| Radiculopathy, radicular pain and referred pain: what are we really talking about? TOM JESSON BA BSc CChertered Physiotrerapist. Connect Heath Pain that radiates from the neck down the arm, or from the back down the leg is a common presentation in clinical practice. However, despite the importance of standardisation in physiotherapy practice, there exists an abundance of terms to describe such symptoms, that may not only be confusing to patients, but may worry them unduly if explanations imply that their body is vulnerable or damaged. Therefore, communicating a diagnosis to the patient in a way that is honest, reassuring and empowering is very important This article also aims to Clarify these terms, explain the pathophysiology behind them, consider their limitations in light of recent developments in pain science UO ay Moai Bret eo) ecu 2To consider these terms in light of eee eng ee PS Ce eC nervy eet ee enor Pouca Introduction In 1941, the rheumatologist Jonas ellgren wrote a paper in The Lancet lamenting that back pain with leg, pain was, in his experience, too often Clagnosed as “sciatic neuritis’ when infact t was nothing of the sort (Keligren 1941), He had performed a series of experiments showing that noxious stimulation of the ligaments and muscles of the spine produced segmental areas of referred pain running down the buttock, eg, shank and foot; areferred pain which he accused the “neurological school” of physicians of cover-diagnosing as nerve pain, Assessing 90 xrays of patients diagnosed with sciatica, Kellgren judged that 50 of them wore in fact suffering referred pain Later, in 1994, the radiologist Pierre Miletie wrote to the journal Radiology on the issue of radicular and refered pain to-asksimaly, “what are we really talking about” (Milete 1994). Like Keligren, Milete accused his colleagues of over diagnosing sciatic nerve root pathology, assuring that any back / leg pain was neurogenic. He pointed ta confusion surrounding the terminology for back / leg pain not only clinically but even at an academic level. "ifwe seak to improve our understanding’ Milette wrote, "tis mandatory to address tis fundamental issue’ Today, despite Kellgren and Milette’s pleas, there is still some confusion about the terms referred pain, radicular pain and radiculopatty. This aticle aims to address this confusion on two levels. First, atthe level of communication between clinician and clinician: in orcer to reduce unwarranted variation in practice itis important to, as Milette put it, be clear what we are really talking about. Second, at the level ‘of communication between clinician ‘and patient: as physiotherapists are becorning more aware of the impact of the words we use, and their power to both harm and heal, we need to improve ‘on our common lexicon so we can ‘explain nerve root pain in a way that is lear, reassuring and empowering, ‘Communication between clinician and clinician BASIC TERMINOLOGY (TABLE 1) Referred pain, or somatic referred pain is MANIFESTATION, MECHANISM ‘SOMATICREFERRED Dull, aching growing anddificlttloalse pal, wth | “The convergence of necceptve afferent on second order neurons a PAIN sninconstent and non-dermatoral pater thespinalcord that alo happen te sutend regions of the lew ib (Bogeuk, 2009) RADICULARPAIN Lancinatig shocking elecefeeing nathinband | Compesslan anda nfammation leads to ectpi Le. spontaneous, albnormal eistharges emanating rom the éorsal rootr ts ganglion RADICULOPATHY Objective neurological signs loss of unetoninretletes, | Compression andar infammation eads to demyelination and axonal poner and sensation. (Not necessrly pa) damage causing reduced impulse conduction aang the neve TABLE: Basic terminology ofthe manifestation and mechanism of pain (Bogduk 2009; Baronet o2016) 46 [ Intouch [ae41 XS PHYSIOTHERAPISTS, WE ARE BECOMING MORE AWARE OF THE IMPACT OF THE WORDS WE USE/? result of nociception (danger messages) arising from the structures of the spine {Bogduk 2008; Baron et of 2016). The proposed mecharism i the “convergence. projection model’ According to this ‘model, afferents ‘rom the lumbar spine and from the lower limb converge on the same second order afferent in the spinal cord, and so the brain cannot