Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RETRACTED ARTICLE: Acute necrotizing myelitis and acute motor axonal neuropathy in a COVID-19 patient.

ABSTRACT:

SUBMITTER: Maideniuc C

PROVIDER: S-EPMC7415129 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

RETRACTED ARTICLE: Acute necrotizing myelitis and acute motor axonal neuropathy in a COVID-19 patient.

Maideniuc Catalina C Memon Anza B AB Memon Anza B AB

Journal of neurology 20200809 2

PMID: 32772172

Similar Datasets

Concomitant Transverse Myelitis and Acute Axonal Sensory-Motor Neuropathy in an Elderly Patient.

Project description:Diagnosing concomitant transverse myelitis (TM) and Guillain-Barré syndrome (GBS) can be challenging. We report a case of an elderly patient presenting with acute sensory and motor disturbances in the four limbs, associated with urinary retention, ophthalmoparesis, facial weakness, and dysarthria. Electrodiagnostic studies were consistent with acute motor sensory axonal neuropathy (AMSAN), and imaging showed a longitudinally extensive tumefactive contrast-enhancing hyperintense spinal cord lesion extending from T6 to the cone. Concomitant AMSAN and TM have not been previously reported in the elderly. Comorbid TM and other GBS variants have been previously reported. Intravenous methylprednisolone, plasma exchange, cyclophosphamide, or combination therapies are usually used, although there are no randomized controlled studies regarding treatment choices.

| S-EPMC5530449 | biostudies-other

Atypical Acute Motor Axonal Neuropathy with Cerebrospinal Pleocytosis Mimicking Myelitis.

Project description: Not available

| S-EPMC5392467 | biostudies-literature

RETRACTED ARTICLE: Homeopathy combat against coronavirus disease (Covid-19).

Project description: Not available

| S-EPMC7272237 | biostudies-literature

RETRACTED ARTICLE: Coronary arteries and aortic valve calcifications in COVID-19.

Project description: Not available

| S-EPMC8783786 | biostudies-literature

Anti-ganglioside antibody internalization attenuates motor nerve terminal injury in a mouse model of acute motor axonal neuropathy.

Project description:In the Guillain-Barré syndrome subform acute motor axonal neuropathy (AMAN), Campylobacter jejuni enteritis triggers the production of anti-ganglioside Abs (AGAbs), leading to immune-mediated injury of distal motor nerves. An important question has been whether injury to the presynaptic neuron at the neuromuscular junction is a major factor in AMAN. Although disease modeling in mice exposed to AGAbs indicates that complement-mediated necrosis occurs extensively in the presynaptic axons, evidence in humans is more limited, in comparison to the extensive injury seen at nodes of Ranvier. We considered that rapid AGAb uptake at the motor nerve terminal membrane might attenuate complement-mediated injury. We found that PC12 rat neuronal cells rapidly internalized AGAb, which were trafficked to recycling endosomes and lysosomes. Consequently, complement-mediated cytotoxicity was attenuated. Importantly, we observed the same AGAb endocytosis and protection from cytotoxicity in live mouse nerve terminals. AGAb uptake was attenuated following membrane cholesterol depletion in vitro and ex vivo, indicating that this process may be dependent upon cholesterol-enriched microdomains. In contrast, we observed minimal AGAb uptake at nodes of Ranvier, and this structure thus remained vulnerable to complement-mediated injury. These results indicate that differential endocytic processing of AGAbs by different neuronal and glial membranes might be an important modulator of site-specific injury in acute AGAb-mediated Guillain-Barré syndrome subforms and their chronic counterparts.

| S-EPMC3287221 | biostudies-literature

An unusual occurrence of opsoclonus and liver enzymes elevation in a patient with acute motor and sensory axonal neuropathy subtype of Guillain-Barre syndrome.

