Low extracellular calcium levels reduce the threshold for depolarization, directly increasing neuromuscular excitability and leading to clinical signs such as tetany and seizures.
The claim is specific and physiologically well-established: extracellular calcium stabilizes voltage-gated sodium channels on nerve membranes. When calcium levels drop (hypocalcemia), these channels open more easily, leading to nerve hyperexcitation. Papers [7] and [8] directly support this physiological relationship, while the other retrieved papers address unrelated topics such as autism, magnesium, or specific channelopathies.