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Thread: More on Central Pain and Neuropathic Pain

  1. #1

    More on Central Pain and Neuropathic Pain

    Is Central Pain neuropathic? Of course. Definitionaly, there is no doubt of this, since neuropathy means "nerve injury pain".

    Is it helpful to CLINICALLY name Central Pain “neuropathic pain”? My own viewpoint is that it is NOT helpful to use "neuropathic pain" for both central and peripheral nerve injury pain.

    My reasons include the following:

    1) The vocabulary is already muddled enough without throwing in the towel and lumping very diverse conditions together

    2) There are clinical tests to differentiate the two (Mitchell test, emotional consequences and distribution of pain on the body surface.

    3) The public must know that Central Pain exists

    4) Doctors should not shotgun meds at Central Pain patients which were designed ONLY for peripheral nerve injury pain

    It has been helpful in my own case to be able to have a DSM (ISDN9) designation number for my specific condition. If nothing else, it put doctors who were unaware Central Pain existed, that it is a distinct disorder. This was most helpful in dealing with the skeptic, who was inclined to think if he hadn’t heard of it, it did not exist.

    Riddoch invented the term Central Pain, calling it a “pain beyond pain” in 1940. Prior to this S Weir Mitchell (1876) termed it “pain of central origin” and developed tests to distinguish it from peripheral nerve injury pain, which assisted him in therapy as well. Dejerine, Eggers, and Roussy (1903) used Mitchell’s terminology but studied CP from stroke to the area of the thalamus. For a time central pain was referred to as thalamic pain, but that term is now reserved for stroke victims.

    That this is a difficult area is shown by the fact that not until recently were clinicians aware that central pain feels different from ordinary pain. (First pointed out by Ron Tasker) The vocabulary was that weak.

    Bowsher proposed to simplify the diagnosis by using the following criteria for central pain:

    Dysesthetic (ie. conveys little or no discriminative information) burning pain following injury to the central nervous system, often with a paradoxical cold component.

    Bowsher was fully aware CP patients have other pain as well, but he was trying to draft a minimal statement to allow easy diagnosis.

    Tasker expanded this slightly by allowing differentiation of pains into spontaneous and evoked, since some CP patients have ONLY spontaneous pain while others show enhancement of one or another of the central pains from various stimuli (sudden cold stimulus or LIGHT touch being the most frequent evokers).

    Peripheral nerves are NOT central nerves. Peripheral nerves can heal and the prognosis is different. Central neurons cannot heal and futile efforts to make them heal frustrate and confuse the patient (and cost money).

    The taxonomy (naming) committee of the IASP reportedly delisted Central Pain, and now just uses the word “Neuropathic pain” for any nerve injury pain.

    I disagree with this because it fails to alert the caregiver to fully elaborated cases of Central Pain, with accompanying need for extensive patient and family counseling, realistic expectations as far as work, dress, and social interaction, and it lumps CP with such things as diabetic neuropathy.

    The dysesthesia of CP is the cardinal feature. There are plenty of other pain aspects of CP such as intermittent lightning pain, and pain in the muscles. However, keeping it simple by holding with Bowsher’s definition helps make the diagnosis. Dejerine said central pain diagnosis was EASY. But the mélange of definitions and confusing vocabularly has now obscured the condition until agreement has vanished, leading to a lumping of CP with peripheral nerve injury pain.

    At present, we think of Central Pain as inflammation (activation by genetic alteration) of TRPV1 receptors in the dorsal horn of the spinal cord by oxidized linoleic acid metabolites 9- and 13-hydroxyoctadecadienoic acid (9- and 13-HODE) .These are known as OLAM, or oxidized linoleic acid metabolites and work is under way to try to treat linoleic metabolites with other fatty acids, such as Omega-3 derived fats. Not only CP but also ordinary heat causes increase in 9 and 13 HODE. They are also manufactured in isolated strips of removed skin subjected to noxious heat.

    CP is neuroinflammation in central neurons, susceptible to input from peripheral sensory neurons, (which may also be manufacturing 9 and 13 HODE). One unexplained mystery is why CP patients also kick out the 9 and 13 HODE in the face of a cold blast, ("cold" being relative since the cold necessary is not painful at all to normals). The similarity in the initiating chemicals, presumed at present to be 9 and 13 HODE, does not indicate a similar response in the brain as in the rest of the body. Therefore I favor retaining different names until we know the mechanisms are in fact the same.
    Last edited by dejerine; 04-18-2013 at 01:05 AM.

  2. #2
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    Quote Originally Posted by dejerine View Post
    Is Central Pain neuropathic? Of course. Definitionaly, there is no doubt of this, since neuropathy means "nerve injury pain".

    Is it helpful to CLINICALLY name Central Pain “neuropathic pain”? My own viewpoint is that it is NOT helpful to use "neuropathic pain" for both central and peripheral nerve injury pain.

