scholarly journals COVID-19 Neuromuscular Involvement in Post-Acute Rehabilitation

2021 ◽  
Vol 11 (12) ◽  
pp. 1611
Author(s):  
Sergio Bagnato ◽  
Manfredi Ferraro ◽  
Cristina Boccagni ◽  
Gianluca Battaglia ◽  
Tiziana D’Agostino ◽  
...  
Keyword(s):  
Critical Illness ◽  
Nerve Injury ◽  
Axonal Neuropathy ◽  
Clinical Signs ◽  
Critical Illness Polyneuropathy ◽  
Common Finding ◽  
Acute Motor Axonal Neuropathy ◽  
Abnormal Gait ◽  
Sensory Motor ◽  
Peroneal Nerve Injury

Background: Coronavirus disease 2019 (COVID-19) is associated with muscle and nerve injuries as a consequence of prolonged critical illness or the infection itself. In this study, we evaluated neuromuscular involvement in patients who underwent post-acute intensive rehabilitation after COVID-19. Methods: Clinical and neurophysiological evaluations, including nerve conduction studies and electromyography, were performed on 21 consecutive patients admitted for rehabilitation after COVID-19. Results: Clinical signs suggesting muscle or nerve involvement (weakness, reduced deep tendon reflexes, impaired sensitivity, abnormal gait) were found in 19 patients. Neurophysiological examinations confirmed neuromuscular involvement in 17 patients: a likely association of critical illness myopathy (CIM) and critical illness polyneuropathy (CIP) was found in 5 patients; CIM alone was found in 4 patients; axonal sensory-motor polyneuropathy was found in 4 patients (CIP in 2 patients, metabolic polyneuropathy in 2 patients); Guillain-Barré syndrome was found in 2 patients (classical demyelinating sensory-motor polyneuropathy and acute motor axonal neuropathy, respectively); peroneal nerve injury was found in 1 patient; and pre-existing L4 radiculopathy was found in 1 patient. Conclusions: Neuromuscular involvement is a very common finding among patients admitted for rehabilitation after COVID-19, and proper investigation should be conducted when muscle or nerve injury is suspected for adequate rehabilitative strategy planning.

Porcine teschovirus, sapelovirus, and enterovirus in Swiss pigs: multiplex RT-PCR investigation of viral frequencies and disease association

2021 ◽  
pp. 104063872110258
Author(s):  
Tamara Stäubli ◽  
Charlotte I. Rickli ◽  
Paul R. Torgerson ◽  
Cornel Fraefel ◽  
Julia Lechmann
Keyword(s):  
Clinical Signs ◽  
Virus Detection ◽  
Common Finding ◽  
Fecal Samples ◽  
High Frequencies ◽  
Reverse Transcription Pcr ◽  
Suckling Piglets ◽  
Porcine Teschovirus ◽  
Fattening Pigs ◽  
Pathology Data

Porcine teschovirus (PTV), sapelovirus (PSV-A), and enterovirus (EV-G) are enteric viruses that can infect pigs and wild boars worldwide. The viruses have been associated with several diseases, primarily gastrointestinal, neurologic, reproductive, and respiratory disorders, but also with subclinical infections. However, for most serotypes, proof of a causal relationship between viral infection and clinical signs is still lacking. In Switzerland, there has been limited investigation of the occurrence of the 3 viruses. We used a modified multiplex reverse-transcription PCR protocol to study the distribution of the viruses in Swiss pigs by testing 363 fecal, brain, and placental or abortion samples from 282 healthy and diseased animals. We did not detect the 3 viruses in 94 placental or abortion samples or in 31 brain samples from healthy pigs. In brain tissue of 81 diseased pigs, we detected 5 PSV-A and 4 EV-G positive samples. In contrast, all 3 viruses were detected at high frequencies in fecal samples of both healthy and diseased pigs. In healthy animals, PTV was detected in 47%, PSV-A in 51%, and EV-G in 70% of the 76 samples; in diseased animals, frequencies in the 81 samples were 54%, 64%, and 68%, respectively. The viruses were detected more frequently in fecal samples from weaned and fattening pigs compared to suckling piglets and sows. Co-detections of all 3 viruses were the most common finding. Based on clinical and pathology data, statistical analysis yielded no evidence for an association of virus detection and disease. Further research is required to determine if pathogenicity is linked to specific serotypes of these viruses.

