Special Issue "Toxic Neuropathy: Mechanisms, Causes, Risk Exposure, Diagnosis, Prevention and Therapeutic Options"

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Toxicology".

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 5609

Special Issue Editors

Dr. Valentina Carozzi
E-Mail Website
Guest Editor
Unità di Neurologia Sperimentale e Centro di Neuroscienze di Milano, Dipartimento di Chirurgia e Medicina traslazionale, Università di Milano-Bicocca, Via Cadore 48, 20900 Monza, Italy
Interests: peripheral neuropathies, antineoplastic drugs, animal models
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Wolfgang Grisold
E-Mail
Guest Editor
Ludwig Boltzmann Institute for Experimental und Clinical Traumatology, Vienna, Austria
Interests: neurotoxicity; peripheral nerve; mechanisms; axonal and myelin damage; risk factors; toxic substances; diagnosis; rehabilitation

Special Issue Information

Dear Colleagues,

The exposure to toxic agents can frequently cause nerve damage leading to neuropathy. These agents may include drugs (antibiotics, antiretroviral agents, cardiac medications, chemotherapy, chloroquine, hydroxychloroquine, lithium, TNF-alpha inhibitors, and warfare drugs, for example), organic solvents, heavy metals, alcohol, biologicals, and other substances.

Most mechanisms of toxic neuropathy include axonal degeneration, impairment of axonal transport, damage of myelin and of peripheral neuron energy metabolism, as well as toxicity at Ranvier node, ion channels, and small fibers. Clinically, patients may suffer from numbness, tingling, pain, walking difficulties, sensory deficits, autonomic and motor disturbances, weakness, and often from neuropathic pain, which make toxic neuropathy difficult to diagnose. Symptoms usually have an insidious onset, sometimes shortly after exposure to toxics.

This Special Issue aims to highlight the research on the established knowledge as well as on open issues regarding toxic neuropathy. Studies that report insights into:

  • The mechanisms of toxic neuropathies of all types and origins (accidental or not accidental exposure to toxic substances) as well as on the evaluation and discussion of the risk factors and susceptibilities (e.g., genetic, environment, patients’ history and social condition, pre-existing neuropathy);
  • The indirect mechanisms of neuropathy development, discussing subtle ways of contracting the disease (e.g., aerosols, environment, nutrition);
  • The diagnosis, preventive strategies, time course of the disease, as well as the available and experimental therapeutic options;
  • The improvement of the awareness of toxic neuropathies and the identification of medical conditions;
  • Rehabilitation, medical, and social solutions

are encouraged. Preclinical and clinical research as well as translational research are welcome.

Authors are invited to submit original research papers, reviews, and short communications with no limitations in terms of number of pages or words. Moreover, tables and figures that can help in summarizing and/or focusing on important issues can be added in support of the text.

Dr. Valentina Alda Carozzi
Prof. Dr. Wolfgang Grisold
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurotoxicity
  • peripheral nerve
  • mechanisms
  • axonal and myelin damage
  • risk factors
  • toxic substances
  • diagnosis
  • rehabilitation

Published Papers (5 papers)

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Research

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Article
Factors Predicting Acute Brain Injury in Cases of Carbon Monoxide Poisoning: A Prospective Registry-Based Study
Toxics 2021, 9(6), 120; https://doi.org/10.3390/toxics9060120 - 27 May 2021
Viewed by 970
Abstract
Carbon monoxide (CO) is one of the most common poisoning substances worldwide. Since acute brain injury (ABI) is an important determinant of the neurological outcome in CO poisoning, screening for patients at a high risk of developing ABI is essential for the proper [...] Read more.
Carbon monoxide (CO) is one of the most common poisoning substances worldwide. Since acute brain injury (ABI) is an important determinant of the neurological outcome in CO poisoning, screening for patients at a high risk of developing ABI is essential for the proper treatment. This study identified predictors of ABI in patients with CO poisoning. This prospective registry-based study was conducted in patients who visited a tertiary care hospital for CO poisoning from August 2016 to June 2020. ABI was defined as the presence of acute hypoxic lesions on diffusion-weighted magnetic resonance imaging. Multiple logistic regression analysis was performed to identify the predictors of ABI. Of 231 patients, 64 (27.7%) showed ABI. Multiple logistic regression analysis showed that a Glasgow Coma Scale (GCS) score <9 at presentation (odds ratio [OR] 3.28, 95% confidence interval (CI) 1.08–10.01), creatinine level >1.2 mg/dL (OR 3.04, 95% CI 1.16–8.01), and C-reactive protein (CRP) level >9.2 mg/L (OR 4.38, 95% CI 1.41–13.65) predicted ABI in cases of acute CO poisoning. In CO poisoning, the GCS score at presentation, and serum creatinine and CRP levels, were useful predictors of ABI, and may help clinicians identify high-risk patients for whom treatment should be prioritized. Full article
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Review

