Background: Blood contamination due to traumatic lumbar puncture presents a diagnostic pitfall in cerebrospinal fluid (CSF) analysis. It is controversially discussed if phagocytosis of erythrocytes which can be found in the CSF after subarachnoid hemorrhage can also develop in vitro in the presence of artificial blood contamination. Furthermore, there is no consensus about the acceptable amount of artificial blood contamination on CSF protein results. Methods: Two measurement series were performed in order to investigate the role of artificial blood contamination on the possible development of erythrophages and siderophages in the CSF: (1) blood contamination was simulated in vitro by adding blood into the CSF. (2) CSF was investigated when blood contamination occurred during a traumatic lumbar puncture. In both types of experiments, CSF including blood was incubated for 24 h and for 72 h at room temperature or at 4°C. In the third measurement series, the effects of artificial blood contamination on CSF protein results were investigated. Blood contamination was simulated in vitro by adding different amounts of blood ending up with five different samples containing erythrocyte counts of 2,500, 5,000, 7,500, 10,000, and 20,000 per μl CSF. Results: Cytological examination revealed no evidence of erythrophages or siderophages in vitro . In contrast, already a low blood contamination (2,500 erythrocytes/μl CSF) led to false pathological results of total protein and albumin. Along with increasing amounts of blood, the frequency of false pathological protein results increased. A blood contamination of 5,000 erythrocytes/μl CSF resulted in a false positive intrathecal IgM production in nearly every fifth patient. In contrast, blood contamination with 5,000 erythrocytes/μl CSF was the acceptable amount of blood which did not lead to a false positive intrathecal synthesis of IgG and IgA. Conclusion: Erythrophages and siderophages do not develop in vitro . An extensive diagnostic work up for the source of blood in the CSF should be performed when erythrophages or siderophages are found in the CSF. The contamination of CSF with increasing volume of blood resulted in falsely elevated CSF protein concentrations. Hence, the amount of blood contamination has to be taken into consideration when interpreting CSF protein measurement results.

To explore the correlations of botulinum toxin (BT) therapy with dysphagia, we wanted to study a group of cervical dystonia (CD) patients with optimised BT therapy during a prolonged period of time to record their dysphagia frequency, severity and duration, to study potential risk factors and try to avoid it by BT application with ultrasound guidance. BT therapy of 75 CD patients (23 males, 52 females, age 60 ± 12 years, BT total dose 303.5 ± 101.5 uMU) was retrospectively analysed for 1 year. BT therapy was optimised prior to the observation period. Dysphagia was noticed by one fifth of the patients. In those patients, it only occurred in about one third of the injection series. It was never associated with a functional deficit and lasted several days to 2 weeks. It was not related to patient age or gender, BT total dose, BT dose in the sternocleidomastoid muscle, BT dose in the sternocleidomastoid and scalenii muscles, by BT therapy with bilateral sternocleidomastoid muscle injections or BT therapy with abobotulinumtoxinA. Ultrasound guidance was not able to prevent it. Further prospective studies will be necessary to study underlying dystonia associated swallowing abnormalities as a potentially predisposing factor.