Myasthenia Gravis and preserved deep tendon reflexes, why?

Question

I saw a patient on rounds the other day w/ MG (Myasthenia Gravis) and it was mentioned that DTR (deep tendon reflexes) are preserved. I've been going over it in my head and I am confused why they would be preserved.

Textbooks are specifically pointing out that in classic MG, DTR is remained and therefore this is one of the findings that we can use to differentiate MG from Lambert–Eaton Myasthenic Syndrome. I am wondering why DTR is remained in classic MG?

ANSWER TO THE QUESTİON:

In MG as in LEMS the afferent limb of the reflex ark is unaffected as is the efferent up until the neuromuscular junction. The explanation of preserved reflexes in MG is that the initial barrage arrives at a rested neuromuscular junction. The initial release of acetylcholine is larger than later in a train of impulses and this is sufficient to overcome any deficit in the number of acetylcholine receptors. Only brief transmission is needed to provide the mechanical response, and this occurs before fatigability can set in. (Source: https://onlinelibrary.wiley.com/doi/abs/10.1002/mus.880180821

Answer 1

During your rotations you will notice that not every disease will show itself with the classic "Textbook" presentation (this actually very rare). Moreover MG can be considered a cluster of different diseases: because of different groups of muscles affected by the disease (e.g. ocular or generalized) or because of pathogenesis (anti achR, anti MusK etc. etc.) - You can read more about it here. So, your pathophysiological reasoning is correct: without any Ach (to be precise, without a satisfactory interaction between Ach and its receptor), you have no DTR. Still, in MG it can be very variable depending on the type of MG that the patient had, on the clinical phase the patient was going through (MG can have a relapsing remitting disease course, as in this case where patients were treated with azathioprine) and even on the medications the patient was on (such as Acetylcholinesterase inhibitors).

So, long story short: in medicine there's no absolute truth and no thing such as 100%. Every piece must be carefully placed in the big frame.

EDIT: I thought in the beginning that the question was going to be more general and less clinical. As of the clinical explanation to why in MG the DTR are spared (opposed to LEMS), here's a good neurophysiological basis for it:

In MG as in LEMS the afferent limb of the reflex ark is unaffected as is the efferent up until the neuromuscular junction. The explanation of preserved reflexes in MG is that the initial barrage arrives at a rested neuromuscular junction. The initial release of acetylcholine is larger than later in a train of impulses and this is sufficient to overcome any deficit in the number of acetylcholine receptors. Only brief transmission is needed to provide the mechanical response, and this occurs before fatigability can set in.

Source: https://onlinelibrary.wiley.com/doi/abs/10.1002/mus.880180821