Saturday, July 20, 2013

Melzack & Katz, Pain. Part 16: Apples are to fruit as cows are to animals as nociceptive input is to pain

The paper, Pain.

Part 15: Prevention of neurobiological hoarding behaviour by dorsal horn and DRG glia is easier than clutter-busting after the fact


It struck me, and it should strike the reader, that Melzack and Katz are completely in agreement with the assertion that nociceptive input is associated with pain, and that nerves are associated with pain, and that keeping nerves quiet with local blocking, etc., during surgery etc., will way reduce the chance that pain post-op will occur or become chronic. Their reference list from 32 to 58 is all about this. 
They get that pain is connected with nociceptive input. 
They simply do not agree that nociceptive input is all there is to pain, an emergent phenomenon not fully understood, that manifests in the brain, that's all.

Let's keep categories straight

They're saying, yes, cows are animals, but no, not all animals are therefore cows. 
Yes, apples are fruit, but no, not all fruits are therefore apples. 
Nociceptive input is not exactly what pain is. Inputs are not exactly the same as the outputs with which they may be linked. 
Let's not perpetuate conceptual error or create categorical error when it comes to something as debilitating as pain, especially pain that has become chronic. Consider nested setshierarchies

You wouldn't call every kind of fruit an apple. You wouldn't call every kind of animal a cow. 
So don't call pain "nociceptive input," or every nociceptive input, pain. Admittedly, the analogy breaks down a little, in that the relation isn't quite as logical or clearcut, but change those labels in text books. They are misleading. 

Emergent properties arise differently at different levels of a system, and treatment models, explanatory models, scientific models should reflect that. So let's be sure we have defined nociceptive input as what it really is - input into another level of a system which creates another something, an emergence, which we might then (more legitimately) call "pain." Furthermore, that "other level" of this system is dealing with way more than just one kind of input at a time. It has to deal with ALL inputs, at once, including its own input from itself. Self. 

Patients in pain are not crazy

The next section is titled, Pain and Psychopathology. The first sentence is, 
"Pains that do not conform to present-day anatomical and neurophysiological knowledge are often attributed to psychological dysfunction." 
This is a scholarly way of saying that if doctors (and therapists) can't find something physically "wrong" that they can blame for the patient's pain, they often end up blaming the patient him or herself - the patient must be crazy. 

"This view of the role of psychological generation in pain persists to this day notwithstanding evidence to the contrary."
One could become sidetracked by examining all the ways human brains default to a vast spectrum of faulty heuristic thinking. But to save time, check out these books some time. 
Mistakes Were Made, But Not By Me
On Being Certain. 

"Psychopathology has been proposed to underlie phantom limb pain, 25 dyspareunia, 59 orofacial pain, 60 and a host of others including pelvic pain, abdominal pain, chest pain and headache. 61  However, the complexity of the pain transmission circuitry described in the previous sections means that many pains that defy our current understanding will ultimately be explained without having to resort to a psychopathological etiology."
Sounds to me like they're saying, let's not be so quick to judge. There are perfectly valid explanations coming along, everyday, and until they're in, don't blame patients for having mysterious pain or label them crazy. 

"Pain that is ‘nonanatomical’ in distribution, spread of pain to non-injured territory, pain that is said to be out of proportion to the degree of injury, and pain in the absence of injury have all, at one time or another, been used as evidence to support the idea that psychological disturbance underlies the pain. Yet each of these features of supposed psychopathology can now be explained by neurophysiological mechanisms that involve an interplay between peripheral and central neural activity.4,60"
Look how far we've already come! 
"Recent data linking the immune and central nervous systems have provided an explanation for another heretofore medically unexplained pain problem. Mirror image pain or allochira has puzzled clinicians and basic scientists ever since it was first documented in the late 1800s.62 Injury to one side of the body is experienced as pain at the site of injury as well as at the contralateral, mirror image point.6,63 Animal studies show induction of a sciatic inflammatory neuritis by peri-sciatic microinjection of immune system activators results in both an ipsilateral hyperalgesia and hyperalgesia at the mirror image point on the opposite side in the territory of the contralateral healthy sciatic nerve.64 Moreover, both the ipsilateral and contralateral hyperalgesia are prevented or reversed by intrathecal injection of a variety of proinflammatory cytokine antagonists.65"
See all previous blogposts on the gliopathy paper, in section 14 and 15 of this blog series (links are above and below).  

