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BackgroundDementia with Lewy bodies (DLB) is a type of dementia often diagnosed in older patients. Since its initial symptoms range from delirium to psychiatric and cognitive symptoms, the diagnosis is often delayed.ObjectivesIn our study, we evaluated the magnetic resonance imaging (MRI) of patients suffering from DLB in correlation with their initial symptoms taking a new pragmatic approach entailing manual measurements in addition to an automated volumetric analysis of MRI.MethodsA total of 63 patients with diagnosed DLB and valid 3D data sets were retrospectively and blinded evaluated. We assessed atrophy patterns (1) manually for the substantia innominata and (2) via FastSurfer for the most common supratentorial regions. Initial symptoms were categorized by (1) mild cognitive impairment (MCI), (2) psychiatric episodes, and (3) delirium.ResultsManual metric MRI measurements revealed moderate, but significant substantia-innominata (SI) atrophy in patients with a psychiatric onset. FastSurfer analysis revealed no regional volumetric differences between groups.ConclusionThe SI in patients with DLB and a psychiatric-onset is more atrophied than that in patients with initial MCI. Our results suggest potential differences in SI between DLB subtypes at the prodromal stage, which are useful when taking a differential-diagnostic approach. This finding should be confirmed in larger patient cohorts.

Additional file 4. Chart review for identification of a postoperative delirium on Day 1-5

Additional file 2: Table S2. Manual measurements and Volumetric results using the Desikan���Killiany���Tourvilleatlas and FastSurfer for patients and control group with T1 MP-RAGE and T1 VIBEsequences.

Additional file 1. Delirium risk assessment

Additional file 3. Outcome-oriented Nursing Assessment (ePA-AC)

Additional file 2. Medical history, cardiovascular risk factors, medication, and sociodemographic data

Additional file 1: Table S1. Demographic and CSF data of patients with dementia with Lewybodies.

Additional file 3: Table S3. Manual measurements and Volumetric results using the Desikan���Killiany���Tourvilleatlas and FastSurfer for patients and control group with T1 MP-RAGE sequences.

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.

Dementia with Lewy bodies (DLB) is the second most common form of dementia and is assumed to be often under- or misdiagnosed, especially in early stages. Here we present a complex case of probable DLB with major depression and alcohol and benzodiazepine dependence in which DLB was ruled out initially. This case highlights the challenging diagnostic workup of DLB patients. Core clinical features can be missing and indicative biomarkers can be negative, especially in early stages of the disease. Initially, Fluorodeoxyglucose positron emission tomography as well as neuropsychological assessment were suspicious for a possible DLB diagnosis in our patient while core clinical criteria were missing and the indicative biomarker 123I-FP-CIT SPECT was negative. Follow up was performed two years later and the patients showed several core and supportive clinical features of DLB and 123I-FP-CIT SPECT showed a pathological pattern. Extensive neuropsychological assessment in combination with PET imaging might provide crucial evidence for DLB even in early stages. If neuropsychology and PET imaging point to an early DLB diagnosis careful follow-up should be performed as core symptoms and indicative biomarkers might appear in later stages of the disease. Open-Access-Publikationsfonds 2020 peerReviewed

Mortality of patients with end-stage renal disease tremendously exceeds that of the general population due to excess cardiovascular morbidity. Large middle-sized molecules (LMM) including pro-inflammatory cytokines are major drivers of uremic cardiovascular toxicity and cannot be removed sufficiently by conventional high-flux (HFL) hemodialysis. We tested the ability of plasma from 19 hemodialysis patients participating in a trial comparing HFL with high cut-off (HCO) membranes facilitating removal of LMM to induce calcification in mesenchymal stromal cells (MSC) functioning as vascular progenitors. HCO dialysis favorably changed plasma composition resulting in reduced pro-calcific activity. LMM were removed more effectively by HCO dialysis including FGF23, a typical LMM we found to promote osteoblastic differentiation of MSC. Protein-bound uremic retention solutes with known cardiovascular toxicity but not LMM inhibited proliferation of MSC without direct toxicity in screening experiments. We could not attribute the effect of HCO dialysis on MSC calcification to distinct mediators. However, we found evidence of sustained reduced inflammation that might parallel other anti-calcifying mechanisms such as altered generation of extracellular vesicles. Our findings imply protection of MSC from dysfunctional differentiation by novel dialysis techniques targeted at removal of LMM. HCO dialysis might preserve their physiologic role in vascular regeneration and improve outcomes in dialysis patients.