SLC25A19 deficiency and bilateral striatal necrosis with polyneuropathy: a new case and review of the literature

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Francesco Porta ◽  
Barbara Siri ◽  
Nicoletta Chiesa ◽  
Federica Ricci ◽  
Lulash Nika ◽  
...  
Keyword(s):  
Axonal Neuropathy ◽  
Clinical Signs ◽  
Leigh Syndrome ◽  
High Dose ◽  
New Variant ◽  
Long Term Follow Up ◽  
Basal Ganglia Involvement ◽  
Biallelic Mutations ◽  
Thiamine Treatment ◽  
Striatal Necrosis

AbstractObjectivesBiallelic mutations in the SLC25A19 gene impair the function of the thiamine mitochondrial carrier, leading to two distinct clinical phenotypes. Homozygosity for the c.530G > C mutation is invariably associated to Amish lethal microcephaly. The second phenotype, reported only in 8 patients homozygous for different non-Amish mutations (c.373G > A, c.580T > C, c.910G > A, c.869T > A, c.576G > C), is characterized by bilateral striatal necrosis and peripheral polyneuropathy. We report a new patient with the non-Amish SLC25A19 phenotype showing compound heterozygosity for the new variant c.673G > A and the known mutation c.373G > A.Case presentationThe natural history of non-Amish SLC25A19 deficiency is characterized by acute episodes of fever-induced encephalopathy accompanied by isolated lactic acidosis and Leigh-like features at magnetic resonance imaging (MRI). Acute episodes are prevented by high-dose thiamine treatment (600 mg/day). As shown in the new case, both mild clinical signs and basal ganglia involvement can precede the acute encephalopathic onset of the disease, potentially allowing treatment anticipation and prevention of acute brain damage. Peripheral axonal neuropathy, observed in 7 out of 9 patients, is not improved by thiamine therapy. In two early treated patients, however, peripheral neuropathy did not occur even on long-term follow-up, suggesting a potential preventive role of treatment anticipation also at the peripheral level.ConclusionsNon-Amish SLC25A19 deficiency is an extra-rare cause of Leigh syndrome responsive to thiamine treatment. Ex adiuvantibus thiamine treatment is mandatory in any patient with Leigh-like features.

Neuroleptic malignant syndrome and acute motor axonal neuropathy after Campylobacter jejuni infection

2009 ◽  
Vol 39 (3) ◽  
pp. 135-138 ◽  
Author(s):  
Y.A. Rajabally ◽  
A. Ramlackhansingh ◽  
M. Fraser ◽  
R.J. Abbott
Keyword(s):  
Neuroleptic Malignant Syndrome ◽  
Campylobacter Jejuni ◽  
Axonal Neuropathy ◽  
Acute Motor Axonal Neuropathy

scholarly journals Acute Motor Axonal Neuropathy Associated with Pandemic H1N1 Influenza A Infection

2010 ◽  
Vol 13 (1) ◽  
pp. 98-100 ◽  
Author(s):  
Marko Kutleša ◽  
Marija Santini ◽  
Vladimir Krajinović ◽  
Dinko Raffanelli ◽  
Bruno Baršić
Keyword(s):  
Influenza A ◽  
Axonal Neuropathy ◽  
H1n1 Influenza ◽  
Pandemic H1n1 ◽  
Acute Motor Axonal Neuropathy ◽  
Pandemic H1n1 Influenza

Acute Motor Axonal Neuropathy Associated with IgM Anti-GM1 following Mycoplasma pneumoniae Infection

1999 ◽  
Vol 41 (3) ◽  
pp. 175-176 ◽  
Author(s):  
J.G. Heckmann ◽  
J.B. Sommer ◽  
A. Druschky ◽  
F.J. Erbguth ◽  
A.J. Steck ◽  
...  
Keyword(s):  
Mycoplasma Pneumoniae ◽  
Axonal Neuropathy ◽  
Acute Motor Axonal Neuropathy
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