Bilateral sixth nerve palsy.
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Abducens Nerve Diseases↗
Biomedical subjects
Robert J Casson
Publications and source records attributed to Robert J Casson.
Effect of cataract on frequency doubling perimetry in the screening mode.
PURPOSE: To determine the effect of cataract on frequency doubling perimetry in the screening mode. METHODS: Frequency doubling technology perimetry in the C-20-5 screening mode was performed prospectively on 34 patients with otherwise healthy eyes before and after phacoemulsification. Cataracts were scored using the LOCS III classification, and the number of missed points (at any level of severity) on the screening field was compared before and after surgery. RESULTS: Nine patients missed at least one point pre-operatively and had no misses post-operatively. Those patients with posterior subcapsular (PSC) cataract were significantly more likely to miss points on the screening frequency doubling technology perimetry than those without posterior subcapsular cataracts (P < 0.001; Fisher exact test). In addition, the degree of posterior subcapsular cataract strongly correlated with the number of missed points pre-operatively (r = 0.97). The degree of nuclear sclerotic cataract did not correlate strongly with the number of missed points (r = 0.26), but the correlation was slightly stronger in the presence of cortical cataract (r = 0.36). CONCLUSION: Advanced age-related cataracts may cause false positive results on the screening frequency doubling technology, and the presence of even mild posterior subcapsular cataract may be a cause of false positive results and should be taken into consideration when interpreting the screening frequency doubling technology perimetry results.
Aged↗
Prevalence of trachoma among a group of Aboriginal school children in remote South Australia.
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Adolescent↗
Refractory glaucoma--here there be dragons.
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Ciliary Body↗
Lash ptosis caused by latanoprost.
PURPOSE: To report a case of lash ptosis caused by latanoprost. DESIGN: Observational case report. METHODS: Retrospective chart review. RESULTS: A 61-year-old, ocular hypertensive man who was using latanoprost OU presented with trichomegaly and bilateral lash ptosis. The lash ptosis had not resolved 6 months after stopping latanoprost, and anterior lamellar repositions were performed. At last follow-up, 8 months after surgery, the lids were in a normal position, but the trichomegaly had reduced only slightly. CONCLUSIONS: Lash ptosis should be considered as a possible complication of latanoprost therapy.
Antihypertensive Agents↗
Monocarboxylate transporter expression remains unchanged during the development of diabetic retinal neuropathy in the rat.
PURPOSE: To determine the effect of diabetes on monocarboxylate transporter (MCT) expression in the rat retina. METHODS: Diabetes was induced in Wistar rats by a single intraperitoneal injection of streptozotocin (62.5 mg/kg). Rats were killed after 10 weeks, and the retinal levels of PKCalpha, bFGF, glial fibrillary acidic protein (GFAP), caspase-3, and MCT1, -2, and -4 were assessed with immunoblot analysis and RT-PCR. Hippocampal samples were used as a comparison. In other animals, the retinas were processed histologically and sections stained for the breakdown of DNA (TUNEL procedure) and for the distribution of MCT1, -2, and -4. RESULTS: Diabetic rats exhibited cataract formation, elevated blood glucose levels, and polydipsia. Retinal levels and distribution of MCT1, 2, and -4 were similar in the diabetic and age-matched control groups; however, the early retinopathy markers bFGF and PKCalpha were significantly elevated in the diabetic retinas but not in the hippocampal samples. ERG recordings showed decreased oscillatory potentials in the diabetic group, and TUNEL staining was most evident in the photoreceptor layer. Activated caspase-3 levels were elevated in the diabetic retina. CONCLUSIONS: The expression of retinal MCT1, -2, and -4 is unaffected after 10 weeks of diabetes in rats. It appears unlikely that diabetic retinal neuropathy is a result of a hyperglycemic induction of altered MCT expression.
Animals↗
The effect of hyperglycemia on experimental retinal ischemia.
OBJECTIVE: To determine the effect of hyperglycemia and intraocular glucose delivery on ischemic retinal injury. METHODS: Experimental diabetes was induced in age- and sex-matched Wistar rats by an injection of streptozocin. The functional and structural retinal injury in these rats after a period of pressure-induced retinal ischemia was compared with the injury in appropriate controls and with rats made hyperglycemic by an injection of systemic glucose. The effect of high intraocular pressure-induced ischemia with the use of several different isotonic substrates in the elevated reservoir (isotonic sodium chloride solution, glucose, 2-deoxyglucose, and lactate) was also determined. Electroretinography, reverse transcriptase polymerase chain reaction, and histologic examination were used to assess the retinal injury. RESULTS: Streptozocin-induced diabetes, glucose injection-induced preexisting hyperglycemia, and intraocular glucose delivery during ischemia markedly reduced the functional and structural ischemic retinal injury. Neither postischemic hyperglycemia nor the intraocular delivery of lactate significantly affected the ischemic injury; however, the intraocular delivery of 2-deoxyglucose significantly exacerbated the retinal injury. CONCLUSION: Preexisting hyperglycemia and the intraocular delivery of glucose markedly attenuate ischemic retinal injury. Clinical Relevance These findings highlight fundamental differences in energy metabolism between brain and retina, have important implications for the pathophysiology of diabetic retinopathy, and may lead to novel therapeutic strategies for ischemic retinopathies.
