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0013-9580&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0013-9580&client=summon