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HelpTest Code DMS2 Dementia, Autoimmune/Paraneoplastic Evaluation, Serum
Ordering Guidance
Multiple neurological phenotype-specific autoimmune/paraneoplastic evaluations are available. For more information as well as phenotype-specific testing options, refer to Autoimmune Neurology Test Ordering Guide.
When more than one evaluation is ordered on the same order number, the duplicate test will be canceled.
For a list of antibodies performed with each evaluation, see Autoimmune Neurology Antibody Matrix.
This test should not be requested for patients who have recently received radioisotopes, therapeutically or diagnostically, because of potential assay interference. The specific waiting period before specimen collection will depend on the isotope administered, the dose given, and the clearance rate in the individual patient. Specimens will be screened for radioactivity prior to analysis. Radioactive specimens received in the laboratory will be held 1 week and assayed if sufficiently decayed or canceled if radioactivity remains.
Necessary Information
Provide the following information:
-Relevant clinical information
-Ordering healthcare professional's name, phone number, mailing address, and e-mail address
Specimen Required
Patient Preparation:
1. For optimal antibody detection, collect specimen before starting immunosuppressant medication or intravenous immunoglobulin treatment.
2. For 24 hours before specimen collection, patient should not receive general anesthetic or take muscle-relaxant drugs.
Supplies: Sarstedt Aliquot Tube, 5 mL (T914)
Collection Container/Tube:
Preferred: Red top
Acceptable: Serum gel
Submission Container/Tube: Plastic vial
Specimen Volume: 4 mL Serum
Collection Instructions: Centrifuge and aliquot serum into a plastic vial.
Forms
If not ordering electronically, complete, print, and send a Neurology Specialty Testing Client Test Request (T732) with the specimen.
Secondary ID
92114Useful For
Investigating new onset dementia and cognitive impairment plus 1 or more of the following using serum specimens:
-Rapid onset and progression
-Fluctuating course
-Psychiatric accompaniments (psychosis, hallucinations)
-Movement disorder (myoclonus, tremor, dyskinesias)
-Headache
-Autoimmune stigmata (personal history or family history or signs of diabetes mellitus, thyroid disorder, vitiligo, poliosis [premature graying], myasthenia gravis, rheumatoid arthritis, systemic lupus erythematosus)
-Smoking history (20 or more pack-years) or other cancer risk factors
-History of cancer
-Inflammatory cerebrospinal fluid
-Neuroimaging findings atypical for degenerative etiology
Profile Information
| Test ID | Reporting Name | Available Separately | Always Performed |
|---|---|---|---|
| ADMSI | Dementia, Interpretation, S | No | Yes |
| AK5IS | AK5 Ab IFA, S | No | Yes |
| AMPCS | AMPA-R Ab CBA, S | No | Yes |
| AMPHS | Amphiphysin Ab, S | No | Yes |
| AGN1S | Anti-Glial Nuclear Ab, Type 1 | No | Yes |
| ANN1S | Anti-Neuronal Nuclear Ab, Type 1 | No | Yes |
| ANN2S | Anti-Neuronal Nuclear Ab, Type 2 | No | Yes |
| ANN3S | Anti-Neuronal Nuclear Ab, Type 3 | No | Yes |
| CS2CS | CASPR2-IgG CBA, S | No | Yes |
