CACNA1H antibodies associated with headache with neurological deficits and cerebrospinal fluid lymphocytosis (HaNDL). (January 2013)

• Record Type: Journal Article
• Authors: Kürtüncü, Murat; Kaya, Dilaver; Zuliani, Luigi; Erdağ, Ece; İçöz, Sema; Uğurel, Elif; Çavuş, Filiz; Ayşit, Neşe; Birişik, Ömer; Vincent, Angela; Eraksoy, Mefkure; Vural, Burçak; Akman-Demir, Gülşen; Tüzün, Erdem
• Is Part Of: Cephalalgia. Volume 33:Number 2(2013)
• Page Start: 123
• Page End: 129
• Publication Date: 2013-01
• Subjects: HaNDL -- headache -- CACNA1H -- voltage-gated calcium channel -- autoantibody; Headache -- Periodicals; 616.8491
• DOI: 10.1177/0333102412463494
• Languages: English
• ISSNs: 0333-1024

Abstract

Background: 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.