Autoantibodies against neuronal surface proteins in spontaneous subarachnoid and intracerebral haemorrhage

Brain autoimmunity has been reported in patients with preceding infection of the central nervous system by herpesviridae. It has been hypothesized that neuronal damage releasing antigens might trigger secondary immune response. The objective of the study was to investigate whether brain damage due to spontaneous subarachnoid haemorrhage (SAH) or intracerebral haemorrhage (ICH) induces reactivity against neuronal surface proteins.

Patients with spontaneous SAH and ICH, who had cerebrospinal fluid (CSF) and serum sampling within 2 weeks after disease onset (baseline) and afterwards at least 10 days later (follow-up), were included. Antibodies against NMDA, GABA-B, AMPA-1/- 2 receptor, LGI1 and CASPR2 were determined by indirect immunofluorescence.

A total of 43 SAH and 11 ICH patients aged 62 (±12) years (65% females) had simultaneous CSF/ serum sampling median 5 and 26.5 days after disease onset. At baseline, all CSF samples were collected via ventricular drainage, at follow-up 20 (37.0%) patients had CSF collection by lumbar puncture because ventricular drain had been already removed. All CSF and serum samples at baseline and follow-up tested negative for antibodies against NMDA, GABA-B, AMPA-1/- 2 receptor, LGI1 and CASPR2.

Immunoreactivity against common neuronal surface proteins was not observed within the early disease course of spontaneous SAH and ICH.