Neuropathic pain is a constant enduring pain with no biological importance unlike nociceptive pain which is reversible and has biological importance of reminding the individual of the presence of danger - hence, acting as a vital sign in a way. 'Mixed pain' syndromes contain some features of nociceptive and some of neuropathic, where it is always relevant to conduct an accurate neurological examination to determine the presence of the different types of pain, and thus optimize the management. 

Dear Yohannes, thank you for your interesting answer, esp. for the statement of "neuropathic pain with no biological importance“. It is true, neuropathic pain has lost any warning function, but neuropathic pain can be distinguished from nociceptive pain based on clinical signs and symptoms; neuropathic pain is very difficult to treat, but I think, there are so many signals of pain and dysaesthesia, that we can modify mixed pain early enough to prevent some chronical neuropathic syndromes, including CRPS.

Dear Karl, thank you for your insightful comments. I share your thoughts. I guess there's some overlap between nociceptive and neuropathic, similar to a spectrum, in addition to 'mixed syndromes'. I agree on the importance of early management in the long run prevention of chronic neuropathic pain syndromes such as CRPS.

Neuropathic pain is due to the damage or physiological change in the nerves casuing noxious stimuli which perceive as burning sensation, pin and needle feeling, contact hypersesnitivity -allodynia. Neurological examination can be normal. In contrast, nociceptive pain is due to the damage to teh tissue and as a result the description of the pain localize to teh area of the tissue damage or physiological change in the tissue.

As neurological examination can be normal in both pain. Therefore the mainly clinical presentation and history of the pain helps in differentiate between neuropathic pain or niccpetive. There are several questionnaire availabel to help to diagnose neuropathic pain as already mentioned DN4. Currently many NHS clinic for diabetic neuropathic pain using LANSS score.

Look for clues such as numbness, tingling, pins and needles sensation  or electrical paresthesia and distribution in a dermatomal (remember, dermatomes have signature areas for hypoesthesia and sensory abnormalities are usually confined to small areas not the entire dermatome; e.g., the medial ankle for L4) or peripheral nerve pattern. Not all neuropathic pain states have these features but if they are present it suggest the pain is neuropathic. Painful numbness (anesthesia dolorous) is also a sign of neuropathic pain. Allodynia can be present but it is not pathognomonic as it is seen in nociceptive pain as well (e.g., sunburn). With a small neuroma the neurologic exam might be completely normal and the pain still be considered neuropathic. Neuropathic pain can have many faces: post stroke/thalamic pain, diabetic peripheral neuropathy, lumbar radiculopathy, trigeminal neuralgia, postherpetic neuralgia, carpel tunnel syndrome, brachial plexus avulsion, etc. so its presentation can vary. 

@Amir: I find your comment in contradiction - at one point you mentioned of the presence of allodynia, hypersensitivity..and then you said neurological exam can be normal. In addition, neuropathic pain also neurolocalizes to its dermatomal distribution. 

I have experience with both DN4 and LANSS, their utility is more for screening methods, not to be used as 'gold standard'. Similar to all neurological problems, an accurate neuro-exam accompanied by meticulous history taking and appropriate investigations offers the best method. 

In Addition: The DN4 (Douleur Neuropathique 4) is one of the mentioned  questionnaires. DN4 has been well validated (and is not difficult at all).

http://www.gloshospitals.nhs.uk/en/Wards-and-Departments/Departments/Pain-Management/Different-Pains/Nerve-Pain/Assessment-of-Nerve-Pain/DN4-Draft/

Do you know the scale "paindetect"?

@Yohannes: I agree with you that clinical history and examination is essential. However neurological examination CAN be normal. Classically if only small fibers disease and large fibers are intact.

Dermatomal distribution is helpful in localise pain however in peripheral neuropathic pain thats not the case.  

@Amir: Okay, I see what you mean, good to clarify. There are a number of disorders that selectively involve large-fibers and result in 'classic' neuropathic pain. This small-fiber large-fiber classification is outdated, has inherent defects, and not fully explanatory.

