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Your partner in autoimmune neurology testing

NEUROLOGY

A WORLD LEADER IN AUTOIMMUNENEUROLOGY

ADVANCED PHENOTYPE-SPECIFICEVALUATIONS

TOP EXPERTS IN THELAB AVAILABLE FORCONSULTATION

We are recognized as leaders in the

diagnosis and treatment of autoimmune

neurologic disorders, one of the most

rapidly evolving fields in modern neurology.

These common disorders target virtually

any structure within the central or peripheral

nervous system.

Our approach to antibody evaluations

ensures a timely diagnosis and complete

picture of a patient’s likelihood of

autoimmune disease compared to single

antibody testing.

Get unparalleled assistance with test

selection, interpretation follow-up, treatment

guidance, and unclassified antibody

findings. Neurologists are available for

consultation seven days a week, providing

interpretive expertise and support.

Improving patient outcomes throughadvanced testing and consultations

Leading the way in autoantibody evaluations

A HISTORY OF INNOVATION AND DISCOVERY

Recognized as a world leader in the diagnosis and treatment of

autoimmune neurologic disorders and demyelinating disease, Mayo

Clinic mounts unmatched resources for uncovering novel syndromes,

developing new diagnostic biomarkers and unique laboratory tests.

The Mayo Clinic Neuroimmunology Laboratory was the first to

introduce comprehensive serological evaluations for the diagnosis of

paraneoplastic neurologic autoimmune disorders, a group of disorders

in which unusual neurologic signs and symptoms are the initial

manifestations of cancer.

The laboratory continues to discover and clinically validate novel

autoantibody profiles that inform neurological decision-making and

guide the search for cancer.

Vanda Lennon, M.D., Ph.D., is the founder of the

Mayo Clinic Neuroimmunology Laboratory. She is also

the Dorothy A. Adair Professor in the Departments of

Laboratory Medicine and Pathology, Neurology, and

Immunology at the College of Medicine at Mayo Clinic.

A RAPIDLY EVOLVING SUBSPECIALTY

Autoimmune neurology has been advanced through discovery,

research, and clinical service for decades. Recent advances

validate that disorders—extending beyond MS—are more common

than traditionally believed. These conditions manifest as disorders

previously thought to be independent and unrelated and thus, are

often treated incorrectly—with devastating consequences for patients.

Meet our team of experts

PARTNER WITH TOP NEUROLOGISTS

Extend your network to include some of the world’s

leading neurology experts. Our laboratories are

directed and run by clinical neurologists who can

provide the guidance you need.

John R. Mills, Ph.D. Sean Pittock, M.D. Andrew McKeon, M.B., B.Ch., M.D.

LABORATORY DIRECTORS

Eoin Flanagan, M.B., B.Ch. Christopher Klein, M.D. Daniel Lachance, M.D.Divyanshu Dubey, M.B.B.S. Anastasia Zekeridou, M.D.

CONSULTANTS

Optimized screening methods

OUR AUTOIMMUNE NEUROLOGY EVALUATIONS USE THE MOST UP-TO-DATE SCREENING METHODOLOGIES AND ARE OPTIMIZED FOR EACH ANTIBODY. EVALUATIONS INCLUDE:

• An indirect immunofluorescence assay, using a tissue or cell-based test. This testing is often used to screen for

paraneoplastic antibodies and antibodies related to encephalitis.

• A flow cytometry assay, used to screen for aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies, which are

relevant in diagnosing transverse myelitis, optic neuritis, and neuromyelitis optica.

• A radioimmunoprecipitation assay, which can detect some ion channel antibodies, including the diagnostics for Lambert-

Eaton syndrome and myasthenia gravis.

Contact a clinical specialist at 855-516-8404 or +1-855-379-3115 (International). See more at mayocliniclabs.com.

