Peripheral nerve involvement in multiple sclerosis: Demonstration by magnetic resonance neurography

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140006/1/ana25068_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/140006/2/ana25068.pd

»Mit Gender-Wissen in die Praxis!« : Studierende berichten von einem Workshop an der Goethe-Universität

Am 22. November 2019 fand der Workshop „Mit Gender-Wissen in die Praxis“ im Seminarpavillon der Goethe-Universität statt. Die Veranstaltung wurde von Dr. Minna Ruokonen-Engler und Dr. Ewa Palenga-Möllenbeck in Kooperation mit dem Cornelia-Goethe-Centrum veranstaltet und aus dem Ruth-Moufang-Fonds vom Zentralen Gleichstellungsbüro und dem Fachbereich Gesellschaftswissenschaften finanziert. Der Workshop zielte darauf ab, Studierenden der Gender Studies sowie Interessierten Einblicke in verschiedene Berufsfelder der Gender Studies zu geben und Studierende mit den Praktiker*innen zu vernetzen..

Etiology of Ischemic Strokes of Patients with Atrial Fibrillation and Therapy with Anticoagulants

Background: Reducing the number of ischemic strokes in patients with atrial fibrillation despite oral anticoagulation remains an important, yet largely unsolved challenge. Therefore, we assessed the etiology of ischemic strokes despite anticoagulation with vitamin K antagonists (VKA) or non-VKA oral anticoagulants (NOACs). Methods: Patients with known atrial fibrillation (AF), treatment with VKA or NOAC, and acute ischemic stroke admitted between 2015 and 2018 (1st half) were identified from the hospital database. Brain imaging data were independently reviewed. An integrated etiologic classification according to the ASCOD system was made. Medication errors (admission INR <2.0 in the VKA- or NOAC-specific concentration <10 ng/mL) or dosage/dosing errors were also analyzed. Results: Of 3610 patients screened, n = 341 were included (VKA, n = 127; NOAC, n = 214). An overall increasing rate of OAC-associated stroke per year was observed. In 95.3% of patients with adequate diagnostic work-up (n = 321/337), at least one additional potential, uncertain, or unlikely non-cardiac cause of stroke was identified. More patients in the VKA than in the NOAC group had a medication error (81/127, 63.8% vs. 102/205, 49.8%; p = 0.013). Conclusions: Stroke risk factors despite atrial fibrillation were highly prevalent. Although less common with NOACs than VKAs, medication errors are still frequent

Quantitative magnetic resonance neurographic characterization of peripheral nerve involvement in manifest and pre-ataxic spinocerebellar ataxia type 3

Background and purposeKnowledge about the exact underlying pathophysiological changes involved in the genesis and progression of spinocerebellar ataxia type 3 (SCA3) is limited. Lower extremity peripheral nerve lesions in clinically, genetically and electrophysiologically classified ataxic and pre-ataxic SCA3 mutation carriers were characterized and quantified by magnetic resonance neurography (MRN).MethodsEighteen SCA3 mutation carriers and 20 age-/sex-matched healthy controls were prospectively enrolled. All SCA3 mutation carriers underwent detailed neurological and electrophysiological examinations. 3 T MRN covered the lumbosacral plexus and proximal thigh to the tibiotalar joint by using T2-weighted inversion recovery sequences, dual-echo relaxometry sequences with spectral fat saturation, and two gradient-echo sequences with and without an off-resonance saturation rapid frequency pulse. Detailed quantification of nerve lesions by morphometric and microstructural MRN markers, including T2 relaxometry and magnetization transfer contrast imaging, was conducted in all study participants.ResultsMRN detected peripheral nerve damage in ataxic and pre-ataxic SCA3. The quantitative markers proton spin density (ρ), T2 relaxation time, magnetization transfer ratio and cross-sectional area were decreased in SCA3, indicating chronic axonopathy. MTR and ρ identified early, subclinical nerve damage in pre-ataxic SCA3 and in SCA3 mutation carriers without polyneuropathy and were superior in differentiating between all subgroups. Additionally, microstructural markers correlated well with clinical symptom scores and electrophysiological results.ConclusionsOur data provide a comprehensive characterization of peripheral nerve damage in SCA3 and assist in understanding the mechanisms of the multisystemic disease evolution. Evidence of peripheral nerve involvement prior to the onset of clinically overt ataxia might have important implications for designing early intervention studies.Peripheral nerve involvement was characterized and quantified in 18 adult ataxic and pre-ataxic spinocerebellar ataxia type 3 (SCA3) mutation carriers in comparison with 20 healthy age- and sex-matched controls by applying high-resolution magnetic resonance neurography (MRN). The quantitative MRN markers proton spin density, T2 relaxation time, magnetization transfer ratio and cross-sectional area were decreased in SCA3, indicating a chronic axonopathy, and correlated well with clinical symptom scores and electrophysiological results. Early subclinical nerve damage in pre-ataxic SCA3 and in SCA3 mutation carriers without polyneuropathy was already evident and detectable by magnetization transfer ratio and proton spin density, having potentially important implications for designing future early intervention studies.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/172786/1/ene15305.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/172786/2/ene15305_am.pd

