Muscle atrophy

Hi everyone

I am new to this forum but certainely not new to the disease! It all started about four years ago with severe fatique then nerve pain then hell looking for a diagnosis and going to tens of doctors...

Anyway due to late diagnosis I have reached a point where it's very difficult for me to walk without the help of someone else, my body is very weak. But since three or four months muscle atrophy has become very visible, especially in my hands, and feet up to my knees. Due to that distal amyotrophy I was convinced I had ALS as also had a lot of muscle twitches which I thought where the typical fasciculations. But due to my sensory symptoms the docs suspected somthing else and that's how CIDP was considered. I have not started treatment yet but I am curious to know: has anybody developped such muscle atrophy? I can't hold my feet straight I guess this is what they call foot drop but mine is clearly due to the atrophy of my ankles..

Thanks a lot for reading!

yes in both legs they have got very skinny and weak but they have started to get stronger with the IVIG treatments

I have atrophy in both thighs and my left arm. I've been going through IVIG and physio therapy but so far I can say it's doing much good. Gary


Yes I have lost considerable muscle mass in my calf muscles which has caused difficulty walking. The forward step we all take requires calf muscles. This "plantar flexion" is necessary to "push off" as you step. I also have the fasciculations. Two years ago this presentation (limping, muscle atrophy plus the twitching) caused one neurologist to suggest I had ALS (Lou Gehrig's). My other neurologist strongly disagreed and time has proven him correct. IVIG has slowed the progression to a "crawl". Specific exercises have helped me a lot. No loss of muscle mass anywhere else. Also, am easily fatigued, have numbness from my knees down but no pain so I am very blessed! mike 64y/o & diagnosed 28 mos ago.

Short answer - yes (lower legs). The battle now is to get those muscles active again without too much upset to the nerves. I was very lucky in that I got early diagnosis and start on IVIg - I still walk OK. BUT - not fast!

As part of my keeping track of progress I have some standard challenges for my legs. I did one yesterday - 25m at marching pace to check reactions. I paid for that for many hours (through the night even....). And that is why I walk slowly but I do believe the IVIg is improving my endurance.

For you - IVIg will (hopefully) stop the nerves getting worse - perhaps even get a little better - but like the others are saying - exercise is important even if it is just holding the muscles from getting worse. By far the biggest challenge is how to get that exercise within your limitations and without upsetting the nerves (too much).

Hang in there!

Thanks a lot everyone for your answers!!

Now my next question is: if CIDP causes that much weakness and muscle atrophy, how do they distinguish it from ALS?

There is a technical paper at . Let us know if you understand what it says.... LOL - good luck!

filmmaker said:

Thanks a lot everyone for your answers!!

Now my next question is: if CIDP causes that much weakness and muscle atrophy, how do they distinguish it from ALS?

Immune demyelinating Neuropathies. Although MMN and CIDP are both demyelinating neuropathies, the differences in their clinical, electrophysiological and immunologic features are more prominent than their similarities. MMN commonly presents with distal asymmetric weakness while in CIDP, proximal symmetric weakness is a more common finding. The remitting and relapsing course that may occur in CIDP is uncommon in the motor neuropathies. Patients with MMN rarely have significant sensory symptoms while in CIDP, sensory signs are the rule. Electrophysiological testing may show conduction block in both conditions. However, other features of demyelination such as prolonged distal latencies and slowed conduction velocities are more prominent in CIDP. Abnormalities in sensory nerve conduction studies are usually seen in CIDP, but not in MMN, unless complicated by another disease process. The spinal fluid examination shows markedly increased protein concentration in the majority of cases of CIDP while this change is rare in patients with MMN. High titer anti-GM1 antibodies as well as more specific patterns of autoantibody reactivity (see above) are common in MMN. In CIDP anti-GM1 antibodies are unusual. Serum autoantibody binding to tubulin is more common. Finally, differences in the frequency of therapeutic response to prednisone and plasma exchange (common in CIDP, but rare in motor neuropathies) define a practical difference in the management of the two disorders.

This is the piece that applies. Gary

thank you very much springmong!!!

Thank you to you both and filmmaker thank you for all your discribitions...then very helpful in understanding what is what and what is going on.


filmmaker said:

thank you very much springmong!!!

It's springmang. Gary -Also check Cochrane Summaries on line.