What other diseases cause muscle wasting in multiple regions of the body?

[gracefullyteaching]

Just curious if anyone knows off the top of their head. Thanks, have a good day!

 

[trfogey]

Various muscular dystrophies and myopathies. Cancer. AIDS. Congestive heart failure. COPD. Anorexia. Inactivity. Various rare neuropathies, usually genetic in origin.

Why do you ask?

 

[trfogey]

Also, Guillan-Barre syndrome and polio.

 

[gracefullyteaching]

Thank you, trfogey. I ask because when I last spoke with the MS specialist by phone, he said that people with MS don't lose muscle. As I pondered the statement today, I thought to ask on the forum.

 

[Alyoop]

The ms specialist is spot on. Wasting only comes when the disease is advanced, and caused by lack of use. Not the atrophy that is seen in als.

 

[trfogey]

The ms specialist is spot on. Wasting only comes when the disease is advanced, and caused by lack of use. Not the atrophy that is seen in als.

No offense intended, Alyoop, but that seems like a distinction without a difference to me. Muscles start atrophying in MNDs after paralysis sets in. By definition, a paralyzed muscle is unable to be used, so you have atrophy from lack of use going on there as well. It's simply occurring at the fascicle level as opposed to the whole muscle at once (as in immobilization atrophy).

If the fascicle gets renervated (the early stages of ALS), the paralysis lifts, the fascicle is usable again, and some of the atrophy may be recovered. If the fascicle doesn't get renervated (the advanced stage of ALS, from the fascicle's point of view), the muscle fibers of the fascicle continue to atrophy until they're fully wasted.

Of course, I could just be nitpicking, but it seems to me that atrophy should be considered a manifestation of "advanced" stage for either disease, at least at the micro level.

 

[Robynnblue]

No offense intended, Alyoop, but that seems like a distinction without a difference to me. Muscles start atrophying in MNDs after paralysis sets in. By definition, a paralyzed muscle is unable to be used, so you have atrophy from lack of use going on there as well. It's simply occurring at the fascicle level as opposed to the whole muscle at once (as in immobilization atrophy).

If the fascicle gets renervated (the early stages of ALS), the paralysis lifts, the fascicle is usable again, and some of the atrophy may be recovered. If the fascicle doesn't get renervated (the advanced stage of ALS, from the fascicle's point of view), the muscle fibers of the fascicle continue to atrophy until they're fully wasted.

Of course, I could just be nitpicking, but it seems to me that atrophy should be considered a manifestation of "advanced" stage for either disease, at least at the micro level.

Not trying to butt in but I guess I am a little, but I always thought once you began to atrophy with ALS, there was no turning back, or am I mis-interpreting what you said trfogey?

Just being my curious self

Robynn:-D

 

[Alyoop]

No your not nit picking. I am just crap at explaining myself. You should know that by now
Robyn just posted while I was writing this ( and icing a cake) and like her I was not aware that paralysis can lift.

 

[Alyoop]

Now I am confused. I asked my husband to read your post trfogey and he said the words sound right if you look at the definition as you wrote it, but the rest of what you wrote was........not going to use his words. Now he has left to have a drink with a mate. I am sitting here laughing, cause I don't know squat

So I will just finish icing my cake and keep out of it.

Aly

PS he was equally as verbal about the "rubbish I had written". Now I am grumpy

 

[trfogey]

Not trying to butt in but I guess I am a little, but I always thought once you began to atrophy with ALS, there was no turning back, or am I mis-interpreting what you said trfogey?

The scale of atrophy I'm talking about is very small -- at the individual muscle fiber level. Here's a very oversimplified explanation for what I mean.

Your muscles are made up of lots of individual fibers. Those fibers are organized into bundles called fascicles. Each fascicle (the root word, by the way, from which "fasciculation" is derived) is connected to nerve fibers from a single lower motor neuron, which tells each individual fiber to contract and when to stop contracting. The LMN-muscle fiber fascicle combination is referred to as a motor unit. The LMN, in turn, is also connected through the spinal cord to an upper motor neuron (in the primary motor cortex of the brain).

As well as I understand it, when a LMN dies, the muscle fascicle it controlled is paralyzed and unable to be used. That means that a number of muscle fibers no longer can get the signal to contract and relax. According to the materials I've read, two things start happening.

First, the body attempts to repair the damage when neighboring LMNs attempt to extend nerve fibers to the "orphaned" muscle fibers. If successful, those muscle fibers are reinnervated and come back online. One of the theories about fasciculations is that they may be the result of these reconnection efforts.

Of course, there's no guarantee that all of the paralyzed muscle fibers will get reinnervated by the neighboring motor neurons, so the more LMNs you have to do the job, the greater the likelyhood of a complete recovery from the denervation. More on that later.

Second, the body starts to reclaim the materials of the muscle fibers that are no longer in use. Some studies have shown that disuse atrophy can begin setting in within hours of the muscle fibers becoming immobilized. And, as anyone who's had a broken limb immobilized in a cast for a few weeks can tell you, it doesn't take long to lose a substantial amount of muscle bulk.

So, you've got two opposing processes occurring simultaneously. In the early stages of ALS, the vast majority of denervated muscle fibers get reinnervated, so apparent atrophy is minimal or non-existent. But, as more LMNs die off, there are fewer remaining LMNs to reinnervate the paralyzed fascicles and the tide slowly turns toward permanent denervation with the consequent permanent paralysis and atrophy.

As I said, oversimplified, but hopefully I didn't make any egregious mistakes. Here's a link that says it better than I did.

Denervation atrophy

 

[trfogey]

Now I am confused. I asked my husband to read your post trfogey and he said the words sound right if you look at the definition as you wrote it, but the rest of what you wrote was........not going to use his words. Now he has left to have a drink with a mate. I am sitting here laughing, cause I don't know squat

So I will just finish icing my cake and keep out of it.

Aly

PS he was equally as verbal about the "rubbish I had written". Now I am grumpy

Somehow, I'm not surprised, :lol: but I'd be interested in what I got wrong, from his point of view. PM it to me if you want, or post it here -- I'm a big boy and can take it. Besides, I'd prefer to learn the right answer.

Especially since I've got a much longer answer to Robynnblue waiting for the moderators' attention that I may have to eat my words on.

 

[olly]

i have odd areas of atrophy..............dont know if its used,disused or partly used:roll:

 

[Kitchener]

Trfogey outlines it pretty much as I understand it. However, the practical impact of this is not that one gets weak with the initial denervation, stronger with the re-inervation, then weak again. Rather it is the re-inervation process that delays the observable impacts of paralysis and atrophy. This is one thing the EMG is looking for and why we take the test. Basically the body is fighting a rear-guard action against the ALS process. When your first battalion of LMN fall, the neighbouring units send over re-inforcements (re-inervation) and the muscle unit continues to operate as normal (patients don't know anything is happening at this stage). This continues until the attacking ALS process gets the upper hand, and eventaully there are too few LMN survivors to hold the fort. The muscle is left with too few neurons effectively attaching to it, with many fascicles or units cut off from their neurons. n this environment they are paralysed as they get no nerve signals, and can't contract or relax. The body recognises that paralysed muscle fibres aren't much good, and reclaims the constituents and so the muscle atrophys, or wastes away. Apologies for mixing medical and military metaphors, bu they are my two biggest interests right now!

 

[gracefullyteaching]

Excellent information, thank you, all.

 

[Alyoop]

Trfogey, I am not going to ask him, he was scathing of both of us and told me he was not going to answer any questions. I was kinda glad he went for a drink. You may be a big boy, but I am not a big girl. lol your explanation makes sense to me. Which I gather is not saying much.