Of course, dermatomal localization is still helpful in peripheral neuropathic pain - it can discern patterns of involvement for e.g. earlier dorsal than solar involvement will help guide to more of non-DSP - since the longest axons are to be affected earlier in DSP.  

@ Donald: Thank you for your answer concerning a dermatome having signature areas for sensory abnormalities usually confined to small areas not the entire dermatome; but its presentation can vary, I agree with you, for neuropathic pain tends to spride out over the dermatom frontiers, esp. in postherpetic and trigiminal neuralgia, but also in many other cases as carpal tunnel syndrome and plexus lesion, thalamic syndrome etc.

Well in agreement with the fact that questionnaires are good for screening but not for diagnosis. Neuropathic pain is due to "lesion or disease of the somatosensory system", hence to detect objectively neuropathic components in a mixed pain syndrome we need objective markers of somatosensory  "lesion or disease". Good neurological exam and sensory testing are essential, but subjective, and are subject to malingering (Shy et al Nurology 2003; ;60:898-904). Only electrophysiology can confirm objectively the existence of something wrong in sensory transmission. If standard neurophysiological exams (EMG, SSEPs) remain normal there are more specialised tests that can tag specifically the pain systems (laser-evoked potentials, nociceptive reflexes, laser-evoked sympathetic responses, axon reflexes, etc) which are being increasingly used in university hospitals. - this paper may help ("Objective pain diagnostics" Neurophysiol Clin 2012; 42(4):187-97) 

@ Luis Garcia-Larrea, thank you very much for your interesting answer. I suppose, the prevalence of neuropathic pain ( >15 million people in Western countries, as you wrote in 2012) is not too high estimated; (in Germany > 5 %).Yes we need objective pain diagnostics by neurophysiology. The conclusion of M Shy et al in Neurology 2003; 60:898-904) was: Malingering and other nonorganic factors can influence the test results. In my opinion, there are many nonorganic factors with dissociative symptoms and also limitations of all psychological tests. Two examples for malignering and self manipulated pain could only be documented by photos (shown in our textbook of Neurology, Thieme Stuttgart 2013, p. 553).

Thanks, I'll try to get the photos. We are orrselves trying to develop physiological tests to disentangle genuine conversion from malingering. 

Thank you again. The question is: Malingerig, psychogenic or neuropathic pain?  Hope you  can open to the page of photos below, seemed to be difficult.

Data Malingerig, psychogenic or neuropathic pain?

Thanks!

Hi Karl,

I'm not sure if you have seen this paper:

NeuPSIG guidelines on neuropathic pain assessment,PAIN - January 2011 (Vol. 152, Issue 1, Pages 14-27, DOI: 10.1016/j.pain.2010.07.031)

It gives a good understanding of where we are and a plan for future research in developing tools for definite diagnosis of NP.

Abstract

This is a revision of guidelines, originally published in 2004, for the assessment of patients with neuropathic pain. Neuropathic pain is defined as pain arising as a direct consequence of a lesion or disease affecting the somatosensory system either at peripheral or central level.Screening questionnaires are suitable for identifying potential patients with neuropathic pain, but further validation of them is needed for epidemiological purposes. Clinical examination, including accurate sensory examination, is the basis of neuropathic pain diagnosis. For more accurate sensory profiling, quantitative sensory testing is recommended for selected cases in clinic, including the diagnosis of small fiber neuropathies and for research purposes.Measurement of trigeminal reflexes mediated by A-beta fibers can be used to differentiate symptomatic trigeminal neuralgia from classical trigeminal neuralgia. Measurement of laser-evoked potentials is useful for assessing function of the A-delta fiber pathways in patients with neuropathic pain. Functional brain imaging is not currently useful for individual patients in clinical practice, but is an interesting research tool. Skin biopsy to measure the intraepidermal nerve fiber density should be performed in patients with clinical signs of small fiber dysfunction.The intensity of pain and treatment effect (both in clinic and trials) should be assessed with numerical rating scale or visual analog scale. For future neuropathic pain trials, pain relief scales, patient and clinician global impression of change, the proportion of responders (50% and 30% pain relief), validated neuropathic pain quality measures and assessment of sleep, mood, functional capacity and quality of life are recommended.

