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  • 1
    Online Resource
    Online Resource
    Adult-Onset Opsoclonus-Myoclonus Syndrome
    American Medical Association (AMA) ; 2012
    In:  Archives of Neurology Vol. 69, No. 12 ( 2012-12-01), p. 1598-
    Details
    In: Archives of Neurology, American Medical Association (AMA), Vol. 69, No. 12 ( 2012-12-01), p. 1598-
    Type of Medium: Online Resource
    ISSN: 0003-9942
    URL: Article
    DOI: 10.1001/archneurol.2012.1173
    RVK:
    XA 10000
    Language: English
    Publisher: American Medical Association (AMA)
    Publication Date: 2012
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  • 2
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    Utility of MRI Enhancement Pattern in Myelopathies With Longitudinally Extensive T2 Lesions
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Neurology: Clinical Practice Vol. 11, No. 5 ( 2021-10), p. e601-e611
    Details
    In: Neurology: Clinical Practice, Ovid Technologies (Wolters Kluwer Health), Vol. 11, No. 5 ( 2021-10), p. e601-e611
    Abstract: To determine whether MRI gadolinium enhancement patterns in myelopathies with longitudinally extensive T2 lesions can be reliably distinguished and assist in diagnosis. Methods We retrospectively identified 74 Mayo Clinic patients (January 1, 1996–December 31, 2019) fulfilling the following criteria: (1) clinical myelopathy; (2) MRI spine available; (3) longitudinally extensive T2 hyperintensity (≥3 vertebral segments); and (4) characteristic gadolinium enhancement pattern associated with a specific myelopathy etiology. Thirty-nine cases with alternative myelopathy etiologies, without previously described enhancement patterns, were included as controls. Two independent readers, educated on enhancement patterns, reviewed T2-weighted and postgadolinium T1-weighted images and selected the diagnosis based on this knowledge. These were compared with the true diagnoses, and agreement was measured with Kappa coefficient. Results Among all cases and controls (n = 113), there was excellent agreement for diagnosis using postgadolinium images (kappa, 0.76) but poor agreement with T2-weighted characteristics alone (kappa, 0.25). A correct diagnosis was more likely when assessing postgadolinium image characteristics than with T2-weighted images alone (rater 1: 100/113 [88%] vs 61/113 [54%] correct, p 〈 0.0001; rater 2: 95/113 [84%] vs 68/113 [60%] correct, p 〈 0.0001). Of the 74 with characteristic enhancement patterns, 55 (74%) were assigned an alternative incorrect or nonspecific diagnosis when originally evaluated in clinical practice, 12 (16%) received immunotherapy for noninflammatory myelopathies, and 2 (3%) underwent unnecessary spinal cord biopsy. Conclusions Misdiagnosis of myelopathies is common. The gadolinium enhancement patterns characteristic of specific diagnoses can be identified with excellent agreement between raters educated on this topic. This study highlights the potential diagnostic utility of enhancement patterns in myelopathies with longitudinally extensive T2 lesions.
    Type of Medium: Online Resource
    ISSN: 2163-0402 , 2163-0933
    URL: Article
    DOI: 10.1212/CPJ.0000000000001036
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2645818-4
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  • 3
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    Glial fibrillary acidic protein immunoglobulin G as biomarker of autoimmune astrocytopathy: Analysis of 102 patients
    Wiley ; 2017
    In:  Annals of Neurology Vol. 81, No. 2 ( 2017-02), p. 298-309
    Details
    In: Annals of Neurology, Wiley, Vol. 81, No. 2 ( 2017-02), p. 298-309
    Abstract: A novel autoimmune central nervous system (CNS) disorder with glial fibrillary acidic protein (GFAP)‐IgG as biomarker was recently characterized. Here, 102 patients with GFAP‐IgG positivity are described. Methods The 102 included patients had: (1) serum, cerebrospinal fluid (CSF), or both that yielded a characteristic astrocytic pattern of mouse tissue immunostaining; (2) confirmation of IgG reactive with specific GFAP isoforms (α, ɛ, or κ) by cell‐based assays; and (3) clinical data available. Control specimens (n = 865) were evaluated by tissue (n = 542) and cell‐based (n = 323) assays. Results Median symptom onset age was 44 years (range = 8–103), and 54% were women. The predominant phenotype (83 patients; 81%) was inflammation of meninges, brain, spinal cord, or all 3 (meningoencephalomyelitis). Among patients, highest specificity for those phenotypes was observed for CSF testing (94%), and highest sensitivity was for the GFAPα isoform (100%). Rare GFAP‐IgG positivity was encountered in serum controls by tissue‐based assay (0.5%) or cell‐based assay (1.5%), and in CSF controls by cell‐based assay (0.9%). Among patients, striking perivascular radial enhancement was