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
[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
{ 2 comments… read them below or add one }
So could you translate that into english for us not so scientifically minded massage therapists? I am on a new cause to make research understandable and applicable to massage therapists and I couldn’t even get through the first sentence.
What is this saying? What does it mean for massage therapists? How can they apply this to their practice?
Thanks
Julie
[Reply]
Stefano Reply:
April 19th, 2010 at 11:51 pm
Dear Julie – thanks for your question. With our study, we wanted to explain why approximately half of the patients with carpal tunnel syndrome report that their symptoms (pain, numbness and tingling) do spread outside the anatomical boundaries of median nerve territory (i.e.: palmar side of thumb, index, middle and half of the ring finger) to involve the territories of another hand nerve (i.e.: the ulnar nerve, which innervates the remaining half of the ring and the small finger).
Moreover, half of CTS patients (not necessarily those who refer hand extramedian spread) report that symptoms spread to the forearm and the arm. If one considers the nervous system as hardwired, there would be two reasons for this extraterritorial spread. The first would be that, at the peripheral nerve level, another nerve/root is damaged, but we excluded this in our patients before including them in the study.
The second is that patients are hysteric, malingering or somatise, but this hypothesis would not be reasonable to explain symptom spread in half of CTS patients simply because hysteria and malingering are not common phenomena.
Another reason, which our data favour, is that dorsal horn sensitization takes place in CTS patients with extramedian spread of symptoms. I will try to explain this point: animal models indicate that when a nerve is damaged, hyperalgesia (i.e.: reduced pain threshold for a variety of stimuli) takes place in the territory innervated by this nerve (this is not very surprising) as well as in neighbouring territories. The reason for these extraterritorial changes is that the representation of our body in the dorsal horn, which are the sensory areas of the spinal cord, is not fixed but may change in response to a variety of condition. Pain, expecially when chronic, is the most powerful reason why the representation of our body may change and sensory fields may expand. This is called spinal sensitization and may even change the quality of our feeling. All of us might have experienced the phenomenon of mechanical allodynia when we touch near border of a wound and feel pain instead of touch. Sensitization may also take place at the peripheral level (pain receptors and nerve fibers) and in the central nervous system. We may hypothesize that these two anatomical levels may contribute to extramedian spread but the study was not aimed at exploring these changes.
From a practical point of view, the take-home message of our study is that there is no need to worry when a patient with a peripheral nerve lesion report symptoms that spread outside the anatomical territory of that given nerve. In the majority of cases there are neither other nerve lesions nor malingering/hysteria but simply spinal sensitization. This means no need for additional tests and no need for psychologic/psychiatric consultation.
Best regards Stefano
[Reply]
Thanks for sharing this great study Stefano and what a good and understandable reply you wrote.
Is it true that the dorsal horn is ultimately controlled by the higher parts of our nervous system? I Have learned that the limbic system for one is part of keeping these pain signals local and that it can fail when there is an emotional component or distress? In that respect one could argue for multidisciplinary therapy.
Of course this assumption is based on colleges neurophysiology I received many years ago, and science must have progressed since.
Could you tell us more about the conditions in these patients that make the pain spread?
[Reply]