Visual evoked potentials study in chronic idiopathic inflammatory demyelinating polyneuropathy

Stojkovic, Tanya; Seze, J. de; Hurtevent, J. F.; Arndt, Carl; Beaume, Anne; Hache, J.-C.; Vermersch, Patrick

doi:10.1016/s1388-2457(00)00478-8

Cited by 43 publications

(48 citation statements)

References 28 publications

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“…The syndrome of simultaneous bilateral optic and peripheral neuropathy is known to occur in nutritional and metabolic disorders such as B12 and folate pathway disorders, and with unclear precise incidence in acute and in chronic polyneuropathies [17][18][19]. The optic nerve can be affected in chronic demyelinating polyneuropathies (CIDP), due to the particular susceptibility to immune-mediated damage of both the peripheral and the optic nerves, which share rather similar proteins functioning as antigens capable of inducing self-reactive T-cell responses [17].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…The optic nerve can be affected in chronic demyelinating polyneuropathies (CIDP), due to the particular susceptibility to immune-mediated damage of both the peripheral and the optic nerves, which share rather similar proteins functioning as antigens capable of inducing self-reactive T-cell responses [17]. Indeed,it has been shown that myelin P1 expressed in peripheral nerves is identical to the central myelin basic protein; in addition, myelin-associated-glycoprotein is common to CNS and to peripheral nerves [17][18][19]. Subclinical visual pathway abnormalities in CIDP patients with and without detectable CNS lesions on MRI were reported by Stojkovic et al [17], who pointed out a lack of concordance between VEP and MRI abnormalities in some patients: of the 8 cases with altered VEPs only 4 had neuroradiological abnormalities.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed,it has been shown that myelin P1 expressed in peripheral nerves is identical to the central myelin basic protein; in addition, myelin-associated-glycoprotein is common to CNS and to peripheral nerves [17][18][19]. Subclinical visual pathway abnormalities in CIDP patients with and without detectable CNS lesions on MRI were reported by Stojkovic et al [17], who pointed out a lack of concordance between VEP and MRI abnormalities in some patients: of the 8 cases with altered VEPs only 4 had neuroradiological abnormalities. The discrepancy between negative MRI results and altered VEPs in CIDP similarly to what happens in multiple sclerosis could be the consequence of transient demyelinating lesions due to blood brain barrier damage that are eventually reversed by treatments [17].…”

Section: Discussionmentioning

confidence: 99%

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Amiodarone neurotoxicity: the other side of the medal

2014

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AbstractThe efficacy of amiodarone is tempered by its toxicity, with 50% of long-term users discontinuing the drug. The non-cardiac side effects of amiodarone may involve central and peripheral nervous system. We studied two patients treated with amiodarone for 46 and 15 months respectively. Both patients exhibited progressive distal extremity weakness, impaired perception, loss of deep reflexes. Electrophysiology identified a widespread, sensorimotor polyneuropathy with features of axonal loss and demyelination. Visual evoked potentials (VEPs) showed prolonged P100 latency bilaterally in absence of visual symptoms or brain magnetic resonance imaging (MRI) abnormalities. Extensive laboratory examinations excluded known causes of peripheral neuropathies. At 21 months after amiodarone withdrawal, P100 latency of case 1 VEPs returned to normal, whereas polyneuropathy continued to progress. In the second patient neuropathy has worsened similarly over 2 years whereas P100 latency of VEPs recovered to normal within 7 months after withdrawal of amiodarone. These findings may suggest different mechanisms of toxicity, which could be due to amiodarone pharmacokinetic and its metabolite effects on the peripheral nerves, as opposed to the optic nerve. We emphasize that use of amiodarone needs monitoring of patients at risk of development side effects.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Amiodarone neurotoxicity: the other side of the medal