Targeted evaluations to expedite diagnosis and treatment of autoimmune encephalopathy

Encephalopathy

Autoimmune CNS

WHAT IS AUTOIMMUNE ENCEPHALOPATHY?Autoimmune encephalopathy extends beyond the classically recognized clinical and radiological spectrum of “limbic encephalitis.” It encompasses a diversity of neurological presentations with subacute or insidious onset, including confusional states, psychosis, delirium, memory loss, hallucinations, movement disorders, sensory or motor complaints, seizures, dyssomnias, ataxias, eye movement problems, nausea, vomiting, inappropriate antidiuresis, coma, dysautonomias, or hypoventilation.

WHEN TO CONSIDER TESTINGConsider autoimmune testing for patients presenting with new-onset encephalopathy (non-infectious or metabolic) and one or more of the following:

• Headache• Autoimmune stigmata (e.g., physical signs or personal/family history of

diabetes, thyroid disorder, vitiligo, prematurely gray hair, myasthenia gravis, rheumatoid arthritis, systemic lupus erythematosus)

• History of cancer• Smoking history (20+ pack years) or other cancer risk factors• Inflammatory cerebrospinal fluid • Neuroimages suggesting inflammation (signal abnormality, limbic or

extra-temporal)• Prior treatment with immune checkpoint inhibitors• Antibody prevalence in epilepsy and encephalopathy (APE2) score is ≥41

AUTOIMMUNE ENCEPHALOPATHY IS INCREASINGLY RECOGNIZEDMany cases of encephalopathy previously considered infectious are now recognized to have an autoimmune cause. In fact, based on a recent Mayo Clinic study, autoimmune encephalitis was found to be as common as infectious encephalitis.2

AUTOIMMUNE VERSUS INFECTIOUS ENCEPHALITIS

Prevalence Rate (per 100,000 people)

AutoimmuneEncephalitis

13.7

11.6

InfectiousEncephalitis

A guide to testing and evaluated antibodies

Encephalopathy

ENC2 | Encephalopathy, Autoimmune Evaluation, Spinal Fluid TAT: 5 days

ENS2 | Encephalopathy, Autoimmune Evaluation, Serum TAT: 7 days

CLINICAL REFERENCES

1 Dubey D, et al. Predictors of neural-specific autoantibodies and immunotherapy response in patients with cognitive dysfunction. J Neuroimmunol. 2018;323:62-72.

2 Flanagan EP, Dubey D, Pittock SJ, et al. Autoimmune encephalitis epidemiology and a comparison to infectious encephalitis. Ann Neurol. 2018 Jan;83(1):166-177.

3 Flanagan EP, Kotsenas AL, Britton JW, et al. Basal ganglia T1 hyperintensity in LGI1-autoantibody faciobrachial dystonic seizures. Neurol Neuroimmunol Neuroinflamm. 2015;2(6):e161.

4 Horta ES, Lennon VA, Lachance DH, et al. Neural autoantibody clusters aid diagnosis of cancer. Clin Cancer Res. 2014;20(14):3862-3869.

5 Linnoila J, Pittock SJ. Autoantibody-associated central nervous system neurologic disorders. Semin Neurol. 2016;36(04):382-396.

6 McKeon A. Autoimmune encephalopathies and dementias. CONTINUUM: Lifelong Learning in Neurology. 2016;22(2, Dementia):538-558.

7 McKeon A, Tracy JA. GAD65 neurological autoimmunity. Muscle & Nerve. January 2017.

8 Pittock SJ, Vincent A. Autoimmune Neurology. Amsterdam: Elsevier; 2016.

9 van Sonderen A, Ariño H, Petit-Pedrol M, et al. The clinical spectrum of Caspr2 antibody-associated disease. Neurology. 2016;87(5):521-528.

10 van Sonderen A, Thijs RD, Coenders EC, et al. Anti-LGI1 encephalitis: clinical syndrome and long-term follow-up. Neurology. 2016;87(14):1449-1456.

