Kürtüncü, MuratKaya, DilaverZuliani, LuigiErdağ, Eceİçöz, SemaUğurel, ElifÇavuş, FilizAyşit, NeşeBirışık, ÖmerVincent, AngelaEraksoy, MefkureVural, BurçakAkman Demir, GülşenTüzün, Erdem10.07.20192019-07-1010.07.20192019-07-102013Kürtüncü, M., Kaya, D., Zuliani, L., Erdağ, E., İçöz, S., Uğurel, E. ... Tüzün, E. (2013). CACNA1H antibodies associated with headache with neurological deficits and cerebrospinal fluid lymphocytosis (HaNDL). Cephalalgia, 33(2), 123-129. https://dx.doi.org/10.1177/03331024124634940333-1024https://dx.doi.org/10.1177/0333102412463494https://hdl.handle.net/20.500.12511/2147WOS: 000312550000006PubMed ID: 23111027Background: Patients with the syndrome of headache with neurological deficits and lymphocytosis (HaNDL) typically present with recurrent and temporary attacks of neurological symptoms and cerebrospinal fluid lymphocytosis. Aim and methods: To identify potential HaNDL-associated antibodies directed against neuronal surface and/or synapse antigens, sera of four HaNDL patients and controls were screened with indirect immunohistochemistry, immunofluorescence, cell-based assay, radioimmunoassay, protein macroarray and enzyme-linked immunosorbent assay (ELISA). Results: Although HaNDL sera did not yield antibodies to any of the well-characterized neuronal surface or synapse antigens, protein macroarray and ELISA studies showed high-titer antibodies to a subunit of the T-type voltage-gated calcium channel (VGCC), CACNA1H, in sera of two HaNDL patients. Conclusion: Our results support the notion that ion channel autoimmunity might at least partially contribute to HaNDL pathogenesis and occurrence of neurological symptoms.eninfo:eu-repo/semantics/openAccessHaNDLHeadacheCACNA1HVoltage-Gated Calcium ChannelAutoantibodyArticle33212312910.1177/0333102412463494Q1Q1