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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A decreased count of retinal photoreceptors all over the fundus and a loss of retinal pigment epithelium cells mainly in the parapapillary region have been reported to be associated with glaucoma. This study addressed the question whether this cell loss in the deep retinal layers may be connected with a change of the choroidal thickness in glaucomatous eyes. Histological sections of 12 eyes with secondary angle closure glaucoma due to a malignant melanoma of the ciliary body and 20 eyes with a malignant choroidal melanoma and normal intraocular pressure were histomorphometrically evaluated. Before enucleation the intraocular pressure was significantly higher in the glaucoma group compared with the control group. Thickness of the choroid was measured at 12 locations from the posterior pole to the fundus periphery. The choroid was significantly thinner in the glaucoma group than in the control group. The decreased choroidal thickness was mainly due to a diminished choroidal vessel diameter. The differences were more marked at the optic disc border than in the fundus periphery. The decreased choroidal thickness in the glaucomatous eyes suggests a reduced choroidal perfusion. It fits with the reported lack of autoregulation of the choroidal blood circulation. Considering the diminished choroidal thickness especially in the parapapillary region, it may be one among other factors explaining the changes of the deep retinal layers in eyes with glaucoma. It indicates that thinning of the choroid, besides the chorioretinal atrophy in the parapapillary region, should be added to the panoply of histological changes in glaucoma.
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PMID:Decreased choroidal thickness in eyes with secondary angle closure glaucoma. An aetiological factor for deep retinal changes in glaucoma? 834 72

Thinning of the posterior sclera may imply that stretching and/or weakening of the sclera plays a role in axial elongation of myopic eyes. We investigated the elastic stress-strain properties of sclera from developing tree shrew eyes made myopic by monocular deprivation (MD) of form vision. Five days of MD induced a relative myopia (mean +/- SEM) of -5.6 D +/- 0.6 D (retinoscopy) and a vitreous chamber elongation (deprived minus control) of 106 +/- 14 microns, n = 10 (ultrasonography). Posterior scleral test samples (2 mm wide) cut from myopic eyes were significantly thinner than their contralateral eye controls (149 +/- 4 microns versus 164 +/- 4 microns, n = 10, P < 0.01) when measured with a force-controlled micrometer. However, posterior sclera from control eyes was significantly thicker than that from age-matched normal eyes (164 +/- 4 microns versus 149 +/- 3 microns, n = 10, P < 0.01). Under uniaxial tension, posterior scleral samples from myopic eyes failed at 18% lower load (162 g versus 198 g) and extended approximately 25% more than controls at a load corresponding to 20 mm Hg intraocular pressure. These differences were largely accounted for by the differences in scleral thickness. Finite element modelling of tree shrew eyes using the material properties summarised above, implies that simple elastic stretching of the sclera accounts for less than 20% of the observed difference in axial length between myopic and contralateral control eyes.
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PMID:Form deprivation myopia: elastic properties of sclera. 852 54

We measured the central corneal thickness and the applanation intraocular pressure (IOP) on 45 Hong Kong Chinese. There was no obvious relationship between these two parameters, as different from other literatures. It could be due to either a limited number of subjects with a high IOP level (only six subjects with IOP > or = 22 mmHg), or Chinese has a thicker central cornea in general. The mean central cornea of our subjects was thicker (566 +/- 36 microns) than some previous findings. Thirty subjects had their intraocular pressure further increased by adopting a 40 degrees head-down posture. Their IOP and topographic corneal thickness were measured again. There was no significant change in the central corneal thickness even though the IOP was elevated by 11.7 mmHg. However the nasal cornea demonstrated a thinning effect (by some 18 microns) during the IOP elevation but it returned to the pre-inverted level after returning to a sitting posture for 5 min. Further investigation with more corneal regions being measured would be valuable to evaluate the in vivo effect of IOP elevation from glaucoma attack on corneal thickness.
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PMID:The effect of an artificially-elevated intraocular pressure on corneal thickness in Chinese eye. 939 Mar 68