NUCLEAR AND CYTOPLASMIC SPECIFICITIES

ANTIBODY SERUM SPINAL FLUID

ANNA-1 (anti-Hu) • •

ANNA-2 (anti-Ri) • •

ANNA-3 • •

AGNA-1 (SOX1) • •

PCA-1 • •

PCA-2 • •

CRMP-5 (anti-CV2) • •

Amphiphysin • •

GAD65 • •

GFAP • •

PLASMA MEMBRANE SPECIFICITIES


NMDA receptor • •

LGI1 • •

CASPR2 • •

AMPA receptor • •

GABA-B receptor • •

DPPX • •

mGluR1 • •

P/Q and N-type calcium channel •

Neuronal ganglionic AChR •

PCA-Tr • •

Abbreviations: AChR, acetylcholine receptor; AGNA, anti-glial/neuronal nuclear antibody; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; ANNA, antineuronal nuclear antibody; CASPR2, contactin-associated protein-like 2; CRMP-5, collapsin response-mediator protein-5; DPPX, dipeptidyl-peptidase-like protein 6; GABA, gamma-aminobutyric acid; GAD65, glutamic acid decarboxylase-65; GFAP, glial fibrillary acidic protein; LGl1, leucine-rich glioma-inactivated 1; NMDA, N-methyl D-aspartate; mGluR1, metabotropic glutamate receptor 1; PCA, Purkinje cell cytoplasmic antibody.


Epilepsy

Targeted evaluations to expedite diagnosis and treatment of autoimmune epilepsy

WHAT IS AUTOIMMUNE EPILEPSY?Autoimmune epilepsy is increasingly recognized in the spectrum of neurological disorders characterized by detection of neural autoantibodies in serum or spinal fluid and responsiveness to immunotherapy. The advent of more sensitive and specific serological detection methods is increasingly revealing previously underappreciated autoimmune epilepsies. Neural autoantibodies specific for intracellular and plasma membrane antigens aid the diagnosis of autoimmune epilepsy, but no single antibody is specific for this diagnosis.

IMPROVING PATIENT OUTCOMES THROUGH AUTOIMMUNE TESTINGIdentifying epilepsy as autoimmune-mediated is crucial because patients may benefit from immune suppression, while traditional antiepileptic therapy may not be effective.

WHEN TO CONSIDER TESTINGConsider autoimmune testing for patients presenting with new-onset epilepsy with incomplete seizure control, duration of less than two years, and one or more of the following:

• Subacute progression (maximal seizure frequency within three months)• Multiple seizure types or faciobrachial dystonic seizures• Antiepileptic drug resistance• Psychiatric accompaniments (psychosis, hallucinations)• Movement disorder (myoclonus, tremor, dyskinesia)• Headache• Cognitive impairment/encephalopathy• Autoimmune stigmata (e.g., physical signs or personal/family history of


• History of cancer• Smoking history (20+ pack years) or other cancer risk factors• Inflammatory cerebrospinal fluid • Neuroimages suggesting inflammation (limbic or extra-temporal)• Prior treatment with immune checkpoint inhibitors• Antibody prevalence in epilepsy and encephalopathy (APE2) score is ≥41

Autoimmune CNS

67%In a Mayo Clinic study of 27 patients with suspected autoimmune

epilepsy treated with immunotherapy, 81% experienced clinical

improvement and 67% became seizure free.

Epilepsy


EPC2 | Epilepsy, Autoimmune Evaluation, Spinal Fluid TAT: 5 days

EPS2 | Epilepsy, Autoimmune Evaluation, Serum TAT: 7 days

CLINICAL REFERENCES


2 Suleiman J, Dale RC. The recognition and treatment of autoimmune epilepsy in children. Dev Med Child Neurol. 2015 May;57(5):431-40.






8 Quek AM, Britton JW, McKeon A, et al. Autoimmune epilepsy: clinical characteristics and response to immunotherapy. Arch Neurol. 2012;69(5):582-593.

