Classification of Radiculopathy and Peripheral Neuropathic Pain
Now before we start I want to state that most of my knowledge regarding this topic has developed from attending lectures/courses/practical sessions with Dr Toby Hall (Specialist Musculoskeletal Physiotherapist). I would encourage anyone reading this post to take any opportunity that arises to attend a course of Toby’s. He is a wealth of knowledge and a fantastic teacher.
So this post is about how we might attempt classification of radiculopathy and peripheral neuropathic pain.
The following is a link to the Manual Concepts website (Toby is a Director). www.manualconcepts.com
One of the comments in relation to my last post was what my thoughts are in relation to management of chronic lumbar radiculopathy.
As discussed in previous posts I feel it is imperative that we diagnose and classify pain types, and where possible subclassify as much as possible to assist in directing treatment approaches for the best management outcome for the patient. So let’s get started:
What predominant pain type is a radiculopathy?
- When we defined the pain types earlier we discussed the following types:
- Nociceptive
- Inflammatory
- Pathological
- Neuropathic
- Functional/Dysfunctional
- Pain associated with chronic radiculopathy is caused by compression or a lesion of a dorsal root or its ganglion. The pain involves pathology of the peripheral nerve trunk hence it is thought to be mainly of neuropathic origin (Mahn et al, 2011).
- The International Association for the Study of Pain (IASP) defines Peripheral Neuropathic pain as:
- Pain caused by a lesion or disease of the peripheral somatosensory nervous system.
- So based on the above a radiculopathy is a Peripheral Neuropathic Pain disorder. Remember though that this doesn’t mean that there cannot be other types of pain(s) associated with a radiculopathy.
How can we diagnose/recognise/classify Peripheral Neuropathic Pain?
The main approaches I am aware of are:
- Smart et al (2012):
- Classify peripheral neuropathic pain based on presence of the 3 following “cluster” of symptoms and signs:
- Pain referred in a dermatomal or cutaneous distribution
- Pain/symptom provocation with mechanical/movement tests (e.g. Active/Passive, Neurodynamic, i.e. SLR) that move, load or compress neural tissue.
- History of nerve injury, pathology or mechanical compromise.
- As the authors report this cluster differs significantly from the criteria contained in many of the existing screening instruments (e.g. LANSS or DN4) for identification of neuropathic pain. They suggest that the reason for this may be that the cluster in their study was mainly derived from physiotherapy/back clinic settings which may represent patients with less severe symptoms than those patients assessed in pain clinics where the screening instruments were devised.
- Classify peripheral neuropathic pain based on presence of the 3 following “cluster” of symptoms and signs:
- Treede et al (2008):
- Grade/Classify Neuropathic Pain via the following criteria.
- 1. Pain in a distinct neuroanatomically plausible distribution
- 2. History suggestive of a relevant lesion/disease affecting the peripheral somatosensory nervous system.
- 3. Demonstration of the neuroanatomically plausible distribution by at least one clinical test of nerve function.
- 4. Demonstration of the relevant lesion or disease by at least one investigation of aetiology.
- The following interpretation of these criteria is then undertaken by the clinician:
- If all 4 criteria are present = definite neuropathic pain
- If 1 and 2 plus 3 or 4 are present = probably neuropathic pain
- If 1 and 2 are only present = possible neuropathic pain
- Grade/Classify Neuropathic Pain via the following criteria.
- Questionnaires:
- As mentioned above, and in previous posts we can also use questionnaires such as:
- LANSS
- DN4 Neuropathic Pain Questionnaire
- PainDETECT
- As mentioned above, and in previous posts we can also use questionnaires such as:
Now all 3 of the above methods used together or separately can certainly give us a strong suggestion of neuropathic pain being present, but……..
How much does this help us clinically?
In my clinical experience it would appear that patients are going to present with neuropathic pain that differs in symptoms and outcomes. What would appear to be needed is a system to differentiate/classify patients with peripheral neuropathic pain into subcategories that will then assist us with management and prognosis.
The following summarises the classification of limb/referred pain devised by Schafer et al (2009, 2011). The authors subclassify patients with lower back and leg symptoms into the following groups. This is my interpretation of the articles and lectures I have attended. Patients are sub classified into 1 of 4 categories. My understanding of this classification approach is that it is hierarchical.
1. Neuropathic Sensory Hypersensitivity
- Peripheral Neuropathic pain with significant presence of peripheral and central pain mechanisms.
- LANSS positive (>12)
- Presence of “positive symptoms/features” such as allodynia, hyperalgesia, hyperpathia etc. These symptoms may also spread to non-anatomically related areas.
- Sensitisation of nerve trunks and signs of reduced nerve conduction can also be present but the key issue is the presence of a positive LANSS and central pain mechanisms/symptoms.
- Poorer prognosis, poor response to physiotherapy/manual therapy. Need medical and/or cognitive behavioural management. May be a role for physiotherapy to play if there are any nociceptive contributions to the pain (e.g. muscle control/flexibility issues) and in the provision of general exercise programs for maintaining conditioning fitness. There may also be a role for us in providing education regarding pain science etc.
