The spectrum of antineuronal autoantibodies in a series of neurological patients.
The aim of the present study is to identify the range of neurological disorders expressing antineuronal antibodies, evaluate the number of different patterns of reactivity that can be detected, and analyse the contribution of these studies to the identification of subgroups of patients. The records of 882 patients were reviewed and their sera and cerebrospinal fluids tested for antineuronal antibodies. Patients were initially divided into four groups according to suspected clinical diagnosis. Autoantibodies were detected by immunohistochemistry, Western blot of gradient-separated neuronal and recombinant proteins and by RIA. Cerebellar degeneration and sensory neuropathies were the most common neurological disorders in which paraneoplastic-related anti-neuronal antibodies were detected. However, in addition to PCA1/anti-Yo and ANNA1/anti-Hu antibodies, we found other reactivities in six patients with cerebellar degeneration: anti-GAD in three females and atypical in the other cases. The widest range of different anti-neuronal antibodies was detected in patients with peripheral sensory neuropathy. Few patients with Stiff-Person syndrome, temporal lobe epilepsy and myoclonus harboured anti-GAD antibodies. Atypical antibodies were detected in single cases with motor neuron disorder and multiple system atrophy. No anti-neuronal antibodies were detected in patients with neurological complications of connective tissue disorders other than Sjögren's syndrome, or in neurological diseases other than motor neuron disease and multiple system atrophy. Our study shows that the spectrum of neurological disorders in which anti-neuronal antibodies can be detected is wider than previously thought. In addition, we found patterns of neuronal staining and Western blot reactivity that differed from those so far reported. This may permit identification of subgroups of patients in whom strategies directed at removing and/or suppressing antibody production could be of some benefit.
Vianello
M
M
Department of Neurological and Psychiatric Sciences, Second Neurological Clinic, University of Padua, via Facciolati 71, Padua 35127, Italy.
Vitaliani
R
R
Pezzani
R
R
Nicolao
P
P
Betterle
C
C
Keir
G
G
Thompson
E J
EJ
Tavolato
B
B
Scaravilli
F
F
Giometto
B
B
D000912:Antibodies, Neoplasm / Q000378:metabolism; D001323:Autoantibodies / Q000276:immunology*; D015153:Blotting, Western / Q000379:methods; D004268:DNA-Binding Proteins / Q000276:immunology / Q000378:metabolism; D051959:ELAV Proteins; D005260:Female; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D009363:Neoplasm Proteins / Q000276:immunology / Q000378:metabolism; D009419:Nerve Tissue Proteins; D009422:Nervous System Diseases / Q000145:classification / Q000276:immunology*; D009474:Neurons / Q000276:immunology*; D016601:RNA-Binding Proteins / Q000276:immunology / Q000378:metabolism; D011863:Radioimmunoassay / Q000379:methods
D000912:Antibodies, Neoplasm; D001323:Autoantibodies; C095184:CDR2 protein, human; D004268:DNA-Binding Proteins; D051959:ELAV Proteins; D009363:Neoplasm Proteins; D009419:Nerve Tissue Proteins; D016601:RNA-Binding Proteins; D005968:Glutamate Decarboxylase