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Deutsches Arzteblatt International Feb 2018
Topics: Critical Pathways; Humans; Polyneuropathies
PubMed: 29478434
DOI: 10.3238/arztebl.2018.0081 -
The Primary Care Companion For CNS... Nov 2022
Topics: Humans; Anorexia Nervosa; Muscular Diseases; Polyneuropathies
PubMed: 36343356
DOI: 10.4088/PCC.21cr03169 -
Molecular Metabolism Jan 2021The lack of effective treatments against diabetic sensorimotor polyneuropathy demands the search for new strategies to combat or prevent the condition. Because reduced...
OBJECTIVE
The lack of effective treatments against diabetic sensorimotor polyneuropathy demands the search for new strategies to combat or prevent the condition. Because reduced magnesium and increased methylglyoxal levels have been implicated in the development of both type 2 diabetes and neuropathic pain, we aimed to assess the putative interplay of both molecules with diabetic sensorimotor polyneuropathy.
METHODS
In a cross-sectional study, serum magnesium and plasma methylglyoxal levels were measured in recently diagnosed type 2 diabetes patients with (n = 51) and without (n = 184) diabetic sensorimotor polyneuropathy from the German Diabetes Study baseline cohort. Peripheral nerve function was assessed using nerve conduction velocity and quantitative sensory testing. Human neuroblastoma cells (SH-SY5Y) and mouse dorsal root ganglia cells were used to characterize the neurotoxic effect of methylglyoxal and/or neuroprotective effect of magnesium.
RESULTS
Here, we demonstrate that serum magnesium concentration was reduced in recently diagnosed type 2 diabetes patients with diabetic sensorimotor polyneuropathy and inversely associated with plasma methylglyoxal concentration. Magnesium, methylglyoxal, and, importantly, their interaction were strongly interrelated with methylglyoxal-dependent nerve dysfunction and were predictive of changes in nerve function. Magnesium supplementation prevented methylglyoxal neurotoxicity in differentiated SH-SY5Y neuron-like cells due to reduction of intracellular methylglyoxal formation, while supplementation with the divalent cations zinc and manganese had no effect on methylglyoxal neurotoxicity. Furthermore, the downregulation of mitochondrial activity in mouse dorsal root ganglia cells and consequently the enrichment of triosephosphates, the primary source of methylglyoxal, resulted in neurite degeneration, which was completely prevented through magnesium supplementation.
CONCLUSIONS
These multifaceted findings reveal a novel putative pathophysiological pathway of hypomagnesemia-induced carbonyl stress leading to neuronal damage and merit further investigations not only for diabetic sensorimotor polyneuropathy but also other neurodegenerative diseases associated with magnesium deficiency and impaired energy metabolism.
Topics: Animals; Cross-Sectional Studies; Diabetes Mellitus; Diabetic Neuropathies; Energy Metabolism; Female; Glycation End Products, Advanced; Humans; Magnesium; Male; Mice; Middle Aged; Mitochondria; Neurons; Polyneuropathies; Pyruvaldehyde; Sensorimotor Cortex
PubMed: 33166742
DOI: 10.1016/j.molmet.2020.101114 -
Der Nervenarzt Feb 2023Neuropathic pruritus is a previously neglected symptom of a wide range of neurological diseases. Peripheral nerve or root compression syndromes, space-occupying... (Review)
Review
Neuropathic pruritus is a previously neglected symptom of a wide range of neurological diseases. Peripheral nerve or root compression syndromes, space-occupying lesions of the central nervous system, chronic inflammatory neurological diseases and polyneuropathy can cause neuropathic pruritus. Even when the identification of the underlying neurological disease is successful, a direct causal treatment is not always possible, hence an effective symptomatic treatment remains the only therapeutic option. The purpose of this review article is to present the current literature on various therapeutic agents and options in the treatment of neuropathic pruritus.
Topics: Humans; Pruritus; Peripheral Nervous System Diseases; Central Nervous System; Polyneuropathies
PubMed: 35951052
DOI: 10.1007/s00115-022-01369-0 -
CMAJ : Canadian Medical Association... Feb 2023
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Neurology Dec 2020To present standardized diagnostic criteria for idiopathic distal sensory polyneuropathy (iDSP) and its subtypes: idiopathic mixed fiber sensory neuropathy (iMFN),... (Review)
Review
OBJECTIVE
To present standardized diagnostic criteria for idiopathic distal sensory polyneuropathy (iDSP) and its subtypes: idiopathic mixed fiber sensory neuropathy (iMFN), idiopathic small fiber sensory neuropathy (iSFN), and idiopathic large fiber sensory neuropathy (iLFN) for use in research.
