Nociceptive vs. neuropathic pain indicators

Figured for my first post, I'd use the collective community of the inter-web to improve my intelligence.  I was asked by our orthopedic division of the Canadian Physiotherapy Association to come up with a way for orthopedic manual therapists to discriminate between nociceptive and neurogenic pain.  I struggled with the distinction for a while, understanding the spirit of it but struggling with the practicalities.  Finally I settled on the nociceptive/neuropathic distinction, as outlined below.

I ran the session with a group of graduate physios at Western, and asked them to generate the list of discriminators (active learning, yay!).  The table below is largely what they came up with, with a few embellishments of my own.  All in all, I'm OK with it, but I have to think the larger pain community could embellish this even further.  So my challenge to you all is to look at the table, and consider for yourself what clinical indicators you do/could use to discriminate pain of a primarily 'uncomplicated' (pardon the term) nociceptive origin from that of a more neuropathic, or in the original lingo, neurogenic origin (read: indicators of neural sensitization, nerve injury, sprouting, ectopic discharge, etc...).  Leave your comments in the space below, and I'll incorporate the good ones into this list.  I'll make the final table available to all on this site.  Cheers!

Here's the start of the brief synopsis I wrote for the manual PTs:

Pain mechanisms

Pain is multi-dimensional, by definition being both a sensory and emotional experience that may or may not be associated with actual tissue damage.  The gate control and neuromatrix theories of pain describe mechanisms through which the experience of pain can be amplified or decreased dependent on a variety of other influences, including genetics, competing stimuli, emotional state and environmental context, among others.   Researchers such as Clifford J. Woolf have suggested that identifying the mechanisms driving a pain experience is important, insofar as such identification can affect decisions regarding treatment and expected outcomes.

Pain is often largely thought of as being broadly classified into two distinct types.  ‘Nociceptive pain’ is driven by activity that starts at the end organ (ie. free nerve ending) of high-threshold afferents in response to stimuli that represent actual or potential tissue damage (ie. chemical, thermal or mechanical).  Conversely, ‘Neuropathic pain’ is pain that occurs as a result of some alteration in the parts of the nervous system that are usually reserved for transmitting high-threshold stimuli to the brain.  This may occur after direct nerve injury, but phenomena such as sensitization or abnormal sensations, which may or may not be due to nerve injury, tend to be lumped into the ‘neuropathic’ pain group as well.  I would argue however, that drawing an absolute distinction between nociceptive and neuropathic pain can be dangerous, especially in the case of chronic pain problems.  Even in the acute pain situation, sensitization can occur in either peripheral or central nociceptive pathways under perfectly normal conditions (see Woolf & Salter 2000), which might manifest as something like secondary hyperalgesia in the absence of frank nerve injury.  Perhaps a better way to conceptualize the two types of pain are as two entities that are present in most all pain states, but one usually moreso than the other (Figure 1).

Figure 1: Conceptualization of nociceptive vs. neuropathic pain


As the neuromatrix theory suggests, pain is an output, one of several possible outputs of the body protective systems, that might or might not occur if the brain interprets incoming stimuli as threatening.  Melzack suggests that both the inputs that drive the pain experience, and the experience of pain itself, can be largely subdivided into three broad categories: sensory-discriminative components, cognitive-evaluative components, and motivational-affective components (Figure 2).  This means that when discussing the mechanisms that drive a pain experience, consideration must be given to sensory components (nociceptive vs. neuropathic) as well as psychosocial components that would affect the ways a person understands and interprets pain, as well as the status of their stress-response system, which is affected by physiological and emotional processes.

Figure 2: The body-self neuromatrix (from Melzack 1999)

In an effort to help clinicians better distinguish between the various mechanisms that may be contributing to their patient’s pain experience, Table 1 attempts to categorize clinical signs and symptoms by the mechanism with which they are most likely associated.  This has occurred with the recognition that all pain experiences are probably driven by each of these mechanisms to a greater or lesser extent.  It is also likely that what would be representative of neuropathic (or neurogenic) pain in one condition is different than that in a different condition.   As an example, Scholz and colleagues (2009) attempted to create and validate a tool to be used to discriminate between low back pain of a primarily nociceptive nature (termed ‘axial pain’ in this case) from that of a more neurogenic nature (termed ‘radicular pain’ in this case).  Their findings indicated that radicular pain could be discriminated from axial pain by things such as increased or decreased sensitivity to non-noxious could stimuli, no change in sensitivity to repeated non-noxious pin-prick, and no change in the response to brushing the skin.  This is in contrast to the identification of frank neuropathic conditions, in which cold sensitivity, wind-up pain (increasing pain with repetitive pin-prick stimulation) and allodynia (pain response to brushing the skin) are diagnostic hallmarks.  This may mean that radicular low back pain is not a neuropathic pain condition, or that it is a neuropathic condition that differs from other neuropathic conditions.  Either way, the list presented in Table 1 should be considered more of a guide rather than an absolute tome of diagnostic criteria for discriminating between the different mechanisms that are most likely influencing any patient’s pain experience.