found on brain magnetic resonance imaging in 53%. Although cases frequently mimicked vasculitis, angiography was uniformly negative, and spinal imaging frequently demonstrated longitudinally extensive myelitic lesions. Diverse neoplasms encountered were found prospectively in 22%. Ovarian teratoma was most common and was predicted best when both N‐methyl‐D‐aspartate receptor–IgG and aquaporin‐4–IgG coexisted (71%). Six patients with prolonged follow‐up had brisk corticosteroid response, but required additional immunosuppression to overcome steroid dependency. Interpretation GFAPα‐IgG, when detected in CSF, is highly specific for an immunotherapy‐responsive autoimmune CNS disorder, sometimes with paraneoplastic cause. Ann Neurol 2017;81:298–309
    Type of Medium: Online Resource
    ISSN: 0364-5134 , 1531-8249
    URL: Issue
    URL: Article
    DOI: 10.1002/ana.v81.2
    DOI: 10.1002/ana.24881
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2037912-2
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  • 4
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    Autoimmune encephalitis epidemiology and a comparison to infectious encephalitis
    Wiley ; 2018
    In:  Annals of Neurology Vol. 83, No. 1 ( 2018-01), p. 166-177
    Details
    In: Annals of Neurology, Wiley, Vol. 83, No. 1 ( 2018-01), p. 166-177
    Abstract: To evaluate the incidence and prevalence of autoimmune encephalitis and compare it to that of infectious encephalitis. Methods We performed a population‐based comparative study of the incidence and prevalence of autoimmune and infectious encephalitis in Olmsted County, Minnesota. Autoimmune encephalitis diagnosis and subgroups were defined by 2016 diagnostic criteria, and infectious encephalitis diagnosis required a confirmed infectious pathogen. Age‐ and sex‐adjusted prevalence and incidence rates were calculated. Patients with encephalitis of uncertain etiology were excluded. Results The prevalence of autoimmune encephalitis on January 1, 2014 of 13.7/100,000 was not significantly different from that of all infectious encephalitides (11.6/100,000; p  = 0.63) or the viral subcategory (8.3/100,000; p  = 0.17). The incidence rates (1995–2015) of autoimmune and infectious encephalitis were 0.8/100,000 and 1.0/100,000 person‐years, respectively ( p  = 0.58). The number of relapses or recurrent hospitalizations was higher for autoimmune than infectious encephalitis ( p  = 0.03). The incidence of autoimmune encephalitis increased over time from 0.4/100,000 person‐years (1995–2005) to 1.2/100,000 person‐years (2006–2015; p  = 0.02), attributable to increased detection of autoantibody‐positive cases. The incidence (2.8 vs 0.7/100,000 person‐years, p  = 0.01) and prevalence (38.3 vs 13.7/100,000, p  = 0.04) of autoimmune encephalitis was higher among African Americans than Caucasians. The prevalence of specific neural autoantibodies was as follows: myelin oligodendrocyte glycoprotein, 1.9/100,000; glutamic acid decarboxylase 65, 1.9/100,000; unclassified neural autoantibody, 1.4/100,000; leucine‐rich glioma‐inactivated protein 1, 0.7/100,000; collapsin response‐mediator protein 5, 0.7/100,000; N‐methyl‐D‐aspartate receptor, 0.6/100,000; antineuronal nuclear antibody type 2, 0.6/100,000; and glial fibrillary acidic protein α, 0.6/100,000. Interpretation This study shows that the prevalence and incidence of autoimmune encephalitis are comparable to infectious encephalitis, and its detection is increasing over time. Ann Neurol 2018;83:166–177
    Type of Medium: Online Resource
    ISSN: 0364-5134 , 1531-8249
    URL: Issue
    URL: Article
    DOI: 10.1002/ana.v83.1
    DOI: 10.1002/ana.25131
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2037912-2
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  • 5
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    Discriminating long myelitis of neuromyelitis optica from sarcoidosis
    Wiley ; 2016
    In:  Annals of Neurology Vol. 79, No. 3 ( 2016-03), p. 437-447
    Details
    In: Annals of Neurology, Wiley, Vol. 79, No. 3 ( 2016-03), p. 437-447
    Abstract: To compare longitudinally extensive myelitis in neuromyelitis optica spectrum disorders (NMOSD) and spinal cord sarcoidosis (SCS). Methods We identified adult patients evaluated between 1996 and 2015 with SCS or NMOSD whose first myelitis episode was accompanied by a spinal cord lesion spanning ≥3 vertebral segments. All NMOSD patients were positive for aquaporin‐4–immunoglobulin G, and all sarcoidosis cases were pathologically confirmed. Clinical characteristics were evaluated. Spine magnetic resonance imaging was reviewed by 2 neuroradiologists. Results We studied 71 patients (NMOSD, 37; SCS, 34). Sixteen (47%) SCS cases were initially diagnosed as NMOSD or idiopathic transverse myelitis. Median delay to diagnosis was longer for SCS than NMOSD (5 vs 1.5 months, p 〈 0.01). NMOSD