METHODS
The Analgesic, Anesthetic, and Addiction Clinical Trial Translations, Innovations, Opportunities and Networks (ACTTION) public-private partnership with the Food and Drug Administration convened a meeting to develop consensus diagnostic criteria for iMFN, iSFN, and iLFN. After background presentations, a collaborative, iterative approach was used to develop expert consensus for new criteria.
RESULTS
An iDSP diagnosis requires at least 1 small fiber (SF) or large fiber (LF) symptom, at least 1 SF or LF sign, abnormalities in sensory nerve conduction studies (NCS) or distal intraepidermal nerve fiber density (IENFD), and exclusion of known etiologies. An iMFN diagnosis requires that at least 1 of the above clinical features is SF and 1 clinical feature is LF with abnormalities in sensory NCS or IENFD. Diagnostic criteria for iSFN require at least 1 SF symptom and at least 1 SF sign with abnormal IENFD, normal sensory NCS, and the absence of LF symptoms and signs. Diagnostic criteria for iLFN require at least 1 LF symptom and at least 1 LF sign with normal IENFD, abnormal sensory NCS, and absence of SF symptoms and signs.
CONCLUSION
Adoption of these standardized diagnostic criteria will advance research and clinical trials and spur development of novel therapies for iDSPs.
Topics: Humans; Nerve Fibers, Myelinated; Nerve Fibers, Unmyelinated; Polyneuropathies; Practice Guidelines as Topic; Small Fiber Neuropathy
PubMed: 33055271
DOI: 10.1212/WNL.0000000000010988 -
Respiratory Medicine Sep 2022Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory syndrome with systemic involvement leading to various cardiovascular, metabolic, and neurological... (Review)
Review
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory syndrome with systemic involvement leading to various cardiovascular, metabolic, and neurological comorbidities. It is well known that conditions associated with oxygen deprivation and metabolic disturbance are associated with polyneuropathy, but current data regarding the relationship between COPD and peripheral nervous system pathology is limited. This review summarizes the available data on the association between COPD and polyneuropathy, including possible pathophysiological mechanisms such as the role of hypoxia, proinflammatory state, and smoking in nerve damage; the role of cardiovascular and metabolic comorbidities, as well as the diagnostic methods and screening tools for identifying polyneuropathy. Furthermore, it outlines the available options for managing and preventing polyneuropathy in COPD patients. Overall, current data suggest that optimal screening strategies to diagnose polyneuropathy early should be implemented in COPD patients due to their relatively common association and the additional burden of polyneuropathy on quality of life.
Topics: Comorbidity; Humans; Peripheral Nervous System Diseases; Polyneuropathies; Pulmonary Disease, Chronic Obstructive; Quality of Life
PubMed: 36029697
DOI: 10.1016/j.rmed.2022.106952 -
Journal of Rehabilitation Medicine Apr 2022Patients with COVID-19 may develop a range of neurological disorders. We report here 4 COVID-19 subjects with intensive care unit-acquired weakness and their functional... (Review)
Review
Patients with COVID-19 may develop a range of neurological disorders. We report here 4 COVID-19 subjects with intensive care unit-acquired weakness and their functional outcome. In addition, a scoping review of COVID-19 literature was performed to investigate this issue. Of the post-COVID-19 patients admitted to our Neuro-Rehabilitation Unit, 4 (3 males, 1 female; mean age 59.2 ± 8.62 years) had intensive care unit-acquired weakness, diagnosed with electromyography. Muscle strength and functional evaluation were performed on all patients with Medical Research Council, Disability Rating Scale and Functional Independence Measure, respectively, at admission, discharge and 6-month follow-up after discharge. Electromyography revealed that 3 subjects had critical illness polyneuropathy and 1 had critical illness polyneuropathy/critical illness myopathy. At follow-up, the 3 subjects with critical illness polyneuropathy reached full recovery. The patient with critical illness polyneuropathy/critical illness myopathy showed moderate disability requiring bilateral ankle foot-orthosis and support for ambulation. The scoping review retrieved 11 studies of COVID-19 patients with intensive care unit-acquired weakness, concerning a total of 80 patients: 23 with critical illness myopathy (7 probable), 21 with critical illness polyneuropathy (8 possible), 15 with critical illness polyneuropathy and myopathy (CIPNM) and 21 with intensive care unit-acquired weakness. Of 35 patients who survived, only 3 (8.5%) reached full recovery. All 3 had critical illness myopathy, but 2 of these had a diagnosis of probable critical illness myopathy. Intensive care unit-acquired weakness commonly occurred in subjects with COVID-19. Recovery was variable and a low percentage reached full recovery. However, the heterogeneity of studies did not allow definitive conclusions to be drawn.
