Sometimes piriformis syndrome (PS) is due to taut band and trigger points (TrPs) activation of MPS in piriformis muscle (PM). Primary MPS often regards the typical overuse syndrome that is named for the structures involved or the common conditions that produce it. PS is an example of primary MPS due to existing TrPs in the contracted piriformis muscle. Although MPS is a localized painful muscle condition, sometimes it may present as widespread body pain due to spread of TrPs: (i) through axial kinetic chain; (ii) through the activation of TrPs in the overloaded or mechanically stressed muscle compensating for the dysfunction of other muscles in the functional muscle units. Sometimes the clinical picture of widespread MPS may be confused with FMS. MPS and FMS may also coexist in the same patient and may share common pathophysiology.

Central sensitization is important in the genesis of both FMS and MPS. It could explain both the physical findings and biomechanical changes that have been documented in fibromyalgia. According to Gerwin 75% of FMS may have significant MPS at one or more times during the course of their illness. In MPS an increase in TrPs Ach release could result in sustained depolarization of the post-junctional membrane of the muscle fiber and produce sustained sarcomere shortening and contracture with increased local energy consumption and reduction of local circulation, producing local ischemia and hypoxia. The localized muscle ischemia stimulates the release of prostaglandins, substance P, bradykinin, capsaicin, serotonin, and histamine that sensitize afferent nerve fibers in muscle. Under pathologic conditions, convergent connections from deep afferent nociceptors to dorsal horn neurons are facilitated and amplified in the spinal cord with pain referral beyond the initial nociceptive region owing to spreading of central sensitization to adjacent spinal segments. At the level of the central nervous system, spinal neuroplastic changes in the second order neuron pool produce a long lasting increase in the excitability of nociceptor pathways. Neurotransmitters involved in the process of central sensitization include substance P, N-methyl-D-aspartate, glutamate, and nitric oxide. In addition, there may be impairments in supraspinal inhibitory descending pain control pathways. Like MPS, there is no significant peripheral pathology in FMS. Central sensitization is the most important CNS aberration in FMS with altered neurotransmitters in serum (decrease serotonin) and CSF (increase substance P).

So, longstanding nociceptive stimuli in PM with resultant sensitization of peripheral nerve could develop CNS sensitization, a manifestation of neuroplasticity or the remodeling of central processes with generalized body ache as seen in FMS. Pain can be provoked in favor of PS using FAIR test, Pace sign, localized tenderness over the right gluteal region and per-rectal examination, alongside digital examination yield fibromyalgia tender areas for FMS diagnosis. I consider PS and FMS are the example of peripheral and central sensitization, respectively.

Suggested Reading: Siddiq MA, Khasru MR, Rasker JJ. Piriformis Syndrome in Fibromyalgia – Clinical Diagnosis and Successful Treatment. Case Rep Rheumatol 2014 http://dx.doi.org/10.1155/2014/893836.