Q: Spasticity, tightness, and CPK

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meli

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Hello All:

I have a couple questions to clarify:

How does spasticity present itself in real life and how is it different from tightness?

Would ALS/MND present with normal CPK & Aldolase if one already feels a loss of strength in limbs? I feel loss of strength in all limbs/hips, but my CPK and Aldolase are in normal range.

Thank you
 
Meli,
I cam only amswer for me...I have (as of rifght now) Paramyotonia Congenita amd UMND. My spastivcity is contimnuous. Similar to people with CP. As of rigfht now, the Baclofen, flexceril, Soma amd Valium havbe not relieved amy of the spasms; but I believe has precvented newer ones to appear. I domn't know about my aldolase levbels (would havbe to look for those results); but my CPK levels were ogff the charts. I know it's not much but I hope this helps.
Kimnberluy
 
Hi-
How does spasticity present itself, how does it feel? I'm trying to figure out if the tight sensation in my hands/fingers- not smooth movement when opening and closing fingers, is spasticity?
 
I donm't have any movement left in my fimngers. On my right hanmd. the fingers are bent at the 2nd kniuclke under but on the othjer hand (no pun intemnded) they are more inm a grip position. If I rememnber right, the left hjand became swollen from lack of use and became difficult to opemn and close. But I also sufgfered a fall dowmn the stairs and broke the 3 middkle kmnuckles. Sorry, I can't help any fuirther.
 
Meli.
I just rereafd thje post and you kmnow the tendons amnd ligaments behind youur knee. Inagime them bent halfway and so tigfht you canm't move it either way. Are thjese spasms in just youur hamds?
 
Spasticity is defined as velocity dependent resistance to passive movement. In layman's terms, if you relax and someone else moves your arm or leg, it resists more the faster they move it. (The web has some good videos of "spastic clasp".) It happens because both the muscle that need to contract and the muscle that need to relax are both getting at least some "contract" signal from the spinal cord.

Obviously, that has effects on us in practice. Someone with spastic legs who tries to walk will fall sometimes, for the same reason that when two people wrestle and one let's go, the other goes flying. Even just the small leg movement to correct a bad step can spastic clasp - nothing happens then it goes all at once, and then you're on the ground. VERY spastic legs operate like walking on stilts, no bending is possible at all, and reduces you to waddling. Other joint spasticity has other effects on our day today. Some spasticity is based on your posture, and it can be used to work around weakness to do activities of daily living. So it is something we experience in many ways.

BUT the important thing to understand is that you can't tell if your stiffness is spastic without a (preferably trained) objective third party. No amount of description of what it feels like will get you there. Many doctors can also recognize a spastic gait, but because that isn't how spasticity is tested, they will still test you via passive movement.
 
What about CPK and Adolase, anyone? I read mixed information, if denervation is there, wouldn't these be abnormal? If denervation is happening, muscle fibers are dying, therefore abnormal values?

What other diseases cause denervation other than mnd/als?
 
hi mom-when I open and close my hands, my hands open and close in a um-smooth sort of manner and some of my finger joints feel tight upon opening and closing. No spasms, as in muscle spasms(if you mean like charlie horse). Just a tight/stiff sensation, even though I can open and close my hands.
 
hi tonahfang-
But why can't spasticity or tightness be differentiated by oneself. Shouldn't it be obvious when it's spasticity vs arthritis joint tightness for example?
I'm just trying to understand how those two are different, because I have daily tightness in both hands, more on right, feel tightness in some joints, while my pinky moves very un-smoothly (jerky movement) when I move it isolated (without moving all my fingers), but moves smoother when I open and close all my fingers at the same time.
 
meli,

There is a difference between "hypertonia", "spasticity" and "rigidity". These are three medical terms that describe three different situations that can appear similar to the untrained observer.

Testing for these conditions require the patient to be relaxed and passive so an accurate assessment can be made of all the movement issues in the muscles and joints. That's why you can't do it yourself.
 
What about CPK and Adolase, anyone? I read mixed information, if denervation is there, wouldn't these be abnormal? If denervation is happening, muscle fibers are dying, therefore abnormal values?

Not necessarily true. Reinnervation may be occurring which prevents the muscle fibers from breaking down.

Information on the CPK and aldolase tests from the MedlinePlus Medical Encyclopedia at n l m dot n i h dot g o v

"High CPK levels may be seen in patients who have:

* Heart attack
* Brain injury or stroke
* Inflammation of the heart muscle (myocarditis)
* Convulsions
* Delirium tremens
* Dermatomyositis or polymyositis
* Electric shock
* Lung tissue death (pulmonary infarction)
* Muscular dystrophies

Additional conditions may give positive test results:

* Hypothyroidism
* Hyperthyroidism
* Pericarditis following a heart attack
* Rhabdomyolysis"

and

"Greater than normal levels of aldolase may be due to:

* Damage to skeletal muscles
* Hepatitis
* Infectious mononucleosis
* Liver, pancreatic, or prostate cancer
* Muscular dystrophy
* Myocardial infarction
* Polymyositis"

Please note that conditions that cause muscle inflammation can also cause elevated CPK and aldolase -- note the presence of muscular dystrophy and polymyositis on both lists.

What other diseases cause denervation other than mnd/als?

Motor nerve denervation -- the only thing that comes to mind is polio. Various forms of mechanical entrapments or impingements can also cause it, along with direct trauma to the nerve itself. Any kind of neuropathy is probably capable of causing denervation.

However, what reason do you have to believe that denervation is going on? Your EMGs were clean.
 
Ok, so here is my best shot, Meli. I think you, and you're not alone in this, have a backwards perspective on spasticity. Spasticity is an external symptom of a particular kind of dysfunction in the spine.

