This is in reaponse to a message from Vic:
There is a large CIDP group on Facebook. There is also http://www.gbs-cidp.org/index.html
There are various treatments. Work for some. Not for others. Stem cell therapy is very much the last resort of treatment.
I know some, like me, minimally afflicted at the moment. And I know some who have a nasty progressive CIDP which reminds me greatly of ALS/Lou Gehrig's Disease in the way it debilitates.
Yes, I surely do understand the pain ... electric shocks/zingers, screaming quads, mushy grape feeling toes, etc.
If your friend is without health insurance, the best option would be Medicaid, for now at least. Should he be one with severe CIDP, he will be able to file for Social Security Disability [ which is different from SSI, which is SS Suplemental Income, which he could apply for now ].
I wish him, and you, the very best of outcomes. Do please keep in touch.
Sunday, August 7, 2011
Tuesday, August 17, 2010
new article and new research ...
7% of general population has Restless Leg Syndrome
40% of CIDP patients have Restless Leg Syndrome
Aug 15
"Prevalence of RLS in CIDP was ascertained by face-to-face interview using validated criteria and compared with that in 28 age-and gender-matched controls. Eleven (39.3%) CIDP patients were diagnosed with RLS, compared with 2 (7.1%) controls (p <0.01). A significant correlation was ascertained between presence of RLS and lower limb weakness, functional disability, and summated compound muscle action potential (CMAP). The prevalence of RLS in CIDP was significantly higher than in controls in our study population, approaching 40%.
Screening for RLS in CIDP patients may be appropriate, particularly in those with weakness, disability, and motor axonal loss in the lower limbs," wrote Y.A. Rajabally and colleagues, University Hospital, Department of Neurology.
The researchers concluded: "Our findings may otherwise suggest the existence of peripheral components to the pathophysiology of RLS in patients with CIDP."
Rajabally and colleagues published their study in Muscle & Nerve (Restless legs syndrome in chronic inflammatory demyelinating polyneuropathy. Muscle & Nerve, 2010;42(2):252-6).
For additional information, contact Y.A. Rajabally, Leicester General Hospital, Dept. of Neurology, Neuromuscular Clinic, University Hospitals of Leicester, Leicester LE5 4PW, UK.
(c) 2010 Health & Medicine Week via NewsRx.com
I'm one who had problems with RLS prior to being diagnosed with CIDP. The meds used for either/both aren't tolerated by me. Nasty side effects. ( no details ... too gross ) I can wait until the RLS starts and take 1/2 a Vicodin, which I've done from "stash" leftover from surgeries, but that's gone and my neuro won't prescribe "narcotics". So -- I'm between a rock and a hard place.
__________________
7% of general population has Restless Leg Syndrome
40% of CIDP patients have Restless Leg Syndrome
Aug 15
"Prevalence of RLS in CIDP was ascertained by face-to-face interview using validated criteria and compared with that in 28 age-and gender-matched controls. Eleven (39.3%) CIDP patients were diagnosed with RLS, compared with 2 (7.1%) controls (p <0.01). A significant correlation was ascertained between presence of RLS and lower limb weakness, functional disability, and summated compound muscle action potential (CMAP). The prevalence of RLS in CIDP was significantly higher than in controls in our study population, approaching 40%.
Screening for RLS in CIDP patients may be appropriate, particularly in those with weakness, disability, and motor axonal loss in the lower limbs," wrote Y.A. Rajabally and colleagues, University Hospital, Department of Neurology.
The researchers concluded: "Our findings may otherwise suggest the existence of peripheral components to the pathophysiology of RLS in patients with CIDP."
Rajabally and colleagues published their study in Muscle & Nerve (Restless legs syndrome in chronic inflammatory demyelinating polyneuropathy. Muscle & Nerve, 2010;42(2):252-6).
For additional information, contact Y.A. Rajabally, Leicester General Hospital, Dept. of Neurology, Neuromuscular Clinic, University Hospitals of Leicester, Leicester LE5 4PW, UK.
(c) 2010 Health & Medicine Week via NewsRx.com
I'm one who had problems with RLS prior to being diagnosed with CIDP. The meds used for either/both aren't tolerated by me. Nasty side effects. ( no details ... too gross ) I can wait until the RLS starts and take 1/2 a Vicodin, which I've done from "stash" leftover from surgeries, but that's gone and my neuro won't prescribe "narcotics". So -- I'm between a rock and a hard place.