| CRMS | CRMP-5-IgG, S | No | Yes |
| DPPCS | DPPX Ab CBA, S | No | Yes |
| GABCS | GABA-B-R Ab CBA, S | No | Yes |
| GD65S | GAD65 Ab Assay, S | Yes | Yes |
| IG5CS | IgLON5 CBA, S | No | Yes |
| LG1CS | LGI1-IgG CBA, S | No | Yes |
| GL1IS | mGluR1 Ab IFA, S | No | Yes |
| GL5IS | mGluR5 Ab IFA, S | No | Yes |
| NCDIS | Neurochondrin IFA, S | No | Yes |
| NMDCS | NMDA-R Ab CBA, S | No | Yes |
| PDEIS | PDE10A Ab IFA, S | No | Yes |
| PCAB2 | Purkinje Cell Cytoplasmic Ab Type 2 | No | Yes |
| PCATR | Purkinje Cell Cytoplasmic Ab Type Tr | No | Yes |
| T46IS | TRIM46 Ab IFA, S | No | Yes |
Reflex Tests
| Test ID | Reporting Name | Available Separately | Always Performed |
|---|---|---|---|
| AGNBS | AGNA-1 Immunoblot, S | No | No |
| AGNTS | AGNA-1 Titer, S | No | No |
| AK5CS | AK5 Ab CBA, S | No | No |
| AK5TS | AK5 Ab IFA Titer, S | No | No |
| AMPIS | AMPA-R Ab IF Titer Assay, S | No | No |
| APHTS | Amphiphysin Ab Titer, S | No | No |
| AMIBS | Amphiphysin Immunoblot, S | No | No |
| AN1BS | ANNA-1 Immunoblot, S | No | No |
| AN1TS | ANNA-1 Titer, S | No | No |
| AN2BS | ANNA-2 Immunoblot, S | No | No |
| AN2TS | ANNA-2 Titer, S | No | No |
| AN3TS | ANNA-3 Titer, S | No | No |
| CRMTS | CRMP-5-IgG Titer, S | No | No |
| DPPTS | DPPX Ab IFA Titer, S | No | No |
| GABIS | GABA-B-R Ab IF Titer Assay, S | No | No |
| IG5TS | IgLON5 IFA Titer, S | No | No |
| MP1BS | MAP1B Immunoblot, S | No | No |
| GL1CS | mGluR1 Ab CBA, S | No | No |
| GL1TS | mGluR1 Ab IFA Titer, S | No | No |
| GL5CS | mGluR5 Ab CBA, S | No | No |
| GL5TS | mGluR5 Ab IFA Titer, S | No | No |
| NCDCS | Neurochondrin CBA, S | No | No |
| NCDTS | Neurochondrin IFA Titer, S | No | No |
| NMDIS | NMDA-R Ab IF Titer Assay, S | No | No |
| PC2TS | PCA-2 Titer, S | No | No |
| PCTBS | PCA-Tr Immunoblot, S | No | No |
| PCTTS | PCA-Tr Titer, S | No | No |
| PDETS | PDE10A Ab IFA Titer, S | No | No |
| T46CS | TRIM46 Ab CBA, S | No | No |
| T46TS | TRIM46 Ab IFA Titer, S | No | No |
| CRMWS | CRMP-5-IgG Western Blot, S | No | No |
Testing Algorithm
If the IFA pattern suggests adenylate kinase 5 protein (AK5) antibody, then AK5 IFA titer and AK5 CBA will be performed at an additional charge.
If the indirect immunofluorescence assay (IFA) pattern suggests antiglial nuclear antibody (AGNA)-1, then the AGNA-1 immunoblot and AGNA-1 IFA titer will be performed at an additional charge.
If the IFA pattern suggests antineuronal nuclear antibody type 1 (ANNA-1), then the ANNA-1 immunoblot, ANNA-1 IFA titer, and ANNA-2 immunoblot will be performed at an additional charge.
If the IFA pattern suggests ANNA-2 antibody, then the ANNA-2 immunoblot, ANNA-2 IFA titer, and ANNA-1 immunoblot will be performed at an additional charge.
If client requests or if the IFA pattern suggests ANNA-3 antibody, then the ANNA-3 IFA titer will be performed at an additional charge.
If the IFA pattern suggests amphiphysin antibody, then the amphiphysin immunoblot and amphiphysin IFA titer will be performed at an additional charge.
If the IFA patterns suggest collapsin response-mediator protein 5 (CRMP-5)-IgG, then the CRMP-5-IgG Western Blot and CRMP-5-IgG IFA titer will be performed at an additional charge.
