Review articleNeuromuscular complications in cancer
Introduction
Neuromuscular complications in cancer have different etiologies in different anatomical regions. Although metastases as the cause of a neuromuscular syndrome are often the primary concern, several other pathogenic causes exist.
CN lesions often have a neoplastic cause, in particular local metastases and meningeal infiltration. Nerve roots can be both damaged by mechanical and neoplastic causes, and the nerve plexi are predominantly affected by neoplastic lesions, and if radiated also radiation effects need to be considered.
Peripheral neuropathies can be caused by paraneoplastic etiologies, usually at the time of diagnosis, during the course of therapy by toxic drug effects and much rarer by infrequent causes such as neoplastic infiltration, metabolic or inflammatory causes.
The neuromuscular junction (NMJ) can be a site of paraneoplastic or dysimmune effects such as in myasthenia gravis, Lambert Eaton myasthenia syndrome (LEMS) or neuromyotonia.
In muscle paraneoplastic and inflammatory lesions dominate. Direct neoplastic involvement is rare. The most frequent type of muscle involvement is cachexia.
Neuromuscular complications can appear as the first sign of cancer, where often a tumor search is needed [1], or appear as a complication during the disease.
An important aspect affecting the impact of neuromuscular complications is associated with age. Pediatric cancer, adult cancer and increasingly geriatric aspects of cancer [2], [3] have a diverse spectrum of complications. This distinction can be based on several issues such as tolerance of treatment, development of persisting or late toxicity, and also the influence of other concomitant diseases.
Section snippets
Neoplastic
Different tumors have different propensities to metastasize at different time points and into different organs (organotropism). Cancer is usually classified into hematological and solid tumors. Both types have the ability to convert from a solid into a liquid state (meningeal carcinomatosis) and vice versa (chloroma or myelosarcoma). Other mechanisms are local compression, focal or diffuse invasion, and even rarer anterograde and retrograde spread along nerves and rarely local tumor or
CN
Anatomically, CN have a cerebral parenchymatous and an intracavitary part within the skull. They have a defined exit through the skull, followed by an extracranial course. The intracavitary part will not be considered here, with the exception of nerve infiltration or compression in leptomeningeal disease, as well as base of the skull tumors. Imaging is useful to demonstrate abnormalities of CNs [8].
Neoplastic lesions of CNs can be caused by a number of intracranial causes such as leptomeningeal
Bone marrow transplantation
BMT a treatment used for the hematological tumors and treatment and other cancers. Side effects from chemotherapy, RT, infections and immune dysregulations due to GVHD are observed. GVHD can be associated with several neuromuscular complications of muscle (myositis) [357], disordered neuromuscular transmission (MG) [358] and neuropathies such as GBS and CIDP [359]. In allogeneic transplantations these complications are more frequent.
Hematopoietic stem cell transplantation is used in the
Summary
Neurologists are important in the management and treatment of patients with systemic cancer. In the PNS a large number of differential diagnoses have to be evaluated, and treatment of neuromuscular symptoms and signs needs different approaches, depending on the etiology of the lesion. As the spectrum of tumor therapies broadens the pathogenetic mechanisms vary. The success of several tumor therapies has increased the number of long term survivors, who may also suffer from previously unknown
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