PURPOSE: To report the long term results of bifocal treatment in nonrefractive accommodative esotropia and to analyze the changes of accommodative convergence to accommodation (AC/A) ratio. METHODS: Sixteen patients treated with bifocal glasses for at least 5 years were evaluated retrospectively. Angle of deviation at near and distance, refractive error, and AC/A ratio by the lens gradient method were analyzed. The changes of AC/A ratios were also compared after dividing the patients according to continuation or cessation of bifocal therapy. RESULTS: Six patients (38%; bifocal stop group, BSG) were able to stop using bifocal glasses at an average age of 10.8 years (range, 6.5 to 15.4 years) during their follow-up. However, the other ten patients (62%; bifocal continue group, BCG) had to continue using bifocal glasses until the final visit, which was 13.8 years on average (range, 11.3 to 18.5 years). The AC/A ratio decreased from time of bifocal prescription to the last visit in both groups, from 4.4 to 2.7 in the BSG and from 5.9 to 4.5 in the BCG. AC/A ratios were significantly higher (p = 0.03) in the BCG than that of the BSG from the beginning of bifocal treatment and this difference was persistent until the final visit (p = 0.03). CONCLUSIONS: The AC/A ratio decreased with age in both groups but was significantly higher throughout the entire follow-up period in the BCG. AC/A ratio at bifocal prescription could be an important factor in predicting response to bifocal treatment.
Accommodation, Ocular/*physiology ; Adolescent ; Child ; Cyclopentolate/administration & dosage ; Esotropia/*physiopathology/*therapy ; *Eyeglasses ; Female ; Humans ; Male ; Phenylephrine/administration & dosage ; Retrospective Studies ; Statistics, Nonparametric ; Tropicamide/administration & dosage

PURPOSE: To maximize effective use of mydriatic drugs through comparing the pupillary dilation effects between 1% tropicamide and 2.5% phenylephrine. METHODS: Fifty people requiring pupillary dilation were divided into 3 groups. Group 1 was treated with one drop of 1% tropicamide in the right eye and one drop of 2.5% phenylephrine in the left eye. Group 2 was treated twice during a 5-minute interval with 1% tropicamide in the right eye. Group 3 was treated twice during a 5-minute interval with 2.5% phenylephrine in the right eye. Groups 2 and 3 were treated with 2.5% phenylephrine and 1% tropicamide in the left eye, administered during a 5-minute interval. The pupillary size was measured in all groups for 40 minutes following eye drops administration. RESULTS: The mean patient age was 15.7 years. Group 1 included 10 patients, and groups 2 and 3 included 20 patients each. Eight patients in group 1 and 16 patients in group 2 developed a larger right pupil. Fourteen patients in group 3 developed a larger left pupil. CONCLUSIONS: Our study showed that 1% tropicamide, with its parasympathetic antagonistic mechanism of action, was more effective at inducing pupillary dilation than 2.5% phenylephrine, and the combination of 1% tropicamide and 2.5% phenylephrine was more effective than multiple drops of single eye drops.
Adolescent ; Adult ; Child ; Child, Preschool ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Female ; Follow-Up Studies ; Humans ; Male ; Muscarinic Antagonists/*administration & dosage ; Mydriatics/*administration & dosage ; Ophthalmic Solutions ; Phenylephrine/*administration & dosage ; Pupil/*drug effects ; Refractive Errors/diagnosis/physiopathology ; Retrospective Studies ; Tropicamide/*administration & dosage ; Young Adult

BACKGROUNDCa(2+) in the central nervous system plays important roles in brain physiology, including neuronal survival and regeneration in rats with injured facial motoneurons. The present research was to study the modulations of intracellular free Ca(2+) concentrations by cholinergic receptors in rat facial nucleus, and the mechanisms of the modulations.

METHODSThe fluorescence intensity of facial nucleus in Fluo-3 AM loaded acute brainstem slices was detected by applying intracellular free Ca(2+) measurement technique via confocal laser scanning microscope. The changes of fluorescence intensity of facial nucleus indicate the average changes of intracellular free Ca(2+) levels of the neurons.

RESULTSAcetylcholine was effective at increasing the fluorescence intensity of facial nucleus. Muscarine chloride induced a marked increase of fluorescence intensity in a concentration dependent fashion. The enhancement of fluorescence intensity by muscarine chloride was significantly reduced by thapsigargin (depletor of intracellular Ca(2+) store; P < 0.01), rather than Ca(2+) free artifical cerebrospinal fluid or EGTA (free Ca(2+) chelator; P > 0.05). And the increase of fluorescence intensity was also significantly inhibited by pirenzepine (M(1) subtype selective antagonist; P < 0.01) and 4-DAMP (M(3) subtype selective antagonist; P < 0.01). In addition, fluorescence intensity was markedly increased by nicotine. The enhancement of fluorescence intensity by nicotine was significantly reduced by EGTA, nifedipine (L-type voltage-gated Ca(2+) channel blocker), dihydro-beta-erythroidine (alpha4beta2 subtype selective antagonist), and in Ca(2+) free artificial cerebrospinal fluid (P < 0.01), but not in the presence of mibefradil (M-type voltage-gated Ca(2+) channel blocker) or thapsigargin (P > 0.05).

CONCLUSIONSThe data provide the evidence that muscarinic receptors may induce the increase of intracellular free Ca(2+) levels through the Ca(2+) release of intracellular Ca(2+) stores, in a manner related to M(1) and M(3) subtypes of muscarinic receptors in rat facial nucleus. Nicotine may increase intracellular free Ca(2+) concentrations via the influx of extracellular Ca(2+)+ mainly across L-type voltage-gated Ca(2+) channels, in a manner related to the alpha4beta2 subtype of nicotinic receptors.

Acetylcholine ; pharmacology ; Aniline Compounds ; administration & dosage ; Animals ; Brain Stem ; cytology ; drug effects ; metabolism ; Calcium ; metabolism ; Diamines ; pharmacology ; Facial Nerve ; cytology ; Female ; Fluorescent Dyes ; administration & dosage ; In Vitro Techniques ; Male ; Microscopy, Confocal ; Motor Neurons ; drug effects ; metabolism ; Muscarinic Agonists ; pharmacology ; Nicotine ; pharmacology ; Nicotinic Agonists ; pharmacology ; Piperidines ; pharmacology ; Pirenzepine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Cholinergic ; metabolism ; Receptors, Muscarinic ; metabolism ; Receptors, Nicotinic ; metabolism ; Tropicamide ; pharmacology ; Xanthenes ; administration & dosage