Startseite Why are some patients with chronic pain from anterior abdominal nerve entrapment syndrome (ACNES) refractory to peripheral treatment with neurectomy?
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Why are some patients with chronic pain from anterior abdominal nerve entrapment syndrome (ACNES) refractory to peripheral treatment with neurectomy?

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Veröffentlicht/Copyright: 1. Januar 2017
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In this issue of the Scandinavian Journal of Pain van Rijckevorse et al. present a study that has several important aspects [1]. This is a study of anterior cutaneous nerve entrapment syndrome (ACNES) and the authors’ aim is to find out why around 25% of the patients are unresponsive to the current treatment algorithm.

1 Nerve entrapment pain often not recognized

Nerve entrapments are frequent causes of chronic pain, but not always recognized and treated correctly. While canalis carpi syndrome is well known, easily diagnosed objectively with nerve conduction velocity reduction, and effectively treated operatively, other entrapment syndromes are controversial both when it comes to diagnosis and treatment. Thus, in a recent article Orlin et al. described high prevalence of nerve entrapments of the lower extremity caused by chronic compartment syndrome [2]. The lack of objective tests is one reason for an ongoing controversy regarding diagnosis and treatment. The anterior tarsal tunnel syndrome and the posterior tarsal tunnel syndrome are further examples.

2 Anterior cutaneous nerve entrapment syndrome (ACNES): 75% respond with less pain to peripheral treatment

Anterior cutaneous nerve entrapment syndrome (ACNES) is another example of a frequently overlooked nerve entrapment syndrome. It is often misdiagnosed as functional abdominal pain [3].

ACNES was described as early as 1926 by Carnett [4]. However, the diagnosis had almost been forgotten when the Dutch group lead by Roumen started studying it more systematically. This group has presented an algorithm for diagnosis and treatment [5]. They have also performed a randomized, blinded study of the surgical intervention supporting the long-term effects of neurectomy [6].

However, they find that around 25% of patients are unresponsive to the current treatment algorithm consisting of local injections (local anaesthetics + corticosteroids) and neurectomy. The present study aims to examine possible causes of this treatment failure. In the present study van Rijckevorsel et al. report on their exploratory study on 50 patients with ACNES using Quantitative Sensory Testing (QST)-methodology and conditioned pain modulation (CPM) with cold-pressor as modulating stimulus [1]. Of these 50 patients 35 were responders and 15 were treatment non-responders.

3 Is central sensitization and generalized hyperalgesia behind no response to peripheral treatment?

They report that those who did not respond to peripheral treatment (local anaesthetic infiltration and neurectomy) had signs of central sensitization and generalized hyperalgesia. This is based on the finding of lower thresholds for pressure pain detection in the group of subjects unresponsive to treatment. No difference was found in pain threshold to electrical stimulation or CPM with cold pressor task as conditioning stimulus.

The authors are careful in stating that this study is exploratory and hypothesis generating and that further research is needed. There are several important aspects to consider.

4 What is central sensitization and generalized hyperalgesia?

This is a difficult and controversial question that is still under debate [7,8,9,10]. The findings of lowered thresholds in a group of subjects do not necessarily mean that central pain processing has changed. The group might have a constitutional lowered threshold due to, e.g. genetic factors [11]. This might explain both the reduced thresholds and susceptibility for chronic pain.

The huge inter-individual variation in pain sensitivity is well known [12]. In epidemiological studies, chronic pain patients have changes in experimental pain, in particular after surpra-threshold pain stimulation and in pain tolerance [13].

We also know that both nerve entrapment and neurectomy leads to changes in the proximal part of the primary neuron with possible phenotype switch which possibly can give rise to spontaneous activity in the primary sensory neuron [14]. Typically, only 10–20% of patients get chronic pain after verified nerve injury – much like the percentage unresponsive after ACNES-treatment [1].

5 Do no-responders have altered pain-modulation systems before treatment?

If our aim is to identify unresponsive subjects before surgery, what we need now are studies with careful examination of the subjects both before and after treatment for entrapment syndrome.


DOI of refers to article: http://dx.doi.org/10.1016/j.sjpain.2016.09.014.



Oslo University Hospital, Department of Pain Management and Research, Pbox 4950 Nydalen, 0424 Oslo, Norway.

  1. Conflict of interest: None declared.

References

[1] van Rijckevorsel DC, Boelens OB, Roumen RM, Wilder-Smith OH, van Goor H. Treatment response and central pain processing in Anterior Cutaneous Nerve Entrapment Syndrome: an explorative study. Scand J Pain 2017;14:53–9.Suche in Google Scholar

[2] Orlin JR, Lied IH, Stranden E, Irgens HU, Andersen JR. Prevalence of chronic compartment syndrome of the legs: implications for clinical diagnostic criteria and therapy. Scand J Pain 2016;12:7–12.Suche in Google Scholar

[3] van Assen T, de Jager-Kievit JW, Scheltinga MR, Roumen RM. Chronic abdominal wall pain misdiagnosed as functional abdominal pain. J Am Board Fam Med 2013;26:738–44.Suche in Google Scholar

[4] Carnett J. Intercostal neuralgia as a cause of abdominal pain and tenderness. Surg Gynecol Obstet 1926;42:8.Suche in Google Scholar

[5] Boelens OB, Scheltinga MR, Houterman S, Roumen RM. Management of anterior cutaneous nerve entrapment syndrome in a cohort of 139 patients. Ann Surg 2011;254:1054–8.Suche in Google Scholar

[6] Boelens OB, van Assen T, Houterman S, Scheltinga MR, Roumen RM. A double-blind, randomized, controlled trial on surgery for chronic abdominal pain due to anterior cutaneous nerve entrapment syndrome. Ann Surg 2013;257:845–9.Suche in Google Scholar

[7] Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011;152:S2–15.Suche in Google Scholar

[8] Woolf CJ. What to call the amplification of nociceptive signals in the central nervous system that contribute to widespread pain? Pain 2014;155:1911–2.Suche in Google Scholar

[9] Hansson P. Translational aspects of central sensitization induced by primary afferent activity: what it is and what it is not. Pain 2014;155:1932–4.Suche in Google Scholar

[10] Cervero F. Central sensitization and visceral hypersensitivity: facts and fictions. Scand J Pain 2014;5:49–50.Suche in Google Scholar

[11] Desmeules J, Chabert J, Rebsamen M, Rapiti E, Piguet V, Besson M, Dayer P, Cedraschi C. Central pain sensitization, COMT Val158Met polymorphism, and emotional factors in fibromyalgia. J Pain 2014;15:129–35.Suche in Google Scholar

[12] Nielsen CS, Stubhaug A, Price DD, Vassend O, Czajkowski N, Harris JR. Individual differences in pain sensitivity: genetic and environmental contributions. Pain 2008;136:21–9.Suche in Google Scholar

[13] Johansen A, Schirmer H, Stubhaug A, Nielsen CS. Persistent post-surgical pain and experimental pain sensitivity in the Tromsø study: comorbid pain matters. Pain 2014;155:341–8.Suche in Google Scholar

[14] Nitzan-Luques A, Devor M, Tal M. Genotype-selective phenotypic switch in primary afferent neurons contributes to neuropathic pain. Pain 2011;152:2413–26.Suche in Google Scholar

Published Online: 2017-01-01
Published in Print: 2017-01-01

© 2016 Scandinavian Association for the Study of Pain

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