Chemical structure of edrophonium
Find information on thousands of medical conditions and prescription drugs.

Edrophonium chloride

Edrophonium is a readily reversible acetylcholinesterase inhibitor. It prevents breakdown of the neurotransmitter acetylcholine and acts by inhibiting the enzyme acetylcholinesterase, mainly at the neuromuscular junction. more...

Home
Diseases
Medicines
A
B
C
D
E
E-Base
Ecstasy (drug)
Edecrin
Edrophonium
Edrophonium chloride
Efavirenz
Effexor
Eflornithine
Elavil
Eldepryl
Elidel
Eligard
Elitek
Elixomin
Elixophyllin
Ellagic acid
Elmiron
Eloxatin
Elspar
Emtriva
Emylcamate
Enalapril
Enalaprilat
Enalaprilat
Endep
Enflurane
Enoxaparin sodium
Entacapone
Enulose
Epi-pen
Epinephrine
Epirubicin
Epitol
Epivir
Epogen
Eprosartan
Ergocalciferol
Ergoloid Mesylates
Ergotamine
Eryc
Eryped
Erythromycin
Esgic
Eskalith
Esmolol
Estazolam
Estazolam
Estrace
Estraderm
Estradiol
Estradiol
Estradiol valerate
Estring
Estrogel
Estrone
Estrostep
Ethacridine
Ethambutol
Ethchlorvynol
Ethosuximide
Ethotoin
Etiracetam
Etodolac
Etopophos
Etoposide
Etorphine
Evista
Exelon
Exemestane
Hexal Australia
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z

Clinical uses

Because its duration of action is only about 10 minutes, edrophonium is used to differentiate myasthenic crisis from cholinergic crisis. In myasthenic crisis, where a person is not able to produce enough neuromuscular stimulation, edrophonium will reduce the muscle weakness. In a cholinergic crisis, where a person has too much neuromuscular stimulation, edrophonium will make the muscle weakness worse.

Edrophonium is available under the trade names Enlon (AstraZeneca), Reversol, and Tensilon.

Read more at Wikipedia.org


[List your site here Free!]


A posthemorrhagic mass, a contralateral polypoid mass, and unilateral laryngeal nerve paresis - Laryngoscopic Clinic - Brief Article
From Ear, Nose & Throat Journal, 2/1/02 by Yolanda D. Heman-Ackah

A 39-year-old female attorney came to the office for an evaluation of long-standing hoarseness (since childhood). She said she felt as though she needed to strain her voice in order to talk, and she complained of vocal fatigue, especially with prolonged speaking. She said that her voice had "never been normal." Even so, she had never had her voice or larynx evaluated prior to our examination.

The woman had been born via a normal vaginal delivery without the use of forceps, and she had no congenital disorders. She had experienced no significant medical illnesses or hospitalizations during her infancy and childhood. She had taken singing lessons for 6 months when she was 15 years old, but she had never received any formal speech therapy. As an adult, she described herself as a nonsinger.

The patient denied odynophonia, dysphagia, odynophagia, throat tickle, chronic cough, chronic throat clearing, and heartburn. Her medical history included mild asthma as a child and a 7-year history of ocular migraines. She had had two pregnancies, both of which culminated in cesarean sections; during one of them, she delivered fraternal twins. Her surgical history included an abdominoplasty. She was allergic to penicillin, she was not taking any medications, and she denied the use of alcohol, tobacco, and recreational drugs.

On examination, her voice was slightly hoarse and slightly breathy. Strobovideolaryngoscopy revealed several laryngeal abnormalities. There was a moderate degree of supraglottic hyperfunction that improved slightly with a voluntary increase in pitch. Abduction was normal bilaterally, but adduction was slightly sluggish on the right and variable on the left. Longitudinal tension was variably sluggish on both sides. The arytenoids and posterior laryngeal mucosa were normal. At the midpoint of the vibratory margin of the left vocal fold, there was a broad-based, ill-defined, fibrotic, posthemorrhagic, vascularized mass (figure 1). There was diffuse stiffness at its base that resulted in a moderately decreased mucosal wave amplitude and waveform in the middle and posterior thirds of the musculomembranous vocal fold. On the right vocal fold, there was a softer, polypoid mass that featured an area of ectasia (figure 2). This mass was also centered in the striking zone, slightly anterior to the mass on the left voca l fold. The mucosal wave on the right was mildly decreased in amplitude and waveform in the middle third of the musculomembranous vocal fold.

The variability in vocal fold mobility was consistent with bilateral paresis, neuromuscular junction dysfunction, or compensatory hyperfunction in response to unilateral paresis. Laryngeal electromyography showed a 20% decreased recruitment response in the left cricothy-roid muscle, which did not improve with Tensilon (edrophonium chloride) testing. These findings were consistent with a left superior laryngeal nerve paresis with compensatory hyperfunction.

The patient underwent voice therapy to strengthen the paretic muscle group and to relieve the compensatory muscle-tension dysphonia. She was happy with her post-therapy voice results. Resection of the vocal fold masses was not performed, and it will be considered only if the patient again becomes dissatisfied with her voice.

From University of Illinois at Chicago (Dr. (Heman-Ackah), Thomas Jefferson Hospital (Ms. Cooney), and the Department of Otolaryngology--Head and Neck Surgery, Thomas Jefferson University, Philadelphia (Dr. Sataloff).

COPYRIGHT 2002 Medquest Communications, Inc.
COPYRIGHT 2002 Gale Group

Return to Edrophonium chloride
Home Contact Resources Exchange Links ebay