Chronic nerve pain: an interview with Professor Sally Lawson

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Please could you give a brief introduction to chronic nerve pain?

Chronic nerve pain results from pathological changes within a nerve that appear to be self-sustaining and thus the pain continues for a long time. The pathological changes can result from partial damage to a nerve and/or inflammation within the nerve. It is this we have studied. They can also result from diseases involving the nerve.

What can cause partial nerve injury that leads to chronic nerve pain?

Partial nerve damage leads to death of some nerve fibres within a nerve, and survival of other fibres. Partial damage can result from crush or stretch of a nerve during an accident, or during surgery sometimes leading to long term postoperative pain. Some lower back pain results from a nerve being compressed or partially crushed, or from a prolapsed disc causing pressure on the nerve and also local inflammation.

Death of some nerve fibres within a nerve also occurs in some diseases, including diabetic neuropathy in patients with advanced diabetes, and also in HIV. Other autoimmune diseases have immune responses within the nerve that cause nerve damage and neuroinflammation. Several chemotherapeutic drugs for cancer cause toxic damage to peripheral nerves. All the above can result in chronic nerve pain.

Do the damaged or surviving nerve fibres cause the pain?

There is growing evidence that degeneration of damaged nerve fibres and particularly of their myelin sheaths, cause neuroinflammation and/or immune system activity, and that this causes greater excitability and firing of the surviving fibres, which contributes to, or results in, chronic pain. Simply, the degeneration of damaged fibres may cause an environment that triggers activity in the surviving fibres. 

By showing changes in subgroups of these surviving neurons that could lead to the different qualities of chronic nerve pain, our study adds support to the view that the surviving fibres are very important in causing chronic nerve pain.

What are the different qualities or types of chronic nerve pain?

Patients experiencing chronic nerve pain describe a combination of different types of pain. The pain may be evoked pain (a stimulus is needed to cause the pain) as in allodynia: intense pain from gentle stimulation such as skin touch (e.g. moving cotton wool across the skin) or hyperalgesia: more pain caused by a normally painful stimulus.

Patients also report spontaneous pain unrelated to any stimulus: either ongoing burning pain or sharp, shooting, stabbing pain. This spontaneous pain is hard to live with as it is unrelenting, sometimes called “unbearable” and makes people feel very unwell and very miserable. People with this type of pain may find they are unable to be comfortable even in bed, which can cause insomnia. Some patients report strange sensations, called paresthesias.

What causes these different qualities of chronic nerve pain?

The reason for these different types of pain has never been fully explained. Key questions are whether the central or peripheral (sensory) nervous systems are responsible and whether the dying or surviving nerve cells in a partially injured nerve are more responsible. Our hypothesis was that it was due to the surviving sensory fibres becoming more excitable due to the pathological changes in the nerve; our findings support this hypothesis.  

What did your research show?

We found changes in several different groups of the surviving sensory nerve cells that could account for the different types of chronic nerve pain. We found:

  • spontaneous ongoing firing in C-fibre nociceptors: we have shown previously that spontaneous pain (probably the burning type pain) is linked to the rate of this firing (Djouhri et al., 2006).
  • spontaneous firing in fast conducting A-fibre nociceptors: this would be likely to cause the spontaneous sharp shooting pain complained of by patients.
  • that A-fibre nociceptors became more excitable; this could contribute to the greater sensitivity to stimuli; if these nociceptors are more easily stimulated, gentle (normally not painful) stimulation could cause pain.
  • finally we found spontaneous firing in subgroups of surviving sensory neurons that normally contribute to the sense of touch. This could cause the strange sensations or paresthesias. 
Thus there are changes in different groups of surviving sensory neurons that could account for the main types of pain and paresthesia reported by patients with chronic nerve pain.

Why has neuropathic pain traditionally been hard to treat clinically?

There are many different views on this. A lack of knowledge about which types of sensory nerve cells contribute to the different aspects of neuropathic pain, may have contributed. For example, many studies in the past focussed on neurons with injured fibres, not those with surviving fibres that we describe here. We hope that our study will help to shift the focus towards the uninjured nerve cells and their contributions to different types of nerve pain.

