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It has been postulated that the mechanisms responsible for the increased pericranial tenderness could be peripheral activation or sensitization of myofascial nociceptors.
Moreover the response system with the standardized corrective action could be peripheral and not central.
It is known that diabetic neuropathy could be peripheral, autonomic, and proximal or focal.
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However, synovitis of peripheral joints could be a peripheral manifestation of disease, and does not correlate with axial joint severity and radiographic progression per se.
NP could be a peripheral cause of migraine but also a manifestation of central mechanisms.
The authors' conclusion was that it could be a peripheral effect of the drug because "sumatriptan is a selective 5-HT (1B/1D) receptor agonist that does not cross the blood brain barrier" [60].
One possible explanation for this difference could be that peripheral nerves in general are more protected and thus less exposed to mechanical stress compared to skeletal muscle fibers.
The same experiment on isolated vascular smooth muscle lends support for our observation that the hypotension could be of peripheral origin.
A strength of this study is that the present findings are the first to highlight that peripheral dopamine could be involved in peripheral pain modulation.
In fact, the notion that matrix-producing cells could be derived from peripheral blood mononuclear cells (PBMCs) peripheral blood cells is not new.
In some patients, the cortical changes could be reversed with peripheral anesthesia.
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CEO of Professional Science Editing for Scientists @ prosciediting.com