myelitis patients were more commonly women, had concurrent or prior optic neuritis or intractable vomiting episodes more frequently, had shorter time to maximum deficit, and had systemic autoimmunity more often than SCS ( p 〈 0.05). SCS patients had constitutional symptoms, cerebrospinal fluid (CSF) pleocytosis, and hilar adenopathy more frequently than NMOSD ( p 〈 0.05); CSF hypoglycorrhachia (11%, p = 0.25) and elevated angiotensin‐converting enzyme (18%, p = 0.30) were exclusive to SCS. Dorsal cord subpial gadolinium enhancement extending ≥2 vertebral segments and persistent enhancement 〉 2 months favored SCS, and ringlike enhancement favored NMOSD ( p 〈 0.05). Maximum disability was similar in both disorders. Interpretation SCS is an under‐recognized cause of longitudinally extensive myelitis that commonly mimics NMOSD. We identified clinical, laboratory, systemic, and radiologic features that, taken together, help discriminate SCS from NMOSD. ANN NEUROL 2016;79:437–447
    Type of Medium: Online Resource
    ISSN: 0364-5134 , 1531-8249
    URL: Issue
    URL: Article
    DOI: 10.1002/ana.v79.3
    DOI: 10.1002/ana.24582
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2037912-2
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  • 6
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    PML diagnostic criteria : Consensus statement from the AAN Neuroinfectious Disease Section
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Neurology Vol. 80, No. 15 ( 2013-04-09), p. 1430-1438
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 80, No. 15 ( 2013-04-09), p. 1430-1438
    Abstract: To establish criteria for the diagnosis of progressive multifocal leukoencephalopathy (PML). Methods: We reviewed available literature to identify various diagnostic criteria employed. Several search strategies employing the terms “progressive multifocal leukoencephalopathy” with or without “JC virus” were performed with PubMed, SCOPUS, and EMBASE search engines. The articles were reviewed by a committee of individuals with expertise in the disorder in order to determine the most useful applicable criteria. Results: A consensus statement was developed employing clinical, imaging, pathologic, and virologic evidence in support of the diagnosis of PML. Two separate pathways, histopathologic and clinical, for PML diagnosis are proposed. Diagnostic classification includes certain, probable, possible, and not PML. Conclusion: Definitive diagnosis of PML requires neuropathologic demonstration of the typical histopathologic triad (demyelination, bizarre astrocytes, and enlarged oligodendroglial nuclei) coupled with the techniques to show the presence of JC virus. The presence of clinical and imaging manifestations consistent with the diagnosis and not better explained by other disorders coupled with the demonstration of JC virus by PCR in CSF is also considered diagnostic. Algorithms for establishing the diagnosis have been recommended.
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0b013e31828c2fa1
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
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  • 7
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    Primary Diffuse Leptomeningeal Gliomatosis
    S. Karger AG ; 2009
    In:  European Neurology Vol. 62, No. 1 ( 2009), p. 16-22
    Details
    In: European Neurology, S. Karger AG, Vol. 62, No. 1 ( 2009), p. 16-22
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Primary diffuse leptomeningeal gliomatosis (PDLG) is a rare presentation of a primary central nervous system glial tumor. 〈 i 〉 Methods: 〈 /i 〉 Four case reports of PDLG in young males aged 14–24 years are presented. These reports are discussed in the context of the existing literature. 〈 i 〉 Results: 〈 /i 〉 The clinical presentation of 4 new cases of PDLG resembled chronic meningitis with and without polyradiculopathy. Spinal fluid studies are typically nondiagnostic, but characteristically show elevated opening pressure, an elevated protein level, and a relative paucity of cellular reaction. An accurate antemortem diagnosis required contrast-enhanced imaging and meningeal biopsy in all 4 of our cases. Treatment strategies including craniospinal radiation and chemotherapeutic approaches, alone or in combination, have not been proven to alter the course of the disease. Initial responses to temozolomide and radiation treatments in all 4 of our cases were promising, resulting in temporary stabilization of the disease and prolonging life expectancy over what was previously reported in the literature. 〈 i 〉 Conclusion: 〈 /i 〉 Total neuroaxis contrast-enhanced MRI scanning is required for directing biopsy confirmation and detecting the extent of the disease. More effective therapeutic strategies are needed, but the combination of temozolomide and radiation therapy may slow disease progression.
