Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review
Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, ref...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Lazzarin, Serena Marita [verfasserIn] Vabanesi, Marco [verfasserIn] Cecchetti, Giordano [verfasserIn] Fazio, Raffaella [verfasserIn] Fanelli, Giovanna Franca [verfasserIn] Volonté, Maria Antonietta [verfasserIn] Genchi, Angela [verfasserIn] Giordano, Antonino [verfasserIn] Martinelli, Vittorio [verfasserIn] Colombo, Sergio [verfasserIn] Beccaria, Paolo [verfasserIn] Mucci, Milena [verfasserIn] Peccatori, Jacopo [verfasserIn] Filippi, Massimo [verfasserIn] Minicucci, Fabio [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Journal of neurology - [Darmstadt] : Steinkopff, 1891, 267(2020), 8 vom: 13. Juni, Seite 2462-2468 |
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| Übergeordnetes Werk: |
volume:267 ; year:2020 ; number:8 ; day:13 ; month:06 ; pages:2462-2468 |
| Links: |
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| DOI / URN: |
10.1007/s00415-020-09988-w |
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| Katalog-ID: |
SPR040338126 |
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| 245 | 1 | 0 | |a Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review |
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| 520 | |a Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. | ||
| 650 | 4 | |a Anti-NMDAR encephalitis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Autoimmune encephalitis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Bortezomib |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a EEG |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Movement disorders |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Vabanesi, Marco |e verfasserin |4 aut | |
| 700 | 1 | |a Cecchetti, Giordano |e verfasserin |4 aut | |
| 700 | 1 | |a Fazio, Raffaella |e verfasserin |4 aut | |
| 700 | 1 | |a Fanelli, Giovanna Franca |e verfasserin |4 aut | |
| 700 | 1 | |a Volonté, Maria Antonietta |e verfasserin |4 aut | |
| 700 | 1 | |a Genchi, Angela |e verfasserin |4 aut | |
| 700 | 1 | |a Giordano, Antonino |e verfasserin |4 aut | |
| 700 | 1 | |a Martinelli, Vittorio |e verfasserin |4 aut | |
| 700 | 1 | |a Colombo, Sergio |e verfasserin |4 aut | |
| 700 | 1 | |a Beccaria, Paolo |e verfasserin |4 aut | |
| 700 | 1 | |a Mucci, Milena |e verfasserin |4 aut | |
| 700 | 1 | |a Peccatori, Jacopo |e verfasserin |4 aut | |
| 700 | 1 | |a Filippi, Massimo |e verfasserin |4 aut | |
| 700 | 1 | |a Minicucci, Fabio |e verfasserin |4 aut | |
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10.1007/s00415-020-09988-w doi (DE-627)SPR040338126 (DE-599)SPRs00415-020-09988-w-e (SPR)s00415-020-09988-w-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lazzarin, Serena Marita verfasserin aut Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. Anti-NMDAR encephalitis (dpeaa)DE-He213 Autoimmune encephalitis (dpeaa)DE-He213 Bortezomib (dpeaa)DE-He213 EEG (dpeaa)DE-He213 Movement disorders (dpeaa)DE-He213 Vabanesi, Marco verfasserin aut Cecchetti, Giordano verfasserin aut Fazio, Raffaella verfasserin aut Fanelli, Giovanna Franca verfasserin aut Volonté, Maria Antonietta verfasserin aut Genchi, Angela verfasserin aut Giordano, Antonino verfasserin aut Martinelli, Vittorio verfasserin aut Colombo, Sergio verfasserin aut Beccaria, Paolo verfasserin aut Mucci, Milena verfasserin aut Peccatori, Jacopo verfasserin aut Filippi, Massimo verfasserin aut Minicucci, Fabio verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 267(2020), 8 vom: 13. Juni, Seite 2462-2468 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:267 year:2020 number:8 day:13 month:06 pages:2462-2468 https://dx.doi.org/10.1007/s00415-020-09988-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 267 2020 8 13 06 2462-2468 |
| spelling |
10.1007/s00415-020-09988-w doi (DE-627)SPR040338126 (DE-599)SPRs00415-020-09988-w-e (SPR)s00415-020-09988-w-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lazzarin, Serena Marita verfasserin aut Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. Anti-NMDAR encephalitis (dpeaa)DE-He213 Autoimmune encephalitis (dpeaa)DE-He213 Bortezomib (dpeaa)DE-He213 EEG (dpeaa)DE-He213 Movement disorders (dpeaa)DE-He213 Vabanesi, Marco verfasserin aut Cecchetti, Giordano verfasserin aut Fazio, Raffaella verfasserin aut Fanelli, Giovanna Franca verfasserin aut Volonté, Maria Antonietta verfasserin aut Genchi, Angela verfasserin aut Giordano, Antonino verfasserin aut Martinelli, Vittorio verfasserin aut Colombo, Sergio verfasserin aut Beccaria, Paolo verfasserin aut Mucci, Milena verfasserin aut Peccatori, Jacopo verfasserin aut Filippi, Massimo verfasserin aut Minicucci, Fabio verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 267(2020), 8 vom: 13. Juni, Seite 2462-2468 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:267 year:2020 number:8 day:13 month:06 pages:2462-2468 https://dx.doi.org/10.1007/s00415-020-09988-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 267 2020 8 13 06 2462-2468 |
