2012
DOI: 10.1002/mus.23464
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Paraneoplastic lower motor neuronopathy associated with Hodgkin lymphoma

Abstract: Paraneoplastic causes should be considered in the differential diagnosis of subacute motor neuronopathy, as the neurological presentation may precede cancer detection. Combinations of lymphoma treatment and immunotherapy may result in a favorable outcome.

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Cited by 38 publications
(26 citation statements)
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“…Specifically, this review concentrates on lymphoma and more-or-less well-defined immune neuropathy subgroups that are caused by humoral and/or cell-mediated immune attacks against either known or undetermined peripheral nerve antigens. The selective approach to this topic entailed careful screening of the literature and the exclusion of reports with variables that interfered with the interpretation of chosen, defined neuropathy subgroups: (a) cryoglobulinemic neuropathy (mechanism is vasculitic ischemic damage to nerves); (b) plasma cell dyscrasias that are not usually classified with the lymphomas [1] e.g., Waldenström's macroglobulinemia/IgM-secreting lymphoplasmacytic lymphoma (although deposits of endoneurial monoclonal IgM secreted by plasma cells may lead to immune-mediated neuropathy) [11][12][13]; (c) "paraneoplastic" primarily sensory [14][15][16] or motor [17][18][19] neuronopathies (immune attack presumably directed at nerve cell body antigens); (d) initial presentation as, or exacerbation of, an acquired inflammatory demyelinating neuropathy but: (1) biological treatment likely contributed significantly to immune dysregulation e.g., rituximab introduction [20] or maintenance therapy [21], or recent completion of a course of alemtuzumab [22]; (2) effects of therapy resulted in severe superimposed immune disturbance e.g., acute tumor lysis syndrome [23], mobilization therapy with "pyrexia of unknown origin" [24], or after autologous bone marrow transplantation [25,26]; (3) preceded by virus infection/reactivation e.g., Varicella zoster reactivation [27], or (4) eventual evidence was found of malignant lymphocytic spread to CSF/nerve roots [28][29][30] or peripheral nerves [31]. A systematic search was conducted of relevant publications using databases such as MEDLINE [PubMed], EMBASE and DynaMed, and included case reports and series, retrospective studies, and reviews.…”
mentioning
confidence: 99%
“…Specifically, this review concentrates on lymphoma and more-or-less well-defined immune neuropathy subgroups that are caused by humoral and/or cell-mediated immune attacks against either known or undetermined peripheral nerve antigens. The selective approach to this topic entailed careful screening of the literature and the exclusion of reports with variables that interfered with the interpretation of chosen, defined neuropathy subgroups: (a) cryoglobulinemic neuropathy (mechanism is vasculitic ischemic damage to nerves); (b) plasma cell dyscrasias that are not usually classified with the lymphomas [1] e.g., Waldenström's macroglobulinemia/IgM-secreting lymphoplasmacytic lymphoma (although deposits of endoneurial monoclonal IgM secreted by plasma cells may lead to immune-mediated neuropathy) [11][12][13]; (c) "paraneoplastic" primarily sensory [14][15][16] or motor [17][18][19] neuronopathies (immune attack presumably directed at nerve cell body antigens); (d) initial presentation as, or exacerbation of, an acquired inflammatory demyelinating neuropathy but: (1) biological treatment likely contributed significantly to immune dysregulation e.g., rituximab introduction [20] or maintenance therapy [21], or recent completion of a course of alemtuzumab [22]; (2) effects of therapy resulted in severe superimposed immune disturbance e.g., acute tumor lysis syndrome [23], mobilization therapy with "pyrexia of unknown origin" [24], or after autologous bone marrow transplantation [25,26]; (3) preceded by virus infection/reactivation e.g., Varicella zoster reactivation [27], or (4) eventual evidence was found of malignant lymphocytic spread to CSF/nerve roots [28][29][30] or peripheral nerves [31]. A systematic search was conducted of relevant publications using databases such as MEDLINE [PubMed], EMBASE and DynaMed, and included case reports and series, retrospective studies, and reviews.…”
mentioning
confidence: 99%
“…Positive anti-GM1 antibody and electrophysiologic evidence of conduction block, temporal dispersion, or prolonged Fwave latency point toward MMN. PMA is generally regarded as a neurodegenerative disease; rarely, it could be due to paraneoplastic process [18,19]. The absence of conventional paraneoplastic antibodies does not exclude a paraneoplastic.…”
Section: Peripheral Nervous System Disordersmentioning
confidence: 98%
“…The absence of conventional paraneoplastic antibodies does not exclude a paraneoplastic. etiology [17,18].…”
Section: Peripheral Nervous System Disordersmentioning
confidence: 98%
“…Although some pathological reports show loss of motor neurons in the anterior horn of the spinal cord, the clinical improvement in some patients suggest the presence of mechanisms affecting neuronal function rather than causing irreversible degeneration. 80 Sensory neuronopathy is caused by damage of sensory neurons in the dorsal root ganglia and is one of the most common and wellcharacterized PNSs, usually occurring in association with SCLC and Hu antibodies. 78 The syndrome typically runs a subacute clinical course with pain and paresthesias in the upper or lower limbs.…”
Section: Paraneoplastic Neuronopathiesmentioning
confidence: 99%