If the AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid 9) receptor antibody cell-binding assay (CBA) result is positive, then the AMPA receptor antibody IFA titer will be performed at an additional charge.
If the contactin-associated protein-like-2 (CASPR2)-receptor antibody CBA result is positive, then the CRMP-5-IgG Western blot will be performed at an additional charge.
If the gamma-aminobutyric acid B (GABA-B) receptor antibody CBA result is positive, then the GABA-B receptor antibody IF titer will be performed at an additional charge.
If the N-methyl-D-aspartate (NMDA)-receptor antibody CBA result is positive, then NMDA receptor antibody IF titer will be performed at an additional charge.
If the IFA pattern suggests PCA-Tr antibody, then the PCA-Tr immunoblot and PCA-Tr IFA titer will be performed at an additional charge.
If dipeptidyl-peptidase-like protein-6 (DPPX) antibody CBA result is positive, then the DPPX IFA titer will be performed at an additional charge.
If the IFA pattern suggests metabotropic glutamate receptor 1 (mGluR1) antibody, then the mGluR1 antibody CBA and mGluR1 IFA titer will be performed at an additional charge.
If the IFA pattern suggests metabotropic glutamate receptor 5 (mGluR5) antibody, then the mGluR5 antibody CBA and mGluR5 IFA titer will be performed at an additional charge.
If the IgLON5 antibody CBA result is positive, then the IgLON5 IFA titer will be performed at an additional charge.
If the IFA pattern suggests neurochondrin antibody, then the neurochondrin antibody CBA and neurochondrin IFA titer will be performed at an additional charge.
If the IFA pattern suggests tripartite motif-containing protein 46 (TRIM46) antibody, then the TRIM46 antibody CBA and TRIM46 IFA titer will be performed at an additional charge.
If the IFA pattern suggests phosphodiesterase 10A (PDE10A) antibody, then the PDE10A antibody IFA titer will be performed at an additional charge.
For more information see Autoimmune/Paraneoplastic Dementia Evaluation Algorithm-Serum.
Special Instructions
Method Name
ADMSI: Technical Interpretation
AMPCS, CS2CS, DPPCS, GABCS, IG5CS, LG1CS, NMDCS, AK5CS, GL1CS, GL5CS, NCDCS, T46CS: Cell Binding Assay (CBA)
AGN1S, AK5IS, AMPHS, ANN1S, ANN2S, ANN3S, CRMS, GL1IS, GL5IS, NCDIS, PCAB2, PCATR, PDEIS, T46IS, AGNTS, AK5TS, AMPIS, AN1TS, AN2TS, AN3TS, APHTS, CRMTS, DPPTS, GABIS, GL1TS, GL5TS, IG5TS, NCDTS, NMDIS, PC2TS, PCTTS, PDETS, T46TS: Indirect Immunofluorescence Assay (IFA)
GD65S: Radioimmunoassay (RIA)
CRMWS: Western Blot (WB)
AGNBS, AMIBS, AN1BS, AN2BS, MP1BS, PCTBS: Immunoblot (IB)
Reporting Name
Dementia, Autoimm/Paraneo, SSpecimen Type
SerumSpecimen Minimum Volume
Serum: 2.5 mL
Specimen Stability Information
| Specimen Type | Temperature | Time |
|---|---|---|
| Serum | Refrigerated (preferred) | 28 days |
| Frozen | 28 days | |
| Ambient | 72 hours |
Reject Due To
| Gross hemolysis | Reject |
| Gross lipemia | Reject |
| Gross icterus | Reject |
Clinical Information
The rapid identification of subacute cognitive decline as autoimmune dementia facilitates optimum treatment with immunotherapy and an expedited search for a limited stage of cancer in some patients. Traditionally, neurologists have been reluctant to consider a diagnosis of an autoimmune cognitive disorder in the absence of delirium. However, some recent case series and clinical-serologic observations have suggested a growing appreciation for autoimmune neurologic disorders presenting with features of a rapidly progressive dementia rather than delirium. These disorders can affect all age groups.