Our spinal cords are the main wiring systems of the body, just like the electric wires strung along telephone poles outside your house are for your neighborhood. Now if your lights in your kitchen all turn off, that's a symptom of a problem. You can instantly perceive there is no light. But the cause of that no light isn't immediately obvious: did you blow a fuse? did your lightbulb die? did the wire to your house get cut by a storm? did you forget to pay your electric bill? or is your neighborhood out of power?

There is no amount of staring at the now-dark ceiling that will tell you that. Instead, you survey the situation. If most of your house has power, but your kitchen doesn't, you probably blew a fuse. If just the lightbulb is out, but the microwave is working, you need a new microwave. If your house is out, but your neighbors have power, you should be looking at your electric bill payments and the wire to your house. If no one in a three block radius has power, we can safely say that your house being out is part of a greater black out.

Tightness, stiffness, jerkiness: those are all symptoms, but they are as unspecific as your kitchen light going out. Your kitchen light will look just as dark no matter why it doesn't have power. Stiffness can be a joint problem, a muscle problem, a neurological problem, or a wearing overly tight gloves problem. Clinical tests are the survey that narrows down the cause of the symptoms.

Back to spasticity:

When you initiate a movement by thinking, two commands are sent out and down the spine. So if I do a bicep curl, a "contract" message is sent to my bicep, making it shorter, and pulling my arm up. For that to suceed, a complimentary "relax" message has to be sent to my tricep, telling it to become longer and looser. This basic contract-relax rythym is how every motor function in your body works.

Spasticity is a spinal problem, a problem in the wiring. When the upper motor neurons are damaged, they don't send those relax/contract messages properly, or in our power analogy: they don't power the bicep and turn the tricep off. Instead, a lot of unfiltered "sparks" of errant contract message/power are sent into the tricep. If your wiring isn't too busted, much more power will be sent to the bicep, so it'll win in the end, the limb moves, but stiffly or jerkily. That stiffness or jerky movement is what we get to see visibly of the poorly working invisible wiring in the spine.

That is why spasticity is measured by passive movement. Passive movement of a relaxed or paralyzed limb should be smooth. If there are all these sparks of contract/go juice, it isn't smooth, the tester has to overcome that flow of power into the muscle that should be relaxing. The faster he tries to move the limb, the harder it will resist. The problem the patient encounters isn't that velocity-dependent resistance itself, but rather the symptoms of the bad wiring it points to.

So all people who have spasticity share this spinal wiring breakdown. But how that looks and feels when we try to do stuff varies. For those of us with upper motor neuron diseases, our UMNs are dying a death by a thousand cuts. Our wires are frayed, insulation missing in many places. Like frayed wiring, our power signals are inconsistent, which means that how stiff we are can vary due to posture or external factors that change spinal position. (Think of tweaking the wire position of a poorly working computer mouse.) Where those thousand cuts are, how much signal they are blocking vs not blocking, no two of us would describe the end result the same way. So we can't tell you how spasticity "feels"... that is very dependent on our individual levels and locations of UMN damage. We aren't in the same boat because of how it feels, but because of the underlying damage to our spines that we share.

Contrast that with a bullet through the spine. If it leaves a small amount of motor pathway intact, that paraplegic may also have spasticity. For most of them, they limbs they have spasticity in are completely paralyzed, incapable of being used intentionally. But the same "go juice" spine malfunction we have they can share. They have no normal use of the limb, no proper signal at all, so spasticity in their life looks like sudden jittery rythmic motions of their legs or feet that knocks their feet off of wheelchair footplates, makes it hard to cath or put their socks on, etc. Bad spasticity for them can knock their whole wheelchair over backwards. In short, it looks nothing like it does for someone with an MND, but it is the same spinal condition. It tests the same way, and they take the same drugs.

So both me and my wheelchair basketball buddy both have spasticity. It looks completely different in each of us, because I have a disease that is killing my UMNs, whereas she got shot in the back 25 years ago. Looking at us, a layman would understandably not guess that the same name problem, the same underlying wiring damage, causes her legs to jitter in her wheelchair and mine to turn into unbendable stilts. Nor would we have ever known by swapping war stories. We each know we have spasticity because we went to a doctor and he explained to us that we were spastic, and how that could impact our day to day lives. It is a particular kind of damage to the spine that produces a speed based resistance to passive movement to everyone who has it, as well as a host of very varied inconveniences that aren't standard from person to person.

Does that clear it up?
 
tokah-Mostly., but, What is considered passive movement and which tests does the neuro do to see/diagnose spasticity? Tkanks.
 
TR- they were normal, but my body isn't. I guess I need more clarification in what an EMG (needle) points to vs what NCS (no needle) points to or point away from. I just want to understand. I keep reading that the needle portion EMG is the standard for looking at MND/als, but what is the NCS add to this study (as they are both done together). I also understand that NCS tests the motor and sensory nerves? EMG(needle) evaluates denervation, does NCS show denervation? Thanks.
 
as always beky you explain these things so well.

meli.
when my pt did my physio even if say one of my legs was relaxed as soon as she tried to move it it would just sieze up,my whole leg would just go rigid.
most of the time its just pain and stiffness of the muscles that i get with the spasms...........


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When you initiate a movement by thinking, two commands are sent out and down the spine. So if I do a bicep curl, a "contract" message is sent to my bicep, making it shorter, and pulling my arm up. For that to suceed, a complimentary "relax" message has to be sent to my tricep, telling it to become longer and looser. This basic contract-relax rythym is how every motor function in your body works
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but as becky said here (dont know how to do the quote thing)sometimes i can feel the spasticity in my legs and it feels like there are being squashed length ways...........stretching the legs really hard does relieve it for the few seconds i can hold the stretch.


as for ck levels ,mine were raised early on when i was tested but i dont know the relevance of this.
 
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