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Mar 1, 2019
My understanding of Neudexta is that the dextromethorphan is what helps PBA. If dextromethorphan is the active ingredient in Neudexta, and quinidine is only there to slow the metabolism of the DM, shouldn't any sustained release form of DM be helpful? Quinidine interacts with other meds that can increase QT interval on ecg, and therefore increase risk of fatal arrhythmia. Also, the branded combination can be prohibitively expensive and present access obstacles for some pALS, as I have read in these forums.

Are there any users here with a pharmacology background who can set me straight? My understanding of the mechanism may be flawed. I plan on asking my neurologist when I see him in a few weeks, but I wonder if anyone here has any insight.

Has anyone tried an alternative like Delsym?
I heard it is more due to a better absorption with the quinidine but I never really explored that to validate.

My sister was told not to crush nuedexta ( which I think was incorrect) and took dextromethorphan. Her take was it helped but was not as effective as nuedexta.

Let us know what your neuro says
No, even "SR" DXM (the standard prep) is not going to yield the same exposure as Nuedexta (DXMQ). The label reports a study where the combo yielded 20x the exposure as DXM alone at Cmax, and TOXNET specifies > twice that for AUC.

DXMQ's DXM half life was ~13h, 7h for the quinidine. DXM unopposed has been clocked at 2-4 hrs.

The label also notes that "~7-10% of Caucasians and 3-8% of African Americans generally lack the capacity to metabolize CYP2D6 substrates and are classified as PMs <poor metabolizers>." It recommends that pts who could be at risk if exposed to quinidine undergo genotyping to determine if they are PMs. If they are, it would make no sense to start the drug since they could not expect benefit.

For those without pertinent risks, the supratherapeutic dosing studies seem fairly persuasive in terms of safety. Obviously the FDA thought so.
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I know of quite a few people who opted out of Nuedexta and are taking DM with success.

I have a heart arrhythmia so I was very interested in the posts I've read on other boards and on FB.

I guess, if and when the time comes, I'll try DM alone. Everyone is different. Even DM might set off SVT/PVCs in me which, in turn, cause me to choke and have irregular breathing.
Yup, DXM alone should have some efficacy -- that's the whole concept. Just that adding the low-dose quinidine gives you more.

The lowest oral dose available for quinidine otherwise is 100mg, which no one here should even consider taking. So Nuedexta, with exclusivity till 2026, though you might see an authorized generic sooner, is the only game in town for the 10mg dose for now.
Thank you all for your responses. I appreciate the anecdotal information as well as this reply that expanded my understanding. Not only does quinidine increase t1/2, but it does so by increasing blood levels of the DM. So the therapeutic level for PBA must be higher than that for cough suppression. It stands to reason!
There has to be other ways to induce/inhibit the cytochrome p450 system than potentially arrhythmogenic meds.
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Well, the data so far show suggest that the 10mg of quinidine should not induce arrhythmia in normal cardiovascular systems where any potential drug and condition interactions have been taken into account.

So for most PBA pts (and some other PALS with bulbar features who have tried it as well, based on available evidence), there seems to be a positive risk/benefit ratio.
Alright, in anticipation of neurologist visit I tried to get ecg. Although I made no voluntary movement, I had my usual amount of fasciculation. I think that, combined with skeletal muscle fibrillation created so much artifact as to render the ecg completely illegible. So QT interval was indeterminate.

my neurologist had a student with him, so I talked with him first. He was unaware that the quinidine is only in Neudexta to inhibit the CYP2D6 metabolism of DXM, but he was very willing to review all of my other meds for CYP2D6 metabolism, and as it turns out, I am taking some meds that are also substrates of that pathway, as well as a different med that is a moderate inhibitor of CYP2D6.

Mexiletine and metoprolol are substrates like DXM, whereas mirabegron is an inhibitor of CYP2D6 metabolism. My doctor was concerned about Rxing the Neudexta without an ecg, but I am already taking another med that acts like the quinidine component. Unfortunately, I do not have data to support it, but DXM alone may be adequate for me.

The moral of the story is be sure of EVERYTHING that all of your meds do. I may have supratherapeutic levels of Mexiletine and metoprolol, but thus far I'm tolerating it well. I am fortunate to not have had arrhythmia or bradycardia. Now that I understand my meds better, I may end up giving plain DXM a try for my PBA symptoms.
DrDark, when you write... "skeletal muscle fibrillation created so much artifact as to render the ecg completely illegible. So QT interval was indeterminate."

(EKG/ECG same)

Not being a doctor myself... are you referring to body wide fasciculation?
DrDark, when you write... "skeletal muscle fibrillation created so much artifact as to render the ecg completely illegible. So QT interval was indeterminate."

(EKG/ECG same)

Not being a doctor myself... are you referring to body wide fasciculation?

Hello, Clearwater. Fibrillation is a chaotic wave form observed when one traces the electrical activity in muscle tissue, like an ecg or an emg.

If someone is shaking, that creates a muscle artifact leading to squiggly lines on the EKG. Makes sense that fasciculations underneath the EKG leads could do this.

Dark, let us know how the DXM works for the PBA symptoms.

For those not familiar, some drugs can interfere with how heart muscle repolarizes (relaxes) after it contracts, and that is measured on the EKG by the QT interval. A longer interval can cause a dangerous heart rhythm called Torsades.

If someone is on drugs that interact in such a way as to raise blood levels of the drug that prolongs the QT interval, that could be problematic.
Karen, I was wondering if DrDark was having fasciculation of the trunk muscles.

I had an EKG and had a fasciculation in my left leg. The EKG came out normal...
I think.

I didn't know that fasciculation anywhere would effect heart rhythm. Thanks.

Ok, back to the very knowledgeable. :)
hello again, Clearwater. I was having fasciculation in my trunk and limbs. Fasciculation is picked up by the ecg, but it has nothing to do with the heart rhythm, that is why I called it " artifact." I was able to see one limb lead clearly, and it appeared to be a normal, sinus rhythm, but all of the other eleven leads looked like a complete staticky mess.
DrDark, it's good to have another person as knowledgeable as you seem to be
contributing to the Forum.

Do you have a medical background? Maybe share some of your background
with us...

Thanks for answering my question to Karen concerning the tubes that go
from the back of the throat to the inner ear (my words) in a previous
Hello, Clearwater. I owe you and Karen an apology for butting in. I saw a teachable moment and in my enthusiasm, I overlooked that you were specifically asking Karen. I am a physician and I miss teaching a lot.
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