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• Patients from a tertiary epilepsy center in routine clinical practice were studied. • NfL was measured in serum with a highly sensitive single molecule array (Simoa). • The vast majority (94 %) of patients with epilepsy did not have increased sNfL values. • The finding of higher sNfL in males with seizure activity should be interpreted with utmost caution. To detect possible neuronal damage due to recurrent isolated seizures in patients with epilepsy in a clinical routine setting. We measured the serum concentrations of neurofilament light chain (sNfL) in 46 outpatients with an at least monthly occurrence (self-reported) of generalized tonic-clonic seizures in the six months prior to the study and in 49 patients who had been seizure free (self-reported) for at least one year. We assigned the patients with seizure activity into groups with moderate and high seizure frequency. We measured sNfL with a highly sensitive single molecule array (Simoa). The majority (94 %) of all patients with epilepsy had sNfL values within the age adjusted reference ranges of our laboratory. Three patients with and three patients without seizure activity (each 3 %) showed elevated sNfL concentrations. Age adjusted sNfL concentrations did not differ significantly between patients with and without seizure activity in the total sample or in the female subgroup. In contrast, NfL concentrations were significantly higher in male patients with seizure activity and highest in the subgroup of those with high seizure activity, but were only above the reference range in two patients. sNfL concentrations did not differ between focal and generalized epilepsies and between genetic and structural etiologies. The sNfL concentrations in patients with epilepsy and healthy patients did not differ significantly. The finding of higher sNfL concentrations in males with self-reported seizure activity should be viewed with utmost caution because the difference was small and only two male patients showed sNfL concentrations above the reference range. [ABSTRACT FROM AUTHOR]

Background: There is no consensus with regard to the nosology and cut‐off values for postural abnormalities in parkinsonism. Objective: To reach a consensus regarding the nosology and cut‐off values. Methods: Using a modified Delphi panel method, multiple rounds of questionnaires were conducted by movement disorder experts to define nosology and cut‐offs of postural abnormalities. Results: After separating axial from appendicular postural deformities, a full agreement was found for the following terms and cut‐offs: camptocormia, with thoracic fulcrum (>45°) or lumbar fulcrum (>30°), Pisa syndrome (>10°), and antecollis (>45°). "Anterior trunk flexion," with thoracic (≥25° to ≤45°) or lumbar fulcrum (>15° to ≤30°), "lateral trunk flexion" (≥5° to ≤10°), and "anterior neck flexion" (>35° to ≤45°) were chosen for milder postural abnormalities. Conclusions: For axial postural abnormalities, we recommend the use of proposed cut‐offs and six unique terms, namely camptocormia, Pisa syndrome, antecollis, anterior trunk flexion, lateral trunk flexion, anterior neck flexion, to harmonize clinical practice and future research. [ABSTRACT FROM AUTHOR]

First, AD patients were explicitly selected based on their CSF profile ("We included 40 patients with a CSF profile indicative of AD."), We read with great interest the publication by de Kort and colleagues.[1] It corroborates our recent finding that compared to total tau, phospho-tau, SP 181 sp and amyloid beta (A ) 40, the marker A 42 (or the A 42/A 40 ratio) discriminates best between control and sporadic cerebral amyloid angiopathy (sCAA) cerebrospinal fluid (CSF) samples.[2] Additionally, de Kort et al's findings also support our conclusion that A 40 and A 42 biomarkers do not differentiate well enough between Alzheimer disease (AD) and sCAA to be useful in clinical routine diagnostics.[2] Therefore, we noticed with the highest interest de Kort's result that combinations of CSF markers A 40 and A 43 with A 38 and A 42 allowed discrimination between sCAA and AD with high confidence.[1] However, these new results are not presented in great detail compared to the confirmatory findings. [Extracted from the article]

Background Clinical key aspects of camptocormia in patients with idiopathic Parkinson's disease ( PD) await further definition. Methods Based on a self-assessment of PD patients, we performed an observational study, asking patients with subjectively felt involuntary forward bending to return a questionnaire and provide photographs showing their axial disorder. Forty-two matched PD patients without subjective signs of camptocormia were recruited as controls. Results The stooped posture of patients with advanced PD without camptocormia is characterized by a forward bending angle of always less than 30 degrees. Of the 145 camptocormia patients in our study, 70% had an angle ≥30 degrees. The patients with a more-severe forward bending angle were more severely affected in daily life than those with an angle of less than 30 degrees. Back pain was more frequent (81% vs. 43%) and more severe in PD patients with camptocormia than in controls. Back diseases in camptocormia PD patients were also significantly more frequent than in the PD control patients (55% vs. 26%). Camptocormia is a relevant burden in everyday life. Seventy-seven percent of patients needed walking aids and 85% reported specific disabilities attributed to camptocormia (e.g. increased risk of falling, dyspnea, problems in eating or swallowing). Conclusions Camptocormia cannot be clinically defined based on the forward bending angle alone, but an angle larger than 30 degrees is only found in camptocormia. Back pain is an essential aspect of camptocormia in PD. Back diseases can be seen as a risk factor in these patients. [ABSTRACT FROM AUTHOR]

Background: Treatment options for spasticity include intramuscular botulinum neurotoxin A (BoNT-A) injections. Both ultrasound (US) or electromyographic (EMG) guided BoNT-A injections are employed to isolate muscles. To date, most studies have included patients naïve to BoNT-A or following a prolonged wash out phase. Objective: To determine the impact of US/EMG guided BoNT-A injections on function in outpatients with spasticity receiving an established re-injection regime. Methods: Thirty patients post-stroke were investigated in a single-blinded, randomized controlled trial using a cross-over design for the EMG and US and a parallel design for the control group. The Modified Ashworth (MAS), Disability Assessment (DAS), Quality of Life (EQ-5D), self-rating scale and Barthel Index were assessed pre- and post-BoNT-A injections of upper limb muscles by a to the injection technique blinded person. Results: MAS improved in arm, finger and upper limb 4 weeks after BoNT-A treatment. The improvement showed no significant differences between the three injection techniques. Barthel Index, DAS and EQ-5D remained unchanged in all groups. Conclusions: This pilot study questions the impact of the instrumental guided injection techniques on everyday functionality in a routine clinical setting with established re-injection intervals. Larger trials are warranted with patients who are under long-term treatment on a regular basis. [ABSTRACT FROM AUTHOR]