THE FIBROMITE WHO CRIES

by Jeanne Hambleton © 2007
NFA Leader Against Pain-Advocate

“It breaks my heart when she cries……” This is the story of Ronald J. Waller, who wrote a touching essay about his wife’s fibromyalgia. Called “She Cries” that can be found with links to his other works on http://rjswritingloft.com together.

Ronald wrote to me saying, “I took on the project, as my wife, Carolyn, suffers from this condition, in the hope that it would help to raise awareness in the arena of fibromyalgia and the silent destruction this demon seeks to inflict upon all who are in it’s grip.”

Ronald has written “She Cries” adding that watching “My best friend, my wife, suffer from this condition compels me to write, inform and continue to learn more about this Demon who not only invades Carolyn’s life but also has affected all who are close to her.

“I am honored and humbled that you want to use these works in your endeavors to educate and inform the medical arena; I never thought my writing would reach so many people on this kind of scale and I could not be more pleased at learning about your efforts. I applaud your efforts and commitment to seeking a better life for those who suffer from Fibromyalgia. I hope we can continue to work together to bring the demon, fibromyalgia, to its knees.”

Ronald’s website questions what is fibromyalgia, outlines the symptoms and discusses the pain which knows no boundaries. He describes Carolyn’s pain in the legs as similar to “burning hot grease” adding even the sheets on the bed leaves her purple with irritation.

He said friends had abandoned her and the common choice of words is, “It’s all in her head”. Doctors shake their heads and wonder what to do next, says Ronald.

Sleepless nights and fibro fog are commonplace. To add to Carolyn’s condition she has endured numerous operations on her back, wrist and knee “not to mention the Mollaret’s Meningitis that she suffered from while in the Army”.

Ronald adds,” To know Carolyn Waller, however, you would not know she suffers these multiple medical issues at first glance. Always quick to smile, always ready to listen to another’s problems, always there to tell that joke, placed just right, to put another at ease. I continue to be amazed at her strength and her courage; it remains an honor to be a part of my wife’s life, and a privilege to be allowed in her inner circle to help as I can.

“Carolyn has been my friend when none other could be found; my supporter as I pursue my dreams as a writer; my guide as I overcome my own demons. This veteran (both from the service and from the battles she wages currently) never fails to leave another better off for having come across her path. I know this as personal fact. I am constantly amazed and humbled by the gift of her love and the generosity she freely gives to others. Maybe this is her best weapon in her fight with FMS.  Fibromyalgia. Have you heard of it? It breaks my heart when she cries….”

A dedicated couple Carolyn describes Ronald as the best husband in the world although he himself is not a well man. He suffers from post concussion head aches, and has severe pain in his joints in his legs and feet from extreme laxtivity, his joints are giving away it is hereditary.  This has left him using a cane inside the house like me and we both use electric wheelchairs when we leave our apartment.  As a matter of fact they are our only means of transportation.  He is on a mess of medications and it is hard for him to write now, but you all have really changed him and made him feel really good and useful.
 
“We spend every minute of every day together and very rarely have words against each other.  I love him with all my heart and was so lucky to find him, wrote Carolyn. At a time of the year when we send  Christmas cards to acquaintances and often sign them ’with love’, I think this story illustrates true love. I wish them both every happiness for the rest of their lives.

You may reach Carolyn at Carolyn_n_ny@yahoo.com and Ronald at rj@rjswritingloft.com if you have any questions.
The full transcript of this dedication can be found on the Internet under http://www.rjswritingloft.com.

Ronald J. Waller is a published disabled writer whose work can be found on
RjsWritingLoft.Com || MyBlog and his website. Written in honor of my wife and best friend it is headed, “For you, Princess.”

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Mutation may cause inherited neuropathy

Contact: Scot Roskelley
scot.roskelley@uchospitals.edu
773-702-6241
University of Chicago Medical Center

Mutations in a protein called dynein, required for the proper functioning of sensory nerve cells, can cause defects in mice that may provide crucial clues leading to better treatments for a human nerve disorder known as peripheral neuropathy, which affects about three percent of all those over age 60.

