The most common cause of Raynaud’s phenomenon is overactivation of the sympathetic nervous system. This causes an increased release of the neurotransmitter norepinephrine, which binds to and activates adrenergic receptors. When the alpha-2 adrenergic receptors on blood vessels are activated, the smooth muscle tissue that lines the blood vessel walls contracts, causing vasoconstriction (a narrowing of blood vessels).
Excessive blood vessel constriction reduces blood flow to the extremities, which causes the characteristic changes in skin color associated with Raynaud’s as well as pain, tingling, and numbness.
There are two main variants of Raynaud’s: primary and secondary. With primary Raynaud’s, the disorder occurs on its own, independent of any underlying condition. In contrast, secondary Raynaud’s is caused by the presence of another underlying condition, such as lupus, scleroderma, or other autoimmune disorders.[1]