Unfortunately, these potentially reversible conditions may be misdiagnosed as being progressive neurodegenerative (currently irreversible) disorders with devastating consequences for the patient. In the evaluation of a patient with cognitive decline, clinicians should consider the possibility of an autoimmune etiology on their list of differential diagnoses. The importance of not overlooking this possibility rests in the experience that these patients have a potentially immunotherapy-responsive, reversible disorder. The development and widespread availability of neural antibody marker testing has changed this perspective so that other presenting symptoms, such as personality change, executive dysfunction, and psychiatric symptoms, are increasingly recognized in an autoimmune context.
Clues that are helpful in identifying patients with an autoimmune dementia can be summarized as a triad of:
-Suspicious clinical features (a subacute onset of symptoms, a rapidly progressive course, and fluctuating symptoms) and radiological findings
-Detection of cerebrospinal fluid (CSF) or serological biomarkers of autoimmunity
-Response to immunotherapy
Detection of neural autoantibodies in serum or CSF serves 2 purposes: to inform the physician of a likely autoimmune etiology and to raise suspicion for a paraneoplastic cause. The neurological associations of neural autoantibodies tend to be diverse and multifocal, although certain syndromic associations may apply. For example, LGI1 (leucine-rich, glioma inactivated 1) antibody was initially considered to be specific for autoimmune limbic encephalitis, but, over time, other presentations have been reported, including rapidly progressive course of cognitive decline mimicking neurodegenerative dementia.
Since neurological presentations are often multifocal and diverse, comprehensive antibody testing is usually more informative than testing for 1 or 2 selected antibodies. Some of the antibodies are highly predictive of an unsuspected underlying cancer. For example, small-cell lung carcinoma (antineuronal nuclear antibody-type 1 [ANNA-1]; collapsin response-mediator protein-5 neuronal [CRMP-5-IgG]), ovarian teratoma (N-methyl-D-aspartate receptor: NMDA-R), and thymoma (CRMP-5 IgG).
Also, a profile of seropositivity for multiple autoantibodies may be informative for cancer type. For example, in a patient presenting with a rapidly progressive dementia who has CRMP-5-IgG, and subsequent testing reveals muscle acetylcholine receptor (AChR) binding antibody, the findings should raise a high suspicion for thymoma. If an associated tumor is found, its resection or ablation optimizes the neurological outcome.
Antibody testing on CSF is additionally helpful, particularly when serum testing is negative, although, in some circumstances, testing both serum and CSF simultaneously is pertinent. Testing of CSF is recommended for some antibodies (eg, NMDA-R antibody and glial fibrillary acidic protein [GFAP]-IgG) because CSF testing is more sensitive and specific.
Reference Values
|
Test ID |
Reporting name |
Methodology |
Reference value |
|
ADMSI |
Dementia, Interpretation, S |
Technical interpretation |
Interpretive report |
|
AK5IS |
AK5 Ab IFA, S |
IFA |
Negative |
|
AMPCS |
AMPA-R Ab CBA, S |
