scholarly journals Toxicity in Peripheral Nerves: An Overview

Toxics ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 218
Author(s):  
Wolfgang Grisold ◽  
Valentina Alda Carozzi
Keyword(s):  
Peripheral Nerves ◽  
Toxic Substance ◽  
Focal Lesions ◽  
Fiber Damage ◽  
Toxic Neuropathy ◽  
Immune Mediated ◽  
Toxic Agents ◽  
Mucous Membranes ◽  
Demyelinating Lesions ◽  
Warfare Agents

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.

scholarly journals Microglial Pruning: Relevance for Synaptic Dysfunction in Multiple Sclerosis and Related Experimental Models

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 686
Author(s):  
Maria Concetta Geloso ◽  
Nadia D’Ambrosi
Keyword(s):  
Multiple Sclerosis ◽  
Neuronal Death ◽  
Environmental Changes ◽  
Experimental Models ◽  
Synaptic Dysfunction ◽  
Synapse Elimination ◽  
Neurodegenerative Process ◽  
Immune Mediated ◽  
Wide Range ◽  
Demyelinating Lesions

Microglia, besides being able to react rapidly to a wide range of environmental changes, are also involved in shaping neuronal wiring. Indeed, they actively participate in the modulation of neuronal function by regulating the elimination (or “pruning”) of weaker synapses in both physiologic and pathologic processes. Mounting evidence supports their crucial role in early synaptic loss, which is emerging as a hallmark of several neurodegenerative diseases, including multiple sclerosis (MS) and its preclinical models. MS is an inflammatory, immune-mediated pathology of the white matter in which demyelinating lesions may cause secondary neuronal death. Nevertheless, primitive grey matter (GM) damage is emerging as an important contributor to patients’ long-term disability, since it has been associated with early and progressive cognitive decline (CD), which seriously worsens the quality of life of MS patients. Widespread synapse loss even in the absence of demyelination, axon degeneration and neuronal death has been demonstrated in different GM structures, thus raising the possibility that synaptic dysfunction could be an early and possibly independent event in the neurodegenerative process associated with MS. This review provides an overview of microglial-dependent synapse elimination in the neuroinflammatory process that underlies MS and its experimental models.

Acute Disseminated Encephalomyelitis

2012 ◽  
Vol 27 (11) ◽  
pp. 1408-1425 ◽  
Author(s):  
Gulay Alper
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acute Disseminated Encephalomyelitis ◽  
Protein Levels ◽  
Demyelinating Disorder ◽  
Immune Mediated ◽  
Elevated Protein ◽  
Demyelinating Lesions ◽  
Diagnostic Difficulties ◽  
The Central Nervous System

Acute disseminated encephalomyelitis is an immune-mediated inflammatory and demyelinating disorder of the central nervous system, commonly preceded by an infection. It principally involves the white matter tracts of the cerebral hemispheres, brainstem, optic nerves, and spinal cord. Acute disseminated encephalomyelitis mainly affects children. Clinically, patients present with multifocal neurologic abnormalities reflecting the widespread involvement in central nervous system. Cerebrospinal fluid may be normal or may show a mild pleocytosis with or without elevated protein levels. Magnetic resonance image (MRI) shows multiple demyelinating lesions. The diagnosis of acute disseminated encephalomyelitis requires both multifocal involvement and encephalopathy by consensus criteria. Acute disseminated encephalomyelitis typically has a monophasic course with a favorable prognosis. Multiphasic forms have been reported, resulting in diagnostic difficulties in distinguishing these cases from multiple sclerosis. In addition, many inflammatory disorders may have a similar presentation with frequent occurrence of encephalopathy and should be considered in the differential diagnosis of acute disseminated encephalomyelitis.