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10.1007/s00415-020-09988-w doi (DE-627)SPR040338126 (DE-599)SPRs00415-020-09988-w-e (SPR)s00415-020-09988-w-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lazzarin, Serena Marita verfasserin aut Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. Anti-NMDAR encephalitis (dpeaa)DE-He213 Autoimmune encephalitis (dpeaa)DE-He213 Bortezomib (dpeaa)DE-He213 EEG (dpeaa)DE-He213 Movement disorders (dpeaa)DE-He213 Vabanesi, Marco verfasserin aut Cecchetti, Giordano verfasserin aut Fazio, Raffaella verfasserin aut Fanelli, Giovanna Franca verfasserin aut Volonté, Maria Antonietta verfasserin aut Genchi, Angela verfasserin aut Giordano, Antonino verfasserin aut Martinelli, Vittorio verfasserin aut Colombo, Sergio verfasserin aut Beccaria, Paolo verfasserin aut Mucci, Milena verfasserin aut Peccatori, Jacopo verfasserin aut Filippi, Massimo verfasserin aut Minicucci, Fabio verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 267(2020), 8 vom: 13. Juni, Seite 2462-2468 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:267 year:2020 number:8 day:13 month:06 pages:2462-2468 https://dx.doi.org/10.1007/s00415-020-09988-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 267 2020 8 13 06 2462-2468 |
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10.1007/s00415-020-09988-w doi (DE-627)SPR040338126 (DE-599)SPRs00415-020-09988-w-e (SPR)s00415-020-09988-w-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lazzarin, Serena Marita verfasserin aut Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. Anti-NMDAR encephalitis (dpeaa)DE-He213 Autoimmune encephalitis (dpeaa)DE-He213 Bortezomib (dpeaa)DE-He213 EEG (dpeaa)DE-He213 Movement disorders (dpeaa)DE-He213 Vabanesi, Marco verfasserin aut Cecchetti, Giordano verfasserin aut Fazio, Raffaella verfasserin aut Fanelli, Giovanna Franca verfasserin aut Volonté, Maria Antonietta verfasserin aut Genchi, Angela verfasserin aut Giordano, Antonino verfasserin aut Martinelli, Vittorio verfasserin aut Colombo, Sergio verfasserin aut Beccaria, Paolo verfasserin aut Mucci, Milena verfasserin aut Peccatori, Jacopo verfasserin aut Filippi, Massimo verfasserin aut Minicucci, Fabio verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 267(2020), 8 vom: 13. Juni, Seite 2462-2468 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:267 year:2020 number:8 day:13 month:06 pages:2462-2468 https://dx.doi.org/10.1007/s00415-020-09988-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 267 2020 8 13 06 2462-2468 |
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10.1007/s00415-020-09988-w doi (DE-627)SPR040338126 (DE-599)SPRs00415-020-09988-w-e (SPR)s00415-020-09988-w-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.90 bkl Lazzarin, Serena Marita verfasserin aut Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. Anti-NMDAR encephalitis (dpeaa)DE-He213 Autoimmune encephalitis (dpeaa)DE-He213 Bortezomib (dpeaa)DE-He213 EEG (dpeaa)DE-He213 Movement disorders (dpeaa)DE-He213 Vabanesi, Marco verfasserin aut Cecchetti, Giordano verfasserin aut Fazio, Raffaella verfasserin aut Fanelli, Giovanna Franca verfasserin aut Volonté, Maria Antonietta verfasserin aut Genchi, Angela verfasserin aut Giordano, Antonino verfasserin aut Martinelli, Vittorio verfasserin aut Colombo, Sergio verfasserin aut Beccaria, Paolo verfasserin aut Mucci, Milena verfasserin aut Peccatori, Jacopo verfasserin aut Filippi, Massimo verfasserin aut Minicucci, Fabio verfasserin aut Enthalten in Journal of neurology [Darmstadt] : Steinkopff, 1891 267(2020), 8 vom: 13. Juni, Seite 2462-2468 (DE-627)242065155 (DE-600)1421299-7 1432-1459 nnns volume:267 year:2020 number:8 day:13 month:06 pages:2462-2468 https://dx.doi.org/10.1007/s00415-020-09988-w lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 267 2020 8 13 06 2462-2468 |
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Enthalten in Journal of neurology 267(2020), 8 vom: 13. Juni, Seite 2462-2468 volume:267 year:2020 number:8 day:13 month:06 pages:2462-2468 |
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Enthalten in Journal of neurology 267(2020), 8 vom: 13. Juni, Seite 2462-2468 volume:267 year:2020 number:8 day:13 month:06 pages:2462-2468 |
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Anti-NMDAR encephalitis Autoimmune encephalitis Bortezomib EEG Movement disorders |
