Stimulated by Constantini et al 2020.[1]
This is another paper from the Italian stable of Maria Adele Giamberardino. So perhaps you have guessed that the V-V stands for viscerovisceral. This is another novel relatively long-term experimental study embedded within actual clinical practice. The rather older but similar clinical experimental study was published some 10 years ago.[2]
V-V stands for viscerovisceral
It was a ground-breaking study in that it provided, for the first time, definitive evidence of the theoretical interactions between co-occuring visceral pain conditions and how these can be modified by treatment of one condition. For example, the average patient with coronary heart disease and gallstones would have more frequent and intense symptoms and greater segmental somatic sensitivity than the average patient with only one of those conditions. Treatment of just one of the two conditions resulted in symptomatic improvements in the other, but only for conditions where there was segmental overlap.
segmental overlap
That is a very brief outline of a huge project described as exemplary in an accompanying editorial by Wilfred Jänig.[3] Jänig being recognised as one of the leading figures in the physiology of the autonomic nervous system, and a former speaker at a BMAS Scientific meeting in Glasgow. I remember walking with him back to his hotel and asking him about the potential physiological mechanism of IV lidocaine (lignocaine when I was a boy) in patients with intractable chronic pain, something I naturally considered to be rather controversial. There is a certain simplistic logic to it if you consider that you are trying to obtain local anaesthesia all over! But in practical terms, blocking nerve transmission in all nerves would be rather bad, even if you could achieve a sufficient dose without a fatal cardiac arrhythmia, which you can’t. He recall that he made a pretty good argument based on his own in vitro research. Unfortunately, I do not recall the details of his physiological argument!
For those interested (probably not so many), Jänig published a rather cautious editorial on the subject at about the same time as our conversation,[4] and I have just found a more contemporary review that combines both mechanistic and clinical research.[5] The bottom line is that I am less sceptical.
a quite fabulous clinical experiment study
So, after that diversion for my limited recollection of conversations with famous physiologists, let’s get back to the subject – a quite fabulous clinical experiment study. The authors have laid the theoretical groundwork for us in a recent review,[6] which I commented on here in December 2019.
They took women suffering from dysmenorrhoea who had a history of symptomatic renal stone(s), and a similar number with just the dysmenorrhoea. They followed them for a year and tracked symptoms and somatic sensitivity (muscle hyperalgesia in the referred pain area). After one year of assessments they took half the comorbid women and performed trigger point injections (TPIs) in the ipsilateral loin related to the previous renal stone(s), and then followed both groups for a further year.
The comorbid group had significantly greater symptom burden than the group with dysmenorrhoea alone, and they both had significant muscle hyperalgesia compared to normal. Following injection of trigger points related to previous renal stones, the symptom burden and muscle sensitivity related to the dysmenorrhoea significantly reduced compared with the group that did not receive TPIs.
The authors give a lovely succinct summary of the significance of their research:
A past pain process from an internal organ can continue enhancing pain expression from a painful disease in another neuromerically connected organ (viscero-visceral hyperalgesia) if secondary myofascial trigger points (TrPs) developed in the referred area at the time of the previous visceral disease. Inactivation of these TrPs reverts the enhancement. Assessment and treatment of TrPs in referred areas from past visceral pain conditions should be systematically carried out to better control pain from current diseases in other viscera.
[1]
Of course we would chose to deactivate TrPs with acupuncture or dry needling rather than an injection, and if you will forgive me, it has been established long ago (near the beginning of my reviewing career) that what you inject into TrPs makes no difference as long as you use a needle of some sort.[7]
References
1 Costantini R, Affaitati G, Fiordaliso M, et al. Viscero‐visceral hyperalgesia in dysmenorrhea plus previous urinary calculosis: role of myofascial trigger points and their injection treatment in the referred area. Eur J Pain 2020;2:ejp.1542. doi:10.1002/ejp.1542
2 Giamberardino MA, Costantini R, Affaitati G, et al. Viscero-visceral hyperalgesia: characterization in different clinical models. Pain 2010;151:307–22. doi:10.1016/j.pain.2010.06.023
3 Jänig W. Visceral pain – still an enigma? Pain 2010;151:239–40. doi:10.1016/j.pain.2010.07.009
4 Jänig W. What is the mechanism underlying treatment of pain by systemic application of lidocaine? Pain 2008;137:5–6. doi:10.1016/j.pain.2008.04.001
5 van der Wal SEI, van den Heuvel SAS, Radema SA, et al. The in vitro mechanisms and in vivo efficacy of intravenous lidocaine on the neuroinflammatory response in acute and chronic pain. Eur J Pain 2016;20:655–74. doi:10.1002/ejp.794
6 Affaitati G, Costantini R, Tana C, et al. Co-occurrence of pain syndromes. J Neural Transm 2019;1:3. doi:10.1007/s00702-019-02107-8
7 Cummings TM, White AR. Needling therapies in the management of myofascial trigger point pain: a systematic review. Arch Phys Med Rehabil 2001;82:986–92. doi:10.1053/apmr.2001.24023
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