Identification of the Involvement of Potassium Channels in Fibromyalgia

Abstract

Fibromyalgia is a central sensitivity syndrome that presents with chronic pain, fatigue, cognitive dysfunction, and disordered sleep. The pathophysiology which due to multisensory hypersensitivity of the central nervous system involves neuronal excitability leading to central sensitization. Treatments of the challenges associated with the complexities of fibromyalgia involve combinations of pharmacological and non-pharmacological therapeutic approaches which often offer limited benefit. Potassium (K + ) channels play a fundamental role in establishing and maintaining stability of neuronal activity. The large molecular diversity and distribution of K + channels support involvement in a broad range of physiological functions. In nociceptive pathways, neuronal hyperexcitability leading to pain sensation has been associated with reduced function of K + channels and loss of cellular control. This article reviews the evidence of involvement of K + channels in fibromyalgia. A potential role both in the pathophysiological processes responsible for the symptoms of fibromyalgia and as therapeutic targets for the management of the condition is considered.

Recent research advances in pain mechanisms in McCune–Albright syndrome thinking about the pain mechanism of FD/MAS

“…K channels are involved in fibromyalgia in FD/MAS, with channels including fast K + channels, potassium leak (KL) channels, KCHN2 voltage-gated potassium channels, and Kv channel autoantibodies. Additionally, it has been found that the water fraction of substance P (SP) is elevated in the cerebrospinal fluid of FD/MAS patients [ 63 ]. Substance P is a mediator of pain, is involved in pain production and transmission signaling, and can also exhibit anti-injury-sensing properties.…”