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Autoimmune dementia is a novel and expanding field which subsumes neuropsychiatric disorders with predominant cognitive impairments due to an underlying autoimmune etiology. Progressive dementias with atypical clinical presentation should trigger a thorough diagnostic approach including testing for neural surface and intracellular antibodies to avoid a delay in accurate diagnosis and initiating appropriate therapy. Here, we present two emerging cases of progressive dementia with co-existing serum autoantibodies against the KCNA2 (potassium voltage-gated channel subfamily A member 2) subunit. We found various cognitive deficits with dominant impairments in the memory domain, particularly in delayed recall. One patient presented a subacute onset of then-persisting cognitive deficits, while the other patient’s cognitive impairments progressed more chronically and fluctuated. Cognitive impairments coincided with additional neuropsychiatric symptoms. Both had a potential paraneoplastic background according to their medical history and diagnostic results. We discuss the potential role of KCNA2 autoantibodies in these patients and in general by reviewing the literature. The pathogenetic role of KCNA2 antibodies in cognitive impairment is not well delineated; clinical presentations are heterogeneous, and thus a causal link between antibodies remains questionable. Current evidence indicates an intracellular rather than extracellular epitope. We strongly suggest additional prospective studies to explore KCNA2 antibodies in specifically-defined cohorts of cognitively impaired patients via a systematic assessment of clinical, neuropsychological, neuroimaging, as well as laboratory and CSF (cerebrospinal fluid) parameters, and antibody studies to (1) determine the epitope’s location (intracellular vs. extracellular), (2) the mode of action, and (3) seek co-existing, novel pathogenetic autoantibodies in sera and CSF.

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IntroductionInfectious ileopectineal bursitis is a rare complication after total hip replacement and is associated mainly with rheumatoid arthritis. The main complications are local swelling and pain, but communication of the inflamed bursa with the joint can occur, leading to subsequent cartilage damage and bone destruction.Case presentationWe report a case of a 47-year-old Caucasian woman without rheumatoid arthritis who reported pain and palsy in her left leg almost one year after total hip replacement. She was diagnosed with an ileopectineal bursitis after total hip replacement, leading to femoral nerve palsy. The diagnosis was obtained by thorough clinical examination, the results of focused computed tomography and magnetic resonance imaging.ConclusionTo the best of our knowledge, this is the first report of non-infectious ileopectineal bursitis in a patient without rheumatoid arthritis as a complication of total hip replacement. This rare case underlines the importance of proper neurologic examination of persistent conditions after orthopedic intervention in otherwise healthy individuals. We believe this case should be useful for a broad spectrum of medical specialties, including orthopedics, neurology, radiology, and general practice.