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Lazzarin, Serena Marita @@aut@@ Vabanesi, Marco @@aut@@ Cecchetti, Giordano @@aut@@ Fazio, Raffaella @@aut@@ Fanelli, Giovanna Franca @@aut@@ Volonté, Maria Antonietta @@aut@@ Genchi, Angela @@aut@@ Giordano, Antonino @@aut@@ Martinelli, Vittorio @@aut@@ Colombo, Sergio @@aut@@ Beccaria, Paolo @@aut@@ Mucci, Milena @@aut@@ Peccatori, Jacopo @@aut@@ Filippi, Massimo @@aut@@ Minicucci, Fabio @@aut@@ |
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The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. 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|
| author |
Lazzarin, Serena Marita |
| spellingShingle |
Lazzarin, Serena Marita ddc 610 bkl 44.90 misc Anti-NMDAR encephalitis misc Autoimmune encephalitis misc Bortezomib misc EEG misc Movement disorders Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review |
| authorStr |
Lazzarin, Serena Marita |
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@@773@@(DE-627)242065155 |
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electronic Article |
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610 - Medicine & health |
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keep |
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aut aut aut aut aut aut aut aut aut aut aut aut aut aut aut |
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springer |
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true |
| illustrated |
Not Illustrated |
| issn |
1432-1459 |
| topic_title |
610 ASE 44.90 bkl Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review Anti-NMDAR encephalitis (dpeaa)DE-He213 Autoimmune encephalitis (dpeaa)DE-He213 Bortezomib (dpeaa)DE-He213 EEG (dpeaa)DE-He213 Movement disorders (dpeaa)DE-He213 |
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ddc 610 bkl 44.90 misc Anti-NMDAR encephalitis misc Autoimmune encephalitis misc Bortezomib misc EEG misc Movement disorders |
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ddc 610 bkl 44.90 misc Anti-NMDAR encephalitis misc Autoimmune encephalitis misc Bortezomib misc EEG misc Movement disorders |
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ddc 610 bkl 44.90 misc Anti-NMDAR encephalitis misc Autoimmune encephalitis misc Bortezomib misc EEG misc Movement disorders |
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Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review |
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Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review |
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Lazzarin, Serena Marita |
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Lazzarin, Serena Marita Vabanesi, Marco Cecchetti, Giordano Fazio, Raffaella Fanelli, Giovanna Franca Volonté, Maria Antonietta Genchi, Angela Giordano, Antonino Martinelli, Vittorio Colombo, Sergio Beccaria, Paolo Mucci, Milena Peccatori, Jacopo Filippi, Massimo Minicucci, Fabio |
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refractory anti-nmdar encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review |
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Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review |
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Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. |
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Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. |
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Abstract Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune disease, characterized by autoantibody-mediated neurotransmission impairment in multiple brain locations. The course of this condition often comprises altered mental status, autonomic dysfunctions, refractory seizures and hyperkinetic movement disorders. Available disease-modifying therapies include corticosteroids, i.v. immunoglobulins, plasma exchange, rituximab and cyclophosphamide. In a subgroup of patients not responding to B-cell depletion, bortezomib, a proteasome inhibitor, has shown promising evidence of efficacy. The time course of recovery from acute phase may be very slow (weeks/months), and only few data are available in literature about the concurrent management of encephalitis-associated movement disorders. We report a case of severe anti-NMDAR encephalitis in a 29-year-old woman, not responsive to first- and second-line treatments, with persistent involuntary motor manifestations. Starting three months after symptom onset, four cycles of bortezomib have been administered; subsequently we observed a progressive improvement of neurological status. Meanwhile, motor manifestations were controlled after the administration of tramadol, a non-competitive NMDA receptor antagonist. |
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Refractory anti-NMDAR encephalitis successfully treated with bortezomib and associated movements disorders controlled with tramadol: a case report with literature review |
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| score |
7.3996468 |