2. Neuropathic Compressive Neuropathy
- Peripheral neuropathic pain with minimal peripheral/central pain mechanism involvement.
- LANSS negative (<12)
- Signs of reduced nerve conduction (needs 2 or more of diminished reflexes, sensation or muscle power).
- Minimal/Nil signs of allodynia etc. Minimal sensitisation of nerve trunk roots (i.e. no significant findings on nerve palpation, NTPT) and if sensitisation is present the presence of reduced nerve conduction would suggest “decompression” treatments e.g. exercises, manual therapy to “open up” the foramina, increase lumbar flexion etc.
- Obviously this group may also present with significant compression of the nerve root that surgical opinion is needed.
3. Peripheral Nerve Sensitivity (PNS)
- Not classified as neuropathic pain as no axonal damage is present.
- Normal nerve conduction.
- No significant central pain mechanisms.
- LANSS negative.
- Evidence of positive findings on mechanical stress of the nerve root. All 3 of the following have to be present:
- positive neural tissue provocation testing (e.g SLR/PKB with increased symptoms with sensitising positions)
- pain on nerve trunk palpation
- active movement loss (e.g. reduced lumbar flexion) with symptoms worsened by sensitising movements (e.g. ankle dorsiflexion, cervical flexion).
- Respond well to “sliders”, neural tissue mobilisation exercises etc.
- I would classify the pain from this presentation as either nociceptive or inflammatory (or a mixture of both). No doubt presentations 1 and 2 above could also have elements of nociceptive/inflammatory pain.
4. Musculoskeletal Pain
- None of the above. Now this type may have some signs of PNS but will not have all 3 of the required positive signs of PNS present.
- Articular or myofascial in origin.
- I think it adds to the Treede et al and Smart et al classifications as it subclassifies patients further. This assists management choices. For example, based purely on the Treede classification we could easily end up with the first 2 groups of Schafer et al’s classification (potentially even the 3rd!) being put in the one basket as neuropathic pain. Given all 3 groups would appear to have different mechanisms, prognosis and treatment requirements I think it is imperative that they be further classified.
The Schafer et al classification appears an excellent way of classifying limb/referred pain, and one that I using/trialling at present. Importantly we must still remember to look at other potential “causes” of this pain occurring or being amplified e.g. control impairments, psychosocial elements etc as this will further assist our management process.
I hope this provides some assistance in the management of radiculopathy. I am happy to provide some example of specific exercises for each classification type if need be.
I also realise that this is probably a contentious topic so happy to listen to opinions/comments!
References:
Mahn F, Hüllemann P, Gockel U, Brosz M, Freynhagen R, Tölle TR, Baron J. Sensory symptom profiles and co-morbidities in painful radiculopathy (sensory profiles in painful radiculopathy). PLoS ONE (2011); 6(5).
Schäfer A, Hall T, Muller G, Briffa K. Outcomes differ between subgroups of patients with low back and leg pain following neural manual therapy: a prospective cohort study. Eur Spine J (2011) 20:482–490.
Smart KM, Blake C, Staines A, Thacker M, Doody C. Mechanisms-based classifications of musculoskeletal pain: Part 2 of 3: Symptoms and signs of peripheral neuropathic pain in patients with low back (+/-leg) pain. Manual Therapy (2012);17:345-351.
About the Author: Mark Gibson
Mark is a Specialist Musculoskeletal Physiotherapist who consults at both Insight Physiotherapy and Pain Options, in Perth, Western Australia. He specialises in the assessment and management of persistent/chronic musculoskeletal pain. In addition to his clinical role he maintains regular involvement in education of the profession having held a Teaching Fellow position at the University of Western Australia for 10 years and regularly presenting at courses and seminars through the Australian Physiotherapy Association and private education sector. Mark is also a Facilitator for the Australian College of Physiotherapists Specialisation Training Program and a Sessional Academic at Curtin University. The views expressed on this blog are his own.Subscribe
If you enjoyed this article, subscribe to receive more just like it.
Great post. Especially regarding the distinction between a dermatomal pain (or dysaesthetic pain) and nerve trunk pain/neural mechanosensitivity and the different prognosis for each. My understanding is severe dysaesthetic pain is usually indicative of axonal damage and thus less amenable to “treatment”.
I have found sensory-TENS to be a useful modality in conjunction with other management strategies in some cases of sensory hypersensitivity secondary to peripheral nerve injury. However it must be used with caution given the presence of altered sensation.
Hi James,
I think you are spot on about the dyaesthetic pain and axonal damage, and subsequently that it is less responsive to treatment. That is one of the reasons why I think the Schafer et al classification is of great assistance as it lets us be more confident in directing certain patients towards physiotherapy management/treatment, whilst perhaps sending others (the Neuropathic Sensory Hypersensitivity group) away from physiotherapy towards pain management etc. Some would debate this though….I think as physios we still have a role to play in management of this group but certainly we are not capable of managing them on our own.