__________________
Sunday, June 20, 2010
Finally!!!
In today's Parade magazine ... finally! ... an admission from the medical establishment ...
"Many people know that cancer can cause profound tiredness, but they may not realize that fatigue can persist in some survivors for years. 'We're not entirely sure, but it may be due to unchecked inflammation in the body' says Dr. Patricia Ganz, a professor at UCLA School of Medicine.
"Treatment could possibly push the immune system into overdrive, and in certain patients the resulting inflammation could increase fatigue 'as if the body were constantly fighting off a bad flu'."
And that immune system response could manifest in many ways, among them, of course, CIDP.
"Many people know that cancer can cause profound tiredness, but they may not realize that fatigue can persist in some survivors for years. 'We're not entirely sure, but it may be due to unchecked inflammation in the body' says Dr. Patricia Ganz, a professor at UCLA School of Medicine.
"Treatment could possibly push the immune system into overdrive, and in certain patients the resulting inflammation could increase fatigue 'as if the body were constantly fighting off a bad flu'."
And that immune system response could manifest in many ways, among them, of course, CIDP.
Saturday, June 19, 2010
sorry! i've been remiss in posting...
I've just found another blog, a good one: neuropathycaregivers.blogspot.com
I've been relatively stable for quite awhile now. But I've suffered one of the side effects of gabapentin: diarrhea. I had been taking gabapentin t.i.d. Neuro said to use Imodium. Internist was aghast. I cut out all fresh veggies. No help there. So I cut back on the gabapentin and that's kept the diarrhea manageable, that and very small salads. But with the cutback came the RLS -- big time! On the nights when that's really nasty, I cut in half a Vicodin I got from my daughter ( dental work for her ... she didn't use the med ) and that takes the edge off the RLS after 10-15 minutes.
I have an appointment with the neuro next week. I'll see what she says, though I doubt much will change.
Pinpricks in toes are kept at bay, as are the electric zingers in the hands. Thighs still burn. I notice less strength in my legs and arms. Am looking into a stationary bike ... I wonder if I'd use it faithfully?
Oh yes, and my toes feel like squishy grapes sitting on the ends of my feet. I have to laugh at that. : )
I've been relatively stable for quite awhile now. But I've suffered one of the side effects of gabapentin: diarrhea. I had been taking gabapentin t.i.d. Neuro said to use Imodium. Internist was aghast. I cut out all fresh veggies. No help there. So I cut back on the gabapentin and that's kept the diarrhea manageable, that and very small salads. But with the cutback came the RLS -- big time! On the nights when that's really nasty, I cut in half a Vicodin I got from my daughter ( dental work for her ... she didn't use the med ) and that takes the edge off the RLS after 10-15 minutes.
I have an appointment with the neuro next week. I'll see what she says, though I doubt much will change.
Pinpricks in toes are kept at bay, as are the electric zingers in the hands. Thighs still burn. I notice less strength in my legs and arms. Am looking into a stationary bike ... I wonder if I'd use it faithfully?
Oh yes, and my toes feel like squishy grapes sitting on the ends of my feet. I have to laugh at that. : )
Saturday, March 20, 2010
T-cells and CIDP?
I do not understand all of this, but my friend had AIDS and T-Cells were a huge issue for him. What does it mean for us? I will be sure to ask my neuro when next I see her.
Centre for Clinical Research, The Royal Brisbane and Women’s Hospital, The University of Queensland, Herston Road, Herston, Queensland 4029, Australia
Received 8 April 2009; accepted 6 July 2009. Available online 25 January 2010.
Abstract
Guillain-Barré syndrome (GBS) is an acquired demyelinating neuropathy, characterized by infiltration of peripheral nerves with macrophages and T cells. There have been reports of antibodies to glycolipids in GBS. We have previously found T cell reactivity to glycolipids in patients with the demyelinating form of GBS. This study was performed to characterize the cytokines produced by these T cells. Peripheral blood lymphocytes from patients with GBS, chronic inflammatory demyelinating polyradiculoneuropathy, healthy control patients and other neuropathies were incubated with the ganglioside GM1 and transferred to enzyme-linked immunospot plates. The average number per well of spot-forming cells (SFC) in the absence of antigen was counted. The average spontaneous SFC number was subtracted from the average SFC number in the presence of GM1, to produce a corrected SFC. There was significantly increased production of interferon-gamma but not interleukin-5 in response to stimulation with the ganglioside GM1. This could indicate that SFC have a role in pathogenesis of disease.
