Recent advances in our understanding of the mechanisms in the cascade of events resulting in retinal cell death in ocular pathologies like glaucoma, diabetic retinopathy and age-related macular degeneration led to the common descriptive term of neurodegenerative diseases of the retina. The final common pathophysiologic pathway of these diseases includes a particular form of metabolic stress, resulting in an insufficient supply of nutrients to the respective target structures (optic nerve head, retina). During metabolic stress, glutamate is released initiating the death of neurones containing ionotropic glutamate (N-methyl-D-aspartat, NMDA) receptors present on ganglion cells and a specific type of amacrine cells. Experimental studies demonstrate that several drugs reduce or prevent the death of retinal neurones deficient of nutrients. These agents generally block NMDA receptors to prevent the action of glutamate or halt the subsequent pathophysiologic cycle resulting in cell death. The major causes for cell death following activation of NMDA receptors are the influx of calcium and sodium into cells, the generation of free radicals linked to the formation of advanced glycation endproducts (AGEs) and/or advanced lipoxidation endproducts (ALEs) as well as defects in the mitochondrial respiratory chain. Substances preventing these cytotoxic events are considered to be potentially neuroprotective.

No abstract

No abstract

Background/aims-The choroid, a low resistance vascular structure carrying 85% of the ocular blood flow, provides nourishment to and removal of potential toxic waste products from the adjacent non-vascularised outer layers of the retina, macula, and optic disc regions. Choroidal perfusion may be reduced in retinitis pigmentosa (RP) and might contribute to retinal pigment epithelium (RPE) degeneration. The aim of this study was to determine whether choroidal perfusion is reduced in RP and whether this is correlated with the stage of disease. Conclusions-OPA can be used neither for early clinical detection of RP nor to follow the natural course of the disease. However, our data show that in advanced stages of RP not only the retina but also the choroidal circulation is aVected. (Br J Ophthalmol 2001;85:678-682) Retinitis pigmentosa (RP) comprises a group of progressive degenerative retinal diseases caused by genetic defects localised on diVerent chromosomes aVecting approximately 1.5 million people worldwide. In the majority of cases, RP leads to blindness at around the age of 60 years. Methods-Ocular

(Br J Ophthalmol 1998;82:758-762)

The results showed the expected drop in IOP. However, capillary optic nerve head blood flow, measured by two different techniques, did not change during therapy. This may be due to the effective autoregulation in human optic nerve head circulation, which seems not to be affected by dorzolamide.

No abstract

Methods: OPA, using the Langham Ocular Blood Flow (OBF) System, applanation intraocular pressure (lOP), systemic blood pressure and heart rate were measured and vasospasm was determined by a fingernail capillary blood flow test.Results: OPA (mmHg) in the LTG patients with a vasospastic reaction (LTG-V, 1.4 ± 0.1, n = 17) was not significantly (p>0.09) different when compared with non-vasospastic LTG patients (LTG-NV, 1.5 ± 0.2, n = 15) but was significantly (p0.05) different when compared with each other, but was significantly (p<0.05) lower when compared with matched coutrol subgroups (15.0 ± 0.3 and 15.2 ± 0.4, respectively). Haemodyuamic para meters were not significautly different from controls. Conclusion:The abnormality in choroidal perfusion indicated by a rednction in OPA in all LTG patients is unrelated to the presence or absence of vasospasm. Quigley et al. 5 did not find a reduction in the number of blood vessels in the optic nerve head region whereas Schwartz6 using fluorescein angiogra phy showed filling defects in this area in glaucoma tous subjects. These findings suggest a connection between LTG and vascular abnormalities.The present study was designed to evaluate a parameter of choroidal perfusion, the ocular pulse amplitude (OPA), in LTG patients with respect to vasospasm.