"Mirror image pain is likely not a unitary phenomenon and other non-immune mechanisms may also be involved.66 For example, human67 and animal evidence68 point to a potential combination of central and peripheral contributions to mirror-image pain since nerve injury to one side of the body has been shown to result in a 50% reduction in the innervation of the territory of the same nerve on the opposite side of the body in uninjured skin.68 Interestingly, while documented contralateral neurite loss can occur in the absence of contralateral pain or hyperalgesia, pain intensity at the site of the injury correlates significantly with the extent of contralateral neurite loss.67 This raises the intriguing possibility that the intensity of pain at the site of an injury may be facilitated by contralateral neurite loss induced by the ipsilateral injury68—a situation that most clinicians would never have imagined possible."
Not a bad idea to treat, or at the very least, examine both sides, if you're a human primate social groomer. And use mirror therapy. And graded motor imagery. 

Here is the authors' final word on this. 
"Taken together, these novel mechanisms that explain some of the most puzzling pain symptoms must keep us mindful that emotional distress and psychological disturbance in our patients are not at the root of the pain. In fact, more often than not, prolonged pain is the cause of distress, anxiety, and depression. This is not to say that psychological and emotion distress do not contribute to pain nor that pain cannot be caused by thoughts and feelings even in psychologically healthy people. But strange and unusual pains should not be taken as a proxy for psychopathology." 
Thank you for spelling it out, clearly, yet again for the 10 millionth time, Melzack..Katz... 
Maybe some day the medical community and health care insurers will actually hear this and get it. 

Why should we take care to avoid blaming the patient for their pain?
"Attributing pain to a psychological disturbance is damaging to the patient and provider alike; it poisons the patient-provider relationship by introducing an element of mutual distrust and implicit (and at times, explicit) blame. It is devastating to the patient who feels at fault, disbelieved and alone."
I.e., it ruins the very relationship upon which everything else in the future of that patient's neuromatrix rests.  Little things like, ...oh... future recovery. See Benedetti for more about that.

Also (if you aren't convinced yet) watch the embedded TED video in this news story, Blaming the Patient, Then Asking Forgivenessin which a doctor describes how he came to realize that "blaming the patient" was a completely wrong path, and severely regrets doing so. 


Previous blogposts

Part 1 First two sentences Part 2 Pain is personal Also Pain is Personal addendum., Neurotags! Pain is Personal, Always.

Part 3a Pain is more than sensation: Backdrop Part 3b Pain is not receptor stimulation Part 3c: Pain depends on everything ever experienced by an individual

Part 4: Pain is a multidimensional experience across time

Part 5: Pain and purpose

Part 6a: Descartes and his era; Part 6b: History of pain - what’s in “Ref 4”?; Part 6c: History of pain, Ref 4, cont.. : There is no pain matrix, only a neuromatrix; Part 6d: History of Pain: Final takedown Part 6e: Pattern theories in the history of pain Part 6f: Evaluation of pain theories Part 6g: History of Pain, the cautionary tale. Part 6h: Gate Control Theory.

Part 7: Gate control theory has stood the test of time: Patrick David Wall;  Part 7bGate control: "The theory was a leap of faith but it was right!"

Part 8: Beyond the gate: Self as mayor Part 8b: 3-ring circus of self Part 8c: Getting objective about subjectivity

Part 9: Phantom pain - in the brain! Part 9b: Dawn of the Neuromatrix model Part 9cNeuromatrix: MORE than just spinal projection areas in thalamus and cortex Part 9d: More about phantom body pain in paraplegics

Part 10: "We don't need a body to feel a body." Part 10b: Conclusion1: The brain generates its own experience of being in a body Part 10c:Conclusion 2: Your brain, not your body, tells you what you're feeling Part 10dConclusion 3: The brain's sense of "Self" can INclude missing parts, or EXclude actual parts, of the biological body Part 10eThe neural network that both comprises and moves "Self" is (only)modified by sensory experience

Part 11We need a new conceptual brain model! Part 11b: Intro to a new conceptual nervous system Part 11c: Older brain models just don't cut it Part 11d: The NEW brain model!

Part 12: Action! 12b: Examining the motor system, first pass. 12c: Motor output and nervous systems - where they EACH came from Part 12d... deeper and deeper into basal ganglia Part 12e: Still awfully deep in basal ganglia Part 12f: Surfacing out of basal ganglia Part 12gThe Action-Neuromatrix 

Part 13: Pain and Neuroplasticity Part 13b: Managing neuroplasticity

Part 14: Side trip out to the periphery! Part 14b: Prevention of pain neurotags is WAY easier than cure Part 14cPW Nathan was an interesting pain researcher  Part 14dBrain glia are from neuroectoderm and PNS glia are from neural crest Part 14e: The stars in our headsPart 14f: Gleeful about glia Part 14g: ERKs and MAPKs and pain Part 14h: glia-fication of nociceptive input 14i: molecular mediators large and small Part 14j: Neurons, calling glia (over, do you read?) Part 14k: Glia calling glia, over. Do you read? Part 14l: satellite cell and neuron cell body interactions, and we're outta here!

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