Brachial Plexitis—Parsonage-Turner Syndrome

2018 ◽  
Author(s):  
Sandra Hearn
Keyword(s):  
Turner Syndrome ◽  
Impression Management ◽  
Peripheral Nerves ◽  
Surgical Intervention ◽  
Sudden Onset ◽  
Accurate Diagnosis ◽  
Advanced Imaging ◽  
Neuralgic Amyotrophy ◽  
Arm Pain ◽  
Immune Mediated

The chapter provides a case-based review of Parsonage-Turner syndrome. Parsonage-Turner syndrome, also known as neuralgic amyotrophy and idiopathic brachial plexitis, represents immune-mediated inflammation of neural structures within the brachial plexus and peripheral nerves of the upper limb. Classic features include sudden-onset shoulder or upper arm pain, followed by weakness in the forequarter or limb. This pattern, in addition to nonmechanical and nonradicular clinical features, should prompt consideration of Parsonage-Turner syndrome diagnosis. The diagnosis is established on clinical grounds, although electrodiagnostic data and advanced imaging can support the impression. Management is conservative. For neurosurgeons, accurate diagnosis of Parsonage-Turner syndrome can avoid unnecessary and inappropriate surgical intervention when symptoms are erroneously ascribed to another cause.

scholarly journals Tracking the evolution of CNS remyelinating lesion in mice with neutral red dye

2019 ◽  
Vol 116 (28) ◽  
pp. 14290-14299 ◽  
Author(s):  
Maryna Baydyuk ◽  
David S. Cha ◽  
Jingwen Hu ◽  
Reiji Yamazaki ◽  
Evan M. Miller ◽  
...  
Keyword(s):  
Neutral Red ◽  
Mass Spectrometry Analysis ◽  
Focal Lesion ◽  
Cns Injury ◽  
Autoimmune Encephalomyelitis ◽  
Spectrometry Analysis ◽  
Immune Mediated ◽  
Demyelinating Lesions ◽  
Demyelinating Disorders ◽  
Red Dye

Animal models of central nervous system (CNS) demyelination, including toxin-induced focal demyelination and immune-mediated demyelination through experimental autoimmune encephalomyelitis (EAE), have provided valuable insights into the mechanisms of neuroinflammation and CNS remyelination. However, the ability to track changes in transcripts, proteins, and metabolites, as well as cellular populations during the evolution of a focal lesion, has remained challenging. Here, we developed a method to label CNS demyelinating lesions by the intraperitoneal injection of a vital dye, neutral red (NR), into mice before killing. We demonstrate that NR-labeled lesions can be easily identified on the intact spinal cord in both lysolecithin- and EAE-mediated demyelination models. Using fluorescence microscopy, we detected NR in activated macrophages/microglia and astrocytes, but not in oligodendrocytes present in lesions. Importantly, we successfully performed RT-qPCR, Western blot, flow cytometry, and mass spectrometry analysis of precisely dissected NR-labeled lesions at 5, 10, and 20 d postlesion (dpl) and found differential changes in transcripts, proteins, cell populations, and metabolites in lesions over the course of remyelination. Therefore, NR administration is a simple and powerful method to track and analyze the detailed molecular, cellular, and metabolic changes that occur within the lesion microenvironment over time following CNS injury. Furthermore, this method can be used to identify molecular and metabolic pathways that regulate neuroinflammation and remyelination and facilitate the development of therapies to promote repair in demyelinating disorders such as multiple sclerosis.

scholarly journals Inflammatory polyradiculoneuropathies: Clinical and immunological aspects, current therapies, and future perspectives

2020 ◽  
Vol 18 ◽  
pp. 205873922094234
Author(s):  
Vincenzo Di Stefano ◽  
Filomena Barbone ◽  
Camilla Ferrante ◽  
Roberta Telese ◽  
Michela Vitale ◽  
...  
Keyword(s):  
Peripheral Nerves ◽  
Axonal Degeneration ◽  
Chronic Inflammatory Demyelinating Polyneuropathy ◽  
Leukocyte Infiltration ◽  
Potential Treatment ◽  
Future Perspectives ◽  
Nerve Roots ◽  
Immune Mediated ◽  
Current Therapies ◽  
Made In

Inflammatory polyradiculoneuropathies are heterogeneous disorders characterized by immune-mediated leukocyte infiltration of peripheral nerves and nerve roots leading to demyelination or axonal degeneration or both. Inflammatory polyradiculoneuropathies can be divided into acute and chronic: Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy and their variants. Despite major advances in immunology and molecular biology have been made in the last years, the pathogenesis of these disorders is not completely understood. This review summarizes the current literature of the clinical features and pathogenic mechanisms of inflammatory polyradiculoneuropathies and focuses on current therapies and new potential treatment for the future.

scholarly journals Heterogeneity of Polyneuropathy Associated with Anti-MAG Antibodies

