About 20 or more years ago, some juicy basic research demonstrated what most aware clinicians and many patients already knew – that injured peripheral neurones were sensitive to adrenaline, or simply, – stress can make a peripheral nerve fire. More recent research in the last 10 years has shown that in the dorsal root ganglia, injured neurones will express more adrenaline sensitive channels and sympathetic fibres will actually sprout allowing more adrenaline to dribble onto the channels (For a reviews see Ramer et al 1999 and/or Pertovaara 2006).
If you combine this with two facts, (a) ion channels are produced in response to need, thus adrenaline sensitivity is the brain’s response to stress and (b) the ion channels will only be in situ for a day or two before they die and are replaced, the simple follow on is that reduction of stress can have a very rapid influence on the sensitivity of peripheral nerves.
Most clinicians will know of the patient who returns for their second visit feeling much better, although little ‘therapy’ might have been carried out or had time to really influence the problems. The probable basis of the improvement was that the clinical intervention was helpful and threat reducing (call it placebo if you wish) resulting in a powerful alteration in billions of ion channels as neural tissue returned to pre-stress ion channel numbers and kind. And of course nerves will move and slide better if the adrenaline reactivity is reduced.
Ramer MS et al (1999) Pain Suppl 6 S111-S120
Pertovaara A (2006) Progress in Neurobiology 80 (2) 53-83