Centre for Clinical Research, The Royal Brisbane and Women’s Hospital, The University of Queensland, Herston Road, Herston, Queensland 4029, Australia
Received 8 April 2009; accepted 6 July 2009. Available online 25 January 2010.
Abstract
Guillain-Barré syndrome (GBS) is an acquired demyelinating neuropathy, characterized by infiltration of peripheral nerves with macrophages and T cells. There have been reports of antibodies to glycolipids in GBS. We have previously found T cell reactivity to glycolipids in patients with the demyelinating form of GBS. This study was performed to characterize the cytokines produced by these T cells. Peripheral blood lymphocytes from patients with GBS, chronic inflammatory demyelinating polyradiculoneuropathy, healthy control patients and other neuropathies were incubated with the ganglioside GM1 and transferred to enzyme-linked immunospot plates. The average number per well of spot-forming cells (SFC) in the absence of antigen was counted. The average spontaneous SFC number was subtracted from the average SFC number in the presence of GM1, to produce a corrected SFC. There was significantly increased production of interferon-gamma but not interleukin-5 in response to stimulation with the ganglioside GM1. This could indicate that SFC have a role in pathogenesis of disease.
Wednesday, February 3, 2010
something promising -- finally !!
well nigh unto a miracle, I'd say ...
there was nothing more than treating the beast prior to what this could mean.
__________
Blood-nerve barrier model allows closer look at diseases affecting peripheral nerves
HOUSTON -- (February 2, 2010) -- The cells regarded as the "gate-keepers" of the barrier between blood circulation and the peripheral nerves have been hard to study and even harder to isolate. However, researchers at Baylor College of Medicine have created a laboratory model that will enable scientists to study a wide variety of diseases affecting peripheral nerves.
They describe their model in the January 2010 issue of the Journal of Neuropathology and Experimental Neurology.
Specialized vascular system
"The barrier is known as the blood-nerve barrier and it regulates how peripheral nerves work. Peripheral nerves connect the central nervous system to the muscles of the limbs and sensory organs. This 'gate keeper' is a specialized vascular system that allows for proper nerve function by enabling the necessary nutrients in blood to flow in and unwanted material out," said Dr. Eroboghene E. Ubogu, assistant professor of neurology and director of the Neuromuscular Immunopathology Research Laboratory at BCM.
Ubogu, who is the senior author on the study, added that very little is known about how the human blood-nerve barrier normally works or how it is altered when the peripheral nerves are diseased. The cells that make up the blood-nerve barrier are hard to study and extract because they are surrounded by a large amount of connective tissue, are present deep within the innermost layers and represent less than 1 percent of all cells found in peripheral nerves.
Ubogu and his research colleagues, including lead author research assistant Nejla Yosef and Dr. Robin H. Xia, a postdoctoral research associate, both in the department of neurology at BCM, began by isolating these specialized blood vessel cells from the sciatic nerve, the largest nerve in the body found at the back of the thighs.
"It started as trial and error since methods for this type of work had not been outlined for human peripheral nerves," Ubogu said. "We looked at how other blood vessel and nerve cells were isolated from humans and other animals and modified those protocols until we achieved our goal."
It took more than six tries of a process involving multiple steps before Ubogu and his team were successful in isolating the blood vessel cells that make up the blood-nerve barrier.
Prior to developing the blood-nerve barrier model, Ubogu and his colleagues used several laboratory methods to verify that these specialized blood vessel cells, called primary human endoneurial endothelial cells, were the cells that formed blood vessels within the innermost layer of peripheral nerves.
Better view of diseases
These cells were grown in laboratory dishes, and used to develop a blood-nerve barrier model system that behaves very similar to what is seen or expected in humans. This model will allow researchers to study how substances dissolved in the bloodstream, large molecules, drugs, microorganisms and white blood cells are able to enter or exit the peripheral nerves and why their movements may be restricted or permitted in times of health or disease.
"We can now see the gate, and if we understand how it is locked, opened and closed, we may be able to treat certain nerve diseases more effectively or even prevent them," said Ubogu.
This model will give researchers a better view of how diseases such as HIV and diabetes affect the peripheral nervous system. Guillain-Barré syndrome and chronic demyelinating inflammatory polyneuropathy (peripheral nerve inflammation that leads to a loss of movement or sensation) are also disorders that can be further investigated because of this research. A better understanding of how drugs get into peripheral nerves is also possible with this model.
