The notion that radiology can image pain is an urban myth. Clinical medicine must not abdicate its role for the simple reason that radiology has a way to go before it can be used to rule in or rule out the existence of pain.
The anguish and bewilderment of a central pain patient who has just been assured that there is no lesion which would account for her claims, is a travesty of medicine we would like to see end. She knows perfectly well she has terrible pain, more terrible and more profound than she has ever experienced. Yet, the nature of the sensations is wildly different from anything she associates with pain. Since she cannot explain her pain, and the magic plastic image stands as “incontrovertible” evidence of her mistake, there is a schism between what she recognizes as true and what she concludes can possibly be true.
How was this point reached? It flowed from simple unawareness of the size of structures to be imaged (<1,5 mm), and a grossly wrong assumption by a radiologist that the markers of motor injury and muscle disorder can serve as markers of pain. This is lumping gone beserk. It is time for a little splitting.
MRI images see, basically, water, at the Larmor excitation frequencies utilized in clinical imaging. Electron spin is not utilized. MRI creates images by using radioexcitation of the nuclei and studying decay of the disturbance in spin, which gives off energy which can be detected in a magnetic field and converted to an image. Currently, the Larmor frequency is aimed at hydrogen, which for technical reasons, means mainly WATER. If pain went sloshing around the nervous system, there might be some reason, a poor one, to think that MRI could see pain. Since pain is, at the root, a frequency of action potentials, one cannot string a violin with a monkey wrench. The radiologist must not write checks which the patient cannot cash.
To speak of the radiologic gold standard of pain, is to speak nonsense, and states an unscientific oxymoron, at least for now. No one would be more grateful for a reliable MRI marker than CP patients. They could stop being lumped with back pain, since the screen would light up whenever a CP sufferer was fed into the “human pencil sharpener” the big, noisy, intimidating MRI machine.
Rapid scanning techniques are helpful, since many with spinal cord injury have slight spasticity, and the noise of the magnet may itself make holding still difficult. If the experts are correct, no pain state matches severe central pain. Patients with CP will be the gold standard of comparison for measuring severity of any other pain state. Some with CP have it over the entire skin surface, in all the muscles, throughout the dura, on the corneas, in the mouth and nose, and in the entire viscera, including bladder, gut, urethra (the bladder burns if they don’t urinate and the urethra burns if they do) and rectum.
How much credibility is to be given those who claim a pain state? Medicine has a tradition since the time of Osler, of listening to the patient, a tradition which is ignored in evalutating chronic pain. If this process had been followed, the Wall/McHenry database of CP descriptors would be unnecessary. Neurosurgeons would speak specifically of the individual CP components and cease reporting “benefit” to “pain”, whatever that is. Burn medicine speaks of the percentage of body affected, and anesthesia speaks of stages of anesthesia, but where is the measurement in the word, “pain”. We can do better than this.
Drug remedies would evaluate “spinothalamic pain” (burning and visceral pain) separately from “posterior column pain” (muscle pains and lancinating pain), and the process would be rational, in an inchoate sense. English has been criticized for having only one word for love, failing to follow even the Greek, which had three such words. Even more is the poverty of the King’s English revealed when find clinicians speaking not of dysesthetic burning, kinesthetic dysesthesia, secondary allodynia, but only of “pain”. This is surely puerile when it comes to nerve injury pain, which shares neither the quality nor the pain descriptors of normal pain.
Who constitutes the group of pain patients under the middle of the bell shaped curve is a matter of debate. According to the pain myth, the centrist group is comprised of physically and psychologically weak individuals who malinger, exaggerate, and generally behave in a blameworthy fashion. The reality is that humans are generally sincere in their desire for good health care, and that malingerers are extremely rare, and represent outliers in the run of medical contacts.
Almost any of what may be called the minor pain states, such as low back pain, whiplash, or repetitive stress syndrome, have extreme detractors, who would define the malady out of existence as a fabrication of misplanced or evil positures of the mind.
Central pain is not one of the conditions with detractors, because it has no tractors in the first place. It is unspoken outside spine hospitals and rehab centers. The rejection of central pain as valid is not an issue because the disease itself is unknown except to specialists in pain medicine. So distant is the condition that it is typically thrown in the bag with back pain, if and when the term comes up, causing little or no curiosity to the listener.
