Vomiting induced alkalosis and hyperventilation induced respiratory alkalosis also cause tetany because of neuronal irritability. Pathophysiology
Hypocalcemia is the primary cause of tetany. Low ionized calcium levels in the extracellular fluid increase the permeability of neuronal membranes to sodium ion, causing a progressive depolarization, which increases the possibility of action potentials. This occurs because calcium ions interact with the exterior surface of sodium channels in the plasma membrane of nerve cells and hypocalcemia effectively increases resting potential (rendering the cells more excitable) since less positive charge is present extracellularly. When calcium ions are absent the voltage level required to open voltage gated sodium channels is significantly altered (less excitation is required). If the plasma Ca2+ decreases to less than 50% of the normal value of 9.4 mg/dl, action potentials may be spontaneously generated, causing contraction of peripheral skeletal muscles. Hypocalcemia is not a term for tetany but is rather a cause of tetany. Diagnosis
French Professor Armand Trousseau (1801–1867) devised the maneuver  of occluding the brachial artery by squeezing, to trigger cramps in the fingers. This is now known as the Trousseau sign of latent tetany.Also, tetany can be demonstrated by tapping anterior to the ear, at the emergence of the facial nerve. A resultant twitch of the nose or lips suggests low calcium levels. This is now known as the Chvostek sign.EMG studies reveal single or often grouped motor unit discharges at low discharge frequency during tetany episodes. References


== External links ==
This creates structural problems throughout the skeletal muscle and in the Z line of the sarcomere, creating the weakness in the muscle. Myopathies with fiber size variation
Myopathies with varying fiber size, such as congenital fiber type disproportion,
occurs when type 1 fibers, the slow twitch fibers involved in sustaining activity, are smaller than type 2 fibers, the fast twitch fibers involved in quick activity. Since smaller type 1 fibers is not associated with nemaline myopathy, the most common type of congenital myopathy, it has not been studied in as great detail as many of the others. However, the smaller type 1 fibers explains why patients typically can participate in activities for shorter periods of time, but struggle with extended activity. Cause
Diagnosis
There are rarely any specific tests for the congenital myopathies except for muscle biopsy. Tests can be run to check creatine kinase in the blood, which is often normal or mildly elevated in congenital myopathies. Electromyography can be run to check the electrical activity of the muscle. Diagnosis heavily relies on muscle pathology, where a muscle biopsy is visualised on the cellular level. Diagnosis usually relies on this method, as creatine kinase levels and electromyography can be unreliable and non-specific. Since congenital myopathies are genetic, there have been advancements in prenatal screenings. Types
The conditions included under the term "congenital myopathy" can vary. One source includes nemaline myopathy, myotubular myopathy, central core myopathy, congenital fiber type disproportion, and multicore myopathy. The term can also be used more broadly, to describe conditions present from birth.