9 Toledano M, Britton JW, McKeon A, et al. Utility of an immunotherapy trial in evaluating patients with presumed autoimmune epilepsy. Neurology. 2014;82(18):1578-1586.







ANNA-3 • •


PCA-2 • •


Amphiphysin • •

GAD65 • •

GFAP • •




LGI1 • •

CASPR2 • •



DPPX • •

mGluR1 • •



PCA-Tr • •



Dementia

Targeted evaluations to expedite diagnosis and treatment of autoimmune dementia

WHAT IS AUTOIMMUNE DEMENTIA?Recent case series and clinical-serological observations have shown that autoimmune encephalopathies do not always present with delirium, but sometimes present as a rapidly progressive dementia. Additionally, some cases may be paraneoplastic.

AN AUTOIMMUNE CAUSE MEANS A POTENTIALLY REVERSIBLE COURSEIf autoimmune dementia is misdiagnosed as an irreversible progressive neurodegenerative disorder, it may delay a correct diagnosis beyond the window of reversibility (6–12 months) and result in devastating consequences for the patient and family. An accurate diagnosis and early-initiated immunotherapy give patients the best possible outcome.

WHEN TO CONSIDER TESTINGConsider autoimmune testing for patients presenting with new-onset dementia or cognitive impairment and one or more of the following:

• Rapid onset and progression• Fluctuating course• Psychiatric accompaniments (psychosis, hallucinations)• Movement disorder (myoclonus, tremor, dyskinesia)• Headache• Autoimmune stigmata (e.g., physical signs or personal/family history of


• History of cancer• Smoking history (20+ pack years) or other cancer risk factors• Inflammatory cerebrospinal fluid • Neuroimaging atypical for degenerative etiology• Prior treatment with immune checkpoint inhibitors• Antibody prevalence in epilepsy and encephalopathy (APE2) score is ≥41

Autoimmune CNS

35%Among Mayo Clinic patients diagnosed with and treated for an

autoimmune dementia, 35% were initially misdiagnosed as having

a neurodegenerative disorder.

Dementia


DMC2 | Dementia, Autoimmune Evaluation, Spinal Fluid TAT: 5 days

DMS2 | Dementia, Autoimmune Evaluation, Serum TAT: 7 days

CLINICAL REFERENCES



3 Flanagan EP, McKeon A, Lennon VA, et al. Autoimmune dementia: clinical course and predictors of immunotherapy response. Mayo Clin Proc. 2010;85(10):881-897.



6 McKeon A. Autoimmune encephalopathies and dementias. CONTINUUM: Lifelong Learning in Neurology. 2016;22(2, Dementia):538-558.









ANNA-3 • •


PCA-2 • •


Amphiphysin • •

GAD65 • •

GFAP • •




LGI1 • •

CASPR2 • •



DPPX • •

mGluR1 • •



PCA-Tr • •



Targeted evaluations to expedite diagnosis and treatment of autoimmune movement disorders

MovementDisorders

Autoimmune CNS

WHAT ARE AUTOIMMUNE MOVEMENT DISORDERS?Autoimmune movement disorders encapsulate a large and diverse group of neurologic disorders occurring either in isolation or accompanying morediffuse autoimmune encephalitic illnesses. Disorders may be ataxic, hypokinetic(parkinsonism), or hyperkinetic (myoclonus, chorea, and other dyskinetic disorders).

PERSONALIZED TREATMENT FOR EACH PATIENTGiven the variety of movement phenomena and disorders, treatment protocols should be individualized for each patient and reflect symptom severity, the type of antibody identified, and the presence or absence of cancer. In addition to oncologic therapy (when appropriate), often treatment involves immunotherapy and symptomatic therapy. Often, early-initiated immunotherapy gives patients the best possible outcomes.