CBA |
Negative |
|
AMPHS |
Amphiphysin Ab, S |
IFA |
Negative |
|
AGN1S |
Anti-Glial Nuclear Ab, Type 1 |
IFA |
Negative |
|
ANN1S |
Anti-Neuronal Nuclear Ab, Type 1 |
IFA |
Negative |
|
ANN2S |
Anti-Neuronal Nuclear Ab, Type 2 |
IFA |
Negative |
|
ANN3S |
Anti-Neuronal Nuclear Ab, Type 3 |
IFA |
Negative |
|
CS2CS |
CASPR2-IgG CBA, S |
CBA |
Negative |
|
CRMS |
CRMP-5-IgG, S |
IFA |
Negative |
|
DPPCS |
DPPX Ab CBA, S |
CBA |
Negative |
|
GABCS |
GABA-B-R Ab CBA, S |
CBA |
Negative |
|
GD65S |
GAD65 Ab Assay, S |
RIA |
≤0.02 nmol/L |
|
IG5CS |
IgLON5 CBA, S |
CBA |
Negative |
|
LG1CS |
LGI1-IgG CBA, S |
CBA |
Negative |
|
GL1IS |
mGluR1 Ab IFA, S |
IFA |
Negative |
|
GL5IS |
mGluR5 Ab IFA, S |
IFA |
Negative |
|
NCDIS |
Neurochondrin IFA, S |
IFA |
Negative |
|
NMDCS |
NMDA-R Ab CBA, S |
CBA |
Negative |
|
PDEIS |
PDE10A Ab IFA, S |
IFA |
Negative |
|
PCAB2 |
Purkinje Cell Cytoplasmic Ab Type 2 |
IFA |
Negative |
|
PCATR |
Purkinje Cell Cytoplasmic Ab Type Tr |
IFA |
Negative |
|
T46IS |
TRIM46 Ab IFA, S |
IFA |
Negative |
Reflex Information:
|
Test ID |
Reporting name |
Methodology |
Reference value |
|
AGNBS |
AGNA-1 Immunoblot, S |
IB |
Negative |
|
AGNTS |
AGNA-1 Titer, S |
IFA |
<1:240 |
|
AK5CS |
AK5 Ab CBA, S |
CBA |
Negative |
|
AK5TS |
AK5 Ab IFA Titer, S |
IFA |
<1:240 |
|
AMPIS |
AMPA-R Ab IF Titer Assay, S |
IFA |
<1:240 |
|
APHTS |
Amphiphysin Ab Titer, S |
IFA |
<1:240 |
|
AMIBS |
Amphiphysin Immunoblot, S |
IB |
Negative |
|
AN1BS |
ANNA-1 Immunoblot, S |
IB |
Negative |
|
AN1TS |
ANNA-1 Titer, S |
IFA |
<1:240 |
|
AN2BS |
ANNA-2 Immunoblot, S |
IB |
Negative |
|
AN2TS |
ANNA-2 Titer, S |
IFA |
<1:240 |
|
AN3TS |
ANNA-3 Titer, S |
IFA |
<1:240 |
|
CRMTS |
CRMP-5-IgG Titer, S |
IFA |
<1:240 |
|
CRMWS |
CRMP-5-IgG Western Blot, S |
WB |
Negative |
|
DPPTS |
DPPX Ab IFA Titer, S |
IFA |
<1:240 |
|
GABIS |
GABA-B-R Ab IF Titer Assay, S |
IFA |
<1:240 |
|
IG5TS |
IgLON5 IFA Titer, S |
IFA |
<1:240 |
|
MP1BS |
MAP1B Immunoblot, S |
IB |
Negative |
|
GL1CS |
mGluR1 Ab CBA, S |
CBA |
Negative |
|
GL1TS |
mGluR1 Ab IFA Titer, S |
IFA |
<1:240 |
|
GL5CS |
mGluR5 Ab CBA, S |
CBA |
Negative |
|
GL5TS |
mGluR5 Ab IFA Titer, S |
IFA |
<1:240 |
|
NCDCS |
Neurochondrin CBA, S |
CBA |
Negative |
|
NCDTS |
Neurochondrin IFA Titer, S |
IFA |
<1:240 |
|
NMDIS |
NMDA-R Ab IF Titer Assay, S |
IFA |
<1:240 |
|
PC2TS |
PCA-2 Titer, S |
IFA |
<1:240 |
|
PCTBS |
PCA-Tr Immunoblot, S |
IB |
Negative |
|
PCTTS |
PCA-Tr Titer, S |
IFA |
<1:240 |
|
PDETS |
PDE10A Ab IFA Titer, S |
IFA |
<1:240 |
|
T46CS |
TRIM46 Ab CBA, S |
CBA |
Negative |
|
T46TS |
TRIM46 Ab IFA Titer, S |
IFA |
<1:240 |
*Methodology abbreviations used:
Cell-binding assay (CBA)
Immunoblot (IB)
Immunofluorescence assay (IFA)
Radioimmunoassay (RIA)Western Blot (WB)
Interpretation
Antibodies specific for neuronal, glial, or muscle proteins are valuable serological markers of autoimmune epilepsy and of a patient's immune response to cancer. These autoantibodies are not found in healthy subjects and are usually accompanied by subacute neurological symptoms and signs. It is not uncommon for more than 1 of the following autoantibodies to be detected in patients with autoimmune dementia:
