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When the pain of carpal tunnel syndrome spreads, we should be thinking dorsal horn not malingering

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Here is an important study.  A couple of Italian Neurologists have investigated people with carpal tunnel syndrome who report that their pain has spread beyond the boundaries of the median nerve.  Unfortunately, such reports are often misinterpreted by clinicians as evidence of malingering, or hysteria.  Well, these fellows did quantitative sensory testing and came up with some groovy results. What is grooviest however, is that when we asked them to write something about their paper here, they were happy to oblige. So, here is what they wrote:

Spread of pain outside boundaries of peripheral nerve is associated with central nervous system hyperexcitability. A psychophysical study in carpal tunnel syndrome

Giampietro Zanette, Stefano Tamburin

The recently revised diagnostic criteria for neuropathic pain (NP) indicate pain with a distinct neuroanatomically plausible distribution (i.e.: a distribution corresponding to that of a peripheral nerve, fascicle, root or to the topographic representation of a body part in the central nervous system) as a mandatory criterion for NP diagnosis [3]. However, in carpal tunnel syndrome (CTS), which represent a very common cause (3% overall prevalence in the general population) of median nerve entrapment at the wrist, patients often report spread of pain and sensory symptoms beyond the boundaries of the sensory distribution of the median nerve. Whole-hand sensory symptoms were documented in up to 70% [1, 4, 5] and proximal spread of sensory symptoms in 45% of CTS patients [6] despite thorough exclusion of other conditions that could have caused extramedian symptoms.

Animal models suggest that NP can extend beyond anatomical borders because of sensitization changes leading to spinal hyperexcitability [2] but human data are lacking. To test whether similar mechanisms would take place in CTS patients with extraterritorial symptoms, we used a psychophysical procedure called quantitative sensory threshold (QST) [7]. During QST, subjects undergo mechanical and thermal stimuli of increasing intensities and are asked to push a button when they begin to feel the stimuli as painful; this intensity represents the pain threshold for that given stimulus. Subjects are also asked to score the severity of pain to the same type of stimuli when their intensity is higher than the pain threshold. QST is non-invasive and allows researchers to explore peripheral and central nervous system hyperexcitability in humans. We found that mechanical and thermal pain threshold were lower (i.e.: less intense stimuli were needed to cause the patient to feel pain) in CTS patients with extramedian spread of symptoms in the hand but not in those with proximal spread [7].

Our data documented spinal sensitization in CTS patients with hand extramedian symptoms. Peripheral and brain sensitization might also have contributed to our findings. These results indicate that a patient with putative NP and symptoms that do not respect an anatomical distribution may have NP and should not be considered as hysteric or malingering. Spinal sensitization, which sometimes may persist after resolution of the peripheral nerve damage, might also explain those CTS patients whose symptoms do not disappear after successful median nerve surgical release.

About Stefano

Stefano Tamburin MD, PhD, is Lecturer in Neurology at the Department of Neurological and Visual Sciences, University of Verona, Section of Rehabilitative Neurology, GB Rossi Hospital, Verona, Italy

If you want to know more about Stefano visit his page at the University of Vernoa.

References

ResearchBlogging.org[1] Caliandro P, La Torre G, Aprile I, Pazzaglia C, Commodari I, Tonali P, & Padua L (2006). Distribution of paresthesias in Carpal Tunnel Syndrome reflects the degree of nerve damage at wrist. Clinical neurophysiology: 117 (1), 228-31 PMID: 16325467

[2] Malan TP, Ossipov MH, Gardell LR, Ibrahim M, Bian D, Lai J, & Porreca F (2000). Extraterritorial neuropathic pain correlates with multisegmental elevation of spinal dynorphin in nerve-injured rats. Pain, 86 (1-2), 185-94 PMID: 10779675

[3] Treede RD, Jensen TS, Campbell JN, Cruccu G, Dostrovsky JO, Griffin JW, Hansson P, Hughes R, Nurmikko T, & Serra J (2008). Neuropathic pain: redefinition and a grading system for clinical and research purposes. Neurology, 70 (18), 1630-5 PMID: 18003941

[4] Wilder-Smith EP, Ng ES, Chan YH, & Therimadasamy AK (2008). Sensory distribution indicates severity of median nerve damage in carpal tunnel syndrome. Clinical neurophysiology: 119 (7), 1619-25 PMID: 18467170

[5] Zanette G, Marani S, & Tamburin S (2006). Extra-median spread of sensory symptoms in carpal tunnel syndrome suggests the presence of pain-related mechanisms. Pain, 122 (3), 264-70 PMID: 16530966

[6] Zanette G, Marani S, & Tamburin S (2007). Proximal pain in patients with carpal tunnel syndrome: a clinical-neurophysiological study. Journal of the peripheral nervous system : JPNS, 12 (2), 91-7 PMID: 17565533

[7] Zanette G, Cacciatori C, & Tamburin S (2010). Central sensitization in carpal tunnel syndrome with extraterritorial spread of sensory symptoms. Pain, 148 (2), 227-36 PMID: 20004060

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