|12-09-2009, 02:57 AM||#1|
Join Date: Jan 2002
central pain and syrinx
Before citing a new article on how central pain develops, I want to give a
Reminder to Everyone: Do not forget to email Dr. Francis Collins, Director of the National Institutes of Health and ask him for some of the eighteen billion stimulus money he was given to be devoted to BASIC pain research. Basic research is done at NIDCR, a division of NIH. Presently, they have six people in the department. They need six hundred.
Dr. Francis Collins email is:
Equally or more effective is to find the names of your elected representatives (by state AND district) and ask THEM to email Dr. Collins. You can quickly find the email of your representatives at this website:
Most congressmen have ended open email so you have tg find out who they are, go their website and use webforms. Some people recommend fax instead, but my senator responds to by email the same as by fax.
Very interesting article by Hemley in J Neurosurg. recently:
Howard Fields began writing about the watershed effect in cord injury decades ago. The spinal arteries and radicular arteries (as well as one in the thoracic area discussed here recently by Dr. Young) push blood into the spinal artery. Then, having done its job, the blood is removed in the venous system. However, with swelling of the cord, there is a tourniquet like effect so that blood entering under higher arterial pressure cannot get OUT via the lower pressure venous system. This leads to a cessation of circulation, obviously NOT good for the cord. The result is tissue hypoxia in the cord. Fields called this the "watershed phenomenon" meaning that the drainage fields were blocked, so no new blood could get in. This idea is behind the attempts to use hyperbaric oxygen immediately after cord injury to try to minimize damge. This is not a popular remedy and rarely available, but I personally interviewed a neurosurgeon researcher who claimed to have restored cord function in rats by use of such a chamber.
Some researchers have noted that this condition is often associated with release of cytotoxic amines, i.e. those associated with the process of inflammation. This has been assumed to have something to do with the proliferation of glia around the neurons of the cord, and the development of central pain. The glia surround neurons and produce things like brain derived neurotrophic factor and nerve growth factor, which attract inflammatory chemicals. Injury anywhere in the body tends to make the area sensitive, or inflammed.
Now, it would appear that this neuroinflammation and associated excess swelling may actually be the cause of cavities of fluid (syrinx) which sometimes forms with cord compression or injury.
In a rat animal model designed to try to figure out what causes cavities (syrinxes) to form, they produced evidence that backup in blood flow in the cord led to fluid being released into the interstitium (substance between harder structures) of the cord and that excitotoxic amines injected into the area caused a syrinx in 16 of the 17 animals. Since it is so common for a syrinx patient to have pain, there seems to be a close link between syrinx, which is more or less the extreme situation, and central pain, which represents the consequences of swelling and neuroinflammation SHORT of causing a syrinx.
It is possible that in very careful autopsy, all of us with central pain, MIGHT have evidence of microsyrinxes, which never coalesced and perhaps eventually left scar tissue, which in the cord is sometimes called "gliosis". No one to my knowledge has ever looked at this. Indeed, I find a virtual absence of the literature on anyone doing very careful autopsies of anyone, or even any animal with central pain. This is surprising.
Examiners in lab animals tend to have something they are looking for and do that much, but an extensive from the ground up autopsy, including chemoarchitectural analysis, I have not seen. Contra this idea are the reports by Patrick Wall and Triggs in Brain which showed people with central pain are more likely to have NO bright lesions on MRI. However, many discrete tiny foci of fluid in the cord would not cause enhancement of signal (bright lesions) on MRI. Cord lesions on MRI tend to look like someone spilled bleach on a photograph. This whiteness is recognized to signify water, as in liquification, or later, scarring by glia.
On my first MRI, there was a white blob big enough for me to see, but the neuroradiologist failed to see it. Another clue is the shape of the cord. Those with injury, instead of a nice oval cord, tend to have slightly dished out areas, which represent collapse of the cord substance. Although my cord was oval elsewhere, at the level of injury it looks like a kidney bean with the concavity facing the front of my body. NONE of this was mentioned on the reading of the films.
Never assume your films have had a thorough going over, unless you pester people, including your neurosurgeon. Complicated though the radiology interpretation may be, it is mostly routine verbage, and you should always ask if there are any areas where the cord is misshapen, or whether any brigher areas appear at any level. Change in cord shape is easily detected by measuring the front to back measurement and comparing it to the side to side measurement. Ligaments attached to the side of the canal maintain the side to side measurement even in severe cord injury. However, the collapse will show up in the front to back measurement. This leads to a drop in the RATIO of the diameter of antero-posterior cord to the lateral diameter of the cord.
It is amazing to me how seldom this ratio is peformed on MRI. It takes less than five seconds for the radiologist to use a mouse to place the cursor at the four points (the measurement is displayed by the software on the screen automatically), but I can hardly find any who do it routinely and I have never even seen an MRI report which gives these very valuable numbers. You can ask your doctor to do it with a ruler on the films, and even if you have no bright spots, a ratio of less than 0.4 means there is significant compression, at a minimum. People differ in cord size so the radiologist should measure ratios at the level above and below your injury to see what the AP/lateral ratio is there. Someone with a cervical cord size of say 13 mm above an otherwise normal appearing cord, and 13 mm below that same area would be abnormal if the area of interest is only 9mm, although 9mm is within the range of normal averages for all humans.
I am aware of a number of films which say something like "there is no significant effacement (touching) of the cord" when if a compression ratio is performed it shows the effacement is indeed significant. Also since the spinal artery and vein run in front of the cord, when there is touching, that means there is no space between cord and the front of the bony spinal canal, so one wonders how the artery and vein find enough space to do their job. Most cord injury is felt actually to represent compression and compromise of the vessels, not the cord itself.
For the money they charge, we deserve a quick compression ratio, as well as a look for any bright (enhancing) areas. The compression ratio does not apply below L1 or L2 where the cord is broken up into many branches which reminded some anatomist of the tail of a horse, the cauda equina area.
Some people feel uninformed about neurons and glia. The Nov Issue of Scientific American has an article which goes into this relative to Chronic pain. Written by Fields.
Last edited by dejerine; 12-09-2009 at 04:14 AM.
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