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Parkinson's disease patients have been shown to have abnormal visually evoked cortical potentials (VEPs) to pattern stimulation. Whereas dopamine is not an important neurotransmitter in the central visual pathways, the retina is rich in dopamine and, together with previous animal and human studies, this suggests that the abnormal VEPs in Parkinson's disease patients may be due to a biochemical and electrophysiological disorder in the retina. This hypothesis has been examined by studying the VEPs and pattern electroretinogram (PERG) of Parkinson's disease patients and matched control subjects. The amplitudes of the cortical and retinal evoked potentials were significantly reduced in Parkinson's disease patients compared with the control subjects and this could not be attributed to any particular feature of the disease or its treatment. There was a significant relationship between the VEP P100 latency and the PERG amplitude. Moreover for those subjects in whom there was an interocular difference in both cortical and retinal evoked potentials, the abnormality was more commonly found in the potentials from the same eye. These findings suggest that the abnormality of the VEP in Parkinson's disease patients is, at least in part, secondary to an abnormality of the retina itself. [ABSTRACT FROM AUTHOR]

Visual evoked potentials (VEPs) were elicited from 29 patients who had experienced a previous attack of acute primary angle closure glaucoma. The VEPs were shown to be abnormal in at least one of the measures (latency, amplitude, contrast threshold, or slope) in 72.4% of affected eyes, whereas only 41.4% indicated obvious optic nerve damage. It is notable that 48.1% of fellow eyes with no (known) history of acute pressure rise also showed some form of VEP abnormality. The possible pathophysiological mechanisms operating in both affected and fellow eyes are discussed. It is concluded that, despite the presence of possible artefactual influences, the results probably reflect the presence of primary angle closure glaucoma. [ABSTRACT FROM PUBLISHER]

Pattern reversal visual evoked potentials (VEPs) have been elicited in 16 female hyperthyroid patients before and after treatment and compared with those from a similar group of age and sex matched control subjects. No effect on latency was seen, and although larger amplitude values were noted in the thyrotoxic group these too were not significant. We would conclude that hyperthyroidism per se has little effect on the pattern reversal VEP, and any observed effect on these potentials is probably due to other factors. [ABSTRACT FROM PUBLISHER]

An electrophysiological investigation of visual evoked potential (VEP) latency and contrast sensitivity was performed in a group of 13 patients who had undergone extracapsular cataract surgery with posterior chamber lens implantation. In spite of good postoperative visual acuity, abnormalities were detected in nine of the group (69%). This study suggests that, even with successfully implanted lenses, there may be a reduction in visual function which could be the result of altered transmission through the plastic lenticulus or fibrosis of the posterior lens capsule, and/or subtle changes in retinal architecture, not observed ophthalmoscopically. [ABSTRACT FROM PUBLISHER]

In recent years it has been shown that it is of considerable clinical value to determine the visual contrast sensitivity function of the patient. This can reveal the wider effects of pathology on the visual system where visual acuity may or may not be affected. There is a comprehensive literature on subjective approaches of obtaining this function in the clinical environment but very little on alternative objective methods. This paper describes the latter approach, which exploits electrophysiological techniques using the visual evoked cortical potential (VECP) to checkerboard onset-offset stimulation. Its application in a variety of disorders of the visual system is described. The importance of selecting the most appropriate stimulus parameters is discussed, and the relative advantages and disadvantages as compared with psychophysical methods are appraised. [ABSTRACT FROM PUBLISHER]

Aims: To describe the phenotype in three family members affected by a novel mutation in the gene coding for the enzyme tissue inhibitor of metalloproteinase-3 (TIMP-3)., Methods: Three members of the same family were seen with a history of nyctalopia and visual loss due to maculopathy. Clinical features were consistent with Sorsby's fundus dystrophy. Exon 5 of the gene coding for TIMP-3 was amplified by the polymerase chain reaction, single strand conformation polymorphism analysis undertaken and exon 5 amplicons were directly sequenced., Results: Onset of symptoms was in the third to fourth decade. Five of six eyes had geographic macular atrophy rather than neovascularisation as a cause for central visual loss. Peripheral retinal pigmentary disturbances were present. Scotopic ERGs were abnormal in all three. Mutation analysis showed a G-->T transversion in all three resulting in a premature termination codon, E139X, deleting most of the carboxy terminal domain of TIMP-3., Conclusions: The patients described had a form of Sorsby's fundus dystrophy which fell at the severe end of the spectrum of this disease. Postulated disease mechanisms include deposition of dimerised TIMP-3 protein.

Purpose: To report on a patient who developed retinal toxicity from an intraocular copper foreign body in the absence of any signs of chalcosis or inflammation., Method: Case report., Result: Removal of the copper foreign body resulted in electroretinographic improvement and the patient has retained good vision., Conclusion: Retinal toxicity from intraocular copper can be subclinical and such foreign bodies should be removed. Removal of the foreign body can be associated with at least partial reversal of retinal toxicity.