Anti-neuronal antibodies associated with headache with neurological deficits and cerebrospinal fluid lymphocytosis

Infectious-immunogenic mechanisms have been proposedfor the pathogenesis of the syndrome of transient headacheand neurological deficits with cerebrospinal fluid lympho-cytosis (HaNDL) [1]. To investigate this assumption, weperformed immunohistochemistry and Western blot studieswith sera and cerebrospinal fluid (CSF) of two HaNDLpatients. Serum and CSF IgGs of both patients showedstrong reactivity with the nuclei of rat central nervoussystem (CNS) cells and proteins extracted from neuro-blastoma cells. This reactivity was not observed withsamples of a sporadic hemiplegic migraine (SHM) patientand 12 migraine patients used as controls. The CNSbinding pattern of HaNDL IgG was easily distinguishablefrom that of other well-known anti-neuronal nuclear anti-bodies (ANNA) such as anti-Hu, anti-Ri, and anti-nuclearantibody (ANA). The presence of an anti-neuronal immuneresponse may support the autoimmune hypothesis as apathogenic factor for HaNDL and should be furtherinvestigated in larger series.To show the presence of a possible autoimmuneresponse in this syndrome, sera and CSF of two HaNDLpatients were investigated for anti-neuronal antibodies.Serum/CSF of a SHM patient, sera from 12 migraine, 2anti-Hu, 2 anti-Ri, 34 ANA positive patients and 30 healthyindividuals were used as controls. All headache patientsfulfilled the clinical criteria established by The Interna-tional Headache Society [2].Transient headache and neurological deficits with cere-brospinalfluidlymphocytosispatientswere35-(H1)and38-year-old (H2) men presenting with three episodes of throb-bing headache, dysphasia/dysarthria, marching righthemiparesis and hemihypoesthesia (H1 only) lasting for 2–9 h. Their CSF revealed increased lymphocytes [496/mm