WHEN TO CONSIDER TESTINGConsider autoimmune testing for patients presenting with a new-onset movement disorder and one or more of the following:

• Fluctuating course• Psychiatric accompaniments (psychosis, hallucinations)• Headache• Autoimmune stigmata (e.g., physical signs or personal/family history of


• History of cancer• Smoking history (20+ pack years) or other cancer risk factors• Inflammatory cerebrospinal fluid• Neuroimages suggesting inflammation (signal abnormality, limbic or

extra-temporal)• Prior treatment with immune checkpoint inhibitors

Patients with autoimmune neurologic disorders may present with multiple movement phenomena, many of which can resemble neurodegenerative disorders, such as Huntington disease. These disorders can manifest in conjunction with autoimmune encephalitic diseases, neoplasms, infections, or be completely idiopathic.

53%of autoimmune cerebellar ataxia

is paraneoplastic.

46%of autoimmune cerebellar ataxia patients improve

with immunotherapy.


MovementDisorders

MDS2 | Movement Disorder Evaluation, Serum TAT: 7 days

MDC2 | Movement Disorder Evaluation, Spinal Fluid TAT: 5 days

CLINICAL REFERENCES

1 Honorat JA, McKeon A. Autoimmune movement disorders: a clinical and laboratory approach. Curr Neurol Neurosci Rep. 2017;17(1):4. doi: 10.1007/s11910-017-0709-2.

2 Jones AL, Flanagan EP, Pittock SJ, et al. Responses to and outcomes of treatment of autoimmune cerebellar ataxia in adults. JAMA Neurol. 2015;72(11):1304–1312. doi:10.1001 jamaneurol.2015.2378.


ANTIBODY SYNDROME SERUM SPINAL FLUID

ANNA-1 (anti-Hu) Chorea, Ataxia • •ANNA-2 (anti-Ri) Chorea, Myoclonus • •ANNA-3 Varies • •AGNA-1 (SOX1) Varies • •PCA-1 Ataxia • •PCA-2 Varies • •CRMP-5 (anti-CV2) Chorea, Myoclonus • •Amphiphysin Stiff-Person Spectrum

Disorders• •

GAD65 Chorea, Myoclonus, Parkinsonism, Stiff-Person Spectrum Disorders, Ataxia

• •


ANTIBODY SYNDROME SERUM SPINAL FLUID

NMDA receptor Dyskinesia, Myoclonus • •LGI1 Parkinsonism • •CASPR2 Ataxia • •DPPX Stiff-Person Spectrum

Disorders• •

mGluR1 Ataxia • •P/Q and N-type calcium channel Ataxia, Chorea •

Neuronal ganglionic AChR Varies •

PCA-Tr Ataxia • •



Myelopathy

Targeted evaluations to expedite diagnosis and treatment of autoimmune myelopathy

WHAT IS AUTOIMMUNE MYELOPATHY?Patients with autoimmune myelopathy present with subacute onset and rapid progression of spinal cord symptoms (weakness, gait difficulties, loss of sensation, neuropathic pain, and bowel and bladder dysfunction). Autoimmune myelopathy evaluation of serum and spinal fluid can assist in the diagnosis and aid distinction from other causes of myelopathy (multiple sclerosis, sarcoidosis, vascular disease). Early diagnosis may assist in diagnosis of occult cancer, prompt initiation of immune therapies, or both.

NOVEL BIOMARKER FOR A TREATABLE MENINGOENCEPHALOMYELITISA novel astrocytic autoantibody, glial fibrillary acidic protein (GFAP), has recently been described by Mayo Clinic as a biomarker of a relapsing autoimmune meningoencephalomyelitis that is responsive to immunotherapies. Seropositivity distinguishes autoimmune GFAP meningoencephalomyelitis from disorders commonly considered in the differential diagnosis.

