Activation of<unk><unk> s may be caused by a number of factors, including acute or chronic muscle overload, activation by other<unk><unk> s (key/satellite, primary/secondary), disease, psychological distress (via systemic inflammation), homeostatic imbalances, direct trauma to the region, collision trauma (such as a car crash which stresses many muscles and causes instant<unk><unk> s), radiculopathy, infections and health issues such as smoking.<unk><unk> s form only in muscles. They form as a local contraction in a small number of muscle fibers in a larger muscle or muscle bundle. These in turn can pull on tendons and ligaments associated with the muscle and can cause pain deep within a<unk>  where there are no muscles. The integrated hypothesis theory states that<unk><unk> s form from excessive release of acetylcholine which produces sustained depolarization of muscle fibers. Indeed, the<unk><unk>  has an abnormal biochemical composition with elevated concentrations of acetylcholine, noradrenaline and serotonin and a lower pH. These sustained contractions of muscle sarcomeres compresses local blood supply restricting the energy needs of the local region. This crisis of energy produces sensitizing substances that interact with some nociceptive (pain) nerves traversing in the local region which in turn can produce localized pain within the muscle at the neuromuscular junction (Travell and Simons 1999). When<unk><unk> s are present in muscles there is often pain and weakness in the associated structures. These pain patterns in muscles follow specific nerve pathways and have been readily mapped to allow for identification of the causative pain factor. Many<unk><unk> s have pain patterns that overlap, and some create reciprocal cyclic relationships that need to be treated extensively to remove them.
Myofascial trigger point
Psychogenic pain
Calpainopathy
Phantom pain
Neurogenic claudication
Nerve compression syndrome
Peroneal strike
Myofascial pain syndrome