Possible second motor neuron damage in neuromyelitis optica

Laemmer, Alexandra B.; Maihöfner, Christian; Gölitz, Philipp; Schwab, Stefan; Lee, D.H.; Linker, Ralf A.; Schramm, Axel

doi:10.1016/j.clinph.2013.08.023

Cited by 8 publications

(5 citation statements)

References 5 publications

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“…[18][19][20][21][22] Our patient had a motor axonal neuropathy, a pattern that has previously been reported and postulated to be due to severe myelitic anterior horn cell involvement. 19 This is a potential mechanism in our case also, given the preserved sensory responses. Other postulated mechanisms include peripheral nervous system damage from direct targeting of peripherally expressed AQP4, or targeting of other, at present unknown, peripheral nerve antibody antigens.…”

Section: Discussionsupporting

confidence: 77%

“…Rare reports of peripheral neuropathy associated with both AQP4-IgG-seropositive and seronegative neuromyelitis optica spectrum disorder exist in adults, although in some of these cases, coexistent medical conditions may have accounted for the neuropathy. [18][19][20][21] To our knowledge, this is the first report of an axonal motor neuropathy in a child with neuromyelitis optica spectrum disorder. The mechanism of peripheral nerve involvement is unclear.…”

Section: Discussionmentioning

confidence: 71%

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Neuromyelitis Optica Spectrum Disorder and Anti-Aquaporin 4 Channel Immunoglobulin in an Australian Pediatric Demyelination Cohort

et al. 2020

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Neuromyelitis optica spectrum disorder is uncommon in children, and often seronegative for aquaporin-4 immunoglobulin G (AQP4-IgG). We conducted a retrospective study of 67 children presenting to a single Australian center with acquired demyelinating syndromes over a 7-year period. All patients were tested for AQP4-IgG. Five children (7.5%) had neuromyelitis optica spectrum disorder. One child was seropositive for AQP4-IgG (1.5%) and had a relapsing disease course with mild residual deficits. She also had a concomitant motor axonal neuropathy that improved with immunosuppressive therapy. Of the remaining 4 children, 3 had a monophasic course and 1 a relapsing course. Two were tested for anti–myelin oligodendrocyte glycoprotein (anti-MOG) antibody and both were seropositive. This study confirms that neuromyelitis optica spectrum disorder is uncommon in children, and that AQP4-IgG seropositivity is rare. Anti-MOG antibodies should be tested in children with neuromyelitis optica spectrum disorder.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 71%

Neuromyelitis Optica Spectrum Disorder and Anti-Aquaporin 4 Channel Immunoglobulin in an Australian Pediatric Demyelination Cohort

et al. 2020

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“…Some cases of possible peripheral nervous system (PNS) involvement in NMOSD have been published. Painful, flaccid paralysis (63), lumbosacral myelitis (132), clinical and electrophysiological second motor neuron involvement (133), and peripheral neuropathy (134, 135) have been described, and radicular pain has been reported to occur in up to 33% (81,136). Recently, a few cases with PNS involvement in MOGAD have been described.…”

Section: Peripheral Nervous System-related Neuropathic Painmentioning

confidence: 99%

Pain in NMOSD and MOGAD: A Systematic Literature Review of Pathophysiology, Symptoms, and Current Treatment Strategies

2020

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Neuromyelitis optica spectrum disorders (NMOSDs) and myelin oligodendrocyte glycoprotein-antibody-associated disease (MOGAD) are autoimmune inflammatory disorders of the central nervous system (CNS). Pain is highly prevalent and debilitating in NMOSD and MOGAD with a severe impact on quality of life, and there is a critical need for further studies to successfully treat and manage pain in these rare disorders. In NMOSD, pain has a prevalence of over 80%, and pain syndromes include neuropathic, nociceptive, and mixed pain, which can emerge in acute relapse or become chronic during the disease course. The impact of pain in MOGAD has only recently received increased attention, with an estimated prevalence of over 70%. These patients typically experience not only severe headache, retrobulbar pain, and/or pain on eye movement in optic neuritis but also neuropathic and nociceptive pain. Given the high relevance of pain in MOGAD and NMOSD, this article provides a systematic review of the current literature pertaining to pain in both disorders, focusing on the etiology of their respective pain syndromes and their pathophysiological background. Acknowledging the challenge and complexity of diagnosing pain, we also provide a mechanism-based classification of NMOSD- and MOGAD-related pain syndromes and summarize current treatment strategies.

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“…Different patterns of involvement have been described such as polyneuropathy, 27,28 radiculopathy, 29 myeloradiculitis, 30 and second motor neuron involvement. 31,32 Recently, vestibulocochlear nerve lesion as a part of CN involvement has been reported for the first time in NMOSDs. 33 Moreover and similarly to our cases, involvement of the transitional region at the spinal root has also been described in a patient presenting with meningoradiculitis.…”

Section: Discussionmentioning

confidence: 99%

Cranial nerve involvement in patients with MOG antibody–associated disease

Cobo‐Calvo¹,

Ayrignac

Kerschen

et al. 2019

Neurol Neuroimmunol Neuroinflamm

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ObjectiveTo describe clinical and radiologic features of cranial nerve (CN) involvement in patients with myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) and to assess the potential underlying mechanism of CN involvement using a nonhuman primate (NHP) model.MethodsEpidemiologic, clinical, and radiologic features from a national cohort of 273 MOG-IgG–positive patients were retrospectively reviewed for CN involvement between January 2014 and January 2018. MOG-IgG binding was evaluated in CNS, CN, and peripheral nerve tissues from NHP.ResultsWe identified 3 MOG-IgG–positive patients with radiologic and/or clinical CN involvement. Two patients displayed either trigeminal or vestibulocochlear nerve lesions at the root level, and the remaining patient had an oculomotor nerve involvement at the root exit and at the cisternal level. Additional CNS involvement was found in all 3 patients. None of the 3 patients' sera recognized MOG expression in CN of NHP.ConclusionCraneal nerve involvement can coexist in patients with MOG antibody disease, although the underlying pathophysiology remains elusive.

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Possible second motor neuron damage in neuromyelitis optica

Cited by 8 publications

References 5 publications

Neuromyelitis Optica Spectrum Disorder and Anti-Aquaporin 4 Channel Immunoglobulin in an Australian Pediatric Demyelination Cohort

Neuromyelitis Optica Spectrum Disorder and Anti-Aquaporin 4 Channel Immunoglobulin in an Australian Pediatric Demyelination Cohort

Pain in NMOSD and MOGAD: A Systematic Literature Review of Pathophysiology, Symptoms, and Current Treatment Strategies

Cranial nerve involvement in patients with MOG antibody–associated disease

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