    My reasons include the following:

    1) The vocabulary is already muddled enough without throwing in the towel and lumping very diverse conditions together

    2) There are clinical tests to differentiate the two (Mitchell test, emotional consequences and distribution of pain on the body surface.

    3) The public must know that Central Pain exists

    4) Doctors should not shotgun meds at Central Pain patients which were designed ONLY for peripheral nerve injury pain

    It has been helpful in my own case to be able to have a DSM (ISDN9) designation number for my specific condition. If nothing else, it put doctors who were unaware Central Pain existed, that it is a distinct disorder. This was most helpful in dealing with the skeptic, who was inclined to think if he hadn’t heard of it, it did not exist.

    Riddoch invented the term Central Pain, calling it a “pain beyond pain” in 1940. Prior to this S Weir Mitchell (1876) termed it “pain of central origin” and developed tests to distinguish it from peripheral nerve injury pain, which assisted him in therapy as well. Dejerine, Eggers, and Roussy (1903) used Mitchell’s terminology but studied CP from stroke to the area of the thalamus. For a time central pain was referred to as thalamic pain, but that term is now reserved for stroke victims.

    That this is a difficult area is shown by the fact that not until recently were clinicians aware that central pain feels different from ordinary pain. (First pointed out by Ron Tasker) The vocabulary was that weak.

    Bowsher proposed to simplify the diagnosis by using the following criteria for central pain:

    Dysesthetic (ie. conveys little or no discriminative information) burning pain following injury to the central nervous system, often with a paradoxical cold component.

    Bowsher was fully aware CP patients have other pain as well, but he was trying to draft a minimal statement to allow easy diagnosis.

    Tasker expanded this slightly by allowing differentiation of pains into spontaneous and evoked, since some CP patients have ONLY spontaneous pain while others show enhancement of one or another of the central pains from various stimuli (sudden cold stimulus or LIGHT touch being the most frequent evokers).

    Peripheral nerves are NOT central nerves. Peripheral nerves can heal and the prognosis is different. Central neurons cannot heal and futile efforts to make them heal frustrate and confuse the patient (and cost money).

    The taxonomy (naming) committee of the IASP reportedly delisted Central Pain, and now just uses the word “Neuropathic pain” for any nerve injury pain.

    I disagree with this because it fails to alert the caregiver to fully elaborated cases of Central Pain, with accompanying need for extensive patient and family counseling, realistic expectations as far as work, dress, and social interaction, and it lumps CP with such things as diabetic neuropathy.

    The dysesthesia of CP is the cardinal feature. There are plenty of other pain aspects of CP such as intermittent lightning pain, and pain in the muscles. However, keeping it simple by holding with Bowsher’s definition helps make the diagnosis. Dejerine said central pain diagnosis was EASY. But the mélange of definitions and confusing vocabularly has now obscured the condition until agreement has vanished, leading to a lumping of CP with peripheral nerve injury pain.

    At present, we think of Central Pain as inflammation (activation by genetic alteration) of TRPV1 receptors in the dorsal horn of the spinal cord by oxidized linoleic acid metabolites 9- and 13-hydroxyoctadecadienoic acid (9- and 13-HODE) .These are known as OLAM, or oxidized linoleic acid metabolites and work is under way to try to treat linoleic metabolites with other fatty acids, such as Omega-3 derived fats. Not only CP but also ordinary heat causes increase in 9 and 13 HODE. They are also manufactured in isolated strips of removed skin subjected to noxious heat.

    CP is neuroinflammation in central neurons, susceptible to input from peripheral sensory neurons, (which may also be manufacturing 9 and 13 HODE). One unexplained mystery is why CP patients also kick out the 9 and 13 HODE in the face of a cold blast, ("cold" being relative since the cold necessary is not painful at all to normals). The similarity in the initiating chemicals, presumed at present to be 9 and 13 HODE, does not indicate a similar response in the brain as in the rest of the body. Therefore I favor retaining different names until we know the mechanisms are in fact the same.

    I agree, and I almost understand your scientific explanation.
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  3. #3

    Stroke of the spine.

    Hi
    I am trying desperately to find some answers and solutions or at least get on the right track for my father. He has recently been informed he had a stroke of the spine. He is in a lot of pain, he can not keep a shirt on and has shooting pain all around his digestive area, he has trouble sleeping and can not function or work. He is also a diabetic, we originally were told it was Painful diabetic neuropathy however an MRI revealed he actually had a stroke in the spine. He is taking a range of meds including lyrica. I would just like some info on where to go from here.
    Do we try acupuncture? Physio?
    Not sure if its the meds but he has also become very emotional constantly crying (I guess the pain would cause this too) He is 52 and generally a very hard man. It is hard to see him like this. Since being diagnosed he has been put on insulin and is slightly better but just slightly. Please if anyone has any info or suggestions I would be very greatful.
    Regards
    Michael

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