Abstract
Limbic encephalitis (LE) is a rare and rather variable disease associated in part with different antibodies. The most frequent antibodies found are directed against NMDA-receptors or proteins of the voltage-gated potassium channels (LGI1, CASPR2). Additionally, in those patients suffering from LE with early and predominant seizures GABAB-receptor (GABAB-R) antibodies could be identified in serum and cerebrospinal fluid (CSF) [ [1] Dogan Onugoren M. Deuretzbacher D. Haensch C.A. Hagedorn H.J. Halve S. Isenmann S. Kramme C. Lohner H. Melzer N. Monotti R. Presslauer S. Schäbitz W.R. Steffanoni S. Stoeck K. Strittmatter M. Stögbauer F. Trinka E. von Oertzen T.J. Wiendl H. Woermann F.G. Bien C.G. Limbic encephalitis due to GABAB and AMPA receptor antibodies: a case series. J. Neurol. Neurosurg. Psychiatry. 2015; 86: 965-972 Crossref PubMed Scopus (104) Google Scholar ]. Since blockade of GABAB-R leads to disinhibition [ [2] Davies C.H. Collingridge G.L. Regulation of EPSPs by the synaptic activation of GABAB autoreceptors in rat hippocampus. J. Physiol. 1996; 496: 451-470 Crossref PubMed Scopus (95) Google Scholar ], the question was raised whether the CSF profile of excitatory and inhibitory neurotransmitters is reflecting pathophysiological mechanisms of the disease.
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