New Study by TNA in the works! Finally

INew study in mice tracks cause of trigeminal neuralgia pain

Mice may help scientists gain insight into the loss of a protective nerve coating that is thought to cause the shocking facial pains of trigeminal neuralgia—the world’s most painful medical problem.

In an effort to develop an animal model for this agonizing human disorder, neuroscientists at the University of Florida are launching studies in mice deficient in a gene that produces myelin, a fatty substance which surrounds nerves like an insulating sheath. The initial year-long study is under way at UF’s McKnight Brain Institute, aided by a grant from TNA-The Facial Pain Association.

Lucia Notterpek, Ph.D., project director, said her team will track the biological events that destroy myelin to the point that nerve impulses cannot be conducted normally. Loss of myelin coating on the trigeminal nerve, close to where it enters the brain, is strongly suspected as a cause of trigeminal neuralgia. Myelin damage has been found in many, but not all, patients with TN pain.

"Through multiple repeated experiments, we will try to figure out the least amount of nerve damage required to initiate myelin damage in both healthy mice and in mice bred with a gene deficiency," Notterpek said. "We hope to determine whether mice deficient in the myelin gene (the PMP22 gene) are more susceptible than normal mice to the loss or erosion of myelin."

Notterpek said myelin damage will be induced in the mice by surgically tying a thread around a nerve (under anesthesia) in order to constrict the nerve. The intent is to reproduce the type of nerve compression found in most patients with trigeminal neuralgia. In textbook cases of the disease, the trigeminal (three-part) nerve, which energizes all areas of the face, is irritated and eroded by an aging or injured artery that sags and presses against the nerve.

The researchers will attempt to correlate myelin damage with behavioral changes, specifically how the mice respond to the application of heat or mild pressure on the area of skin innervated by the injured nerve.

The outcome of this study may lay the groundwork for testing various pain-relieving treatments, including nerve-protective medications or by "patching" missing segments of myelin with myelin-producing cells derived from mouse stem cells. Notterpek said the study also may aid understanding and treatment of muscular sclerosis, in which small areas of myelin are damaged.

Notterpek, professor and chair of the UF Department of Neuroscience, earned her Ph.D. in neuroscience from the University of California at Los Angeles and completed postdoctoral training in neurobiology at Stanford University.

Good news. Maybe one day we can all live without pain. And we won’t have to worry about our children or parents suffering with this pain.

Hi Michelle, can I ask where you got this info from? i’d love to read the original forward it on to others if possible?
Thanks, Susan.… is the web address from the TNA web pages and I also seen it on a yahoo group that I am n for TN as well.

Susan said:

Hi Michelle, can I ask where you got this info from? i’d love to read the original forward it on to others if possible?
Thanks, Susan.

Thank-you!!! xx

I’m that mouse!!!

Well not really… but I have only one copy of the PMP22 gene, or rather one of my chromosome 17s has that gene missing, so my nerves have a deficiency in that gene. It’s a hereditary disease called HNPP (hereditary neuropathy with liability to pressure palsies). As a result my peripheral nerves are susceptible to easy break down of myelin. I heard one geneticist describe PMP22 as being like the jam in a swiss roll, if the jam is too thin (too little PMP22) then it gets squished out too easily, leaving areas with no jam, in myelin terms this makes it break off because it is uncompacted, (not enough jam to hold it together), and a bit lousy at conducting nerve impulses…

I will follow this study with great interest.


and that was a boatload of info.
Just on the U of F! Cloned foal birth, ‘adult’ stem cells, regenerating…
No one should ever have this pain! Not even a mouse, bob

I did wonder why they just don’t ask those with HNPP, and leave the mouse alone. It seems a bit odd to me that they are trying to ascertain whether PMP22 deletion makes nerves more susceptible to demyelination through relatively minor trauma, when that is already known from the Human disease.
The trouble those with HNPP have is that of ascertainment bias, most doctors, who have never heard of it, rely on a 50 year old description of HNPP, and often dismiss symptoms such as hearing loss, TN, and other cranial neuropathies as being something else.
If anything this research will show whether or not Trigeminal nerves are affected in the disease HNPP, which according to some human studies has already been reported.
I find it all quite puzzling…