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wow i hope everything is ok and the emg is still normal i sure hate when neuros arent helpful, they just are blank.. really i guess bc they just dont know i had a muscle biopsy done last week, she told me sometimes its so early with symtoms starting off the test are just not sensitive to pick anything up yet, i read this on a site called the Awaji criteria something new that fascilitions can be used now to detect als without giveing false positve testing. you should give it a read very interesing.

You've misunderstood what you've read and oversimplified what you did understand of what you read. Fasciculations alone are not evidence of ALS because there are many kinds of fasciculations. There are specific type of fasciculations, combined with other electrophysiological evidence of denervation/renervation and clinical signs of lower motor neuron problems that combine to narrow the diagnostic field toward ALS, not just fasciculations alone.

The original El Escorial criteria for diagnosing ALS required some specific electrophysiological abnormalities -- fibrillations and positive sharp waves -- to be present to sustain the diagnosis of Laboratory Supported Probable ALS. Those abnormalities were not always detectable in some ALS patients, which prevented those patients from being able to participating in many clinical trials despite displaying obvious, unmistakable, and profound disability and progression caused by ALS. The Awaji criteria are designed to provide additional ways to conclude electrophysiologically that there is a neurogenic process at work in a given muscle.

For everyone else, especially the undiagnosed who might have been alarmed by munecagirl22's deceptive (wittingly or not) characterization of the Awaji criteria, here's a paper that explains the technical stuff that our hopelessly confused young lady left out.
 

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Am I reading that incorrectly (entirely possible) or does section 9.1 suggest that nerve conduction studies can help to diagnose upper motor neuron problems?
 
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Am I reading that incorrectly (entirely possible) or does section 9.1 suggest that nerve conduction studies can help to diagnose upper motor neuron problems?

Not the usual type of nerve conduction studies that are performed on the limbs, using the electrodes on the skin. The upper motor neurons are in your brain. The test described in section 9.1 uses magnetic fields on the skull to evoke an electrical signal in your brain that is sent from the upper motor neuron through the spinal cord to the lower motor neuron and out to the muscle, where it can be detected. Abnormal conductivity might reveal problems with the UMN, providing that everything else along the conduction path is functioning properly.

The standard NCV test that the neuro does won't help diagnose UMN problems and it's not designed to.
 
Good lord; never heard of that one before.
 
Trfogey, well thanks for a better understanding, i mean i read thru it and my understanding was differnt, but you correctd me so yah thanks for explaining it better. or how i misinterupted it, iam not the only one tho so i dont feel too bad

wow what a differnt ncv test ive not heard of that one either. wonder when drs use that one?
 
Trfogey: the Al Awaji criteria just says that fasciculations in a muscle in person with suspected ALS can be considered as indication of denervation - if there are clinical or other signs.

We therefore propose that the presence of fasciculation potentials
(FPs) in a muscle identified as showing needle EMG features of neurogenic change should serve as evidence of ongoing denervation, equivalent in importance to fibs-psw. This criterion would obviate the need for the often difficult search for fibs-sw in patients with clinically evident features of ALS; in particular, in cranial-innervated muscles and muscles of normal bulk and strength.


But again, person with fasciculations only or with non als specific changes does not have to worry:
Thus FPs only achieve diagnostic significance for ALS in the context of a clinically suspected
diagnosis.


E.g. if person has weakness and denervation in leg and arm and only fasciculations in trunk, according to El Escorial, it its not classified officialy as ALS. Instead Al Awaji recognizes that fasciculations in such a context are the same signifficance as fibrillations/PSW so one can get official ALS diagnosis earlier and so enroll to trials earlier.
If this is what you said, I am sorry, I did not get it from your post.
 
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Trfogey: the Al Awaji criteria just says that fasciculations in a muscle in person with suspected ALS can be considered as indication of denervation - if there are clinical or other signs.