WHEN TO CONSIDER TESTINGConsider autoimmune testing for patients presenting with spinal cord symptoms and one or more of the following:

• Rapid onset and progression• Fluctuating course• Autoimmune stigmata (e.g., physical signs or personal/family history of


• History of cancer• Smoking history (20+ pack years) or other cancer risk factors• Inflammatory cerebrospinal fluid • Neuroimaging atypical for degenerative etiology• Prior treatment with immune checkpoint inhibitors

Autoimmune CNS

40% In a Mayo Clinic study, 40% of patients with GFAP-IgG

were found to have co-existing antibodies.

Myelopathy


MAC1 | Myelopathy, Autoimmune Evaluation, Spinal Fluid TAT: 5 days

MAS1 | Myelopathy, Autoimmune Evaluation, Serum TAT: 7 days

CLINICAL REFERENCES

1 Dubey D, Flanagan EP, Pittock SJ, et al. Clinical, radiologic, and prognostic features of myelitis associated with myelin oligodendrocyte glycoprotein autoantibody. JAMA Neurol. 2018 Dec 21. doi: 10.1001/jamaneurol.2018.4053.

2 Zalewski NL, Flanagan EP. Autoimmune and paraneoplastic myelopathies. Semin Neurol. Jun;38(3):278-289. doi: 10.1055/s-0038-1660856.

3 Fang B, Lennon VA, McKeon A, et al. Autoimmune glial fibrillary acidic protein astrocytopathy: A novel meningoencephalomyelitis. JAMA Neurol. 2016 Nov 1;73(11):1297-1307.

4 Flanagan EP, McKeon A, Hinson SR, et al. Glial fibrillary acidic protein immunoglobulin G as biomarker of autoimmune astrocytopathy: Analysis of 102 patients. Ann Neurol. 2017 Feb;81(2):298-309.

5 Keegan BM, Lennon VA, Pittock SJ. Autoimmune myelopathy associated with collapsin response-mediator protein-5 immunoglobulin G. Ann Neurol. 2008 Apr;63(4):531-4.

6 Weinshenker BG, Lennon VA, Wingerchuk DM, et al. Neuromyelitis optica IgG predicts relapse after longitudinally extensive transverse myelitis. Ann Neurol. 2006 Mar;59(3):566-9.





ANNA-3 • •


PCA-1 • •

PCA-2 • •


Amphiphysin • •

GAD65 • •

GFAP • •



AQP4 • •

MOG •

DPPX • •

mGluR1 • •


PCA-Tr • •



DIAGNOSING DEMYELINATING DISEASESApproximately 80% of patients with NMO are seropositive for aquaporin-4 (AQP4)-IgG. In the remaining 20% of patients, myelin oligodendrocyte glycoprotein (MOG)-IgG is detected in up to a third. Detection of MOG-IgG is diagnostic of central nervous system (CNS) inflammatory demyelination, where the clinical phenotype (NMOSD, optic neuritis, transverse myelitis, ADEM) may be similar, but the immunopathology (astrocytopathy versus oligodendrogyopathy) and clinical outcome (worse versus better) is different.

SIMILAR CHARACTERISTICS. DIFFERENT TREATMENTS.Although NMOSD and MOG-opathies can have very similar clinical and radiologic characteristics to MS, the appropriate treatments differ significantly:

• While NMOSD and MOG-opathies are treated by immunosuppressant therapy, MS is treated by immunomodulation therapy, which may worsen NMOSD.

• For patients who are AQP4 positive, optimal immunosuppressive therapy should be initiated as soon as possible (a negative result in a subject where NMOSD is suspected should receive follow-up in 3 to 6 months).