2014

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“…Also, as a result of the presence of demyelination, ipsilateral HF components of the VEP appear to show differential latency changes with earlier waves (e.g., N75 and the "leading descending limb" of the P100) showing less marked delays than the later potentials (e.g., the "trailing ascending limb" of the P100 and the N145 wave) [9]. It is shown that pattern reversal stimulation was an effective diagnostic technique in identifying delays in VEP due to demyelination [10,11,12]. This effectiveness has been consistent with and confirmed by our findings.…”

Section: Discussionmentioning

confidence: 99%

Combination of High-Dose Intravenous Immunoglobulins and Itraconozole in Treating Chronic Mycotic Demyelinating Optic Neuritis

Anyanwu

Vojdani

2003

The Scientific World JOURNAL

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Mycotic demyelinating optic neuritis is a neurological disorder of the visual system caused by mycotoxins released by indoor toxic molds. Although the health effect of indoor toxic mold on the population worldwide is now one of the "emerging diseases", its involvement in chronic demyelinating optic neuritis has not been reported. Most of the neurological and immunologic abnormalities associated with toxic mold mycotoxins are very difficult to treat successfully, especially neural demyelination of the central and peripheral nervous systems. This paper presents the case of a 42-year-old white female, in whom chronic demyelinating optic neuritis with persistent visual defects due to chronic exposure to toxic molds was diagnosed at the age of 34 years. In spite of all the therapeutic services given to her for over 8 years, her illness persisted and was difficult to treat. However, we successfully treated her with a combination of intravenous immune globulin (IVIG) and itraconozole (Sporanox) when all other treatment modalities failed. This is probably the first report where persistent toxic mold-induced neurological and immunologic disorders were successfully treated with a combination of itraconozole and IVIG.

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Optic, trigeminal, and facial neuropathy related to anti‐neurofascin 155 antibody

Ogata

Inamizu

et al. 2020

Ann Clin Transl Neurol

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Objective: To characterize the frequency and patterns of optic, trigeminal, and facial nerve involvement by neuroimaging and electrophysiology in IgG4 antineurofascin 155 antibody-positive (NF155 +) chronic inflammatory demyelinating polyneuropathy (CIDP). Methods: Thirteen IgG4 NF155 + CIDP patients with mean onset age of 34 years (11 men) were subjected to neurological examination, blink reflex, and visual-evoked potential (VEP) testing, and axial and/ or coronal T2-weighted head magnetic resonance imaging (MRI). Results: Among 13 patients, facial sensory impairment, facial weakness, and apparent visual impairment were observed in three (23.1%), two (15.4%), and two (15.4%) patients, respectively. All 12 patients tested had blink reflex abnormalities: absent and/or delayed R1 in 11 (91.7%), and absent and/or delayed R2 in 10 (83.3%). R1 latencies had strong positive correlations with serum anti-NF155 antibody levels (r = 0.9, P ≤ 0.0001 on both sides) and distal and F wave latencies of the median and ulnar nerves. Absent and/or prolonged VEPs were observed in 10/13 (76.9%) patients and 17/26 (65.4%) eyes. On MRI, hypertrophy, and high signal intensity of trigeminal nerves were detected in 9/ 13 (69.2%) and 10/13 (76.9%) patients, respectively, whereas optic nerves were normal in all patients. The intra-orbital trigeminal nerve width on coronal sections showed a significant positive correlation with disease duration. Interpretation: Subclinical demyelination frequently occurs in the optic, trigeminal, and facial nerves in IgG4 NF155 + CIDP, suggesting that both central and peripheral myelin structures of the cranial nerves are involved in this condition, whereas nerve hypertrophy only develops in myelinated peripheral nerve fibers.

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Visual evoked potentials study in chronic idiopathic inflammatory demyelinating polyneuropathy

Cited by 43 publications

References 28 publications

Amiodarone neurotoxicity: the other side of the medal

Amiodarone neurotoxicity: the other side of the medal

Combination of High-Dose Intravenous Immunoglobulins and Itraconozole in Treating Chronic Mycotic Demyelinating Optic Neuritis

Optic, trigeminal, and facial neuropathy related to anti‐neurofascin 155 antibody

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