Did you read section 4 of the document I linked, Blizna? Quoting from the document that I linked, section 4:

Although FPs have long been recognised as a characteristic feature of ALS, they can be seen in normal muscles (benign fasciculations) and they are not invariably noted in all muscles in ALS patients. However, there are certain features of FPs in ALS that confirm their importance and allow them to be distinguished from benign FPs. FPs associated with neurogenic disease, especially ALS, show a complex morphology, and often exhibit instability when studied with a high band pass filter and a trigger delay line, which reveals increased jitter with blocking of some components, indicating their origin from reinnervated motor units (Janko et al., 1989; de Carvalho and Swash, 1997). Although particularly characteristic of ALS, unstable FPs also occur in other progressive neurogenic disorders. In contrast, those seen in healthy muscles (benign fasciculations) are simple in morphology, are stable and are always recorded in the context of normal voluntarily activated MUPs. FPs therefore have a clear and relevant impact on the diagnosis of ALS , a feature long recognised in clinical neurology.

It is obvious that ALS cannot be diagnosed purely on the basis of a finding of FPs. Thus FPs only achieve diagnostic significance for ALS in the context of a clinically suspected diagnosis. Stable FPs of simple morphology occur in benign conditions, and FPs of complex morphology occur in many other neurogenic conditions ( Rosenfeld, 2000 ). The occurrence of FPs in other neurogenic disorders, for example in peripheral neuropathies, is an example of the importance of clinical context in diagnosis. This lack of specificity applies also to the presence of fibs-sw. While fibs-sw are never a benign finding they are found in any disease in which there is denervation or muscle damage. However, when FPs and/or fibs-sw are found in conjunction with chronic neurogenic abnormalities, in the context of a diffuse or root-related disorder with superimposed upper motor neuron signs, they assume critical significance and suggest ALS as the diagnosis. We recognise a theoretical possibility that utilizing FPs in this way in the diagnostic process may decrease the diagnostic specificity that a muscle is affected by ALS, but we note that the evidence suggests that this change in diagnostic criteria, applied to the existing Airlie House criteria, would allow patients to be appropriately diagnosed earlier in their disease course, so providing diagnostic clarity for those patients, who may be severely affected by the disease, but do not currently meet accepted EMG diagnostic criteria. We note also that, in general , abnormal spontaneous activity persists in weak muscles throughout the disease
course.

Finally, we stress that, since there is as yet no specific diagnostic test for ALS (Pradat et al., 2007), it is wise to reassess a diagnosis of ALS during the disease course, especially if there are any atypical features, or lack of
progression.

As I said in my previous post, the fasciculations that are to be used under the Awaji criteria are of a specific nature (complex waveform and unstable) and are accompanied by other EMG signs of chronic denervation/reinnervation (the large and giant MUPS, decreased recruitment, etc.), along with clinical signs of upper motor neuron problems.

So, to answer your initial statement, no, the report doesn't say that any type of fasciculation in a muscle is evidence of denervation in person with a suspected case of ALS -- it is much more restricted than that (specific types of fasciculations accompanied by electrophysiological signs of chronic denervation/reinnervation). See the guidelines in Table 1 of the paper -- #2 "EMG features of chronic neurogenic change must be found," and #4 "In the presence of chronic neurogenic change on needle EMG in ALS, fasciculation potentials (FPs), preferably of complex morphology, are equivalent to fibrillations and positive sharp waves (fibs-sw) in their clinical significance." Thus, the types of fasciculations typical of BFS -- stable, simple morphology, normal MUPs -- are, in fact, specifically excluded from the Awaji criteria, as are complex, unstable FPs unaccompanied by signs of chronic denervation/reinnervation.

Please note that the authors do not include any fasciculations in this category that are not detected by EMG and are merely visually observed. They are very precise in what they include and what they don't. We should respect that and we should neither put words in their mouths, nor oversimplify what they said to include things that they specifically excluded.

