Terminal latency index in neuropathy with antibodies against myelin‐associated glycoproteins

Lupu, Vitalie D.; Mora, Carlos A.; Dambrosia, Jim; Meer, Jacob; Dalakas, Marinos C.; Floeter, Mary Kay

doi:10.1002/mus.20678

Cited by 48 publications

(33 citation statements)

References 35 publications

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“…Several electrophysiological studies have shown that anti-MAG/SGPG neuropathy presents with disproportionate distal slowing of the motor nerve conduction, prolongation of DL, and a low terminal latency index without conduction block [12, 13, 14, 15]. These findings were consistent with those in the median nerve of our patient.…”

Section: Discussionsupporting

confidence: 90%

Rituximab Improves Subclinical Temporal Dispersion of Distal Compound Muscle Action Potential in Anti-MAG/SGPG Neuropathy Associated with Waldenström Macroglobulinemia: A Case Report

Kodaira

Yamamoto²

2013

Case Rep Neurol

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Patients with anti-myelin-associated glycoprotein (MAG)/sulfated glucuronyl paragloboside (SGPG) neuropathy associated with Waldenström macroglobulinemia show demyelinating neuropathy, but the temporal dispersion of distal compound muscle action potential (CMAP) in motor nerve conduction studies (NCS), which represents heterogeneous demyelination at the motor nerve terminal, is rare. We report on a 70-year-old man with anti-MAG/SGPG neuropathy associated with Waldenström macroglobulinemia; he had a 2-year history of mild dysesthesia of the foot sole without any motor symptoms. He showed marked temporal dispersion of distal CMAP in the tibial nerve with other demyelinating findings in the NCS. The temporal dispersion of distal CMAP in the tibial nerve improved significantly, and motor function was again normal 1 year after rituximab monotherapy. The temporal dispersion of distal CMAP in anti-MAG/SGPG neuropathy is rare, but it could occur from an early stage when the patients show mild or no motor symptoms. Rituximab therapy before secondary axonal degeneration has great potential to reverse the effects of the demyelination including the temporal dispersion of distal CMAP, and to prevent the deterioration of neuropathy in anti-MAG/SGPG neuropathy.

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Section: Discussionsupporting

confidence: 90%

Rituximab Improves Subclinical Temporal Dispersion of Distal Compound Muscle Action Potential in Anti-MAG/SGPG Neuropathy Associated with Waldenström Macroglobulinemia: A Case Report

Kodaira

Yamamoto²

2013

Case Rep Neurol

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“…Therefore, only MUNEs from the median nerve were assessed for treatment effect. TLI measures were calculated for each nerve to determine if there was excessive slowing in the distal segment relative to proximal nerve segments 26…”

Section: Methodsmentioning

confidence: 99%

Do A‐waves help predict intravenous immunoglobulin response in multifocal motor neuropathy without block?

et al. 2011

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“…Action tremor can be a prominent feature 130131. The electrophysiologic features include extremely prolonged distal motor and sensory latencies representing distal demyelination 132133. Pathologically, there is segmental demyelination with IgM and complement deposits in the myelin sheaths and widened outer myelin lamellae 134.…”

Section: Differential Diagnosis Of Sensory Ataxiamentioning

confidence: 99%

Diagnosis and management of sensory polyneuropathy

Gwathmey

Pearson

2019

BMJ

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Sensory polyneuropathies, which are caused by dysfunction of peripheral sensory nerve fibers, are a heterogeneous group of disorders that range from the common diabetic neuropathy to the rare sensory neuronopathies. The presenting symptoms, acuity, time course, severity, and subsequent morbidity vary and depend on the type of fiber that is affected and the underlying cause. Damage to small thinly myelinated and unmyelinated nerve fibers results in neuropathic pain, whereas damage to large myelinated sensory afferents results in proprioceptive deficits and ataxia. The causes of these disorders are diverse and include metabolic, toxic, infectious, inflammatory, autoimmune, and genetic conditions. Idiopathic sensory polyneuropathies are common although they should be considered a diagnosis of exclusion. The diagnostic evaluation involves electrophysiologic testing including nerve conduction studies, histopathologic analysis of nerve tissue, serum studies, and sometimes autonomic testing and cerebrospinal fluid analysis. The treatment of these diseases depends on the underlying cause and may include immunotherapy, mitigation of risk factors, symptomatic treatment, and gene therapy, such as the recently developed RNA interference and antisense oligonucleotide therapies for transthyretin familial amyloid polyneuropathy. Many of these disorders have no directed treatment, in which case management remains symptomatic and supportive. More research is needed into the underlying pathophysiology of nerve damage in these polyneuropathies to guide advances in treatment.

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Terminal latency index in neuropathy with antibodies against myelin‐associated glycoproteins

Cited by 48 publications

References 35 publications

Rituximab Improves Subclinical Temporal Dispersion of Distal Compound Muscle Action Potential in Anti-MAG/SGPG Neuropathy Associated with Waldenström Macroglobulinemia: A Case Report

Rituximab Improves Subclinical Temporal Dispersion of Distal Compound Muscle Action Potential in Anti-MAG/SGPG Neuropathy Associated with Waldenström Macroglobulinemia: A Case Report

Do A‐waves help predict intravenous immunoglobulin response in multifocal motor neuropathy without block?

Diagnosis and management of sensory polyneuropathy

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