Animals↗
Retinal ischemia: mechanisms of damage and potential therapeutic strategies.
Retinal ischemia is a common cause of visual impairment and blindness. At the cellular level, ischemic retinal injury consists of a self-reinforcing destructive cascade involving neuronal depolarisation, calcium influx and oxidative stress initiated by energy failure and increased glutamatergic stimulation. There is a cell-specific sensitivity to ischemic injury which may reflect variability in the balance of excitatory and inhibitory neurotransmitter receptors on a given cell. A number of animal models and analytical techniques have been used to study retinal ischemia, and an increasing number of treatments have been shown to interrupt the "ischemic cascade" and attenuate the detrimental effects of retinal ischemia. Thus far, however, success in the laboratory has not been translated to the clinic. Difficulties with the route of administration, dosage, and adverse effects may render certain experimental treatments clinically unusable. Furthermore, neuroprotection-based treatment strategies for stroke have so far been disappointing. However, compared to the brain, the retina exhibits a remarkable natural resistance to ischemic injury, which may reflect its peculiar metabolism and unique environment. Given the increasing understanding of the events involved in ischemic neuronal injury it is hoped that clinically effective treatments for retinal ischemia will soon be available.
Animals↗
The effect of retinal ganglion cell injury on light-induced photoreceptor degeneration.
PURPOSE: To determine the effect of optic nerve transection (ONT) and excitotoxic retinal ganglion cell (RGC) injury on light-induced photoreceptor degeneration. METHODS: Age- and sex-matched rats underwent unilateral ONT or received intravitreal injections of N-methyl-D-aspartate (NMDA). The fellow eye received sham treatment, and 7 or 21 days later each eye was subjected to an intense photic injury. Maximum a- and b-wave amplitudes of the flash electroretinogram (ERG) were measured at baseline, after the RGC insult, and 5 days after the photic injury. Semiquantitative reverse transcription-polymerase chain reaction analysis and immunoblot analysis were used to assess rod opsin mRNA and rhodopsin kinase protein levels and to measure defined trophic factors 7 or 21 days after ONT or injection of NMDA. Structural changes after the insults were determined histologically and immunohistochemically. RESULTS: ONT caused time-dependent reductions in the mean a- and b-wave amplitudes. Seven days after intravitreal NMDA the b-wave amplitude was reduced, but the a-wave was unaffected. ONT and NMDA injection attenuated the light-induced reductions in the a- and b-wave. Rod opsin mRNA levels and rhodopsin kinase protein levels were also significantly greater in the axotomized and NMDA-treated eyes compared with the sham-treated fellow eyes after the photic injury. Structural protection in the RGC-injured eyes was also evident histologically. Fibroblast growth factor (FGF)-2, ciliary neurotrophic factor (CNTF), and glial fibrillary acidic protein (GFAP) were significantly upregulated after ONT and NMDA. CONCLUSIONS: ONT and intravitreal injection of NMDA protect against subsequent photic injury. This protection may relate to the activation of retinal glial cells and the possible action of trophic factors such as FGF-2 and CNTF.
Animals↗
The monocarboxylate transport inhibitor, alpha-cyano-4-hydroxycinnamate, has no effect on retinal ischemia.
Glial-derived monocarboxylate lactate is thought to be an important energy source for neurons during brain activation or in hypoxia-ischemia. Treatment with alpha-cyano-4-hydroxycinnamate (4-CIN), a monocarboxylate transporter inhibitor, has been recently reported to exacerbate delayed neuronal damage in a rat model of cerebral ischemia, an effect ascribed to inhibition of lactate/pyruvate transport. Since monocarboxylate transporters are abundant in the retina, we examined the effect of 4-CIN administration on the outcome of high intraocular pressure-induced retinal ischemia in rats. Retinal ischemic damage was assessed by changes in the electroretinogram (ERG), the retinal localization of choline acetyltransferase (ChAT) and neuronal nitric oxide synthase (nNOS) immunoreactivities, and the loss of retinal mRNA for Thy-1. Intraperitoneal or intravitreal administration of 4-CIN had no effect on the ERG or the localization of ChAT and nNOS immunoreactivities in either the control retina or a retina subjected to ischemia/reperfusion. In addition, intravitreal injection of 4-CIN had no effect on ischemia-induced reduction of retinal mRNA levels for Thy-1. These results provide no evidence to support the view that blockade of lactate uptake and/or pyruvate entry into mitochondria for oxidative metabolism has an influence on the outcome of retinal ischemia/reperfusion.
