Subacute peripheral and optic neuropathy syndrome with no evidence of a toxic or nutritional cause

Allen, David C.; Riordan-Eva, Paul; Paterson, Ross W.; Hadden, Robert D.M.

doi:10.1016/j.clineuro.2013.01.002

Cited by 6 publications

(5 citation statements)

References 13 publications

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“…Neuropathic Pain in Acute and Subacute Neuropathies Erythromelalgia (78,79) Subacute peripheral and optic neuropathy syndrome (80,81) Hereditary motor and sensory neuropathy (MPZ mutation) (82) peripheral NP, radicular pain, meningism, headache, muscular pain secondary to bad posture, visceral pain, and arthralgias (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)83). Pain can be acute, subacute, or chronic and it may appear in all GBS variants (e.g., mild GBS, pure motor GBS, pure sensory GBS, etc), albeit patients with MFS tend to show significantly reduced incidence of acute neuropathic pain (84).…”

Section: Methodsmentioning

confidence: 99%

“…Subacute peripheral and optic neuropathy syndrome occurs mainly in metabolic disorders (e.g., B12 or folic acid or copper or thiamine deficiency) and alcoholism. Genetic susceptibility to the syndrome involving mitochondrial DNA mutations is strongly suspected (80,81). The syndrome is characterized by a predominantly sensory distal symmetric painful neuropathy affecting the lower limbs more than the upper limbs.…”

Section: Acute/subacute Neuropathies Due To Deficienciesmentioning

confidence: 99%

“…In some cases, marked ataxia denote concomitant ganglionopathy. Visual symptoms may precede or follow the peripheral neuropathy in a period of one month after onset, which is pathognomonic for the syndrome (80,81).…”

Section: Acute/subacute Neuropathies Due To Deficienciesmentioning

confidence: 99%

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Neuropathic Pain in Acute and Subacute Neuropathies: A Systematic Review

Artemiadis¹,

Zis

2018

Pain Phys

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Background: Neuropathic pain (NP) is a common symptom caused by lesions or diseases of the somatosensory nervous system. Acute/subacute peripheral neuropathies (APN) are rare, however can be particularly painful. Objectives: The aim of this systematic review was to estimate the incidence of NP in APN and overview the various etiologies of such neuropathies. Study Design: Systematic review. Setting: Medline search. Methods: We hand-searched Medline for observational studies published between 1995 and 2017. Results: Our search strategy identified 1,400 papers. Of these, 70 met our inclusion criteria and were included in this review. Out of a total of 2,341 patients, 1,139 patients were diagnosed with NP (pooled incidence of NP 48.7%). In Guillain-Barré syndrome (GBS), the commonest cause of APN, the pooled estimate of NP was 34.8%. Other causes of painful APN include immunemediated, vasculitic, metabolic, nutritional, toxic, paraneoplastic, and infectious. Limitations: An important limitation was that GBS accounted for the majority of patients with APN, as such the calculated incidence reflected mainly this disease entity. Another important limitation was that very few studies targeted primarily NP. Thus, it is highly likely that observational studies reporting NP were missed. Finally there could always be a publication bias due to underreporting and gray literature. Conclusions: NP is a cardinal manifestation of APN. The use of validated diagnostic tools and accepted diagnostic criteria of NP is recommended for both clinical and research purposes. Key words: Neuropathic, pain, acute, subacute, neuropathy, polyneuropathy, frequency, incidence

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Section: Methodsmentioning

confidence: 99%

Section: Acute/subacute Neuropathies Due To Deficienciesmentioning

confidence: 99%

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Neuropathic Pain in Acute and Subacute Neuropathies: A Systematic Review

Artemiadis¹,

Zis

2018

Pain Phys

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“…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%

“…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%

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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Clinical electrophysiology of the optic nerve and retinal ganglion cells

Marmoy

Viswanáthan

2021

Eye

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Clinical electrophysiological assessment of optic nerve and retinal ganglion cell function can be performed using the Pattern Electroretinogram (PERG), Visual Evoked Potential (VEP) and the Photopic Negative Response (PhNR) amongst other more specialised techniques. In this review, we describe these electrophysiological techniques and their application in diseases affecting the optic nerve and retinal ganglion cells with the exception of glaucoma. The disease groups discussed include hereditary, compressive, toxic/nutritional, traumatic, vascular, inflammatory and intracranial causes for optic nerve or retinal ganglion cell dysfunction. The benefits of objective, electrophysiological measurement of the retinal ganglion cells and optic nerve are discussed, as are their applications in clinical diagnosis of disease, determining prognosis, monitoring progression and response to novel therapies.

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Subacute peripheral and optic neuropathy syndrome with no evidence of a toxic or nutritional cause

Cited by 6 publications

References 13 publications

Neuropathic Pain in Acute and Subacute Neuropathies: A Systematic Review

Neuropathic Pain in Acute and Subacute Neuropathies: A Systematic Review

Amiodarone neurotoxicity: the other side of the medal

Clinical electrophysiology of the optic nerve and retinal ganglion cells

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