The etiology of glaucoma is most probably multifactorial. This study intended to investigate the asymmetry in intraocular pressure (IOP) and that in retinal nerve fiber layer (RNFL) thickness in normal-tension glaucoma patients. Two diurnal tension curves, obtained within 3 months and counting at least five IOP readings each, including an early morning IOP measurement upon awaking, were obtained in 15 normal-tension glaucoma patients. None of the patients received IOP-lowering therapy. IOP asymmetry was present in at least three readings and was always in the same direction. The optic nerve was imaged in both eyes in each patient by means of confocal scanning laser ophthalmoscopy (Heidelberg Retina Tomograph). The interocular difference in RNFL thickness and the RNFL cross-sectional area were correlated with the interocular difference in IOP by means of Spearman's rank correlation factor. Nine female and 6 male normal-tension glaucoma patients (mean +/- SD age was 62. 4 +/- 16.9 years) were included in this study. Interocular IOP asymmetry varied between 0.30 and 4 mm Hg. Strong negative correlations were found between interocular asymmetry in IOP and interocular asymmetry in RNFL thickness asymmetry (R = -0.652, p = 0. 0083) and interocular asymmetry in RNFL cross-sectional area (R = -0. 702, p = 0.0034). The present results demonstrate for the first time a more marked thinning of the neuroretinal nerve fiber layer in the eye with the higher IOP in normal-tension glaucoma patients.
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PMID:Asymmetry in intraocular pressure and retinal nerve fiber layer thickness in normal-tension glaucoma. 1042 Jan 4

Accurate Australian glaucoma prevalence has been provided by two population-based studies: the Blue Mountains Eye Study (BMES) and the Melbourne Visual Impairment Project (MVIP). Both stud es defined glaucoma as the presence of matching optic disc cupp ng with rim thinning and g aucomatous field defects demonstrated on automated perimetry Combining 'definite' and 'probable' rates, the glaucoma prevalence in persons aged 50 and over, age-standardized for the 2000 projected Australian population, was 2.70% (BMES) and 3.13% (MVIP), including rates for 'definite' glaucoma of 2.12% (BMES) and 2.50% (MVIP). The number of Australians aged 50 and over in the year 2000 with g aucoma could be estimated as from 144 000 persons (BMES) to 167 000 persons (MVIP). Assuming similar age-specific rates, the number of Austral ans aged 50 and over in the year 2030 wth glaucoma could be estimated as from 307 000 persons (BMES) to 337 000 persons (MVIP). Ocular hypertens on (OH) was defined as present in subjects without glaucoma wth intraocular pressure (IOP) of more than 21 mmHg, including treated subjects with 'normal' examination IOP The age-standardized OH prevalence was 5.15% (BMES), which projects to 275000 Australians with OH in 2000, increasing to 513000 in 2030.
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PMID:Projected number of Australians with glaucoma in 2000 and 2030. 1098 83

Glaucoma is a leading cause of irreversible blindness in the world. Currently, glaucoma is diagnosed as a progressive optic neuropathy with characteristic optic disc and nerve fiber layer damage, usually associated with loss of visual function. The intraocular pressure (IOP) is the most important risk factor for the disease, although a significant proportion of patients do not have elevated IOP. Other risk factors include older age, African descent, myopia and family history of the disease. The ophthalmoscopic examination of the optic disc is essential to identify the signs of glaucomatous optic neuropathy, such as increased cupping, neuroretinal rim thinning or optic disc hemorrhages. Glaucomatous visual field loss usually starts in the periphery, and loss of central vision does not occur until late in the course of the disease. Visual function is most commonly assessed by standard automated perimetry; however, as many as 50% of nerve fibers can be lost before the appearance of visual field defects in this test. Newer technologies have been developed to find more sensitive ways to detect early glaucoma using both functional (short-wavelength automated perimetry and frequency-doubling perimetry) and structural (scanning laser topography, optical coherence tomography and scanning laser polarimetry) measurements. The management of glaucoma is based on lowering the intraocular pressure to prevent further optic nerve damage. Currently, there are five major classes of medications that are used to lower the intraocular pressure: Beta-adrenergic antagonists, adrenergic agonists, parasympathomimetics, prostaglandin-like analogues and carbonic anhydrase inhibitors. The goal of therapy is to maintain adequate vision for patients during their lifetime, keeping in mind the possible adverse effects of the drugs. If additional lowering of IOP is indicated or if medication fails to sufficiently lower the IOP, laser trabeculoplasty is usually the next step. If IOP is still not adequately controlled, incisional glaucoma surgery is indicated. Neuroprotective agents, which directly protect the optic nerve in glaucoma, are being evaluated in clinical trials.
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PMID:Medical backgrounders: glaucoma. 1258 21