Topics: Aged; COVID-19; Critical Illness; Female; Humans; Intensive Care Units; Male; Middle Aged; Muscle Weakness; Muscular Diseases; Polyneuropathies
PubMed: 34935988
DOI: 10.2340/jrm.v53.1139 -
Autoimmunity Dec 2024Immune-mediated demyelinating polyneuropathies (IMDPs) are rare disorders in which dysregulated adaptive immune responses cause peripheral nerve demyelinating... (Review)
Review
Immune-mediated demyelinating polyneuropathies (IMDPs) are rare disorders in which dysregulated adaptive immune responses cause peripheral nerve demyelinating inflammation and axonal injury in susceptible individuals. Despite significant advances in understanding IMDP pathogenesis guided by patient data and representative mammalian models, specific therapies are lacking. Significant knowledge gaps in IMDP pathogenesis still exist, e.g. precise antigen(s) and mechanisms that initially trigger immune system activation and identification of large population disease susceptibility factors. The initial directional cues for antigen-specific effector or autoreactive leukocyte trafficking into peripheral nerves are also unknown. An overview of current animal models, with emphasis on the experimental autoimmune neuritis and spontaneous autoimmune peripheral polyneuropathy models, is provided. Insights on the initial directional cues for peripheral nerve tissue specific autoimmunity using a novel Major Histocompatibility Complex class II conditional knockout mouse strain are also discussed, suggesting an essential research tool to study cell- and time-dependent adaptive immunity in autoimmune diseases.
Topics: Animals; Disease Models, Animal; Humans; Mice; Neuritis, Autoimmune, Experimental; Mice, Knockout; Autoimmunity; Polyneuropathies; Adaptive Immunity; Histocompatibility Antigens Class II
PubMed: 38850571
DOI: 10.1080/08916934.2024.2361745 -
Arquivos de Neuro-psiquiatria Mar 2022Polyneuropathies are characterized by a symmetrical impairment of the peripheral nervous system, resulting in sensory, motor and/or autonomic deficits. Due to the... (Observational Study)
Observational Study
BACKGROUND
Polyneuropathies are characterized by a symmetrical impairment of the peripheral nervous system, resulting in sensory, motor and/or autonomic deficits. Due to the heterogeneity of causes, an etiological diagnosis for polyneuropathy is challenging.
OBJECTIVE
The aim of this study was to determine the main causes of polyneuropathy confirmed by electrodiagnostic (EDX) tests in a tertiary service and its neurophysiological aspects.
METHODS
This observational cross-sectional study from a neuromuscular disorders center included individuals whose electrodiagnostic tests performed between 2008 and 2017 confirmed a diagnosis of polyneuropathy. Through analysis of medical records, polyneuropathies were classified according to etiology and neurophysiological aspect.
RESULTS
Of the 380 included patients, 59.5% were male, with a median age of 43 years. The main etiologies were: inflammatory (23.7%), hereditary (18.9%), idiopathic (13.7%), multifactorial (11.1%), and diabetes (10.8%). The main electrophysiological patterns were axonal sensorimotor polyneuropathy (36.1%) and "demyelinating and axonal" sensorimotor polyneuropathy (27.9%). Axonal patterns showed greater etiological heterogeneity, with a predominance of idiopathic and multifactorial polyneuropathy, while demyelinating and "demyelinating and axonal" polyneuropathies had a significantly fewer etiologies, with a predominance of hereditary and inflammatory polyneuropathies.
CONCLUSION
The main causes of polyneuropathy confirmed by EDX test in this study were those that presented a severe, atypical and/or rapidly progressing pattern. Other causes were hereditary and those that defy clinical reasoning, such as multiple risk factors; some polyneuropathies did not have a specific etiology. EDX tests are useful for etiological diagnosis of rare polyneuropathies, because neurophysiological patterns are correlated with specific etiologies.
Topics: Adult; Axons; Cross-Sectional Studies; Electrodiagnosis; Female; Humans; Male; Neurophysiology; Physical Examination; Polyneuropathies
PubMed: 34816968
DOI: 10.1590/0004-282X-ANP-2020-0561