Published diagnostic criteria for functional (psychogenic) movement disorders (FMDs) include psychiatric symptoms and some historical variables to affect the threshold between categories of ...diagnostic certainty. Clinically
probable
and
possible
categories, however, do not suffice to rule in FMD or rule out complex organic movement disorders and therefore are of little practical help. In contrast, a handful of
unequivocal and reliably incongruent or inconsistent
clinical features in each functional movement phenotype, when present, allow a
clinically definite
diagnosis of FMD, regardless of any psychiatric symptom. We suggest that the use of phenotype-specific clinically definite FMD diagnostic criteria will increase inter-rater reliability and minimize false-positive diagnostic errors. This process involves the ascertainment of core (mandatory) examination features instead of supportive but insufficiently sensitive historical, psychiatric, and inconsistent examination features.
Obituary for Jan O. Aasly (1950–2022) Farrer, Matthew J.
Movement disorders,
September 2022, 2022-09-00, 20220901, Letnik:
37, Številka:
9
Journal Article
John Q. Trojanowski, MD, PhD (1946–2022) Hurtig, Howard I.; Standaert, David G.
Movement disorders,
June 2022, 2022-Jun, 2022-06-00, 20220601, Letnik:
37, Številka:
6
Journal Article
Wearable systems that monitor muscle activity, store data and deliver feedback therapy are the next frontier in personalized medicine and healthcare. However, technical challenges, such as the ...fabrication of high-performance, energy-efficient sensors and memory modules that are in intimate mechanical contact with soft tissues, in conjunction with controlled delivery of therapeutic agents, limit the wide-scale adoption of such systems. Here, we describe materials, mechanics and designs for multifunctional, wearable-on-the-skin systems that address these challenges via monolithic integration of nanomembranes fabricated with a top-down approach, nanoparticles assembled by bottom-up methods, and stretchable electronics on a tissue-like polymeric substrate. Representative examples of such systems include physiological sensors, non-volatile memory and drug-release actuators. Quantitative analyses of the electronics, mechanics, heat-transfer and drug-diffusion characteristics validate the operation of individual components, thereby enabling system-level multifunctionalities.
Advanced Directives for Hastened‐Death? Russell, James A.
Movement disorders,
April 2022, 2022-Apr, 2022-04-00, 20220401, Letnik:
37, Številka:
4
Journal Article
Movement disorders are a common feature of autoantibody-associated diseases. Balint et al. provide a novel phenotype-oriented algorithmic approach to guide diagnosis. They review the underlying ...pathophysiology and point out parallels between immune-mediated and genetic conditions presenting with similar phenotypes. They consider future directions such as personalised immunotherapy.
Abstract
Movement disorders are a prominent and common feature in many autoantibody-associated neurological diseases, a group of potentially treatable conditions that can mimic infectious, metabolic or neurodegenerative disease. Certain movement disorders are likely to associate with certain autoantibodies; for example, the characteristic dyskinesias, chorea and dystonia associated with NMDAR antibodies, stiff person spectrum disorders with GAD, glycine receptor, amphiphysin or DPPX antibodies, specific paroxysmal dystonias with LGI1 antibodies, and cerebellar ataxia with various anti-neuronal antibodies. There are also less-recognized movement disorder presentations of antibody-related disease, and a considerable overlap between the clinical phenotypes and the associated antibody spectra. In this review, we first describe the antibodies associated with each syndrome, highlight distinctive clinical or radiological 'red flags', and suggest a syndromic approach based on the predominant movement disorder presentation, age, and associated features. We then examine the underlying immunopathophysiology, which may guide treatment decisions in these neuroimmunological disorders, and highlight the exceptional interface between neuronal antibodies and neurodegeneration, such as the tauopathy associated with IgLON5 antibodies. Moreover, we elaborate the emerging pathophysiological parallels between genetic movement disorders and immunological conditions, with proteins being either affected by mutations or targeted by autoantibodies. Hereditary hyperekplexia, for example, is caused by mutations of the alpha subunit of the glycine receptor leading to an infantile-onset disorder with exaggerated startle and stiffness, whereas antibodies targeting glycine receptors can induce acquired hyperekplexia. The spectrum of such immunological and genetic analogies also includes cerebellar ataxias and some encephalopathies. Lastly, we discuss how these pathophysiological considerations could reflect on possible future directions regarding antigen-specific immunotherapies or targeting the pathophysiological cascades downstream of the antibody effects.
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