"I would like research collaborations to grow from these findings," Ubogu said. "The hope is that labs already studying peripheral nerve function and disease will be able to use the model to further their work."
All researchers are with the Neuromuscular Immunopathology Research Laboratory at BCM.
The study was supported Guillain-Barré Syndrome/Chronic Inflammatory Demyelinating Polyradiculoneuropathy Foundation International Research Grant and by the BCM New Investigator Start-Up Program.
there was nothing more than treating the beast prior to what this could mean.
__________
Blood-nerve barrier model allows closer look at diseases affecting peripheral nerves
HOUSTON -- (February 2, 2010) -- The cells regarded as the "gate-keepers" of the barrier between blood circulation and the peripheral nerves have been hard to study and even harder to isolate. However, researchers at Baylor College of Medicine have created a laboratory model that will enable scientists to study a wide variety of diseases affecting peripheral nerves.
They describe their model in the January 2010 issue of the Journal of Neuropathology and Experimental Neurology.
Specialized vascular system
"The barrier is known as the blood-nerve barrier and it regulates how peripheral nerves work. Peripheral nerves connect the central nervous system to the muscles of the limbs and sensory organs. This 'gate keeper' is a specialized vascular system that allows for proper nerve function by enabling the necessary nutrients in blood to flow in and unwanted material out," said Dr. Eroboghene E. Ubogu, assistant professor of neurology and director of the Neuromuscular Immunopathology Research Laboratory at BCM.
Ubogu, who is the senior author on the study, added that very little is known about how the human blood-nerve barrier normally works or how it is altered when the peripheral nerves are diseased. The cells that make up the blood-nerve barrier are hard to study and extract because they are surrounded by a large amount of connective tissue, are present deep within the innermost layers and represent less than 1 percent of all cells found in peripheral nerves.
Ubogu and his research colleagues, including lead author research assistant Nejla Yosef and Dr. Robin H. Xia, a postdoctoral research associate, both in the department of neurology at BCM, began by isolating these specialized blood vessel cells from the sciatic nerve, the largest nerve in the body found at the back of the thighs.
"It started as trial and error since methods for this type of work had not been outlined for human peripheral nerves," Ubogu said. "We looked at how other blood vessel and nerve cells were isolated from humans and other animals and modified those protocols until we achieved our goal."
It took more than six tries of a process involving multiple steps before Ubogu and his team were successful in isolating the blood vessel cells that make up the blood-nerve barrier.
Prior to developing the blood-nerve barrier model, Ubogu and his colleagues used several laboratory methods to verify that these specialized blood vessel cells, called primary human endoneurial endothelial cells, were the cells that formed blood vessels within the innermost layer of peripheral nerves.
Better view of diseases
These cells were grown in laboratory dishes, and used to develop a blood-nerve barrier model system that behaves very similar to what is seen or expected in humans. This model will allow researchers to study how substances dissolved in the bloodstream, large molecules, drugs, microorganisms and white blood cells are able to enter or exit the peripheral nerves and why their movements may be restricted or permitted in times of health or disease.
"We can now see the gate, and if we understand how it is locked, opened and closed, we may be able to treat certain nerve diseases more effectively or even prevent them," said Ubogu.
This model will give researchers a better view of how diseases such as HIV and diabetes affect the peripheral nervous system. Guillain-Barré syndrome and chronic demyelinating inflammatory polyneuropathy (peripheral nerve inflammation that leads to a loss of movement or sensation) are also disorders that can be further investigated because of this research. A better understanding of how drugs get into peripheral nerves is also possible with this model.
"I would like research collaborations to grow from these findings," Ubogu said. "The hope is that labs already studying peripheral nerve function and disease will be able to use the model to further their work."
All researchers are with the Neuromuscular Immunopathology Research Laboratory at BCM.
The study was supported Guillain-Barré Syndrome/Chronic Inflammatory Demyelinating Polyradiculoneuropathy Foundation International Research Grant and by the BCM New Investigator Start-Up Program.
Tuesday, January 12, 2010
it's been awhile...
I've been doing quite well, really. But now my arms have lost strength, so muscle mass must be waning there, too. Today my thighs aren't just "burning", they're very very painful, with jabbing pains. So while I thought I was in a slight remission, and I probably was in such, I am now obviously relapsing. Not unexpected, I suppose, but I'd pushed it to the back of my mind.
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