Literature DB >> 12451192

Acral paresthesias in the Andes and neurology at sea level.

O Appenzeller1, P K Thomas, S Ponsford, J L Gamboa, R Cáceda, P Milner.   

Abstract

BACKGROUND: Thirty-nine percent of permanent altitude dwellers in the Andes experience acral paresthesias.
METHODS: Clinical examinations, sural nerve biopsies, and electrodiagnostic studies on peripheral nerves were performed on 15 men. Ten Cerro de Pasco (CP) natives living at 4,338 meters were biopsied. Three of these subjects had no burning feet/burning hands (BF/BH); three had BF/BH; and four had chronic mountain sickness (CMS), a maladaptation syndrome resulting from living in the Andes, all with BF/BH. Three patients with CMS were biopsied in Lima within hours after leaving CP. Two normal Lima natives were biopsied in Lima. Symptom scores for BF/BH and CMS score ratings were used. The nerves were assayed for Na+, K+ adenosine triphosphatase (ATPase), cytochrome oxidase (CO), substance P (SP), and endothelin (ET).
RESULTS: Low ATPase was inversely related to symptom scores and CMS scores (p < 0.001). Patients with CMS biopsied in normoxia (Lima) had ATPase levels similar to those of controls. Nerve motor conduction velocities and sensory action potentials were normal. CO was inversely related to age (p < 0.03) and no relation of SP to any variable was found. ET levels were lower in sea level natives (p = 0.04).
CONCLUSIONS: Acral paresthesias are associated with low ATPase in peripheral nerves. Lower ET levels of sea level natives likely reflect lowered release from vasa nervorum.

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Year:  2002        PMID: 12451192     DOI: 10.1212/01.wnl.0000034761.86543.a1

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


  2 in total

1.  Chronic mountain sickness score was related with health status score but not with hemoglobin levels at high altitudes.

Authors:  Gustavo F Gonzales; Julio Rubio; Manuel Gasco
Journal:  Respir Physiol Neurobiol       Date:  2013-06-11       Impact factor: 1.931

2.  A painful neuropathy-associated Nav1.7 mutant leads to time-dependent degeneration of small-diameter axons associated with intracellular Ca2+ dysregulation and decrease in ATP levels.

Authors:  Harshvardhan Rolyan; Shujun Liu; Janneke Gj Hoeijmakers; Catharina G Faber; Ingemar Sj Merkies; Giuseppe Lauria; Joel A Black; Stephen G Waxman
Journal:  Mol Pain       Date:  2016-11-07       Impact factor: 3.395

  2 in total

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