Change in muscle hardness after trigger point injection and physiotherapy for myofascial pain syndrome.

Assessment and treatment of masticatory myofascial pain syndrome (MPS) are not standardized and remain controversial. We examined whether muscle hardness was useful for evaluating masticatory MPS and analyzed the effectiveness of treatments such as stretching and massage (SM) and trigger point injection (TPI). Twenty healthy volunteers and 20 MPS patients were enrolled. MPS patients were divided into TPI and SM treatment groups. Hardness of masticatory muscle with a taut band (TB) and change in hardness were evaluated after SM and TPI treatments. Hardness values were significantly higher in muscle including a TB (TB point) than in the muscle of healthy controls. Visual analogue scale scores were significantly lower after SM and TPI treatments, and hardness of the TB point was significantly lower after SM but not after TPI. These results suggest that measurement of muscle hardness, including the TB, is useful for evaluating masticatory MPS. However, TPI analgesia might not be caused by change in muscle hardness. The mechanisms underlying the effects of SM and TPI on reducing pain in MPS may differ and thus warrant further research.

Enhancement of ERK phosphorylation and photic responses in Vc/C1 neurons of a migraine model.

Although it is well known that migraine pain is enhanced by photic stimulation of the eye, the mechanisms underlying this response are not yet understood. Noxious stimulation to the dura is known to activate trigeminal spinal subnucleus caudalis and upper cervical spinal cord (Vc/C1) neurons, causing migraine pain. Intense photic stimulation to the eye is also known to activate certain Vc/C1 neurons, thus increasing migraine pain. In this study, we hypothesized that Vc/C1 neurons receiving noxious dural input would be further activated by intense photic stimulation, resulting in the enhancement of migraine pain. However, mechanisms underlying the interactions between dural and photic sensory information in Vc/C1 neurons is unknown. To evaluate the above hypothesis, we studied phosphorylated extracellular signal-regulated kinase (pERK) -immunoreactive (IR) cells in Vc/C1 in dural mustard oil (DMO)-administrated rats. The change in neuronal excitability of Vc/C1 nociceptive neurons receiving input from the dura in DMO rats was examined and tested if those neurons were modulated by intense flush light stimulation. There were many pERK-IR cells in the lateral portion of Vc/C1 after MO administration to the dura. Flashlight presentation to the eye in DMO rats caused an enhancement of ERK phosphorylation in Vc/C1 neurons and pERK-IR cells were significantly suppressed after intracisternal administration of MEK1 inhibitor PD98059. Dura-light sensitive (DL) neurons were recorded in the lateral portion of Vc/C1 and photic responses of DL neurons were significantly enhanced following dural MO administration. These findings indicate that DL Vc/C1 neurons in DMO rats intensified their responses to intense photic stimulation and that ERK phosphorylation in Vc/C1 neurons receiving noxious dural input increased with intense photic stimulation, suggesting that Vc/C1 nociceptive neurons are involved in the enhancement of dural nociception associated with intense light stimulation.

Fractalkine signaling in microglia contributes to ectopic orofacial pain following trapezius muscle inflammation.

Fractalkine (FKN) signaling is involved in mechanical allodynia in the facial skin following trapezius muscle inflammation. Complete Freund's adjuvant (CFA) injection into the trapezius muscle produced mechanical allodynia in the ipsilateral facial skin that was not associated with facial skin inflammation and resulted in FKN but not FKN receptor (CX3CR1) expression, and microglial activation was enhanced in trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1-C2). Intra-cisterna magna anti-CX3CR1 or anti-interleukin (IL)-1ß neutralizing antibody administration decreased the enhanced excitability of Vc and C1-C2 neurons in CFA-injected rats, whereas intra-cisterna magna FKN administration induced microglial activation and mechanical allodynia in the facial skin. IL-1ß expression and p38 mitogen-activated protein kinase phosphorylation were enhanced in activated microglia after CFA injection. The excitability of neurons whose receptive fields was located in the facial skin was significantly enhanced in CFA-injected rats, and the number of cells expressing phosphorylated extracellular signal-regulated kinase (pERK) following noxious mechanical stimulation of the facial skin was significantly increased in Vc and C1-C2. We also observed mechanical allodynia of the trapezius muscle as well as microglial activation and increased pERK expression in C2-C6 after noxious stimulation of the trapezius muscle in facial skin-inflamed rats. These findings suggest that FKN expression was enhanced in Vc and C1-C2 or C2-C6 following trapezius muscle or facial skin inflammation, microglia are activated via FKN signaling, IL-1ß is released from the activated microglia, and the excitability of neurons in Vc and C1-C2 or C2-C6 is enhanced, resulting in the ectopic mechanical allodynia.

Cervical plexus block helps in diagnosis of orofacial pain originating from cervical structures.

Headache associated with cervical lesions is called cervicogenic headache and involves the occiput but not the orofacial region. However, patients occasionally present with orofacial pain accompanied by neck symptoms. This study investigates whether orofacial pain can originate from the neck and whether cervical plexus block can help in diagnosis. We enrolled eight patients suffering from chronic orofacial pain that had not been relieved by dental treatment. Radiographic and magnetic resonance imaging revealed abnormal findings in the neck in seven of them. To identify the origin of the orofacial pain, we firstly blocked peripheral sensory input from the oral cavity and surrounding tissues, followed by that from deep cervical structures. We injected local anesthetics around the painful orofacial region, then to the tender points in the masticatory and superficial cervical muscles (trigger point injection), and consequently around the cervical plexus. Pain was assessed using a pain relief score compared with pre-treatment control values. Local anesthesia in the painful oral region provided insufficient relief whereas trigger point injection significantly relieved pain. The amount of pain relief generated by the deep cervical plexus block was more significant than that produced by any other procedures. We conclude that certain types of orofacial pain originate from cervical structures and that a deep cervical plexus block can be helpful in differentially diagnosing such pain.