ciscriminate between the two sources of input when they are projected up. As @ result, the brain creates a pain experience for both, even thoug” the lumbar spine is the only significant source of nociception. Tiss the same ‘mechanism by which visceral refered pain, like the shoulder and arm pain of @ heart attack, is assumed to work Somatic referred pain is dull, ching, gnawing and difficult to localise (Bogduk 2008). Figure 1 illustrates the results of Kellgren’s (1941) aforementioned experiments to find the referred pain pattems for each spinal segment. Rodicular pain isa result of an action potential emanating from the axon ofa nerve at the dorsal root, orat the nerve root ganglion, as opposed to resulting from stimulation ofthe nerve's peripheral terminals (Bogduk 2003; Baron etal 2016). Ths discharge is heterospecific, @ barrage of AB, Ad and C fibre discharges, and so technically itis not nociceptive a hs! a FIGURE: Patterns of somatic referred pain evoked by noxious stimulation of the Inerspinous ligaments atthe segments Indicated. Based on Kellen (1941) FIGURE 2: An ilustration of the lancinating quality of radicular pain travelling into the lower limb along a narrow band Figure 2 illustrates the result of Kellgren’s 1941) experiments to induce radicular pain. The subjects reported this pain as a lancinating, shocking, electric sensation, The pathophysiological processis complex. Compression of the nerve, whether by isc or ts exudate, or by forarinal stenosis, everses the downward pressure gracient necessary to maintain the nerve's blood supply causingittto become ischaemic. One ‘way in which this leds to pain is by causing Schwann cell death and demyelination, which exposes a portion cof axon from where spontaneous action potentials can emanate to be processed by the brain and experienced as pain (Schmid 2015). Another way in which compression and ischaemia lead to pain i by inciting intrareural inflammation, which aloneis sufficient tosensitise 2 nerve to movement (Dilley etal 2005) and can spread tothe spinal cord and the brain (Albrecht etal 2018). In addition, intraneural inflammation impairs axonal transport so thation channel components being transported along the nerve bunch up in one place, creating @ "hot spot” of excitability (Dilley etal 2013) The mechanisms of radicular pain are Not fully understood and more complex than is suggested by the neat description here; for a more comprehensive ‘explanation see Schmid (2015). As figure 1 demonstrates, experimentally induced radicular pain manifests in a clear line that approximates the territory innervated by the affected nerveroct. Clinically, however, tre boundaries of radicular pain are less clear. Bove etal (2008) found shat, of 25 patients with lumbar radicular pain, all but ‘one reported multidermatomal pain Similarly, Furman & Johnson (2018) foundithat only radicular pain on the anterior, medial and lateral thigh had any correlation with its nerve root, origin, whereas buttock, gluteal and calf pain had none (igure 3). The none dermatomal presentation of radicular painis likely because intraneural inflammation nas the potential to spread to the dorsal horn and beyond, which ‘would sensitise neighbouring nerves {Scheid eta! 20132}; and because nerve roots have multiple intrathecal anastomosis (cross linkeges) (Furman & Johnson 2018) Radiculopatty isthe objective loss of function of a nerve resulting from cdarmage to the nerve root (Bogduk 2009; Baron etal 2016). This manifests clinically 2s loss of muscle power, reflex response, and the sensation of light touch, hot /cold response and response to pinprick. As discussed, @ compressive insultto the nerve can set off a chain events that cause it to become demyelinated and inflamed, in © FIGURE 3: An illustration ofthe variation of induced radicular pain distribution in multiple patients, Based on Furman & Johnson (2018) aaretes | No164] Autums 2078 | 974/THE CLINICIAN SHOULD MAKE A DIAGNOSIS OF RADICULOPATHY BASED ON AN ACCUMULATION OF SIGNS RATHER THAN JUST ONE!” some cases there may also be axonal cogeneration (Merskey & Bogduk 2012) Anerve inthis poor ste of health cannot readily conduct action potentials, leading to the loss of function we call