In regards to TENS, Nijs et al (2011) conclude from a review on management of Central Sensitisation (CS) that TENS can be beneficial as it:
– activates large diameter afferent fibers, which in turn activate descending nociceptive inhibitory mechanisms, however;
– widespread and poorly localized chronic pain states are less likely to be suitable for treatment by TENS.
Obviously this refers to management of CS, although I would strongly suggest that patients within the Neuropathic Sensory Hypersensitivity group are likely to have CS.
Reference:
Nijs J, Meeus M, Van Oosterwijck J, Roussel N, De Kooning M, Ickmans M, Matic M (2011). Treatment of central sensitization in patients with ‘unexplained’ chronic pain: what options do we have? Expert Opin. Pharmacother. 12(7): 1087-1098.
Thanks again for your input.
Cheers
Mark
Hi Mark
Nice post, as its made me realise I have some knowledge gaps! I have been on the NOI Group mobilisation of the nervous system course and read the associated book by David Butler. I was under the impression that pain on nerve palpation was due to the presence of abnormal impulse generating sites which are lesions within the axon. If this were the case then where does “Peripheral nerve sensitivity” come in?
For example, a patient I saw today: dog yanked on its lead – traction force to arm // pain in radial nerve distribution. No significant/overt factors for central sensitization although she is the “on the go”, apical breathing type, so some sensitizing chemistry likely. Conduction tests normal but pain on palpation along the nerve (including referring down to the distal forearm) and restricted neck movements and positive ULTTs. From your understanding it looks like you would consider this “Peripheral nerve sensitivity” ie no actual nerve pathology / not neuropathic pain? My understanding from my NOI Group course is… AIGs / neuropathic pain. Responds to massage / container tissue and interface mobilisation (as I understand it) by aiding clearing of swelling / improving pressure gradients within the nerve and so improving blood supply and axoplasmic flow.
I would expect a similar presentation with similar treatment plan for a “Neuropathic Compressive Neuropathy” (ie I have not got as far as sub-classifying these patients yet). Can you set me straight? As you say, its great if we can classify these patients further to determine different management. Can nerves be painful on palpation without AIGs – thinking now if the nervi nervorum were stuck in an area of raised pressure and tissue hypoxia this could sensitise them.
Any pointers / thoughts / replies appreciated. A little confused now but that’s not always a bad thing.
James
Hi Mark. Writing this again as my last post with questions seems to have disappeared…
I have been on the NOI Group “mobilisation of the nervous system” course and read the related David Butler book…
I have a patient: dog yanked hard on lead, traction force to arm // pain in radial nerve line. All conduction tests normal, ULTTs provocative, nerve trunk palpation painful and also causes pain to radiate down the forearm, Cx AROM restricted and sore on palpation, responds positively to massage up the arm and Cx mobs / treating the nerve-container tissue interfaces. My understanding is/was that this pain is due to a nerve lesion and subsequent development of “abnormal impulse generating sites” – this is the cause of pain on nerve palpation. Positive response to massage and interface mobilisation is due to a) improving pressure gradients around the nerve which enables better axoplasmic flow and b) better blood flow/supply which improves the pH around the nerve which aids lesion healing…
…Now as I am writing this I am considering… hypoxia around the nerve would irritate the nervi-nervorum – inflammatory pain – would this then be a cause of pain on palpation?
My point is/was going to be that my above case study you would classify as PNS – ie no lesion, whereas I had considered this to be due to a nerve lesion (although not a “compressive” neuropathy). Is my very recent thinking about nervi-nervorum being a source of pain due to inflammation how you explain PNS – have I just answered my own question?
Any pointers much appreciated – a little confused now.
Regards – James
Hi James,
Sorry for the delay…….I have been a little busy! Both of your comments have now been put up onto the site.
It is a confusing topic!
I personally think the better way to classify “nerve” pain is the Schafer et al classification system. It is, from my perspective, purely based on symptoms and clinical examination, but I don’t mind that as thinking about things like AIG’s hurts my head!
Rather than go into it in detail here, I will email you through some articles on the above classification system.
My interpretation of your patient example is that he/she is suffering from peripheral nerve sensitisation. But this is assuming his/her neuro examination is normal and he/she does not have a high score on a neuropathic screening tool.
Anyway, I hope the articles will help. But then please come back with any further queries/comments and I can go into more detail.
Thanks again for taking the time to comment. Apologies for my tardiness in replying.
Cheers
Mark
Very useful post Mark, still useful 5 years down the track! and so many James’s appear to read your posts also.
Thanks James……..and all of the other James’ that are regular readers!
This information was a real “game changer” for my clinical practice. There has also been some other great articles recently. This one being top of the list in my opinion:
https://www.ncbi.nlm.nih.gov/pubmed/27903159
Cheers
Gibbo