Article NeuPSIG guidelines on neuropathic pain assessment

Thank you, this is an important source, indeed, the German revision of guidelines (2012) is using it, too.

a few short comments: there are different versions of neuropathic pain scales (all of which do not crrelate very well, and their value may thus be limited), which mostly agree on that neuropathic pain can be discriminated by the presence of a multiplicity of pain descriptors (rather than singular for nociceptive pains).

The nerve damage precipitates incresed expression of the TRPV1 receptor all along the nerves affected making these axons more sensitive to thermal and chemical stimulation.

This enhanced sensitivity drives an exaggerated spinal plasticity (which depends on input from TRPV1-positive nociceptor, c.f. Ziegler et al. BRAIN 1999, Magerl et al. BRAIN 2001)

This precipitates a broad hypersensitivity for all nociceptive modalities, but patterns may vary in patients depending on the balance of peripheral and spinal (or higher central factors. You may profit from a recent paper on analysis of sensory changes in >1200 neuropathic pain patients by the German Research Network on Neuropathic Pain (DFNS) Maier et al. PAIN 2010

There is a recent paper on polymorphisms in TRP receptors, which identified a snp in the TRPV1 gene, which was associated with a lack of nociceptive sensitization (i.e. suggesting that a presumed dysfunctional TRPV1 receptor prevents the nociceptive systems from hypersensitivity) (Binder et al. PLoS ONE 2011; so some bad may actually turn into good

two papers attached

hope that his helps to get ideas for your paper, best wishes, Walter Magerl

Vielen Dank für Ihren wichtigen Beitrag mit den interessanten Artikeln und  beste Grüße nach Heidelberg

One of the good way to diagnose neuropathic pain is to make a distincition between: Spontaneous neuropathic pain and/or touch-evoked neuropathic pain. Touch-evoked neuropathic pain are either STATIC mechanical allodynia (SMA) or DYNAMIC mechanical allodynia (brush-evoked allodynia). The clinical examination sign of SMA is the allodynography. http://doc.rero.ch/lm.php?url=1000,43,2,20080507152616-JF/rouiller_sma.pdf. One of the etiology of SMA is always A-beta neurofibers lesions.

(I am not a clinician, I am neurobiologist) I would not separate spontaneous neuropathic pain and evoked neuropathic pain. C- and A- fibers after nerve lesion develop spontaneous as well as evoked mechano- and thermosensitivity. 

Dear Colleague, I unfortuantely desagree. Some patients present a condition with only touch-evoked neuropathic pain. Some others Some patients present a condition with spontaneous neuropathic pain AND touch-evoked neuropathic pain. finally, some others present a condition with only spontaneous neuropathic pain. I agree taht the etiologies of both are C-neurofibers damaged and/or A-beta neurofibers.

In my opinion there is a certain contradiction concerning the definition of spontaneous chronical neuropathic pain.

This is indeed so. 

This description fit with the patient's complaint of: spontaneous burning pain, spontaneous radiating pain, spontaneous throbbing pain, etc. It doesn't exist any correlation between spontaneous pain and their Activities Daily Living (ADL). This concept of spontaneous neuropathic pain has been published for the first time by the group of P. Hansson:

Hansson, P. (2003). Difficulties in stratifying neuropathic pain by mechanisms. Eur J Pain, 7, 353-357.

The French Society for the Study of Pain uses it:

Mick, G., Pellat, J.M. & Guastella, V. (2013). Aspects diagnostiques et thérapeutiques des douleurs neuropathiques. Doul & Analg, 26, 139-151.

Bouhassira D and Attal N. Douleurs neuropathiques (2ème éd.). Paris : Arnette-Wolters Kluwer France ; 2012, p. 220.