In addition, the study of spontaneous pain and the underlying spontaneous firing in the surviving nociceptors has been under-researched. Now more research groups are examining spontaneous pain and its causes and clinical trials of potential novel pharmaceutical treatments are beginning to include evaluation of spontaneous pain.

What methods of pain relief do patients with chronic pain currently use?

Many people find pain relief with drugs available over the counter, including the non-steroidal anti-inflammatory drugs (NSAIDS) such as paracetamol/acetaminophen, aspirin, and ibuprofen. If these do not provide adequate relief, it is important to consult a physician who prescribe a variety of drugs including: the NSAID diclofenac/volterol, gabapentin or pregabalin, lidocaine patches, opioids, tramadol or tricyclic antidepressants.

These have all been shown to be effective but their efficacy varies between patient and the use of some is limited by adverse side effects. There are other treatment options, but treatment is often not fully effective, leaving an urgent need for development of more effective neuropathic pain therapeutics.

How will your recent research allow for more effective pain killers to be developed?

A greater focus on the uninjured sensory nerve that may cause the different types of nerve pain could contribute to novel approaches tp cpntrolling different aspects of this pain.

How do you think the understanding of chronic nerve pain will develop?

In animal experiments there has been much excellent research on particular protein receptors on nerve fibres that respond to different types of stimulation (i.e. to different thermal, chemical or mechanical stimulation). A combination of these receptors may need to be targeted by drugs to combat effectively the different aspects of chronic nerve pain.

There are other approaches that involve tackling the inflammation or the immune system in the periphery (the last approach is still in its infancy), or targeting the central nervous system (CNS) because it becomes hyperexcitable during this chronic pathological pain, or using the body’s own inhibitory CNS pathways to limit the pain. In small numbers of patients, neuropathic pain results from a mutation in a specific protein channel. The discovery of such mutations may lead to very specific therapies for these patients.

In the sensory neurons it is clear that there are two main types of ion channels that control nerve fibres excitability. Simply put the Na+ channels are the main excitatory machinery of a nerve fibre while the K+ channels tend to be inhibitory or stabilising. It is becoming clear that some of these K+ channels limit the amount of pain that we feel. Perhaps these internal control mechanisms could be increased to limit chronic nerve pain.

The more we understand about the specific mechanisms in different types of sensory nerve cells contributing to, and controlling, their excitability and thus this pain, the more likely it is that these mechanisms can be utilised or modulated therapeutically to limit or block the neuropathic pain.

What plans do you have for further research into this field?

My colleagues Dr. Cristian Acosta, Roger Watkins and I are currently engaged in seeking answers to the following questions:

  • What causes the undamaged C-fibre nociceptors to fire spontaneously and cause ongoing spontaneous pain?
  • Which subdivisions of these neurons are able to fire spontaneously?
  • What controls whether they fire spontaneously and how rapidly they fire? This is important as the level of pain is related to the rate of the firing.
  • What natural mechanisms (such as K+ channel subtypes) do we have that limit this spontaneous firing? Can these perhaps be enhanced?

Dr. Laiche Djouhri, the lead author on our recent paper, now at University of Liverpool, is pursuing different questions related to the types of K+ channels involved in spontaneous firing in subtypes of sensory neuron in pathological pain.

Where can readers find more information?

About Professor Sally Lawson

Sally Lawson BIG IMAGEProfessor Sally Lawson is Emeritus Professor in the School of Physiology and Pharmacology, Medical Sciences Building, University of Bristol.

After a Physiology degree and Neuroscience PhD at Bristol University, she was on the staff from 1977. She has been running a group researching primary sensory neurons and their contributions to chronic pain since 1980, with continuous funding from sources including the BBSRC, the MRC and for the last 20 years, the Wellcome Trust.

Her research group has examined electrophysiological and chemical properties of primary sensory neurons with different sensory properties. This led to studies of how subgroups of sensory neurons change their properties to become spontaneously active, more excitable, and contribute to chronic pathological pain of peripheral origin.

Her group are currently examining the role of K+ leak channels in sensory neurons in chronic pathological pain, and the factors contributing to the spontaneous firing in nociceptors that results in spontaneous pain.

