Refractory topiramate-induced angle-closure glaucoma in a man: a case report.

INTRODUCTION: Topiramate is a sulphonamide derivative indicated in the treatment of epilepsy and migraine. A known adverse affect is an idiosyncratic reaction that results in angle-closure glaucoma. We describe a patient with bilateral glaucoma related to topiramate that showed some unusual clinical features. CASE PRESENTATION: A 39-year-old Caucasian man presented with acute angle-closure glaucoma; he initially presented with intractable headaches after being treated with an escalating dose of topiramate. Clinical signs included elevated intraocular pressure that was initially refractory to treatment, shallow anterior chambers, and extensive bilateral choroidal effusions. After treatment with intravenous methylprednisolone, in conjunction with conventional glaucoma treatment, there was rapid reduction of intraocular pressure, gradual delayed resolution of the choroidal effusion and induced myopic shift; and eventually a good outcome without optic nerve damage. CONCLUSION: This case illustrates the importance of recognizing this entity in a non-ophthalmic setting and that intravenous methylprednisolone may be useful in the treatment of the condition when it is not responsive to conventional treatment. In addition, it is important to recognize that complete resolution of visual symptoms from the myopic shift may be delayed, despite normalization of intraocular pressure.

Tamoxifen increases methamphetamine-evoked dopamine output from superfused striatal tissue fragments of male mice.

The antiestrogen, tamoxifen (TMX), has been shown to function as a neuroprotectant against the nigrostriatal dopaminergic (NSDA) neurotoxin, methamphetamine (MA), within male mice. In the present report, we examined the effects of a combined infusion of TMX and MA within superfused striatal tissue fragments of male mice as an approach to understand some of the bases for TMX to function as a NSDA neuroprotectant within male mice. In Experiment 1, a coinfusion of TMX at 1, 10, or 100 pg/ml were all equally effective in increasing MA-evoked dopamine (DA) output as compared with a 0 pg/ml (control) dose. In Experiment 2, we tested whether this effect of TMX was specific for MA-evoked DA output by coinfusing TMX with a depolarizing concentration of potassium chloride (K+ -30 mM). No statistically significant differences were obtained between superfusions of striatal tissue fragments stimulated with K+ in the presence or absence of TMX (100 pg/ml). In Experiment 3, we assessed whether these effects of TMX may be exerted upon the dopamine transporter (DAT) by coinfusing DA (1 microM) in the presence or absence of TMX (100 pg/ml). No differences in DA recovery rates were obtained between superfusions performed in the presence or absence of TMX. Taken together, these results show that the striatum of male mice is very sensitive to the modulatory effects of TMX upon MA-evoked DA output. These effects of TMX appear to be relatively specific for MA-evoked DA output, as K+ -stimulated DA was not altered by TMX, and do not appear to exert these effects by altering dopamine transporter function.