radiculopathy. Radiculopathy isnot a pain condition atall it isa diagnosis that refers only to oss of nerve function and mayor may not be painful (Merskey & Bogduk 2012} NOTES ON MAKING A DIAGNOSIS In orderto diagnose a radiculopathy (as ‘opposed to radicular pain), we need to see objective loss of nerve function, but itis important to rernember that many of our tests for the loss of function of a nerve have imperfect specificity, ie, will turn up false positives (Tawa et al 2017) This implies that the clinician should make a diagnosis of raciculopathy based con an accumulation of signs rather than just one (Tawa et a! 2027) When it comes to differentiating between radicular and referred pain there isno clear and validated method, although recent work suggests that a cluster of 1. pain below the knee 2. leg pain worse than back pain 3. positive neurodynamic test 4. the report of pins and needles is strongly associated with nerve root, involvement (Stynes et a! 2018), As previously discussed, radicular pain is not necessarily @"line” of pain and rarely follows dermatomal pattems (Furman & Johnson 2018}, In cases of doubt, the Internationa: Association forthe Stucy of Pain (WASP) suggests simply documenting “Lower limb pain” (Merskey & Bogdiuk 2012) When documenting findings from an objective assessment, table? illustrates how it might be helpful to make the istinction between gain and loss of function (Schmid et al 20134}. IMPORTANT CAVEATS Having presented a classical way of categorising low back / leg pain and neck farm pain it should be noted that, to make @ pain diagnosis based on an underlying mechanism like “radicular” ‘ferred isto reformulate something complex anc emergent into something simple and linear, and as such is perilous. ‘The distinction between different kinds of axial /limb pain is not clear; for example, nerve entrapment pain isnot necessarily neuropathic, asnervi nervorum (the nerves subserving the nerve trunk) can bea source of naciception (Tebseira eta! 2016) Additionally, radicular and referred mechanisms can co-exist. Seemingly non-neuropathic pain can feature “occult” neuropathic symptoms (Spahr et al 2017, and, ofcourse, painitselfis a higher construct. None ofthe above mecharisms “are” pain until this information reaches, the brain (Brodal 2017) Indeed, itis arguably not necessary to consider underlying mechanisms 2 al They may in fact distract from variables like expectations, disability and pain severity, wihich appear to be more important for the prognosis and management of many musculoskeletal conditions (Crofteta! 2015; Konstantinow eta! 2017), but such considerations have to be held against the practical need for clinicians to communicate clearly and productively with each other, and between disciplines. For this reason, classification, though awkward, is arguably necessary Just es importantly, we must a'so consider how we communicate such labels 2s radicular pain and radiculopathy with patients. Communication between clinician and patient The clinical presentation of radicular pain has little association with “incings ‘on imaging (Karppinen et a! 2001), but ine survey of people with a history of cervical radiculopathy, Weber et a! (2017) found that 67% believed an MRI is more importart than clinical findings inthe decision-making process for their condition, and 47% said they would be willing to undergo surgery based on “abnormal” findings on an MRIlone, evenif they had no or’ Itis no surprise that patients appear to have a biomedical uncerstanding of radicular pain and radiculopathy, they share that perspective with much of the medical and allied health professions and with society at large. For our patients’ sake, physiotherapists must promote amore evidence-based and less threatening understanding of these conditions (Moseley & Butler 2017). This is.adelicate matter as there isa fineline between de-threatening a condition and trivialsing it DEFINITION _| MANIFESTATION. TED BY MECHANISM ‘oan ‘nermal Parzesthesia, spontaneous pa, hyperagesla | Newredynamietests,Spurin’s | Demyelnatien, axonal degeneration cexctabilty and allodyria, ypereteia,muscespasm | tes, Tinestst, pan on sane neuroinflammtion| palpation Loss Regucedimpulse | Hypoesthesia anzestesa, weaker/absent_ “Hard neuro" defies, pinpiek, | Demyelnaton axonal degeneration conduction relees, museiewesknes,reiced sensation hot col testing TABLE 2: Distinguishing between gain and loss of function during objective assessment butmotneuroinismmation| 48 | Intouch | arrciesThere sno script for patient education, and where passible it should be tallored to the individual’ prior knowledge and belief. That said, the following learning aims are likely to appea” in mast explanations of cervical racicular pain and radiculopathy. Its often possible to provide them in ar “online commentary” tw the objective assessment, to save the patient 2 lecture at the end CONCEPTS TO EMPHASISE (TABLE 3) Since Victorian times, nerves have been thought of as a weak-point in our bodies, tre slightest darnage to which spels disaster (Bourke 2014). Patients may, therefore, benefit from knowing. that nerves are big, tough structures with the dura mater and epineurium forming layer of protection around them (Moseley & Butler 2017), Patients. may also be pleased to hear that, like any other part of the body, nerves also. like movement; a good stretch disperses inflammation and helos provide them with lots of oxygen, The terms “trapped” and “pinches nerves are probably nocebic, and in any event unlikely to be accurate given that the nerve root ganglion takes up just cone third of the space in the outlet holes between the vertebrae, meaning that it potentially has room to move even after significant degenerative changes (Moseley & Butler 2017). Research by ‘Schmid et a (20136) has shown that mile compression, rather than tight constriction, is sulficient to induce nerve pain in rats, 0 “compressed’ or "crowded" are more appropriate words to Use. Indeed, itis neuroinflarmmation that is likely to be more associated with the patient’s symptoms than nerve reat compression (Albrecht et «412018; El Barzouhi et a! 2013), and an explanation in these terms would frame the issue accurately as a normal pathophysialogical process, ie. inflamed as opposed to an aberrant biomechanical event, ie. trapped Where a patient has radicular pain with no objective oss of function, itis important to reassure them that there is no evidence that the nerveis damaged, but that it does appear to be irtated Where there are signs of radiculopathy, i.e. loss of nerve function, itisimportant to be honest, ie. advise that this implies demyelination and axonal degeneration rather than offer blind reassurance that “there is no damage’, which is arguably unethical, However, the patient may benefit rom hearing that thisis common and normal, and that neural tissue, Uke any other soft tissue, is capable of healing and rebuilding. There is some evidence that loss of nerve function, as long as itis not progressive, isnot particularly relevant for prognosis; indeed, itmay be an indicator of z better than average outcome asit implicates a disc protrusion, whic” has a good chance of resolving spontaneously (Konstantinow eta! 2017} There's an opportunity to link nerve pair to the patients wider health ane wellbeing. Expiain to the patient that nerves are connected to the brain and made of the same stuffso, ifthe brain is stressed or overworked, the nerve might CONCEPTS TO EMPHASISE “THE NERVES ARE CONNECTED TO THE BRAIN, SO IF THE BRAIN |S STRESSED, THE NERVE MIGHT NOT GET THE CHANCE TO CALM DOWN EITHER not get a chance to calm down either, This means taking time to relax and sleep walls part of rehab. With regard to ‘exercise, although central sensitisation isa theoretical concern when exercise is painful (Woolf 2004}, there is no reason to think that even vigorous movement will cause structural damage to the nerve, Nerve pain appears to cause patients more distress than somatic pain (Spahr eto! 201) Patt of the reason for this may be that, for the patient, itis a strange sensation. By explaining that it is the nerve’ job to send information about the body and its surroundings to the brain, and that when the neve isinritated it can stat firing off a ot of useless information thatis similar to white noise, the patient can be reassured that, although they might feel al sorts of sensations from thenerve, the