-Plasma membrane antibodies (N-methyl-D-aspartate [NMDA] receptor; 2-amino-3-[5-methyl-3-oxo-1,2-oxazol-4-yl] propanoic acid [AMPA] receptor; gamma-amino butyric acid [GABA-B] receptor); these autoantibodies are all potential effectors of dysfunction
-Neuronal nuclear autoantibody, type 1 (ANNA-1) or type 3 (ANNA-3)
-Neuronal or muscle cytoplasmic antibodies (amphiphysin, Purkinje cell antibody-type 2 [PCA-2], collapsin response-mediator protein-5 neuronal [CRMP-5-IgG], or glutamic acid decarboxylase [GAD65] antibody)
Cautions
Negative results do not exclude autoimmune dementia or cancer.
This test does not detect Ma1 or Ma2 antibodies (also known as MaTa). Ma2 antibody has been described in patients with brainstem and limbic encephalitis in the context of testicular germ cell neoplasms. Scrotal ultrasound is advisable in men who present with unexplained subacute encephalitis.
Intravenous immunoglobulin (IVIg) treatment prior to the serum collection may cause a false-positive result.
Clinical Reference
1. Sechi E, Flanagan EP. Diagnosis and management of autoimmune dementia. Curr Treat Options Neurol. 2019;21(3):11. Published 2019 Feb 27. doi:10.1007/s11940-019-0550-9
2. Bastiaansen AEM, van Steenhoven RW, de Bruijn MAAM, et al. Autoimmune encephalitis resembling dementia syndromes. Neurol Neuroimmunol Neuroinflamm. 2021;8(5):e1039. Published 2021 Aug 2. doi:10.1212/NXI.0000000000001039
3. Flanagan EP, Geschwind MD, Lopez-Chiriboga AS, et al. Autoimmune encephalitis misdiagnosis in adults. JAMA Neurol. 2023;80(1):30-39. doi:10.1001/jamaneurol.2022.4251
4. Orozco E, Valencia-Sanchez C, Britton J, et al. Autoimmune encephalitis criteria in clinical practice. Neurol Clin Pract. 2023;13(3):e200151. doi:10.1212/CPJ.0000000000200151
5. Bastiaansen AEM, van Steenhoven RW, Te Vaarwerk ES, et al. Antibodies associated with autoimmune encephalitis in patients with presumed neurodegenerative dementia. Neurol Neuroimmunol Neuroinflamm. 2023;10(5):e200137. Published 2023 Jun 13. doi:10.1212/NXI.0000000000200137
Method Description
Cell-Binding Assay:
Patient specimen is applied to a composite slide containing transfected and nontransfected EU90 cells. After incubation and washing, fluorescein-conjugated goat-antihuman IgG is applied to detect the presence of patient IgG binding.(Klein CJ, Lennon VA, Aston PA, et al. Insights from LGI1 and CASPR2 potassium channel complex autoantibody subtyping. JAMA Neurol 2013;70[2]:229-234; package insert: IIFT: Neurology Mosaics, Instructions for the indirect immunofluorescence test. EUROIMMUN; FA_112d-1_A_UK_C13, 02/25/2019)
Indirect Immunofluorescence Assay:
The patient's specimen is tested by a standardized immunofluorescence assay that uses a composite frozen section of mouse cerebellum, kidney, and gut tissues. After incubation with the specimen and washing, fluorescein-conjugated goat-antihuman IgG is applied. Neuron-specific autoantibodies are identified by their characteristic fluorescence staining patterns. Specimens that are scored positive for any neuronal nuclear or cytoplasmic autoantibody are titrated. Interference by coexisting non-neuron-specific autoantibodies can usually be eliminated by serologic absorption.(Honorat JA, Komorowski L, Josephs KA, et al. IgLON5 antibody: Neurological accompaniments and outcomes in 20 patients. Neurol Neuroimmunol Neuroinflamm. 2017;4[5]:e385. Published 2017 Jul 18. doi:10.1212/NXI.0000000000000385)