This is not to disparage back pain, which is its own problem. Back pain is nearly a scandal. It would appear that only one doctor, Bogduk in New Zealand knows anything about the trigger point anatomy of back pain. Particularly disappointing is the unscientific approach to the facet joints. These joints, where the vertebrae above, articlulate atop and behind the vertebrae beneath, are known to produce Substance P, CGRP (see CGRP elsewhere at this site, using Search), and to have the characteristic fibers of chronic pain. (see Kallakuri et al, Spine. 2004 Jun 1;29(11):1182-6). However, the facets have been ignored in favor of the disc, in front. The back of the human body is not imaginary and neither is pain in the facet. However, the failure to scientifically evaluate the facet element of back and neck pain, which has to contribute to the large number not helped by disc surgery, is appalling.
The benefit to facet syndrome of lesioning of the medial branch of the posterior ramus of the spinal nerve which supplies the facet is of very short duration in relief, perhaps only one month. Lesioning with electrocautery or freezing is not the answer, at least as it is currently performed. Lesioning of the posterior ramus itself is dangerous since placement of the needle risks entry into blood vessel compartments. Takeup of local anesthetic can send it to the brain, causing seizures or stroke. Actual cautery is even more technically unfeasible. Steroids, aimed at reducing inflammation generally give insufficient relief, or at least relief of short duration.
Obsessed with malingering, some clinicians give bogus injections to see if the patient is giving accurate information, but this is surely unique in medicine, and if so as to be confident of actually hitting the facet compartment, with CT, causes exposure to unnecessary radiation. Furthermore, it makes the false assumpton that it is the patient who must be in question, rather than the technique and the operator. Given the erratic benefit wtth any technique, it is hardly sound to assume that failure of the technique is evidence of unreliable information on the part of the patient.
Certain centers use ultrasound with cold (cryotherapy) to lesion the medial branch, but the probe is rather large and questions exist about the reach of the procedure. Many of those who are good at the radiology do not perform blocks and many who perform blocks do not have access to CT fluoroscopy. Given the number of affected patients, which will only grow when the facet is more commonly evaluated, improvements in surgical management are badly needed.
Radiologic study of the facet can only be done reliably with CT fluoroscopy, yet few institutions provide this, despite the fact that it provides significant reduction in radiation exposure. The beam “locks on” to the image, so that adjustments in needle placement can be mentally calculatd, rather than runninga continuous scan. Low radiation energiews are sufficiently informative for this technique, allowing less radiation to the senstive nervous system than with traditional CT.
Instead of wringing of the hands and uttering the dictum that “pain correlated poorly with imaging”, the solution is not to disparage the patient, but to improve the quality of imaging, and to include electrophysiologic studies so no one is groping around in the dark. Presently, the facet patient can either opt for ongoing dangerous exposures to radiation, with very brief relief, or else must resort to marginal or even “quack” medicine. How a specialist thinks they have worked up back or neck pain without careful analysis of the facet is a mystery. It will surely be corrected in the next generation.
The sloppy evaluation, and general skepticism toward back pain creates a loose attitude toward other more serious pain states,as if pain, in general, is a minor issue, and is better left alone, to avoid getting sucked into the psychopathology of the patient. Dcotors should wash their hands, but not in this fashion. If they aren’t happy with the imaging, let them fix it. Then, and only then, are they doing the job. The poser is not the patient, but the person who studies films which cannot possibly detect pain, and make declaratory statements on that basis. In the meantime, the CP patient can only distance themselves from back pain, although were are at base, sympathetic. The mystery which taints back pain, swallows us completely. Since back pain is nearly universal, the back pain patient is at least credited with “something”. The CP patient is not so fortunate.
There is an assumption that chronic pain is chronic pain and the particular flavor is of not much interest. The important concept here is that CHRONIC PAIN IS NOT NECESSARILY NERVE INJURY PAIN. Nociception (normal pain) and neuropathy are simply not the same thing. Nociception involves pain from some stimulus. In neuropathy however, the injured nerve has become hypersensitive to the point where sustained firing occurs in the nerve without any stimulus whatever.
In many instance, such as evoked burning dyssesthesia, the injured nerve fires spontaneously, but even greater pain is capable of being elicited when any stimulus, noxious or not is applied. As mentioned elsewhere, S. Weir Mitchell discovered, as early as the American Civil War, that in pain of central origin, there is a 20-30 second delay between the time of stimulus and the time light touch elicits burning pain; whereas, in peripheral nerve injury the pain is instantaeous. The cause of Mitchell’s delay is unknown.