Animals↗
The effect of ischemic preconditioning on light-induced photoreceptor injury.
PURPOSE: To determine whether ischemic preconditioning (IPC) upregulates certain retinal survival factors and to assess the protective effect of retinal IPC against light-induced photoreceptor degeneration. METHODS: Albino rats underwent IPC induced by raising the intraocular pressure in one eye to 120 mm Hg for 5 minutes. The fellow eye underwent sham treatment. Basic fibroblast growth factor (bFGF), ciliary neurotrophic factor (CNTF), brain-derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), and Bcl-2 were measured after 6 and 48 hours, by the reverse transcription-polymerase chain reaction and immunoblot analysis. Other preconditioned rats received 48 hours of photic injury (2000 lux) 24 hours after IPC. The a- and b-wave amplitudes of the flash electroretinograms were measured 5 days later, followed by analysis of rhodopsin mRNA levels and histology. The influence of adenosine A1 receptor blockade was assessed. RESULTS: bFGF, GFAP, and Bcl-2 were upregulated after IPC. BDNF was not upregulated. The marked reduction of the a- and b-wave amplitudes and the structural injury to the photoreceptors induced by the photic insult were significantly reduced by IPC. The protection afforded by IPC was not influenced by adenosine A1 antagonism. CONCLUSIONS: IPC upregulates bFGF, GFAP, and Bcl-2 and protects photoreceptors against light-induced injury. These factors may be involved in the protective response.
Animals↗
Long-term effect of cataract surgery on intraocular pressure after trabeculectomy: extracapsular extraction versus phacoemulsification.
PURPOSE: To compare the effect of phacoemulsification with intraocular lens (IOL) implantation on long-term intraocular pressure (IOP) control in glaucoma patients who had previous trabeculectomy with the effect on IOP control in similar patients after extracapsular cataract extraction (ECCE) with IOL implantation. SETTING: Oxford Eye Hospital, Oxford, England. METHODS: Twenty-eight consecutive patients who had phacoemulsification with IOL implantation (phaco group) at least 3 months after trabeculectomy were identified from hospital records, and 28 patients who had ECCE with IOL implantation (ECCE group) were matched retrospectively to the phaco group with respect to age, sex, diagnosis, and IOP. In both groups, the IOP before cataract extraction was compared with the IOP at intervals up to 2 years after cataract extraction. A Kaplan-Meier survival analysis was performed. RESULTS: The mean IOP in the phaco group did not differ significantly from the mean IOP before cataract extraction at any interval. Twelve months after cataract extraction, the mean IOP in the ECCE group was significantly higher than preoperatively (P =.01); however, the mean IOP did not differ between groups over time (P =.704). There was significantly better long-term IOP control in the phaco group as determined by Kaplan-Meier survival analysis and the log-rank test (P =.038). CONCLUSION: After trabeculectomy, phacoemulsification provided better long-term IOP control than ECCE; however, the mean IOP was not significantly lower.
Aged↗
Four-year review of open eye injuries at the Royal Adelaide Hospital.
PURPOSE: To review the epidemiology of penetrating eye injuries and ruptured globes presenting to the Royal Adelaide Hospital, South Australia. METHODS: A retrospective case review over a 4-year period. RESULTS: There were 109 penetrated or ruptured globes in 105 patients. The average age was 41 years and 80.2% were men. Over half were from rural areas. The commonest cause of injury was hammering metal followed by motor vehicle accidents. Falls in the elderly were the commenest cause of globe ruptures. A final visual acuity of 6/12 or better was found in 40% of eyes and no perception of light in 27%. CONCLUSIONS: At the Royal Adelaide Hospital, the predominant referral centre for serious ocular injury in South Australia, approximately 25 open globe injuries are encountered a year. Although the epidemiology of these injuries was found to be similar to those previously reported in Victoria and rural New South Wales, differences were thought to reflect to the ageing population of South Australia. Rupture of an old, healed large-incision cataract extraction wound was the commonest cause of ruptured globe. An effective preventive strategy to reduce the incidence of severe ocular trauma has yet to be implemented. The concept of a national population-based severe ocular trauma database is considered.
Adult↗
Possible role of excitotoxicity in the pathogenesis of glaucoma.
Excitotoxicity describes the process of neuronal injury by excess stimulation of amino acid receptors. This form of insult was first described in the retina, and subsequently has been shown to be an important component of the pathogenesis of ischaemic and traumatic injury in the central nervous system. Furthermore, there is increasing evidence that excitotoxicity is involved in several chronic neurological conditions, and anti-excitotoxic treatment has already been approved for some of these conditions. A large-scale trial is currently underway that will determine the efficacy of an anti-excitotoxic drug (memantine) in the management of glaucoma. This review provides an overview of neurotransmission and the mechanisms of excitotoxicity. The evidence for excitotoxicity as a component of certain neurological diseases, including glaucoma, is discussed.
Animals↗