Radioimmunoassay:
(125)I-labeled recombinant human antigens or labeled receptors are incubated with patient specimen. After incubation, anti-human IgG is added to form an immunoprecipitate. The amount of (125)I-labeled antigen in the immunoprecipitate is measured using a gamma-counter. The amount of gamma emission in the precipitate is proportional to the amount of antigen-specific IgG in the specimen. Results are reported as units of precipitated antigen (nmol) per liter of patient specimen.(Griesmann GE, Kryzer TJ, Lennon VA. Autoantibody profiles of myasthenia gravis and Lambert-Eaton myasthenic syndrome. In: Rose NR, Hamilton RG, eds. Manual of Clinical and Laboratory Immunology. 6th ed. ASM Press; 2002:1005-1012; Walikonis JE, Lennon VA. Radioimmunoassay for glutamic acid decarboxylase [GAD65] autoantibodies as a diagnostic aid for stiff-man syndrome and a correlate of susceptibility to type 1 diabetes mellitus. Mayo Clin Proc. 1998;73[12]:1161-1166; 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)
Western Blot:
Neuronal antigens extracted aqueously from adult rat cerebellum, full-length recombinant human collapsin response-mediator protein-5 (CRMP-5), or full-length recombinant human amphiphysin protein is denatured, reduced, and separated by electrophoresis on 10% polyacrylamide gel. IgG is detected autoradiographically by enhanced chemiluminescence.(Yu Z, Kryzer TJ, Griesmann GE, et al. CRMP-5 neuronal autoantibody: marker of lung cancer and thymoma-related autoimmunity. Ann Neurol. 2001;49[2]:146-154; Dubey D, Jitprapaikulsan J, Bi H, et al. Amphiphysin-IgG autoimmune neuropathy: A recognizable clinicopathologic syndrome. Neurology. 2019;93[20]:e1873-e1880. doi:10.1212/WNL.0000000000008472)
Immunoblot for AGNA-1, amphiphysin, ANNA-1, ANNA-2, and PCA-Tr:
All steps are performed at room temperature (18 to 28° C) utilizing the EUROBlot One instrument. Diluted patient sample is added to test strips (strips containing recombinant antigen manufactured and purified using biochemical methods) in individual channels and incubated for 30 minutes. Positive samples will bind to the purified recombinant antigen and negative samples will not bind. Strips are washed to remove unbound antibodies and then incubated with anti-human IgG antibodies (alkaline phosphatase-labelled) for 30 minutes. The strips are again washed to remove unbound anti-human IgG antibodies and nitroblue tetrazolium chloride/5-bromo-4-chloro-3-indolylphosphate (NBT/BCIP) substrate is added. Alkaline phosphatase enzyme converts the soluble substrate into a colored insoluble product on the membrane to produces a black band. Strips are digitized via picture capture on the EUROBlot One instrument and evaluated with the EUROLineScan software.(O'Connor K, Waters P, Komorowski L, et al. GABAA receptor autoimmunity: A multicenter experience. Neurol Neuroimmunol Neuroinflamm. 2019;6[3]:e552. doi:10.1212/NXI.0000000000000552)
Immunoblot for MAP1B:
Test strips are incubated with appropriately diluted sample, prepared to meet the assay's required end-dilution for each specimen type. Samples and controls are added directly to the strips, ensuring they are fully covered with dilution buffer, then mixed gently and incubated for 60 minutes at room temperature on a rocking platform. After incubation, the strips undergo a series of wash steps using diluted wash buffer, followed by a 30-minute incubation with a ready-to-use alkaline phosphatase-labeled IgG conjugate. The strips are washed again using the same procedure, then incubated with a ready-to-use substrate solution for 20 minutes at room temperature. The reaction is stopped by rinsing with distilled water through several wash cycles. Strips are then placed on absorbent material and allowed to dry fully, generally requiring at least two hours. Results are interpreted only after the strips have dried completely, and dried strips are stored protected from light.(Package insert: PCA-2 line assay. ravo Diagnostika GmbH; 05/2023)
Day(s) Performed
Report Available
8 to 12 daysSpecimen Retention Time
2 daysPerforming Laboratory
Mayo Clinic Laboratories in Rochester
Test Classification
This test was developed and its performance characteristics determined by Mayo Clinic in a manner consistent with CLIA requirements. It has not been cleared or approved by the US Food and Drug Administration.CPT Code Information
86255 x 21
86341
84182 AGNBS (if appropriate)
86256 AGNTS (if appropriate)
86255 AK5CS (if appropriate)
86256 AK5TS (if appropriate)
86256 AMPIS (if appropriate)
86256 APHTS (if appropriate)
84182 AMIBS (if appropriate)
84182 AN1BS (if appropriate)
86256 AN1TS (if appropriate)
84182 AN2BS (if appropriate)
86256 AN2TS (if appropriate)
86256 AN3TS (if appropriate)
86256 CRMTS (if appropriate)
84182 CRMWS (if appropriate)
86256 DPPTS (if appropriate)
86256 GABIS (if appropriate)
86256 IG5TS (if appropriate)
84182 MP1BS (if appropriate)
86255 GL1CS (if appropriate)
86256 GL1TS (if appropriate)
86255 GL5CS (if appropriate)
86256 GL5TS (if appropriate)
86255 NCDCS (if appropriate)
86256 NCDTS (if appropriate)
86256 NMDIS (if appropriate)
86256 PC2TS (if appropriate)
84182 PCTBS (if appropriate)
86256 PCTTS (if appropriate)
86256 PDETS (if appropriate)
86255 T46CS (if appropriate)
86256 T46TS (if appropriate)
LOINC Code Information
| Test ID | Test Order Name | Order LOINC Value |
|---|---|---|
| DMS2 | Dementia, Autoimm/Paraneo, S | 94696-2 |
| Result ID | Test Result Name | Result LOINC Value |
|---|---|---|
| 61516 | NMDA-R Ab CBA, S | 93503-1 |
| 61518 | AMPA-R Ab CBA, S | 93489-3 |
| 61519 | GABA-B-R Ab CBA, S | 93428-1 |
| 606950 | IgLON5 CBA, S | 96478-3 |
| 623395 | mGluR5 Ab IFA, S | In Process |
| 623399 | AK5 Ab IFA, S | In Process |
| 615867 | Neurochondrin IFA, S | 101452-1 |
| 616445 | TRIM46 Ab IFA, S | 105525-0 |
| 620068 | PDE10A Ab IFA, S | 103842-1 |
| 34255 | Dementia, Interpretation, S | 69048-7 |
| 64279 | LGI1-IgG CBA, S | 94287-0 |
| 64281 | CASPR2-IgG CBA, S | 94285-4 |
| 64933 | DPPX Ab CBA, S | 94676-4 |
| 64928 | mGluR1 Ab IFA, S | 94347-2 |
| 89080 | AGNA-1, S | 84927-3 |
| 81722 | Amphiphysin Ab, S | 72327-0 |
| 80150 | ANNA-1, S | 33615-6 |
| 80776 | ANNA-2, S | 43187-4 |
| 83137 | ANNA-3, S | 43102-3 |
| 83077 | CRMP-5-IgG, S | 72504-4 |
| 81596 | GAD65 Ab Assay, S | 94345-6 |
| 83138 | PCA-2, S | 84925-7 |
| 83076 | PCA-Tr, S | 84926-5 |
| 618894 | IFA Notes | 48767-8 |