problem itslfs ikely to be minor and quite localised, Equally, the worrying symptom of night painis easily explained; blood pressure drops at night, and when thisis combined with the individual © Big and tough, wth aprotective covering Nove, bene and stretch with the rest the body Enjoy movement Aworkoutgves them good stretch, disperses ay inflammation and brings them atesh blows supply TRAPPED" NERVES Even fyou ose some space theres plenty spare Nerves are sldey ane bendy ~ they are almost mpassible to pinch, “would be like picking up ychee with chopsticks More cromded out or eamressea than tapped Zings and zaps co not mean that a nerves injured ~ mare ley ee sentive Mostpsinlal never are sor, but ale Ifthenerveisn dings job aswell asi usually does, then ust ke muscles and ligaments, canrepalrand recover ‘UNUSUAL SYMPTOMS Night pains normal: tis because of 021 bloodpressure and eften because you alasleepin an auhward postion Touchy nerves ror al hey possibiycan tothe brain = sometimes werd ane wonder‘ things Theres usualy thing wreng with the ate you feethe pain TABLE: Explanatory statements of nerve concepts (Moseley & Butler 2017}, agretes | No64] Autumn 2078 [19“4 DROP IN BLOOD PRESSURE, COMBINED WITH AN ODD SLEEPING POSITION, CAN RESULT IN A TEMPORARY ISCHAEMIA TO THE NERVE, AND EXPLAIN NIGHT PAIN’! sleeping in an odd position, it can result in a temporary ischaemia to the nerve (Moseley & Butler 2017), With regard to prognosis, the assumption that radicular pain has a ‘avourable natural history's not borne out by the literature. Although some reviews ere optimistic (Casey 2011; Wong 2014), a recent high-quality tal (F608 patients with back /leg pain, inprimary care, found that just 5596 reported a 30% or more improvement in cone year (Konstantinou et a 2017). This study also identified factors associated with improved disability: shorter pain Curation, lower leg pain intensity, fewer other symptoms associated with back and leg pain e.g, ‘atigue,stif joints, poor sleep, (oss of strength), and belief that the problem will be short lived (Konstantinou eta! 2017). Clinicians are, however, nt yet in a position to be confident forecasting an outcome for an individval. Patients can be counselled that there isa good chance their pain will ‘ully resolve, but they need to know that there is also a good chance it may not Conclusion This article began by asking the cuestion: ‘what are we talking about really?” when we talk about axial / mb pain. As demonstrated, there are quite clea cferences between radicular pain, radiculopathy and referred pain; although the clinician should maintain a healthy scepticism ofthe veracity and usefulness of any mechanism based pain diagnosis. When it comes Caplan Sean) Coareeteey to explaining these conditions to our patients, there are many ways to glve ‘them hope for the future and confidence that they are safe to move; although we should not, in our enthustasmn, be ‘tempted to give exalanations that are false. ‘To reiterate Pierre Milette's statement of 24 years ago: “Ifwe seek to improve ‘our understanding, itis mandatory ‘to address this fundamental issue” hope this article has made a small contribution to that effort. About the author ‘Tom graduated as a physiotherapist from Northumbria University in 2017 ‘and has been working and training as ‘a Musculoskeletal Physiotherapist at Connect Health since then, Heis also an apprentice with the Chews Health team, Before becoming a physiotherapist, Tom ‘worked as an English teacher in Seoul, South Korea. References Albrecht D, Ahmed 5, Aetner N, Bora R, Cohen-Adad J, Deng H, Houle T, Opalacz A, Roth $, Melo M, Chen L, Mao J, Hooker J Loggia M, Zhang. Neuroinflamation of the spinal cord and nerve roots in enronic radicular pain patiens, PAIN 2018;155(5}'$68- sr BaroaR, Binder A cal N, Casale R, Dickenson A Treede R, Neuropathiclow back ain in clinica practice. European Journal of Poin 2018;20(6)851-8/3 BogdUk On the definitions and physiology oftback pain, referred pain, and radicular ain, Pain 2009;147(1)17-19 Bourke J. The Story of Poin. Oxford University Press 2014 Bove G, Zaheer A, Baja Z Subject've nature ‘flower limb radicular pain. 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