Hope that clears things up for you.
 
trfogey: Thanks, I have overlooked the fasciculations disctinction..strange still as previously papers said that its not possible to distinquish between malignant and benign fasciculations just based on their appearance.
I am still in touch with one of the Al Awaji criteria authors. dr. Carvalho, who spent so much time telling me what I have is benign that I have sent him a bottle of Becherovka (quite known in Europe :).
What I wanted to say was just that nobody should be scared as I know many people who were terrified when read that fasciculations can have the signifficance as psw/fibs.
Thanks for explanation ;)
 
This is a general comment about Awaji & how it applies to the undiagnosed:

My Neurologist is one of the authors of trfogey's link. I have several muscles with chronic denervation/reinervation (big MUPs &/or polyphasic MUPs) + visible fasciculations (clinically seen, but not detected on EMG). My neurologist confirmed that this is very favorable for me. As a result. my tentative diagnosis is Peripheral Nerve Hyperexcitability (Due to abnormal repetitive nerve stimulation) coupled with a Radiculopathy & another Polyradiculopathy (Due to the big/polyphasic MUPs). So, I can confirm that in the absence of fascics showing up on the EMG, they are treated as separate from the chronic neurogenic change (big/polyphasic MUPs). The tendency is to look for a common cause of multiple symptoms, but that is not always the case.

Take it from me...these are subtle nuances that will drive you crazy if you over-analyze. If you look at my earlier posts you will see examples of how a lack of general knowledge coupled with too much information can lead to unnecessary anxiety.

I'm not 100% worry-free, but I am 99.9% worry-free, which means that I have a much higher probability of being run over by a bus when I step outside the door today (and I live on a dirt road). Sometimes that 0.1% gets a bit bigger than it should, but I think it is human nature to fear the worst.

In my case, my neuro has left my diagnosis open-ended and will follow up with another EMG. This is very conservative & I'm hoping for a final diagnosis of Cramp Fasciculation Syndrome when I have my one-year follow up EMG on Oct 11th. Yes, I will be stressed when he sticks the needle into the muscles that I know had neurogenic changes... No I will not let this stress rule over my life for the next month.

I think it is fine to do research on medical problems, but try not to cherry pick symptoms & diagnostic results and make them fit in a box. As my knowledge has increased, my anxiety has decreased. Thanks to everyone on here who works to help me & my fellow sufferers of medical anxiety.
 
TRfogey, yes that is right thats how i was thinking in my mind the fasic depends on the MUP motor unit potentials so pretty much if you have them shown up like i had in mine, you can ask if when the fasci showed up with it just a little mup or a great big one... thats my intetterpation of it anyways

must be hard for neuros and others to diagnosis because really they have only one test to detect als, only one right now, and ofcourse a clinical exam, as someone stated before if its so east to detect we would all have an emg and be done with it. Or others who have a als diagnosis on clinical exam only with clear emgs early on in a diagnosis process... but rare dieases just dont get that sorta attention unfortunley:(.. hopefuly things will change.. nuero mucular. nervous system disorders, iam sure there are like many that people have (maybe myself included) who will never get a diagnosis and its something off the wall werid going on in our bodies..
 
munecagirl, please watch what you post. That line of "diagnosis of ALS and clear EMG" is just going to serve to terrify people needlessly. Those with a diagnosis of ALS don't have CLEAR EMGs. They might not all show the specific things one would expect--but they are not NORMAL EMGs.

Why do you persist in comments that seem intent on illiciting fear in others? Obviously, hundreds of comments to your multiple threads have not convinced you that a CLEAN EMG means no ALS--but don't spread your opinions as fact here, please.
 
Just to be clear, in my opinion...It is hard to diagnose ALS because they do not want false positives. Who wants to be given a death sentence & then have it reversed. Good in the end, but bad in the beginning. All possibilities must be exhausted before a diagnosis is given. Clearly there are UMN variants that are probably more difficult to pin down, but these are very rare.

However, if your neuro says no to ALS, unless s/he is totally incompetent then believe him/her. If you doubt the competence, then get a 2nd opinion & believe that Dr. Don't think that your self-diagnosis is better than theirs' based on some google searches.

