I think I finally came across some information that can help us feel potentially more at ease about the symptoms:
Reversible oropharyngeal dysphagia secondary to cricopharyngeal sphincter achalasia in a patient with myasthenia gravis: a case report
"Bulbar weakness and fatigue resulting in dysphagia and dysarthria is common in myasthenia gravis. In chronic MG it is often assumed that these symptoms herald an exacerbation of the patient's disease and doses of cholinergic agents and immunomodulatory therapies may be increased, along with initiation of plasma exchange. A case is presented in which dysphagia was refractory to standard MG therapy, leading to the subsequent discovery of cricopharyngeal sphincter achalasia as the primary cause of the patient's symptoms rather than an assumed myasthenia gravis exacerbation. The patient's dysphagia resolved after esophageal dilatation. Cricopharyngeal sphincter achalasia is a common disorder producing dysphagia in the elderly and needs to be considered in the evaluation of a myasthenic patient with worsening dysphagia when standard myasthenia gravis therapy fails. Discussion of myasthenia gravis, cholinergic therapy and cricopharyngeal sphincter achalasia is undertaken. Clinicians are encouraged to consider non-neurologic causes of worsening dysphagia in the myasthenic patient." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2827116/
Here's a video outlining Cricopharyngeal Sphincter Achalasia (not specifically from the perpective of MG but still educational): https://www.youtube.com/watch?v=qmY1XEOmm6s
On a personal note, doing a traditional barium swallow at the height of my symptoms did not catch any throat abnormalities.
According to some info I came across, the traditional barium swallow follows the bolus as it travels from mouth to stomach. But for MG'ers, the fluoroscopy camera focus needs to be on oral manipulation of the bolus. Without that distinction in how the exam is conducted, we're set up for another false negative test result. (Yet another example of the medical establishment's failure in the face of "MG: the best understood autoimmune disease".)
Here's an excerpt on how VFSS should be conducted for MG:
"Myasthenia gravis affects acetylcholine receptors at neuromuscular junctions and leads to severe muscle fatigue (8). Dysphagia should be provoked during VFSS by the administration of food materials or the use of procedures. Once the muscles are fatigued, VFSS may reveal slow, weak tongue movements, oropharyngeal pooling, reduced tongue base retraction, reduced epiglottic motility, delayed pharyngeal phase initiation, vallecular residue, and nasal regurgitation (30,37). Some patients may benefit from anticholinesterase or immunosuppressant medications (8). Xerostomia can be seen and further impairs chewing and swallowing (38). Eaton-Lambert syndrome is clinically similar to myasthenia gravis but is usually related to an underlying malignancy (8).
Abnormal swallowing in myasthenia gravis or Eaton-Lambert syndrome can be due to disrupted lingual propulsion, difficulty initiating the swallow, reduced epiglottic motility, vallecular residue, nasal regurgitation, and fatigue when stressed or repeatedly challenged to swallow." http://radiographics.rsna.info/content/26/1/e22.full
Finally, here are some of the terms I used if you want to continue researching on your own:
Generic term: neurogenic dysphagia. Apparent somewhat interchangeable terms: Cricopharyngeus Dysfunction, Cricopharyngeal spasm, Upper Esophageal Sphincter (UES) Dysfunction, Cricopharyngeal Sphincter Achalasia