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Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox
Calcium is essential for both neurotransmitter release and muscle contraction. Given these important physiological processes, it seems reasonable to assume that hypocalcemia may lead to reduced neuromuscular excitability. Counterintuitively, however, clinical observation has frequently documented hy...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4374060/ https://www.ncbi.nlm.nih.gov/pubmed/25810356 http://dx.doi.org/10.1177/1759091415578050 |
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author | Han, Pengcheng Trinidad, Bradley J. Shi, Jiong |
author_facet | Han, Pengcheng Trinidad, Bradley J. Shi, Jiong |
author_sort | Han, Pengcheng |
collection | PubMed |
description | Calcium is essential for both neurotransmitter release and muscle contraction. Given these important physiological processes, it seems reasonable to assume that hypocalcemia may lead to reduced neuromuscular excitability. Counterintuitively, however, clinical observation has frequently documented hypocalcemia’s role in induction of seizures and general excitability processes such as tetany, Chvostek’s sign, and bronchospasm. The mechanism of this calcium paradox remains elusive, and very few pathophysiological studies have addressed this conundrum. Nevertheless, several studies primarily addressing other biophysical issues have provided some clues. In this review, we analyze the data of these studies and propose an integrative model to explain this hypocalcemic paradox. |
format | Online Article Text |
id | pubmed-4374060 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-43740602015-03-31 Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox Han, Pengcheng Trinidad, Bradley J. Shi, Jiong ASN Neuro Review Article Calcium is essential for both neurotransmitter release and muscle contraction. Given these important physiological processes, it seems reasonable to assume that hypocalcemia may lead to reduced neuromuscular excitability. Counterintuitively, however, clinical observation has frequently documented hypocalcemia’s role in induction of seizures and general excitability processes such as tetany, Chvostek’s sign, and bronchospasm. The mechanism of this calcium paradox remains elusive, and very few pathophysiological studies have addressed this conundrum. Nevertheless, several studies primarily addressing other biophysical issues have provided some clues. In this review, we analyze the data of these studies and propose an integrative model to explain this hypocalcemic paradox. SAGE Publications 2015-03-23 /pmc/articles/PMC4374060/ /pubmed/25810356 http://dx.doi.org/10.1177/1759091415578050 Text en © The Author(s) 2015 http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution 3.0 License (http://www.creativecommons.org/licenses/by/3.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (http://www.uk.sagepub.com/aboutus/openaccess.htm). |
spellingShingle | Review Article Han, Pengcheng Trinidad, Bradley J. Shi, Jiong Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox |
title | Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox |
title_full | Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox |
title_fullStr | Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox |
title_full_unstemmed | Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox |
title_short | Hypocalcemia-Induced Seizure: Demystifying the Calcium Paradox |
title_sort | hypocalcemia-induced seizure: demystifying the calcium paradox |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4374060/ https://www.ncbi.nlm.nih.gov/pubmed/25810356 http://dx.doi.org/10.1177/1759091415578050 |
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