e
aphagia. The same filling of the pyriform sinuses will be noted, but
as the larynx is usually anesthetic also, it may be that no cough is
produced when secretions overflow into it.

_Etiology_.--1. Toxic paralysis as in diphtheria.
2. Functional paralysis as in hysteria.
3. Peripheral paralysis from neuritis.
4. Central paralysis, usually of bulbar origin.
Embolism or thrombosis of the posterior cerebral artery is a
reported cause in two cases. Lues is always to be excluded as the
fundamental factor in the groups 3 and 4. Esophageal paralysis is not
uncommon in myasthenia gravis.

_Esophagoscopic findings_ are those of absence of the normal
resistance at the cricopharyngeus, flaccidity and lack of sensation of
the esophageal walls, and perhaps adherence of particles of food to
the folds. The hiatal contraction is usually that normally
encountered, for this is accomplished by the diaphragmatic
musculature. In paralysis of sensation, the reflexes of coughing,
vomiturition and vomiting are obtunded.

_Diagnosis_.--Hysteria must not be decided upon as the cause of
dysphagia, until after esophagoscopy has eliminated paralysis.
Dysphagia after recent diphtheria should suggest paralysis of the
esophagus. The larynx, lips, tongue, and pharynx also, are usually
paralyzed in esophageal paralysis of bulbar origin. The absence of the
cricopharyngeal resistance to the esophagoscope passed without
anesthesia, general or local, is diagnostic.

_Treatment_.--The internist and neurologist should govern the basic
treatment. Nutrition can be maintained by feeding with the
stomach-tube, which meets no resistance to its passage. Should this be
contraindicated by ulceration of the esophagus, gastrostomy should be
done.

LUES OF THE ESOPHAGUS

_Esophageal syphilis_ is a rather rare affection, and may show itself
as a mucous plaque, a gumma, an ulceration, or a cicatrix. Cicatricial
stenosis developing late in life without history of the swallowing of
escharotics or ulcerative lesions is strongly suggestive of syphilis,
though the late manifestation of a congenital stenosis is a
possibility.

_Esophagoscopic appearances_ of lues are not always characteristic. As
in any ulcerative lesion, the inflammatory changes of mixed infections
mask the basic nature. The mucous plaque has the same appearance as
one situated on the velum, and gummata resemble those seen in the
mucosa elsewhere. There is nothing characteristic in luetic