Diagnosis of acute neuropathies

Crone, C; Krarup, Christian

doi:10.1007/s00415-007-0532-9

Cited by 13 publications

(8 citation statements)

References 150 publications

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“…Here, new onset polyneuropathy was present at the initial presentation, when new distal paresis and severe pain in the extremities became contemporaneously evident with renal failure and renal anemia 3 weeks after cardiac catheterization. The close temporal association and the fact that another etiology for the initial polyneuropathy was not present strongly point toward CCE as the underlying cause of the polyneuropathy in our patient [11]. The initial presentation of an asymmetric polyneuropathy and the histopathological finding in the nerve biopsy matches with the findings in a previously published case [9].…”

Section: Discussionsupporting

confidence: 84%

Polyneuropathy Associated with Cholesterol Crystal Embolism

et al. 2009

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Section: Discussionsupporting

confidence: 84%

Polyneuropathy Associated with Cholesterol Crystal Embolism

et al. 2009

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“…Causes of painful peripheral neuropathies are numerous, however, occasionally patients might suffer from idiopathic (of unknown etiology) painful neuropathies (11,12). This article focuses solely on acute and subacute peripheral neuropathies.…”

Section: Immune-mediated Acute/subacute Neuropathiesmentioning

confidence: 99%

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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“…3,4 Phase cancellation due to the variable diameter and conduction velocity of fibers that make up a peripheral nerve is an important factor involved in distal versus proximal CMAP amplitude reduction. 12 Axonal regeneration and defective remyelination can alter the normal distribution of nerve fiber diameter and conduction velocity.…”

Section: Case Reportmentioning

confidence: 99%

Persistent multifocal pseudo‐conduction blocks in vasculitic neuropathy without antiganglioside antibodies

Ahdab¹,

Michel²,

Neves³

et al. 2009

Muscle and Nerve

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A woman presented with severe multifocal acute axonal neuropathy due to necrotizing vasculitis. Six years later, electrophysiological examination revealed features suggestive of persistent conduction block (CB) with increased temporal dispersion (ITD) affecting the right median and tibial nerves. A clinical case characterized by multifocal CBs that were observed several years after an initial episode of vasculitic neuropathy was recently reported. The occurrence of CBs paralleled clinical deterioration and was attributed to superimposed antiganglioside antibody-mediated demyelination. In contrast, our patient was clinically stable and did not have antiganglioside antibodies. Nerve conduction studies showed pseudo-CBs rather than true CBs. We suggest that pseudo-CBs with ITD can reveal heterogeneous axonal regeneration as a sequel of a severe multifocal vasculitic neuropathy. This condition should be distinguished from the occurrence of pseudo-CB in the acute phase of vasculitis or from superimposed immune-mediated demyelination. Muscle Nerve 40: 290-293, 2009.

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Diagnosis of acute neuropathies

Cited by 13 publications

References 150 publications

Polyneuropathy Associated with Cholesterol Crystal Embolism

Polyneuropathy Associated with Cholesterol Crystal Embolism

Neuropathic Pain in Acute and Subacute Neuropathies: A Systematic Review

Persistent multifocal pseudo‐conduction blocks in vasculitic neuropathy without antiganglioside antibodies

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