A brief word on the distinction between neuropathic and neurogenic is warranted.  In literal terms, neurogenic pain is pain that has its genesis in nerve activity, and is really an umbrella term.  Neuropathic pain, considered pain due to nerve (neuro) illness/injury (pathos), would fit under the umbrella of neurogenic pain.  Continuing with this literal string of interpretation, nociceptive pain would also fit under the umbrella of neurogenic pain, in that the genesis of all somatic nociceptive stimuli occurs with depolarization of a nerve.  Neurogenic pain is probably more easily distinguished from pain of a purely psychogenic origin, than it is from pain of a nociceptive origin.  I realize this is a somewhat pedantic argument, and I understand the spirit of the distinction that Jones and Rivett (2004) are trying to draw between the two, but in practice the distinction between nociceptive and neurogenic pain could become confusing.  From a physiotherapy perspective, the desire is to identify clinical indicators (signs or symptoms) that would suggest that pathological alterations have occurred somewhere along the course of the nociceptive pathway, anywhere from end organ to cerebrum.  This may include activation-dependent sensitization of peripheral nociceptors (where activating a high-threshold afferent leads to short-lived sensitivity to subsequent stimuli) through to phenotypic alterations in nerve expression (ie. Altered neurotransmitter release, abnormal axon-axonal connections, distorted body maps and the like).  Now, on with the table.


Neuropathic or neurogenic pain



Pain tends to be described as achey or dull, sometimes sharp or stabbing with aggravating movements


Patients are generally able to localize the area of their pain fairly well as it doesn’t tend to move around.


The local area is sensitive to pressure (primary hyperalgesia)


The pain tends to behave in fairly stereotypical, predictable ways.


Pain may be associated with other signs of mechanical dysfunction, such as crepitus, popping or edema.


The pain should be aggravated with movement in one or more directions in a predictable fashion, that is, the magnitude of pain increase should be fairly consistent across repeated movements, and may actually decrease.  Conversely, there should also be a position or movement that does not increase the pain, and may decrease it.


Pain that is more nociceptive is most likely to be present in the acute stage of injury.


The pain should be affected by NSAIDs


Purely speaking, as the stimulus causing the pain subsides (ie. inflammation, tissue healing), the pain should also subside.

Pain tends to be described as shooting, burning, crawling, electrical, shocking, freezing



Patients may have greater difficulty delineating the area of their pain, as it may move or grow and shrink.


The pain is not responsive to conventional anti-inflammatory therapies.  Anti-convulsants and anti-depressants are often needed.


There is often little relationship between movement and pain.  Pain can sometimes worsen without movement.


Pain may be present despite no obvious signs of tissue dysfunction.


Associated findings are common, such as weakness, paraesthesia, pins & needles, or frank paralysis of the affected body part.


Wind-up pain (temporal summation) is often present – increasing pain in response to repetitive low-level stimulation.


Cold hypersensitivity is uncommon, as is vibration hyposensitivity.


May see elevated scores on neuropathic screening questionnaires, including the S-LANSS, DN4, PainDETECT and StEP.


Pain tends to be labile rather than constant.


Other than in situations of frank nerve trauma, neuropathic/neurogenic pain is more likely after the pain has been present for some time (ie. subacute/chronic).


Signs that may indicate neurogenic pain of a more peripheral origin:


Positive signs of adverse neural dynamics, especially with simultaneous compression over peripheral nerves.


Pain may be more localized to a particular sensory innervation of the affected nerve.  This may include pain along the path of the nerve (ie. causalgia), or pain in the dermatomal area of innervation.


Objective signs of disturbed nerve conduction are likely (ie. EMG, nerve conduction studies).


Signs that may indicate neurogenic pain of a more central origin:


Pain is more likely to be strongly influenced by anxiety, viewing the injured part, emotional distress.


Patient may have difficulty identifying the affected body part, which may manifest as difficulty drawing the part, difficulty with mental manipulation of the body part (ie. hand laterality), or stating that the body part feels somehow outside or disconnected from themselves.


Pain is more likely to spread to other unaffected body parts.  This may manifest as sensitivity to cold or pressure stimuli beyond the borders of the original injury (secondary hyperalgesia), pain in the same part on the contralateral side (mirror pain), or sensitivity in areas completely remote from the area of symptoms (widespread hypersensitivity).

Patient has a difficult time conceptualizing their pain.  Manifests as:

  • Unknown cause
  • Unknown outcome
  • Unknown aggravating/ easing factors


Pain that affects self-identity.  For example, interferes with leisure, important life roles, work or other activities that define the person.


Patient demonstrates anger, frustration or impatience beyond what would be considered normal given the condition.


Low expectations for improvement


Sense of hopelessness or helplessness.


Patient can’t disengage from the pain, rumination, constantly thinking about the pain


Believes that only external influences affect the pain (ie. fate, god, therapists, doctors)


Describes a sense of injustice or victimization – ‘why me?’


Bad experiences with similar types of pain/injury in the past


Elevated scores on emotional screening questionnaires.  There are several of these and I won’t list them here.  EXTREME caution should be exercised with their administration and interpretation.  Ask me if you’d like more information or guidance on this particular issue.

Feeling of being disbelieved


Reactions of important others that promote either distress (’oh my god that’s awful!’) or dependence (‘poor baby, let me help you so you don’t injure yourself’)


Prevailing cultural beliefs about pain, injury and pain behaviours.


Lack of alternative opportunities for work or leisure.


Stress from other sources: family, marital, financial, work, etc…


Age and gender (these could conceivably go in any of these columns)


Sense of entitlement, either entitled to treatment, entitled to sympathy, entitled to financial compensation, etc…


A physical environment that does not allow for modification of activities (ie. stairs, lifting, seasonal duties)


A work environment that does not support pain and injury, or is hostile towards it. 


Sense of being constantly judged, observed and evaluated, or the target of skepticism from others.


Actively involved in litigation – you cannot get better if you have to constantly prove your are ill.