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Laurent Magy ◽  
Raphaël Kaboré ◽  
Stéphane Mathis ◽  
Prisca Lebeau ◽  
Karima Ghorab ◽  
...  
Keyword(s):  
Peripheral Nerves ◽  
Monoclonal Gammopathy ◽  
Demyelinating Neuropathy ◽  
Laboratory Findings ◽  
Electrodiagnostic Testing ◽  
Immune Mediated ◽  
Chronic Inflammatory Demyelinating Neuropathy ◽  
Myelin Associated Glycoprotein ◽  
Demyelinating Peripheral Neuropathy ◽  
Self Antigen

Polyneuropathy associated with IgM monoclonal gammopathy and anti-myelin associated glycoprotein (MAG) antibodies is an immune-mediated demyelinating neuropathy. The pathophysiology of this condition is likely to involve anti-MAG antibody deposition on myelin sheaths of the peripheral nerves and it is supposed to be distinct from chronic inflammatory demyelinating neuropathy (CIDP), another immune-mediated demyelinating peripheral neuropathy. In this series, we have retrospectively reviewed clinical and laboratory findings from 60 patients with polyneuropathy, IgM gammopathy, and anti-MAG antibodies. We found that the clinical picture in these patients is highly variable suggesting a direct link between the monoclonal gammopathy and the neuropathy. Conversely, one-third of patients had a CIDP-like phenotype on electrodiagnostic testing and this was correlated with a low titer of anti-MAG antibodies and the absence of widening of myelin lamellae. Our data suggest that polyneuropathy associated with anti-MAG antibodies is less homogeneous than previously said and that the pathophysiology of the condition is likely to be heterogeneous as well with the self-antigen being MAG in most of the patients but possibly being another component of myelin in the others.

scholarly journals Leukoencephalopathy in a Cat Due to Accidental Cyanide Poisoning

1966 ◽  
Vol 3 (3) ◽  
pp. 190-195 ◽  
Author(s):  
Seymour Levine ◽  
Ludwig W. Geib
Keyword(s):  
White Matter ◽  
Substantia Nigra ◽  
Corpus Callosum ◽  
Anterior Commissure ◽  
Cerebral Hemispheres ◽  
Cerebral White Matter ◽  
Cyanide Poisoning ◽  
Focal Lesions ◽  
Metal Plating ◽  
Demyelinating Lesions

A cat was accidentally poisoned by cyanide in a metal plating factory. It developed symmetrical necrotizing and demyelinating lesions involving most of the central white matter of the cerebral hemispheres, corpus callosum, anterior commissure, as well as focal lesions in globus pallidus, substantia nigra, cerebellum and hippocampus. This one animal had lesions in most of the areas previously known to be affected by cyanide in various species, and it also demonstrated the predilection of this poison for cerebral white matter.

Essential thrombocythemia in a dog: case report and literature review

1998 ◽  
Vol 34 (3) ◽  
pp. 197-203 ◽  
Author(s):  
MC Bass ◽  
AE Schultze
Keyword(s):  
Platelet Count ◽  
Essential Thrombocythemia ◽  
Conservative Therapy ◽  
Systematic Investigation ◽  
Study Group ◽  
Platelet Morphology ◽  
Immune Mediated ◽  
Mucous Membranes ◽  
Criteria For Diagnosis ◽  
Hydroxyurea Therapy

A 10.5-year-old, castrated male shih tzu was presented for evaluation of weakness, pica, and pallor of the mucous membranes. A hemogram indicated an inflammatory leukogram and a regenerative anemia with spherocytosis and thrombocytosis. The dog responded well to conservative therapy for immune-mediated hemolytic anemia (IMHA). However, the thrombocytosis did not resolve. Serial hemograms were characterized by persistent thrombocytosis (platelet count, 577,000 to 1,200,000/microl) with abnormal platelet morphology. A systematic investigation ruled out causes of physiological and reactive thrombocytoses. A diagnosis of essential thrombocythemia was made by fulfilling the criteria of the Polycythemia Vera Study Group of the National Cancer Institute. The marked thrombocytosis was nonresponsive to hydroxyurea therapy. The dog remains healthy despite the marked increase in the number of circulating platelets. A review of causes of thrombocytoses in humans and animals is presented, and the criteria for diagnosis of essential thrombocythemia are examined.

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