Contact lens-induced keratitis resembling central toxic keratopathy syndrome.

PURPOSE: To document a case of contact lens-induced keratitis resembling central toxic keratopathy syndrome. METHODS: A 23-year-old female developed an acute, central, stromal haze subsequent to soft contact lens overwear. Slit lamp examination revealed corrugated stromal "mud cracks," as seen in stage IV diffuse lamellar keratitis (DLK). This was accompanied by relative corneal thinning and flattening with a hyperopic shift of approximately 6 diopters. RESULTS: Eight weeks after discontinuing contact lens wear and after a 2-week tapering regimen of topical steroids, she had partial resolution of the central haze, partial increase in corneal thickness, steepness, and decrease in hyperopic shift. CONCLUSION: The authors present a case with a history of soft contact lens overwear and a clinical presentation notably similar to the central toxic keratopathy syndrome, which has recently been reported after laser refractive surgery.

Descemet detachment after femtosecond-laser-assisted placement of intrastromal ring segments in pellucid marginal degeneration.

We report the case of a 46-year-old man with pellucid marginal degeneration who had uneventful placement of Intacs intrastromal corneal ring segments (Addition Technology) in the left eye because of poor best spectacle-corrected visual acuity and contact lens intolerance. The IntraLase femtosecond laser (IntraLase Corp.) was used to create the channels for the 2 ring segments. Initially, there was subjective visual improvement and the Intacs segments were well positioned. One week after surgery, corneal edema secondary to a large inferior Descemet membrane detachment was seen. The Intacs segments were removed, and an air bubble was placed in the anterior chamber. The Descemet detachment did not resolve, and penetrating keratoplasty was eventually performed.

The therapeutic effects of intravitreal bevacizumab in a patient with recalcitrant idiopathic polypoidal choroidal vasculopathy.

We describe the clinical course of a patient with therapy refractory polypoidal choroidal vasculopathy (PCV) who was treated with intravitreal bevacizumab (IVB). Prior treatments included photodynamic therapy and intravitreal pegaptanib with poor therapeutic response. Within four weeks of follow-up after a single IVB, the visual acuity improved from count fingers to 20/400 coincident to resolution of subretinal fluid. The visual acuity demonstrated sustained improvement and the macula remained without exudation for 12 months post treatment. Intravitreal injection of bevacizumab should be studied as an effective and relatively inexpensive option for patients with active polypoidal choroidal vasculopathy.

A neurobehavioral systems analysis of adult rats exposed to methylazoxymethanol acetate on E17: implications for the neuropathology of schizophrenia.

BACKGROUND: As a test of plausibility for the hypothesis that schizophrenia can result from abnormal brain, especially cerebral cortical, development, these studies examined whether, in the rat, disruption of brain development initiated on embryonic day (E) 17, using the methylating agent methylazoxymethanol acetate (MAM), leads to a schizophrenia-relevant pattern of neural and behavioral pathology. Specifically, we tested whether this manipulation leads to disruptions of frontal and limbic corticostriatal circuit function, while producing schizophrenia-like, region-dependent reductions in gray matter in cortex and thalamus. METHODS: In offspring of rats administered MAM (22 mg/kg) on E17 or earlier (E15), regional size, neuron number and neuron density were determined in multiple brain regions. Spontaneous synaptic activity at prefrontal cortical (PFC) and ventral striatal (vSTR) neurons was recorded in vivio. Finally, cognitive and sensorimotor processes mediated by frontal and limbic corticostriatal circuits were assessed. RESULTS: Adult MAM-E17-exposed offspring showed selective histopathology: size reductions in mediodorsal thalamus, hippocampus, and parahippocampal, prefrontal, and occipital cortices, but not in sensory midbrain, cerebellum, or sensorimotor cortex. The prefrontal, perirhinal, and occipital cortices showed increased neuron density with no neuron loss. The histopathology was accompanied by a disruption of synaptically-driven "bistable membrane states" in PFC and vSTR neurons, and, at the behavioral level, cognitive inflexibility, orofacial dyskinesias, sensorimotor gating deficits and a post-pubertal-emerging hyper-responsiveness to amphetamine. Earlier embryonic MAM exposure led to microcephaly and a motor phenotype. CONCLUSIONS: The "MAM-E17" rodent models key aspects of neuropathology in circuits that are highly relevant to schizophrenia.

Prospective randomized trial of trimethoprim/sulfamethoxazole versus pyrimethamine and sulfadiazine in the treatment of ocular toxoplasmosis.