Peripheral neuropathy results from damage to the nerves and nerve processes that are located outside the brain and spinal cord. Symptoms include pain in the hands and arms, legs and feet–sometimes constant and quite severe–as well as progressive numbness and weakness in the arms and legs. Despite its prevalence, little is known about the precise causes of the disease or how to prevent or treat it.

In the December 26, 2007, issue of the Journal of Neuroscience, however, researchers at the University of Chicago Medical Center show that mice with mutations in only one copy of a gene coding for one part of dynein protein have severe defects in proprioception, the ability to perceive the spatial orientation of body parts.

These defects caused a significant reduction in the number of sensory nerve cells in affected mice. They also caused early-onset locomotion problems in the mice’s hind legs, a defect that appears to be quite similar to some human neuropathies.

“This gene codes for part of a multi-protein complex,” said study author Brian Popko, PhD, Jack Miller Professor in Neurological Diseases at the University of Chicago Medical Center. “So a mutation in any of these proteins, or disruption in the function of this multi-protein complex through some other mechanism, could also lead to very similar abnormalities” in human patients with sensory neuropathies.

Mutations in the gene for dynein heavy chain 1, Dync1h, led to movement defects in the hind legs of mice. These defect resembled human neuropathies, said Popko, particularly some forms of Charcot-Marie-Tooth disease and hereditary sensory neuropathy.

Charcot-Marie-Tooth disease is one of the most common inherited neurological disorders, affecting approximately 1 in 2,500 people in the United States. It is characterized by loss of muscle tissue and touch sensation, predominantly in the feet and legs. In CMT, both the sensory nerves that carry signals from receptors in the extremities to the brain and spinal cord, as well as motor nerves that relay signals from the brain and spinal cord to the limbs and internal organs are affected.

Hereditary sensory neuropathy affects predominantly sensory nerves. Symptoms included sensation loss, decreased or absent reflexes, foot deformities and various anatomic features.

Dynein appears to be a likely suspect, the authors report. Although it is found throughout the body, Dynein plays an important role in the transport of cargo within axons, the elongated extension of nerve cells that transmit signals from one neuron to another. Dynein is crucial for survival, because mice that lack dynein or have mutations in both Dync1h copies die before birth.

Although dynein is important for the whole body, defects are found only in sensory neurons, and predominantly in hind limbs.

“The key question is why”” said Popko. “This mutation may affect transport proteins in all neurons, but perhaps the region that is mutated is more important for the proteins that it transports in sensory neurons, whereas other regions could play a role in motor neurons. Also, mutations in different regions of this protein seem to have different effects. That may be due to differences in the cargo-binding domains.”

Affected neurons in mice and in patients with sensory neuropathies have very long axons. Such neurons that transmit signals over huge distances depend on dynein, the “cargo-transporter” to carry molecules from the tip of the axon to the neuron’s cell bodies. If the cargo-transporter is somehow disturbed, Popko said, like in the case of mutations in Dync1h gene, neurons that transmit signals over “long distances” will suffer more.

“It’s very common for neuropathies to affect neurons with the longer axons, for example those that innervate the legs and feet,” says Popko. It has been previously suggested that hereditary sensory neuropathy might be connected with disabled trafficking along the axons. There have been mutations found in two genes that form a complex essential for survival of sensory neurons, and this complex is thought to be transported along the neurons by dynein.

“This study lays the groundwork for the search for disruptions of this cargo transporting complex in human patients with sensory neuropathy”, write the authors in their paper.

They are already looking at human patients for similar mutations. And they’re working further on answering new questions, including: what are the binding partners of dynein that are disrupted in diseases, and why does this affect sensory and not motor neurons”

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This work was supported in part by a grant from the Miriam and Sheldon Adelson Program in Neural Repair and Rehabilitation. Additional authors of the paper include Xiang-Jun Chen, Eleni N. Levedakou, Kathleen J. Millen, Robert L. Wollmann and Betty Soliven of the University of Chicago.

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