Chemotherapy-Induced Peripheral Neuropathy: Mechanisms and Clinical Assessment

Mapping Intimacies ◽

10.5772/intechopen.100495 ◽

2021 ◽

Author(s):

Jordi Casanova-Mollà

Keyword(s):

Sensory Neurons ◽

Motor Neurons ◽

Clinical Assessment ◽

Neuromuscular Transmission ◽

Immune Checkpoint Inhibitors ◽

Checkpoint Inhibitors ◽

Sensory Nerve ◽

Nerve Fibers ◽

Sensory Loss ◽

Autonomic Nerves

Antineoplastic drugs may be neurotoxic and the clinical features frequently include distal sensory loss and neuropathic pain. This is related to a direct damage in sensory neurons and non-selective degeneration of sensory nerve fibers. Due to different mechanisms, there are agents that affects also motor or autonomic nerves. In the case of immune checkpoint inhibitors, an inflammatory response attacks the muscle, motor neurons or neuromuscular transmission. We present an easy-to-read article to understand first symptoms of chemotherapy-induced neuropathy (CIN) with describing each agent and the course of neuropathy as well as the clinical assessment with neurophysiological techniques. In addition, skin biopsy allows us to examine histological changes such as reinnervation. Neuroprotection with antioxidant therapy is possible but more effort in this field is needed.

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Motor unit involvement in human acute Chagas' disease

Arquivos de Neuro-Psiquiatria ◽

10.1590/s0004-282x1989000300005 ◽

1989 ◽

Vol 47 (3) ◽

pp. 283-286 ◽

Cited By ~ 5

Author(s):

O. R. Benavente ◽

O. Ledesma Patiño ◽

L. Baez Peña ◽

H. Lugones ◽

E. Kalala ◽

...

Keyword(s):

Motor Unit ◽

Chagas Disease ◽

Neuromuscular Transmission ◽

Sensory Nerve ◽

Nerve Fibers ◽

Acute Stage ◽

Repetitive Stimulation ◽

Muscle Involvement ◽

Sharp Waves ◽

Acute Chagas Disease

Thirty five patients with acute Chagas' disease who demonstrated parasitaemia at the time of the investigation were submitted to a detailed electromyographical study. With their muscles at rest, 12 patients showed fibrillation potentials and/or positive sharp waves. On volitional contraction, 7 had short duration motor unit potentials (MUPs) and low polyphasic MUPs. On motor and sensory nerve fibers conduction studies, 20 disclosed values below the lower control limit within one or more nerves. Finally, 12 patients produced a muscle, decremental response on nerve supramaximal repetitive stimulation. The findings signal that primary muscle involvement, neuropathy and impairement of the neuromuscular transmission, either isolated or combined, may be found in the acute stage of human Chagas' disease.

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Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Journal of Clinical Medicine ◽

10.3390/jcm10071537 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1537

Author(s):

Shuja Sheikh ◽

Usman Alvi ◽

Betty Soliven ◽

Kourosh Rezania

Keyword(s):

Myasthenia Gravis ◽

Acetylcholine Receptors ◽

Neuromuscular Transmission ◽

Immune Checkpoint Inhibitors ◽

Kinase Inhibitors ◽

De Novo ◽

Checkpoint Inhibitors ◽

Postsynaptic Membrane ◽

Neuromuscular Disorder ◽

Immune Homeostasis

Myasthenia gravis (MG) is an autoimmune neuromuscular disorder which is characterized by presence of antibodies against acetylcholine receptors (AChRs) or other proteins of the postsynaptic membrane resulting in damage to postsynaptic membrane, decreased number of AChRs or blocking of the receptors by autoantibodies. A number of drugs such as immune checkpoint inhibitors, penicillamine, tyrosine kinase inhibitors and interferons may induce de novo MG by altering the immune homeostasis mechanisms which prevent emergence of autoimmune diseases such as MG. Other drugs, especially certain antibiotics, antiarrhythmics, anesthetics and neuromuscular blockers, have deleterious effects on neuromuscular transmission, resulting in increased weakness in MG or MG-like symptoms in patients who do not have MG, with the latter usually being under medical circumstances such as kidney failure. This review summarizes the drugs which can cause de novo MG, MG exacerbation or MG-like symptoms in nonmyasthenic patients.

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