OBJECTIVE: To compare the efficacy of the classic treatment of ocular toxoplasmosis (pyrimethamine, sulfadiazine, and prednisolone) with a regimen consisting of trimethoprim/sulfamethoxazole (co-trimoxazole) plus prednisolone. DESIGN: Prospective randomized single-blind clinical trial. PARTICIPANTS: Fifty-nine patients with active ocular toxoplasmosis were randomly assigned to 2 treatment groups: 29 were treated with pyrimethamine/sulfadiazine, and 30 patients received trimethoprim/sulfamethoxazole. INTERVENTION: Treatment consisted of 6 weeks' treatment with antibiotics plus steroids. Antitoxoplasmosis antibodies (immunoglobulin M [IgM] and IgG) were measured using an enzyme-linked immunosorbent assay. MAIN OUTCOME MEASURES: Changes in retinochoroidal lesion size after 6 weeks' treatment, visual acuity (VA) before and after intervention, adverse drug reactions during follow-up, and rate of recurrence. RESULTS: Active toxoplasmosis retinochoroiditis resolved in all patients over 6 weeks' treatment, with no significant difference in mean reduction of retinochoroidal lesion size between the 2 treatment groups (61% reduction in the classic treatment group and 59% in the trimethoprim/sulfamethoxazole group, P = 0.75). Similarly, no significant difference was found in VA after treatment between the 2 groups (mean VAs after treatment were 0.12 logarithm of the minimum angle of resolution [logMAR] [20/25] in the classic treatment group and 0.09 logMAR [20/25] in the trimethoprim/sulfamethoxazole group, P = 0.56). Adverse effects were similar in both groups, with one patient in each suffering from any significant drug side effects. The overall recurrence rate after 24 months' follow-up was 10.16%, with no significant difference between the treatment groups (P = 0.64). CONCLUSIONS: Drug efficacies in terms of reduction in retinal lesion size and improvement in VA were similar in a regimen of trimethoprim/sulfamethoxazole and the classic treatment of ocular toxoplasmosis with pyrimethamine and sulfadiazine. Therapy with trimethoprim/sulfamethoxazole seems to be an acceptable alternative for the treatment of ocular toxoplasmosis.

Excimer laser surgery for correction of ametropia after cataract surgery.

PURPOSE: To review the cases of patients who had excimer laser refractive surgery to correct unintentional or undesired ametropia after cataract extraction with intraocular lens (IOL) implantation. SETTING: Wilmer Laser Vision Correction Center, Wilmer Eye Institute, Baltimore, Maryland, USA. METHODS: In this retrospective noncomparative review of consecutive cases, the Wilmer Laser Vision Correction Center's database was searched for patients who had laser in situ keratomileusis or photorefractive keratectomy to correct ametropia after cataract extraction with IOL implantation. RESULTS: Using the Visx Star excimer laser system (Visx, Inc.), 11 procedures were performed in 11 eyes of 10 patients a mean of 47 months (range 2 to 216 months) after cataract extraction with IOL implantation. Except for 1 patient with a silicone plate lens, all patients received 3-piece poly(methyl methacrylate) lenses. The mean age at time of excimer treatment was 75 years (range 70 to 81 years). Before laser surgery, the mean spherical equivalent of patient eyes was -3.76 diopters (D) +/- 2.50 (SD) (range -6.50 to +0.75 D), spherical refraction ranged from -9.00 D to plano, and the highest cylindrical refraction was +5.50 D. At last follow-up (mean 12.2 months; range 1 to 38 months), the mean manifest spherical equivalent was -0.88 +/- 1.43 D (range -2.75 to +2.13 D). Changes in mean manifest spherical equivalent were highly significant (P = .03, Wilcoxon signed rank test for paired values). There was no difference between targeted and achieved postoperative refraction (P = .34, Wilcoxon test). Increasing age was correlated with a hyperopic shift (r = 0.525, P = .05). All patients were satisfied with their final uncorrected visual acuity (UCVA), which improved in every case. Except for 1 patient in whom an epiretinal membrane developed, best spectacle-corrected visual acuity remained unchanged or improved. CONCLUSIONS: In this series of patients, who were a few decades older than the typical excimer laser candidate, laser refractive surgery was a safe, effective, and predictable method to correct ametropia after cataract extraction with IOL implantation. It may be a viable, noninvasive alternative to intraocular surgery, which has potential complications. Although satisfactory for all patients, final UCVA was not as high as that reported in laser refractive surgery patients in general, and this result may be because of prior cataract extraction with IOL implantation or increased age.