April Cashin-Garbutt

Written by

April Cashin-Garbutt

April graduated with a first-class honours degree in Natural Sciences from Pembroke College, University of Cambridge. During her time as Editor-in-Chief, News-Medical (2012-2017), she kickstarted the content production process and helped to grow the website readership to over 60 million visitors per year. Through interviewing global thought leaders in medicine and life sciences, including Nobel laureates, April developed a passion for neuroscience and now works at the Sainsbury Wellcome Centre for Neural Circuits and Behaviour, located within UCL.


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  1. dave dave United States says:

    Ms Lawson is promoting an occupational strategy of more and more biomedical research -and that research has lead to more knowledge but not better results for people in pain. Ms Lawson should know as late as 2008 Patricia Grady of the pain consortium indicated neuropathic pain has been neglected in research. We as a Nation should not regard researchers opinion as being expert but should view them as interested in continuing to serve their own need to continue to do more and more research ad infinitum without being democratically accountable to the public. If Ms Lawson was very concerned about neuropathic pain she might speak to better methods of research like the Brunswick Lens Model, Systems Biology. But as one American reporter indicated- biomedical research has been as rewarding as the AIG bailout. Its time researchers be held to a higher standard- the public good. Instead they wish to continue to serve their curiosity at the publics expense.

  2. dave dave United States says:

    More biomedical research is wasteful and serves the curiosity of researchers.much more then it helps people in pain

    • TDS TDS United States says:

      Dave, are you a pain patient? I read the entire interview and although this specific woman seems to be motivated honestly my opinion is mixed. My question is why/how is this so difficult for the medical research community so difficult to adequately answer nerve pain and treat it effectively? How many millions/billions of dollars spent and our so called advanced society is no further along in discovering cures and treatments than we were 50 years ago? Millions suffer in pain and are told to take Tylenol ?? Our medical community is a joke when it comes to answering this and other conditions of the human body!! I am a pain patient can you tell?

  3. Philip Power Philip Power Ireland says:


    I guess what we should be praying for is for some of these medical people to be struck down with neuropathy, maybe when they have to suffer 7/24, they just might begin to look for a real cure. I was diagnosed with Diabetes & within a week I had Diabetic neuropathy symptoms in both feet. I have heard that the drugs I was given to bring down my dangerously high blood sugar, caused the neuropathy. Has anyone ever heard of cases like mine. I was 58 when diagnosed.

  4. Michelle Deciantis Michelle Deciantis United States says:

    I am currently still in a definative diagnosis phase, 13 yrs and thought to be hereditary Ataxia and Upper Motor Neuron disease of unknown origin or type.  I am in a clinical trial at NIH for exome sequencing looking at other options such as, HSP etc.  The pain (neurogenic as per my doctors).  Has got to be one of the most difficult.  With Lyrica and Oxycodone, I still live daily with a 4-5 pain level.  And too many Neurologist do not understand this pain is much different than typical pain.  I mean I have the sensory deficits and neuropathy in both lower extremities.  But the neurgenic pain is systemic, relentless, and I am praying they can find something within the CNS, a main shut off valve of sorts.   Thank you for continuing your research.

  5. Lisa .Manville Lisa .Manville United States says:

    When my symptoms first began my doctor told me to stop wearing tight jeans, I did. When that didn't help he said I must stop sleeping on that side, the other side has a titanium hip I don't like to sleep on. He sent me to a doctor who sent me to test for blood clots in my legs. I let time go by between visits because I was frustrated that they didn't seem to understand my problem. I finally mentioned to my orthopedic surgeon the symptoms and he sent me to the correct doctor. I will never forget what it felt like to have her tell me what my symptoms were. 4 years after meeting her and getting a correct diagnosis I moved 1200 miles away. My story has a moral, don't wait for the doctor to figure out what's wrong, hound them because by the time I learned why I have nerve pain, much less what it is, I was told the damage is too far gone for treatment. I could not function without pain meds and gabapentin helps me sleep at night.

  6. Heather Pendley Heather Pendley United States says:

    I  can guarantee that my husband condition would stump everyone, he was electructed almost 3 years ago, his hands and legs twitch, his hands swell, now his hands are starting to turn red on occurance the rain cold makes him worse, he can barley walk or stand for long periods of time, I can't touch his lower back cause it hurts him to much, MRI ct scand xrays show nothing and emgs don't really show much, he's seen a neurologist an orthopedic surgeon and no one seems to be able to help him

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
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