scholarly journals Seizures associated with antibodies against cell surface antigens are acute symptomatic and not indicative of epilepsy: insights from long-term data

Author(s):  
Anna Rada ◽  
Robert Birnbacher ◽  
Claudio Gobbi ◽  
Martin Kurthen ◽  
Albert Ludolph ◽  
...  

Abstract Background Clinicians have questioned whether any disorder involving seizures and neural antibodies should be called “(auto)immune epilepsy.” The concept of “acute symptomatic seizures” may be more applicable in cases with antibodies against neural cell surface antigens. We aimed at determining the probability of achieving seizure-freedom, the use of anti-seizure medication (ASM), and immunotherapy in patients with either constellation. As a potential pathophysiological correlate, we analyzed antibody titer courses. Methods Retrospective cohort study of 39 patients with seizures and neural antibodies, follow-up ≥ 3 years. Results Patients had surface antibodies against the N-methyl-d-aspartate receptor (NMDAR, n = 6), leucine-rich glioma inactivated protein 1 (LGI1, n = 11), contactin-associated protein-2 (CASPR2, n = 8), or antibodies against the intracellular antigens glutamic acid decarboxylase 65 kDa (GAD65, n = 13) or Ma2 (n = 1). Patients with surface antibodies reached first seizure-freedom (88% vs. 7%, P < 0.001) and terminal seizure-freedom (80% vs. 7%, P < 0.001) more frequently. The time to first and terminal seizure-freedom and the time to freedom from ASM were shorter in the surface antibody group (Kaplan–Meier curves: P < 0.0001 for first seizure-freedom; P < 0.0001 for terminal seizure-freedom; P = 0.0042 for terminal ASM-freedom). Maximum ASM defined daily doses were higher in the groups with intracellular antibodies. Seizure-freedom was achieved after additional immunotherapy, not always accompanied by increased ASM doses. Titers of surface antibodies but not intracellular antibodies decreased over time. Conclusion Seizures with surface antibodies should mostly be considered acute symptomatic and transient and not indicative of epilepsy. This has consequences for ASM prescription and social restrictions. Antibody titers correlate with clinical courses.

2021 ◽  
Vol 10 (28) ◽  
pp. 2131-2133
Author(s):  
Krishnan Balagopal

Limbic encephalitis (LE) is a clinical syndrome characterized by the progressive development of neuropsychiatric symptoms including personality changes, memory loss followed by seizures, autonomic dysfunction, and involvement of the medial temporal lobes.1 Limbic encephalitis most commonly presents secondary to an autoimmune aetiology which can be further subclassified into autoimmune and paraneoplastic. Autoimmune LE can be classified according to the presence of autoantibodies into two categories. The first one is associated with antibodies to intracellular neuronal antigens and the other with antibodies to cell surface antigens.2 Intracellular antigens include Hu, Ma2, Collapsin response - mediator protein 5 (CRMP - 5) and cell surface antigens like the voltage-gated potassium channel (VGKC), N - methyl - D - aspartate receptor (NMDA) and others. The autoimmune form of LE is important because it can be treated with immunotherapy if detected early. We present a case of a patient with recurrent vertigo followed by progressive cognitive dysfunction and involuntary movements. She was diagnosed with autoimmune limbic encephalitis associated with glutamic acid decarboxylase (GAD) 65 antibodies. Her symptoms showed improvement following immunomodulatory therapy.


Author(s):  
K. Chien ◽  
I.P. Shintaku ◽  
A.F. Sassoon ◽  
R.L. Van de Velde ◽  
R. Heusser

Identification of cellular phenotype by cell surface antigens in conjunction with ultrastructural analysis of cellular morphology can be a useful tool in the study of biologic processes as well as in diagnostic histopathology. In this abstract, we describe a simple pre-embedding, protein A-gold staining method which is designed for cell suspensions combining the handling convenience of slide-mounted cell monolayers and the ability to evaluate specimen staining specificity prior to EM embedding.


1993 ◽  
Vol 16 (10) ◽  
pp. 1054-1056
Author(s):  
Dai SASAKI ◽  
Satoshi KOSUNAGO ◽  
Takeshi MIKAMI ◽  
Tatsuji MATSUMOTO ◽  
Masuko SUZUKI

1971 ◽  
Vol 134 (4) ◽  
pp. 857-870 ◽  
Author(s):  
Darcy B. Wilson ◽  
Dianne H. Fox

The proliferative reactivity of lymphocytes from rat donors maintained under germfree or conventional conditions was examined in mixed lymphocyte cultures stimulated with allogeneic and xenogeneic cell surface antigens. The results show (a) that lymphocytes from conventionally maintained rats are less reactive to human, hamster, guinea pig, and mouse cell surface antigens than to the major H alloantigens, and (b) that lymphocytes from germfree rats display no demonstrable reactivity to xenogeneic cells, but are quantitatively normal in their response to allogenic cells. The conclusion drawn from these observations is that the circulating lymphocyte pool of an individual consists of a greater proportion of cells reactive to H alloantigens of other members of the same species than to the xenogeneic cellular antigens of members of other species and that this large number of cells is not generated by a mechanism involving immunization to cross-reactive environmental antigens.


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