Tardy posterior interosseous nerve palsy resulting from residual dislocation of the radial head in a Monteggia fracture: a case report

<p>Abstract</p> <p>Introduction</p> <p>We report an extremely rare case of tardy posterior interosseous nerve palsy that developed 40 years after unreduced anterior dislocation of the radial head in a Monteggia fracture.</p> <p>Case presentation</p> <p>A 46-year-old Asian woman was diagnosed with tardy posterior interosseous nerve palsy resulting from residual dislocation of the radial head in a Monteggia fracture. The patient remembered that she had sustained a fracture to the right elbow when she was 6 years old but could not remember the details of either the injury or its treatment. Intra-operatively, the posterior interosseous nerve was compressed at the radial head, wrapped around the medial side of the radial neck, and ran into the distorted supinator muscle, and was stretched. We therefore excised the radial head and performed neurolysis. The function of the right hand was normal at a follow-up examination 8 months after surgery.</p> <p>Conclusion</p> <p>We theorize that excessive repeated motion with loss of elasticity of surrounding tissues because of long-term dislocation of the radial head may cause delayed posterior interosseous nerve palsy. It is necessary to make an accurate diagnosis and render proper treatment when a Monteggia fracture occurs, making sure that the radial head does not remain dislocated, to avoid possible posterior interosseous nerve palsy due to excessive pronation and supination even several decades later.</p

Pattern Alignment Effects in Through-Wafer Bulk Micromachining of (100) Silicon

Precise alignment of the mask patterns relative to wafer crystallographic orientation is critical in the fabrication of many MEMS devices. Slight misalignment between the two can create striations and other defects in the etched sidewalls using an orientation dependent etchant such as potassium hydroxide (KOH). This paper focuses on the characterization of the resultant geometries due to the deliberate misalignment of photolithographically defined patterns relative to the (110) plane in (100) orientation silicon. The surface roughness of the etched (111) sidewall are characterized using optical microscopy, scanning electron microscopy and profilometry

Genotype-phenotype correlations, dystonia and disease progression in spinocerebellar ataxia type 14

Spinocerebellar ataxia type 14 is a rare form of autosomal dominant cerebellar ataxia caused by mutations in protein kinase Cγ gene. Clinically, it presents with a slowly progressive, mainly pure cerebellar ataxia.Using next generation sequencing, we screened 194 families with autosomal dominant cerebellar ataxia and normal polyglutamine repeats. In-depth phenotyping was performed using validated clinical rating scales neuroimaging and electrophysiological investigations.We identified 25 individuals from 13 families carrying pathogenic mutations in protein kinase Cγ gene. A total of 10 unique protein kinase Cγ gene mutations have been confirmed of which 5 are novel and 5 were previously described. Our data suggest that the age at onset is highly variable; disease course is slowly progressive and rarely associated with severe disability. However, one third of patients presented with a complex ataxia comprising severe focal and/or task-induced dystonia, peripheral neuropathy, parkinsonism, myoclonus, and pyramidal syndrome. The most complex phenotype is related to a missense mutation in the catalytic domain in exon 11.We present one of the largest genetically confirmed spinocerebellar ataxia type 14 cohorts contributing novel variants and clinical characterisation. We show that although protein kinase Cγ gene mutations present mainly as slowly progressive pure ataxia, more than a third of cases had a complex phenotype. Overall, our case series extends the phenotype and suggests that protein kinase Cγ gene mutations should be considered in patients with slowly progressive autosomal dominant cerebellar ataxia, particularly when myoclonus, dystonia, or mild cognitive impairment are present in the absence of polyglutamine expansion. © 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society