Hypocalcemia-induced seizure: demystifying the calcium paradox.
Bottom Line: 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.
Affiliation: Barrow Neurological Institute, Dignity Health St Joseph's Hospital and Medical Center and Medical Center, Phoenix, AZ, USA PengCheng.Han@dignityhealth.org.Show MeSH
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Mentions: The inverse relationship between extracellular calcium and neuronal excitability could be explained by several complementary molecular events (summarized in Table 1 and Figure 2). External calcium inhibits NALCNs, shifts the voltage dependency of voltage-gated Na+ channels, stabilizes CNG channels, reduces inward current through AMPA channels, and depresses the release of excitatory neurotransmitters. Conversely, it enhances transient K+ current and KCa channels and perhaps potentiates GABA sensitivity. Some of these modulatory effects may depend on CaSR while others may require calcium influx. It is these processes that we theorize may help shed light on the calcium paradox and lead to further understanding of the mechanisms behind production of seizures through hypocalcemia.Figure 2.
Affiliation: Barrow Neurological Institute, Dignity Health St Joseph's Hospital and Medical Center and Medical Center, Phoenix, AZ, USA PengCheng.Han@dignityhealth.org.