• For patients who are MOG positive, immunosuppressive therapy may be justified as soon as possible; follow-up in 6 to 12 months is recommended as persistence of MOG-IgG seropositivity predicts a relapsing course.1

A GUIDE TO ORDERING AQP4/MOG TESTING

DemyelinatingDiseases

Distinguish a spectrum of autoimmune demyelinating diseases from MS

Autoimmune CNS

OPTIC NERVE OR SPINAL CORD INVOLVEMENT

SYMPTOMS OUTSIDE OPTIC NERVE OR SPINAL CORD

DEFINITELY ORDER

When either a long spinal cord lesion

is present or multiple episodes of optic

neuritis occur

When any symptoms below are present

in combination with either optic neuritis

or spinal cord lesions, or when acute

disseminated encephalomyelitis

is suspected

CONSIDER ORDERING

When either a short spinal cord lesion

is present or single episode of optic

neuritis occur

When any of the following symptoms

are present:

• Area postrema syndrome: episode

of otherwise unexplained hiccups

or nausea and vomiting

• Acute brainstem syndrome

• Symptomatic narcolepsy or acute

diencephalic clinical syndrome with

NMOSD-typical diencephalic

MRI lesions

• Symptomatic cerebral syndrome

with NMOSD-typical brain lesions

DemyelinatingDiseases

A guide to testing and methodology

CDS1 | CNS Demyelinating Disease Evaluation, Serum TAT: 5 days

NMOFS | Neuromyelitis Optica (NMO)/Aquaporin-4-IgG Fluorescence-Activated Cell Sorting (FACS) Assay, Serum TAT: 5 days

MOGFS | Myelin Oligodendrocyte Glycoprotein (MOG-IgG1) Fluorescence-Activated Cell Sorting (FACS) Assay, Serum TAT: 5 days

CLINICAL REFERENCES

1 Peschl P, Bradl M, Hoftberger R, et al. Myelin oligodendrocyte glycoprotein: deciphering a target in inflammatory demyelinating diseases. Front Immunol. 2017;8:529.

2 Waters PJ, Pittock SJ, Kommorwski L, et al. A multicenter comparison of MOG-IgG cell-based assays. Neurology. 2019 Mar 12;92(11):e1250-e1255.

3 Waters PJ, McKeon A, Leite MI, et al. Serologic diagnosis of NMO: a multicenter comparison of aquaporin-4-IgG assays. Neurology. 2012;78(9):665-671.

4 Pittock SJ, Lucchinetti CF. Neuromyelitis optica and the evolving spectrum of autoimmune aquaporin-4 channelopathies: a decade later. Ann N Y Acad Sci. 2016;1366(1):20-39.

5 Hyun JW, Woodhall MR, Kim SH, et al. Longitudinal analysis of myelin oligodendrocyte glycoprotein antibodies in CNS inflammatory diseases. J Neurol Neurosurg Psychiatry. 2017;88(10):811-817.

6 Waters PJ, McKeon A, Leite MI, et al. Serologic diagnosis of NMO: a multicenter comparison of aquaporin-4-IgG assays. Neurology. 2012;78(9):665-671.

7 Reindl M, Jarius S, Rostasy K, Berger T. Myelin oligodendrocyte glycoprotein antibodies: How clinically useful are they? Curr Opin Neurol. 2017;30(3):295-301.

FACS: A SUPERIOR METHOD OF TESTINGMayo Clinic has developed the only fluorescence activated cell sorting (FACS) live cell-binding assay that is currently available in the U.S. for antibody detection of AQP4 and MOG. FACS is recommended by international leaders in neuroimmunology for its increased sensitivity and specificity.

AQP4 by FACSThe likelihood of having a false-positive result with ELISA methodology is at least 5x greater when compared with the Mayo Clinic cell-binding assay.3

SENSITIVITY3 SPECIFICITY

FACS LIVE CELL-BINDING ASSAY

>80% >99%

ELISA 60–65% 99%

INDIRECT IMMUNOFLUORESCENCE

50–55% >99%

MOG by FACSA recent study found that live cell-based methodologies had superior PPVs to the fixed cell assays, indicating that positive results in these assays are more reliable indicators of MOG autoimmune spectrum disorders.2

Your partner in autoimmune neurology testing › ... › 07 › Autoimmune-Neurology-Br… ·...

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Transcript of Your partner in autoimmune neurology testing › ... › 07 › Autoimmune-Neurology-Br… ·...