Clinical Reasoning: Burning hands and feet

Chan, Amanda C.; Wilder-Smith, Einar

doi:10.1212/wnl.0000000000001559

Cited by 5 publications

(7 citation statements)

References 10 publications

(8 reference statements)

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“…(Republished with permission from Chan AC, Wilder‐Smith E. Clinical reasoning: burning hands and feet. Neurology 2015;84:e146–152) . [Color figure can be viewed in the online issue, which is available at http://wileyonlinelibrary.com.…”

Section: Resultsmentioning

confidence: 99%

Small fiber neuropathy: Getting bigger!

2016

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Etiological and clinical heterogeneity of small fiber neuropathy (SFN) precludes a unifying approach and necessitates reliance on recognizable clinical syndromes. Symptoms of SFN arise from dysfunction in nociception, temperature, and autonomic modalities. This review focuses on SFN involving nociception and temperature, examining epidemiology, etiology, clinical presentation, diagnosis, pathophysiology, and management. Prevalence of SFN is 52.95 per 100,000 population, and diabetes and idiopathic are the most common etiologies. Dysesthesia, allodynia, pain, burning, and coldness sensations frequently present in a length-dependent pattern. Additional autonomic features in gastrointestinal, urinary, or cardiovascular systems are frequent but poorly objectified. SFN is diagnosed by intraepidermal nerve fiber density and quantitative sensory and autonomic tests in combination with normal nerve conduction. Pathophysiological understanding centers on sodium channel dysfunction, and genetic forms are beginning to be understood. Treatment is directed at the underlying etiology supported by symptomatic treatment using antidepressants and anticonvulsants. Little is known about long-term outcomes, and systematic cohort studies are needed.

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Section: Resultsmentioning

confidence: 99%

Small fiber neuropathy: Getting bigger!

2016

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“…A further limitation of the study includes variability of the investigations performed and clinical parameters for each patient, which may lead to missing data. Although a standardized approach to SFN patients was utilized, 22 parts of the clinical evaluation may be customized by the managing neurologist depending on the patient's presentation, leading to the inevitable possibility of missing data. Missing data would be excluded in the subgroup analysis, which would lead to a smaller sample size, hence a higher rate of type II error 40 .…”

Section: Discussionmentioning

confidence: 99%

Novel Autoantibodies in Idiopathic Small Fiber Neuropathy

Chan

Wong

Chong

et al. 2021

Annals of Neurology

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Objective: Small fiber neuropathy (SFN) is clinically and etiologically heterogeneous. Although autoimmunity has been postulated to be pathophysiologically important in SFN, few autoantibodies have been described. We aimed to identify autoantibodies associated with idiopathic SFN (iSFN) by a novel high-throughput protein microarray platform that captures autoantibodies expressed in the native conformational state. Methods: Sera from 58 SFN patients and 20 age-and gender-matched healthy controls (HCs) were screened against >1,600 immune-related antigens. Fluorescent unit readout and postassay imaging were performed, followed by composite data normalization and protein fold change (pFC) analysis. Analysis of an independent validation cohort of 33 SFN patients against the same 20 HCs was conducted to identify reproducible proteins in both cohorts. Results: Nine autoantibodies were screened with statistical significance and pFC criteria in both cohorts, with at least 50% change in serum levels. Three proteins showed consistently high fold changes in main and validation cohorts: MX1 (FC = 2.99 and 3.07, respectively, p = 0.003, q = 0.076), DBNL (FC = 2.11 and 2.16, respectively, p = 0.009, q < 0.003), and KRT8 (FC = 1.65 and 1.70, respectively, p = 0.043, q < 0.003). Further subgroup analysis into iSFN and SFN by secondary causes (secondary SFN) in the main cohort showed that MX1 is higher in iSFN compared to secondary SFN (FC = 1.61 vs 0.106, p = 0.009). Interpretation: Novel autoantibodies MX1, DBNL, and KRT8 are found in iSFN. MX1 may allow diagnostic subtyping of iSFN patients.

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“…Indeed, burning feet has been the eponym used both for familial and sporadic cases. [26][27][28] Further clinical presentations have been proposed, from focal neuropathy underlying the cases of burning mouth syndrome 20 29 or pain after inguinal hernia repair, 30 in which the distribution of symptoms respected the neuroanatomical distribution, to a non-length dependent presentation reflecting the primary involvement of DRG neurons in paraneoplastic and non-malignant immune-mediated diseases and genetic syndromes. 31 32 The intrinsic limitations of routine nerve conduction studies, psychophysical measurement of thermal thresholds, painrelated evoked potentials and autonomic function evaluation for achieving the diagnosis of SFN in individual patients have been overcome by skin biopsy at the ankle essentially for one reason: the possibility to provide an objective morphometric assessment of the target fibres in the body region corresponding to the symptoms.…”

Section: What Is Sfn?mentioning

confidence: 99%