If peripheral neuropathy and central pain cannot be considered equivalent, nociception and neuropathy may be compared even less. It is therefore unscientific for doctors to group nerve injury pain with chronic nociceptive pain. This mistake is behind the knee-jerk combination of the two in the doctor’s mind.
This is not to say we think nociception is well handled. It is not. In the area of back pain, for example, it is fashionable to say radiology does not correlate well with pain, and to assume that cuts against those who claim pain. There is no basis for affording radiology such omniscience. Radiology has not yet reached the position where is should be considered a gold standard of pain, or any standard, since the imaging of pain is limited to functional MRI (fMRI) or PET scans, which have very crude ways of addressing it.
Both of these modalities are getting better, as is tensor imaging. We welcome this progress as a way of putting distance between ourselves and those with nociception. Frankly, there is so little understanding of nerve injury that radiologists themselves have sometimes been guilty of assuming that radiology, which assesses structure, can also assess function. This would only be true, at best, if the structures involved, and the damage to those structures, were larger than 1.5 millimeters, since that is the resolving limit of MRI.
It is no wonder that clinicians sometimes have the mistaken view that MRI should see pain, since clinicians are not generally aware that the spinothalamic tract is less than 1.5 mm and that it is not a discrete bundle but is like telephone wire, composed of a large number of fibers which spread out so they can contact other nerve tracts. They are even unaware that there are TWO spinothalamic tracts, the ventral and the lateral. Nor do they know which sensations are carried in the two discrete tracts.
Even less are they aware that Patrick Wall, a great pain anatomist, was able to demonstrate in 1985 that there are at least SEVEN spinothalamic tracts from which are made up the traditional TWO. The great Ron Tasker, a brilliant neurosurgeon in Toronto, was the first to discover the true function of the spinothalamic tract as it carries nerve injury pain. His work produced “Tasker’s Rule”, which is that injury anywere in the neuraxis (the CNS) can produce similar pain. What neurosurgeons generally do not know is that Tasker himself, through laborious research, pointed out how these similar pains DIFFER. Above all, Tasker did not speak in one word to describe the central PAINS (plural). Integration by the brain is responsible for the remarkably pure signal we call normal pain, of which there is no clearer sensation. DISintegration through injury creates the spray and bizarre quality of the central pains.
Doctors are more typically aware that pain is also carried in the posterior columns, but again, they are unaware of the nature of pain which is carried in the posterior columns. Even if radiology could image pain, clinicians are not prepared to receive this knowledge unless they recognize the different manifestations of nerve injury pain. Radiology does not exist in a vacuum. It make sense only as it is put in a context of clinical signs and symptoms.
If evoked pain is under consideration, there is little sense in running an fMRI scan if the patient is almost naked in a cool room. Let them put clothing and shoes on the individual and raise the temperature a bit, if they wish to image evoked dysesthesia. This is self evident but missing because of the radiology/clinical medicine GAP.
They are also unaware that the eomatosensory evoked potential tests only a part of the anterior portion of the posterior columns, and NOT the entire tract. Thus we see the folly of assuming MRI can spot all or even most cases of nerve injury. That job belongs to the clinician who can recognize central pain by the very unique clinical picture. Dejerine and Roussy were quick to point out that malingerers claim total numbness in an affected extremity or part, whereas in pain of central origin, the defect is only in superficial sensibilities, pain, touch, temperature, and the loss is always partial, with a worsening distally. The PARTIAL loss of sensation is in the same area as the pain, which pain does NOT respond to opiates. This description shows that Dejerine and Roussy were focusing on the spintothalmic pains and not the lancinating and muscle pains which travel in the posterior columns.
Finally, radiologists themselves are unaware that Triggs and Wall showed in “Brain” that with visible bright lesions (the whitish cast on MRI which is causd by water, or the swelling in the area of cord or brain injury), the patient is UNLIKELY to have pain. This was also true of radiologic evidence of scarring, or gliosis. Where the MRI Is positive, the most likely picture is NO sensation, or numbness. Central Pain requires PARTIAL injury. Those with central pain typically had no bright lesion. It is therefore nonsense to write off CP to the imagination in a patient with no bright lesion.