    Type of Medium: Online Resource
    ISSN: 0014-3022 , 1421-9913
    URL: Article
    DOI: 10.1159/000216838
    RVK:
    XA 10000
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2009
    detail.hit.zdb_id: 1482237-4
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  • 8
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    Optic Disc Edema in Glial Fibrillary Acidic Protein Autoantibody–Positive Meningoencephalitis
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Journal of Neuro-Ophthalmology Vol. 38, No. 3 ( 2018-09), p. 276-281
    Details
    In: Journal of Neuro-Ophthalmology, Ovid Technologies (Wolters Kluwer Health), Vol. 38, No. 3 ( 2018-09), p. 276-281
    Abstract: Glial fibrillary acidic protein (GFAP) autoantibody–positive meningoencephalitis is a newly described entity characterized by a corticosteroid-responsive meningoencephalomyelitis. Some patients with GFAP autoantibody–positive meningoencephalitis have been found to have optic disc edema, which has previously not been well characterized. Methods: We performed a retrospective, observational case series of Mayo Clinic patients found to have GFAP-IgG and optic disc edema from January 1, 2000, to December 31, 2016. We identified 40 patients with GFAP-IgG seropositivity by tissue-based immunofluorescence and cell-based assay. Patients were screened for the following inclusion criteria: 1) serum, cerebrospinal fluid, or both that yielded a characteristic astrocytic pattern of mouse tissue immunostaining with confirmation of IgG reactive with specific GFAPα isoform by cell-based assay; 2) meningoencephalitis or encephalitis; and 3) optic disc edema. We excluded those with coexisting aquaporin-4-IgG or insufficient clinical information. Results: Ten patients had optic disc edema and met inclusion criteria. The median age was 39.5 years and 60% were men. Visual acuity was unaffected and disc edema was bilateral in all cases. Mild vitreous cell was noted in 3 patients. The optic disc edema resolved with corticosteroid treatment but resulted in mild optic atrophy in 2 patients. The median lumbar puncture opening pressure was 144 mm H 2 O (range, 84–298 mm H 2 O). Brain MRI revealed radial perivascular enhancement in all except 1 patient. Fluorescein angiography was available for 1 patient with optic disc edema, which showed leakage from the venules. Conclusions: Patients with GFAP autoantibody–positive meningoencephalitis can have optic disc edema that can mimic papilledema. The cause of the optic disc edema remains uncertain, but most patients did not have raised intracranial pressure.
    Type of Medium: Online Resource
    ISSN: 1070-8022
    URL: Article
    DOI: 10.1097/WNO.0000000000000593
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2062798-1
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  • 9
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    Glial fibrillary acidic protein IgG related myelitis: characterisation and comparison with aquaporin-4-IgG myelitis
    BMJ ; 2019
    In:  Journal of Neurology, Neurosurgery & Psychiatry Vol. 90, No. 4 ( 2019-04), p. 488-490
    Details
    In: Journal of Neurology, Neurosurgery & Psychiatry, BMJ, Vol. 90, No. 4 ( 2019-04), p. 488-490
    Type of Medium: Online Resource
    ISSN: 0022-3050 , 1468-330X
    URL: Article
    DOI: 10.1136/jnnp-2018-318004
    RVK:
    XA 10000
    Language: English
    Publisher: BMJ
    Publication Date: 2019
    detail.hit.zdb_id: 1480429-3
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  • 10
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    Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy : A Novel Meningoencephalomyelitis
    American Medical Association (AMA) ; 2016
    In:  JAMA Neurology Vol. 73, No. 11 ( 2016-11-01), p. 1297-
    Details
    In: JAMA Neurology, American Medical Association (AMA), Vol. 73, No. 11 ( 2016-11-01), p. 1297-
    Type of Medium: Online Resource
    ISSN: 2168-6149
    URL: Article
    DOI: 10.1001/jamaneurol.2016.2549
    Language: English
    Publisher: American Medical Association (AMA)
    Publication Date: 2016
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