If you still have unexplained symptoms after multiple opinions, please accept that an answer may not be there and shift your focus to the management of your symptoms. Most treatments are for symptoms not diseases, so regardless of having a disease name you can still treat the symptoms. If you can live with the symptoms, then live happily.
 
davegud,

It's good to see you back and thanks for relating your experiences with these issues. As always, I'm also hoping and praying that your October EMG continues to support the PNH/BCFS diagnosis.

munecagirl22,

A clinical neurological examination is a test and it will detect symptoms of ALS when the disease reaches the clinical level, so your statement that there is only one test for ALS is simply not true. A person with clinically suspected ALS will have pathologically abnormal reflexes. A person with clinically suspected ALS will have pathologically abnormal muscle tone. A person with clinically suspected ALS will have muscles that have pathologically abnormal problems with movement -- spasticity, weakness, uneven or absent ability to contract or stretch, inability to move a joint through its full range of motion.

A muscle biopsy is also a test that finds particular pathological problems that are specific to ALS, so we have a second instance that disproves your statement that there is no test for ALS. The muscle biopsy in an ALS patient will show particular muscle abnormalities, specifically a certain pattern of muscle atrophy.

Finally, there is the test of progression. Over time, ALS symptoms will get worse and they will move into other parts of the body. That progression is typically quite rapid. An afflicted limb can go from initial symptoms to profoundly crippled to total paralysis in a few months. All you have to do to verify that is to read some of the PALS and CALS stories around here. You'll see just how quickly limb problems go from minor annoyances to total disability with this disease. Perhaps then you'll understand why your complaints of having problems that haven't changed for nearly a year lead us to discount your claims that those problems sound "just like ALS." We've seen members go from mildly afflicted in one limb to total quadriplegia in a year, and it's very typical for us to see a person with a slightly weak grip in one hand completely lose the use of that hand and arm (and sometimes both arms) in a year, so your non-progressing issues just don't match up with what we know about ALS and MNDs.

I'll issue you the same challenge that I've issued to other hard-headed folks -- if you really are convinced that what you have is ALS or another MND, then stop reading about onset and diagnosis and start reading about the disease pathology and progression. If you do have ALS, it's information you need to know, so it won't hurt you to get a head start on it. And while you're reading and learning this new material, you'll have plenty of new signs and problems you can monitor yourself for.
 
. . . and for further clarification aimed at dispelling more misinformation disseminated by a certain individual on this forum who just won't GIVE IT A REST:

Fasciculations as seen on an EMG and the motor unit potential (MUP) have absolutely nothing to do with each other (i.e. one doesn't affect the other). They are measures of two completely different things.

Furthermore, MUP's are found on all EMG's (unless the muscle and nerve are completely destroyed). What distinguishes a normal MUP from an abnormal MUP is the size and duration of the MUP. On top of that, if the MUP is abnormal, it certainly doesn't mean someone has ALS; abnormal MUP's can happen for a gazillion different reasons (so too can fasciculations, by the way).


Andy

It's been awhile since I've heard from you. Hang in there and let me know if there is anything I can do to help. Take care in the meantime.
 
Good to be back Trfogey. I mostly lurk now just to keep tabs on the latest news. I'm also reassured by seeing how silly some people can be (like I was) stressing over the same things again and again that their Dr. already told them not to worry about.

On a side note: For anyone that wants the magnetic brain stimulation to test for UMN hyper-excitability, you'll have to travel to Australia...I don't recommend it. My Dr. had some experimental test that is only done in the UK. I participated in the test as an "independent researcher" for my curiosity only/ not for diagnostic purposes. I had hoped to be cleared of that last .1% of my worry. The test results were exactly half way between the normal control group and the ALS group... Within the confidence interval of either group.......... More tests does not = answers in every case.

Andy, sorry I'm hijacking your post. Good luck getting answers.
 
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