Project description:BackgroundAcute motor and sensory axonal neuropathy (AMSAN) is a subtype of Guillain-Barré syndrome (GBS) differentiated by nerve conduction studies (NCS) and characterized by symmetric ascending paralysis often involving respiratory muscles. While opsoclonus, which is involuntary chaotic rapid eye movements, is not a common manifestation of GBS. Moreover, little published data are available on the relation between liver enzymes elevation and GBS.Case presentationA 42-year-old man presented to Al Mouwassat University Hospital with weakness in all limbs and dyspnea. Examination showed an elevated respiratory rate, hyporeflexia, and decreased strength of upper and lower limbs. Analysis of cerebrospinal fluid revealed an albuminocyto-dissociation suggesting the diagnosis of GBS and subsequent plasmapheresis. NCS confirmed a diagnosis of AMSAN. Elevation in liver enzymes was noticed prompting further exploration with no positive findings. Despite treatment efforts, the patient developed severe dyspnea, deterioration in cognitive abilities, and opsoclonus with a normal brain MRI. Unfortunately, he developed respiratory failure which lead to his death.ConclusionIn this case, we highlight the occurrence of opsoclonus which is a rarely-encountered manifestation of GBS, in addition to an unexplained elevated liver enzyme, the thing that could contribute to larger research to further comprehend the pathophysiology of GBS.

| S-EPMC8932169 | biostudies-literature

Late-onset sensory-motor axonal neuropathy, a novel SLC12A6-related phenotype.

Project description:We describe five families from different regions in Norway with a late-onset autosomal-dominant hereditary polyneuropathy sharing a heterozygous variant in the SLC12A6 gene. Mutations in the same gene have previously been described in infants with autosomal-recessive hereditary motor and sensory neuropathy with corpus callosum agenesis and mental retardation (Andermann syndrome), and in a few case reports describing dominantly acting de novo mutations, most of them with onset in childhood. The phenotypes in our families demonstrated heterogeneity. Some of our patients only had subtle to moderate symptoms and some individuals even no complaints. None had CNS manifestations. Clinical and neurophysiological evaluations revealed a predominant sensory axonal polyneuropathy with slight to moderate motor components. In all 10 patients the identical SLC12A6 missense variant, NM_001365088.1 c.1655G>A p.(Gly552Asp), was identified. For functional characterization, the mutant potassium chloride cotransporter 3 was modelled in Xenopus oocytes. This revealed a significant reduction in potassium influx for the p.(Gly552Asp) substitution. Our findings further expand the spectrum of SLC12A6 disease, from biallelic hereditary motor and sensory neuropathy with corpus callosum agenesis and mental retardation and monoallelic early-onset hereditary motor and sensory neuropathy caused by de novo mutations, to late-onset autosomal-dominant axonal neuropathy with predominant sensory deficits.

| S-EPMC9976957 | biostudies-literature

RETRACTED ARTICLE: Advances in Diagnosis of Endometrial Hyperplasia.

Project description: Not available

| S-EPMC6801245 | biostudies-literature

βIV Spectrinopathies Cause Profound Intellectual Disability, Congenital Hypotonia, and Motor Axonal Neuropathy.

Project description:βIV spectrin links ankyrinG (AnkG) and clustered ion channels at axon initial segments (AISs) and nodes of Ranvier to the axonal cytoskeleton. Here, we report bi-allelic pathogenic SPTBN4 variants (three homozygous and two compound heterozygous) that cause a severe neurological syndrome that includes congenital hypotonia, intellectual disability, and motor axonal and auditory neuropathy. We introduced these variants into βIV spectrin, expressed these in neurons, and found that 5/7 were loss-of-function variants disrupting AIS localization or abolishing phosphoinositide binding. Nerve biopsies from an individual with a loss-of-function variant had reduced nodal Na+ channels and no nodal KCNQ2 K+ channels. Modeling the disease in mice revealed that although ankyrinR (AnkR) and βI spectrin can cluster Na+ channels and partially compensate for the loss of AnkG and βIV spectrin at nodes of Ranvier, AnkR and βI spectrin cannot cluster KCNQ2- and KCNQ3-subunit-containing K+ channels. Our findings define a class of spectrinopathies and reveal the molecular pathologies causing nervous-system dysfunction.

| S-EPMC5992132 | biostudies-literature

Challenges in Identifying the Retracted Status of an Article.

Project description: Not available

| S-EPMC8243230 | biostudies-literature