Thursday, 3 December 2015

Neuropathic Pain What is it

Pain is a very difficult symptom to manage notably neuropathic pain which is a problem caused by damage to spinal nerves, such that the pain occurs without any logical cause. I lifted this off the web

Neuropathic pain is caused by damage to- or dysfunction of- the peripheral and central nervous system, rather than stimulation of pain receptors. It can involve any level of the nervous system and in neuropathic pain the nerve fibres may be damaged, dysfunctional or injured. The impact of injury includes a change in nerve function both at the site of injury (e.g. the spinal cord) and areas around the injury. This leads to incorrect signals being sent to the brain. The brain perceives that these signals are coming from pain receptors in the skin or organs where in fact this is not the case. Phantom pain following limb amputation is a good example of this.

People commonly use abnormal adjectives to describe painful and non-painful sensations such as ‘shooting’, ‘burning’, ‘tingling’ and ‘numbness’. In people with neuropathic pain, there are three types of changes that can occur: painful symptoms, visible skin changes and loss of sensation.

Painful symptoms
Neuropathic pain commonly results in ‘spontaneous’ pains. Some of these sensations appear to have a ‘life of their own’ and are bizarre. Sensations include abnormally painful responses to an ordinary physical stimulus (evoked pain); and spontaneous pain – which occurs in the absence of a stimulus. There are two types of spontaneous pain: continuous and paroxysmal.
Continuous pain– is a steady, ongoing sensation which is often felt in the skin. It is sometimes described as burning, cutting, pricking, tingling, “pins and needles” and stabbing. If it is felt in the deep tissues, it is usually described as cramping, throbbing, crushing or aching.
Paroxysmal pain – this is an intermittent pain that usually is not associated with any precursor and described as shooting, lancinating, jabbing or stabbing in nature.Paroxysmal attacks or paroxysms (from Greek παροξυσμός) are a sudden recurrence or intensification of symptoms, such as a spasm or seizure.

Evoked pains are usually exaggerated responses to innocuous events that do not cause pain in people with ‘normal’ pain pathways:
Allodynia - pain that comes on from simple contact that is not normally painful. This is divided into mechanical allodynia (e.g. clothes touching the skin) and thermal allodynia (e.g. cool breeze against the skin).
Paraesthesia and dysaesthesia – absence or impairment of the senses especially touch
Hyperpathia - a prolonged duration of pain following a painful event.
Hyperalgesia - hypersensitivity to mildly painful events – knocks, for instance.

Other sensations can include physical contact in one area of the skin resulting in painful sensations in another (trigger zone pain), or pain that radiates down a whole leg or arm (referred pain).

Skin changes

In people with neuropathic pain, there may be visible changes in the skin in the area that overlies the painful area. Mechanisms underlying these changes that may accompany neuropathic pain are not well understood and are complex. The expected changes include the skin being pinker or redder than other areas; or more blue, mottled and dusky-looking. The changes that occur are largely due to alterations in blood flow. As well as colour changes; the skin can look waxy, dry, puffy or swollen with a reduction in hair and nail growth.

Loss of sensations

Areas affected by neuropathic pain can be numb to touch. Nerve damage from injury or disease processes can lead to loss of normal sensation. The nerves that are the most prone to damage (from diseases like diabetes) are those carrying temperature sensations; and hence the assessment involves testing for sensation, pain and temperature. The loss of normal input from the anaesthetic area may cause a failure of the normal gating process and promote central sensitisation in an effort to gain information from the affected area. Such amplification may result in the paroxysmal presentation of pain in a non-sensate area.

Making the diagnosis

 A diagnosis is usually made using a combination of the patient’s report, a clinical examination and sensory nerve testing. Often, quantitative sensory testing is performed. Although these tests might highlight areas of abnormal sensation, the tests themselves cannot prove or disprove that a person is suffering with pain caused by the nerve damage.(Eur J Neurol 11(3):153-62). 

Managing neuropathic pain

Before considering what is available in terms of managing this type of pain, it is important to stress that any underlying condition that may be implicated should be assessed and managed. For instance, mechanical pressure (e.g. by spinal discs on spinal roots) causing the neuropathic symptoms may require surgery. Improvements in diabetic control can improve symptom progression in diabetic neuropathy but cannot reverse damage.

It may be useful to consider two approaches to managing pain of neuropathic origin:
Non-pharmacological Treatment of Neuropathic Pain)
Physical methods- desensitisation, mirror-box therapy, rehabilitative physiotherapy
Psychological techniques such as Mindfulness, ACT, CBT
Patient education
Pharmacological measures
Non-opioid analgesics and NSAIDs
Antidepressants
Anticonvulsants
Opioids
Topical preparations
Specialist treatments
IV management (lidocaine, ketamine)
Complex, multimodal treatment approaches e.g. residential intense pain managemnet programs
Invasive techniques – nerve blocks, deinnervation, etc

The following may be useful in identifying what should be considered in managing people with neuropathic pain:

Clinically, it is important to stress that neuropathic pain is a difficult problem, often resistant to multiple therapies; and requires patience and understanding by both the person affected and health care professional. Treament is best with a collaborative approach to therapy; and ideally, there should be frequent reassesment of treatment response, disease progression and careful evaluation of quality of life indicators.

7 comments:

  1. It so good to finally get the confirmation that the redness on the palms of my hands is not normalbut caused by neuropathy. I knew it! Thank you, you made my day.

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  2. Worse thing ever neuropathic pain. I hate it. Hopefully as MS progresses and some of these nerves finally die the pain will improve?

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    1. Good question that deserves an answer.

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  3. Ketamine!?! Wow, that's what ravers took in the fields of Manchester circa 1991.

    Now it's being prescribed to MSers ... and horses, of course.

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  4. Almost all chronic pain is neuropathic pain according to my notes from a presentation by Dr. Pradeep Chopra who specializes in anesthesiology, has an interventional pain management practice, and also teaches medicine at Brown University.

    He spoke about treating Complex Regional Pain Syndrome (CRPS) successfully using low-dose naltrexone (LDN) at a 2013 conference. Dr. Chopra attributed the success of LDN to its reduction of pro-inflammatory cytokines. An effective drug for neuropathic pain relates to glial cells; this type of pain isn’t a problem of nerves, it is a problem of glial cells releasing cytokines according to my notes from Chopra’s presentation.

    Dr. Chopra presented brief case histories of some of his patients who got immediate relief from chronic pain using LDN. Please don’t misunderstand, he did not say all his patients got overnight relief using LDN! He said that some did and some after years of trying many other treatments. A few of those successes were literally overnight, yes, in one night some found pain was vastly reduced.

    He will again be speaking about chronic pain issues and the use of LDN at an up-coming conference in Orlando, FL this February 19, 20, and 21. Chopra is scheduled to leadoff the conference Friday morning. Info can be Googled, if desired.

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  5. Does pain worsen as nerves begin to "die off"? What would explain sudden worsening burning pain for PPMSer?

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  6. Oh crikey I hope not!
    I reckon it has to be this low grade background microglia inflammation /demylination causing positive symptoms in progressive MS (rather than the full on adaptive Tcell/B cell immune response as with RRMS). Dead axons cannot conduct at all. End of. Fact. Dead. No signal no pain. At least I hope so! This is what keeps me going.
    We're too far down the blog for this to be read, question for the next unrelated blog comments slot?

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