The neuroprotective effect of MCI-9042 (Mitsubishi Pharma Corporation) was investigated on glutamate-induced retinal ganglion cell (RGC) death in vitro and on rat retinal ischemia in vivo. RGCs were purified from retinal cells isolated from 6-day-old Wistar rats and cultured in serum-free media. After application of 25 microM glutamate, the viability of RGCs treated with or without several serotonin 2 (5-HT(2)) receptor antagonists: MCI-9042, M-1 (a major metabolite of MCI-9042), ketanserin, and LY-53857; was evaluated by calcein-acetoxymethyl ester staining. Retinal ischemia was induced by intraocular pressure (IOP) elevation (130 mmHg, 50 min). Rats were intraperitoneally injected with MCI-9042 at a dose of 3, 30 mg/kg or base at 30 min before and just after ischemia-reperfusion. Retinal damages were evaluated by histology, morphometric analysis and electroretinograms (ERGs) recordings at 7 days after ischemia-reperfusion. 25 microM glutamate decreased the number of viable RGCs to about 60 to 65% of untreated RGCs. MCI-9042, M-1, ketanserin, and LY-53857 significantly reduced glutamate-induced RGC death at concentrations of more than 100 nM, 1 nM, 1 microM and 100 nM, respectively. Ischemia-reperfusion caused thinning of the thickness between the inner plexiform layer and the outer plexiform layer and attenuation of a-and b-waves in ERG recordings. The intraperitoneal injection of MCI-9042 significantly reduced morphological and functional damages in retinal ischemia. Our data demonstrate that 5-HT(2) receptor antagonists including MCI-9042 and M-1 have the neuroprotective effects in cultured RGCs and that MCI-9042 protects against ischemic retinal diseases.
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PMID:Effect of MCI-9042, a 5-HT2 receptor antagonist, on retinal ganglion cell death and retinal ischemia. 1263 9

The excimer laser keratorefractive surgery inevitably compromises structural integrity of the cornea by the surgical tissue subtraction and loss of integrity of Bowman's membrane. Forward shift of the cornea is commonly seen after both photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK). Antero-posterior movement of the cornea is evaluated by measuring the posterior corneal elevation with the scanning-slit corneal topography (Orbscan). Eyes with thinner cornea, higher intraocular pressure, and higher myopia requiring greater laser ablation were more predisposed to forward shift of the cornea. After PRK, there was a trend toward progressive forward shift of the cornea, but the progression stabilized 6 months after surgery. Because progressive thinning and expansion of the cornea were not observed during the one-year observation period after PRK, the forward shift of the cornea does not represent true ectasia. Forward shift of both corneal surfaces would add to the tendency toward myopic regression after excimer laser surgery.
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PMID:Corneal forward shift after excimer laser keratorefractive surgery. 1275 56

Current best practice for primary open-angle glaucoma case-finding comprises history-taking, disc examination, intraocular pressure measurement and suprathreshold visual field analysis (SVFA). An alternative case-finding technique was formulated replacing SVFA with computerised quantitative disc assessment, using the Heidelberg retinal tomograph II (HRT II). Each approach was adopted by four optometrists who screened 29 POAG and 37 normal patients. Average sensitivities and specificities were similar in the two groups [sensitivity 71% (SVFA) vs 69% (HRT II); specificity 94% both groups]. Our inclusion of pre-perimetric glaucoma cases limited the sensitivity of the optometrists in this study. There was evidence to suggest that the optometrists tended to miss early changes at the optic disc such as disc haemorrhage, nerve fibre layer defects and subtle neuroretinal thinning.
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PMID:Sensitivity and specificity of two glaucoma case-finding strategies for optometrists. 1282 24

The SmartLens tonometer (ODC, Zurich, Switzerland) is a contact lens that allows continuous measurement of intraocular pressure (IOP), in addition to estimating pulse amplitude. IOP measurements taken with the Smartlens tonometer showed a good correlation with Goldmann tonometry. Nevertheless, there was a mean difference of 3.5 mmHg (p<0.01) in intraocular pressure between the two methods, with a significant overestimation by Smartlens tonometry compared with Goldmann tonometry in normal individuals. Preliminary results demonstrated that IOP measurements are not statistically affected by the thinning of the cornea induced by LASIK surgery.
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PMID:[I have tested it for you....the Smartlens]. 1464 26


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