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Review
Considerations for a Reliable In Vitro Model of Chemotherapy-Induced Peripheral Neuropathy
Toxics 2021, 9(11), 300; https://doi.org/10.3390/toxics9110300 - 11 Nov 2021
Cited by 1 | Viewed by 811
Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) is widely recognized as a potentially severe toxicity that often leads to dose reduction or discontinuation of cancer treatment. Symptoms may persist despite discontinuation of chemotherapy and quality of life can be severely compromised. The clinical symptoms of CIPN, [...] Read more.
Chemotherapy-induced peripheral neuropathy (CIPN) is widely recognized as a potentially severe toxicity that often leads to dose reduction or discontinuation of cancer treatment. Symptoms may persist despite discontinuation of chemotherapy and quality of life can be severely compromised. The clinical symptoms of CIPN, and the cellular and molecular targets involved in CIPN, are just as diverse as the wide variety of anticancer agents that cause peripheral neurotoxicity. There is an urgent need for extensive molecular and functional investigations aimed at understanding the mechanisms of CIPN. Furthermore, a reliable human cell culture system that recapitulates the diversity of neuronal modalities found in vivo and the pathophysiological changes that underlie CIPN would serve to advance the understanding of the pathogenesis of CIPN. The demonstration of experimental reproducibility in a human peripheral neuronal cell system will increase confidence that such an in vitro model is clinically useful, ultimately resulting in deeper exploration for the prevention and treatment of CIPN. Herein, we review current in vitro models with a focus on key characteristics and attributes desirable for an ideal human cell culture model relevant for CIPN investigations. Full article
Review
Pathomechanisms of Paclitaxel-Induced Peripheral Neuropathy
Toxics 2021, 9(10), 229; https://doi.org/10.3390/toxics9100229 - 22 Sep 2021
Cited by 8 | Viewed by 1267
Abstract
Peripheral neuropathy is one of the most common side effects of chemotherapy, affecting up to 60% of all cancer patients receiving chemotherapy. Moreover, paclitaxel induces neuropathy in up to 97% of all gynecological and urological cancer patients. In cancer cells, paclitaxel induces cell [...] Read more.
Peripheral neuropathy is one of the most common side effects of chemotherapy, affecting up to 60% of all cancer patients receiving chemotherapy. Moreover, paclitaxel induces neuropathy in up to 97% of all gynecological and urological cancer patients. In cancer cells, paclitaxel induces cell death via microtubule stabilization interrupting cell mitosis. However, paclitaxel also affects cells of the central and peripheral nervous system. The main symptoms are pain and numbness in hands and feet due to paclitaxel accumulation in the dorsal root ganglia. This review describes in detail the pathomechanisms of paclitaxel in the peripheral nervous system. Symptoms occur due to a length-dependent axonal sensory neuropathy, where axons are symmetrically damaged and die back. Due to microtubule stabilization, axonal transport is disrupted, leading to ATP undersupply and oxidative stress. Moreover, mitochondria morphology is altered during paclitaxel treatment. A key player in pain sensation and axonal damage is the paclitaxel-induced inflammation in the spinal cord as well as the dorsal root ganglia. An increased expression of chemokines and cytokines such as IL-1β, IL-8, and TNF-α, but also CXCR4, RAGE, CXCL1, CXCL12, CX3CL1, and C3 promote glial activation and accumulation, and pain sensation. These findings are further elucidated in this review. Full article
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Review
Toxicity in Peripheral Nerves: An Overview
Toxics 2021, 9(9), 218; https://doi.org/10.3390/toxics9090218 - 11 Sep 2021
Cited by 2 | Viewed by 913
Abstract
Introduction to a collection. This article is intended to introduce a collection of papers on toxic neuropathies. Toxic neuropathies can be caused by a variety of substances and by different mechanisms. Toxic agents are numerous and can be distinguished between drugs, recreational agents, [...] Read more.
Introduction to a collection. This article is intended to introduce a collection of papers on toxic neuropathies. Toxic neuropathies can be caused by a variety of substances and by different mechanisms. Toxic agents are numerous and can be distinguished between drugs, recreational agents, heavy metals, industrial agents, pesticides, warfare agents, biologic substances and venoms. Toxic agents reach the nervous system by ingestion, transcutaneously, via the mucous membranes, parenterally and by aerosols. The most frequent types are cumulative toxicities. Other types are acute or delayed toxicities. Pathogenetic mechanisms range from a specific toxic substance profile causing axonal or demyelinating lesions, towards ion channel interferences, immune-mediated mechanisms and a number of different molecular pathways. In addition, demyelination, focal lesions and small fiber damage may occur. Clinically, neurotoxicity presents most frequently as axonal symmetric neuropathies. In this work, we present a panoramic view of toxic neuropathy, in terms of symptoms, causes, mechanisms and classification. Full article
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Review
The Role of Protein Adduction in Toxic Neuropathies of Exogenous and Endogenous Origin
Toxics 2021, 9(5), 98; https://doi.org/10.3390/toxics9050098 - 29 Apr 2021
Cited by 1 | Viewed by 828
Abstract
The peripheral (axonal) neuropathy associated with repeated exposure to aliphatic and aromatic solvents that form protein-reactive γ-diketones shares some clinical and neuropathological features with certain metabolic neuropathies, including type-II diabetic neuropathy and uremic neuropathy, and with the largely sub-clinical nerve damage associated with [...] Read more.
The peripheral (axonal) neuropathy associated with repeated exposure to aliphatic and aromatic solvents that form protein-reactive γ-diketones shares some clinical and neuropathological features with certain metabolic neuropathies, including type-II diabetic neuropathy and uremic neuropathy, and with the largely sub-clinical nerve damage associated with old age. These conditions may be linked by metabolites that adduct and cross-link neuroproteins required for the maintenance of axonal transport and nerve fiber integrity in the peripheral and central nervous system. Full article
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