Rigidity percolation control of the brittle-ductile transition in disordered networks

In ordinary solids, material disorder is known to increase the size of the process zone in which stress concentrates at the crack tip, causing a transition from localized to diffuse failure. Here, we report experiments on disordered 2D lattices, derived from frictional particle packings, in which the mean coordination number $\langle z \rangle$ of the underlying network provides a similar control. Our experiments show that tuning the connectivity of the network provides access to a range of behaviors from brittle to ductile failure. We elucidate the cooperative origins of this transition using a frictional pebble game algorithm on the original, intact lattices. We find that the transition corresponds to the isostatic value $\langle z \rangle = 3$ in the large-friction limit, with brittle failure occurring for structures vertically spanned by a rigid cluster, and ductile failure for floppy networks containing nonspanning rigid clusters. Furthermore, we find that individual failure events typically occur within the floppy regions separated by the rigid clusters

Correlation between deep motor branch T2-signal (y-axis) and its electrical conduction time in ms (x-axis).

<p>Electrical conduction time through the deep motor branch was measured as distal motor latency to its most distal target muscle which is the first dorsal interosseus muscle (IOD I). Note how the empirical data (black dots) strongly correlate (R² = −0.8; p<0.001) in a non-linear fashion (non-linear fit of asymptotic growth, red dashed line). This finding indicates that nerve T2-signal and electrical nerve conduction show a distinctive behavior under physiological and pathological condition, in that the former exhibits its largest dynamic range near the normative reference value of dml IOD I (which is given in the literature at 3–5 ms), and that electrical conduction exhibits its largest dynamic range in severe pathological states (>5 ms). This may point toward a strong diagnostic value of nerve T2-signal as a novel marker for the early detection of nerve injury.</p

Representative findings of nerve T2-signal increase on single subject level.

<p>one GCS patient with isolated motor symptoms (left column), another with combined motor and sensory symptoms (middle column), both compared to one asymptomatic control (right column). Three image sections from distal (A) to proximal (C) are given and image positions indicated on the anatomical schematic drawing on the left (with permission from The Journal of Bone and Joint Surgery, Volume 51, pages 1095–1103). The deep motor branch at the level of the hook of the hamate is encircled in red and found in the upper image row (A = slice position 10). Just distal to the bifurcation of the ulnar nerve motor and sensory branches are encircled in red and green, respectively (middle image row, B, slice position +3). Just proximal to the bifurction the ulnar nerve trunk is encircled in yellow (lower image row, B = slice position -3). In GCS with isolated motor symptoms (left column, GCS motor only) increased nerve T2-signal was most noticeable within the deep motor branch (red arrow) and extended over a short distance proximally into the ulnar nerve trunk (yellow circle in C), while the T2-signal was normal within the superficial sensory branch (green arrow). In case of combined motor and sensory symptoms both distal ulnar nerve branches clearly show an incresed nerve branch T2-signal (red and green circle without arrows in level B, middle column, GCS motor+sensory).</p