The Chvostek sign is a clinical indicator involving a muscular response to gentle mechanical stimulation. It helps healthcare professionals understand a patient’s physiological state, pointing to heightened nerve responsiveness and potential underlying conditions.
Understanding the Chvostek Sign
A positive Chvostek sign manifests as twitching or spasm of the facial muscles. This reaction, an ipsilateral facial spasm, occurs on the same side of the face where the stimulus is applied. The facial nerve (Cranial Nerve VII or CN VII) is involved. When activated, muscles around the nose, lips, and eyebrows contract sporadically, particularly around the corner of the mouth, nose, or eye.
How the Chvostek Sign is Elicited
Eliciting the Chvostek sign involves a precise technique. A healthcare professional gently taps the patient’s cheek about two centimeters in front of the ear, directly over the facial nerve. This light tap can be delivered with a reflex hammer or fingertips. The professional then observes the facial muscles for involuntary contractions. If no twitching occurs, the patient has a negative Chvostek sign.
What a Positive Chvostek Sign Indicates
A positive Chvostek sign is associated with hypocalcemia, a condition of low blood calcium levels. Calcium plays a role in nerve signaling and muscle contraction; its deficiency increases nerve and muscle cell excitability. Low calcium makes neurons less stable and more prone to spontaneous firing. This heightened neuromuscular irritability can cause muscle spasms or tetany. However, it is not a perfectly reliable indicator; it can be observed in 10-25% of individuals with normal calcium levels and may be absent in some patients with hypocalcemia.
The Physiological Basis of the Chvostek Sign
The physiological basis for a positive Chvostek sign involves how low calcium levels affect nerve and muscle cell excitability, especially the facial nerve. Calcium ions are important for stabilizing nerve cell membranes. They bind to voltage-gated sodium channels, proteins controlling sodium ion flow into the cell. This binding influences the channel protein’s electrical state, regulating the voltage needed to open the sodium gate.
When extracellular calcium decreases, this stabilizing effect diminishes. Sodium channels become more easily activated, opening at more negative membrane potentials. This increased sodium permeability makes the nerve fiber more excitable, lowering its depolarization threshold. Consequently, peripheral nerves, including the facial nerve, may discharge spontaneously or react with exaggerated responses to mechanical stimulation, causing the characteristic twitching.