7,651 research outputs found

    Professor Edwin W. Briggs

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    Professor Edwin W. Brigg

    Professor Edwin W. Briggs

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    Professor Edwin W. Brigg

    How do I manage functional visual loss

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    Functional visual loss is a subtype of functional neurological disorder (FND) and is a common cause of visual impairment seen in both general and neuro-ophthalmological practice. Ophthalmologists can generally diagnose functional visual loss reasonably confidently but often find it harder to know what to say to the patient, how to approach, or even whether to attempt, treatment. There is little evidence-based treatment despite studies showing up to 60% of adults having impactful symptoms on long-term follow-up. The last 20 years has seen large changes in how we understand, approach, and manage FND more widely. In this article, we set out our practical approach to managing functional visual loss which includes : 1) Make a positive diagnosis based on investigations that demonstrate normal vision in the presence of subjectively impaired vision, not just because tests or ocular exam is normal; 2) Explain and label the condition with an emphasis on these positive diagnostic features, not reassurance; 3) Consider eye or brain comorbidities such as migraine, idiopathic intracranial hypertension or amblyopia; 4) Consider working with an orthoptist using diagnostic tests in a positive way to highlight the possibility of better vision; 5) Develop simple treatment strategies for photophobia; 6) Consider psychological factors and comorbidity as part of assessment and therapy, but keep a broader view of aetiology and don't use this to make a diagnosis; 7) Other treatment modalities including hypnotherapy, transcranial magnetic stimulation and more advanced forms of visual feedback are promising candidates for functional visual loss treatment in the future.</p

    Nuclei in Strongly Magnetised Neutron Star Crusts

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    We discuss the ground state properties of matter in outer and inner crusts of neutron stars under the influence of strong magnetic fields. In particular, we demonstrate the effects of Landau quantization of electrons on compositions of neutron star crusts. First we revisit the sequence of nuclei and the equation of state of the outer crust adopting the Baym, Pethick and Sutherland (BPS) model in the presence of strong magnetic fields and most recent versions of the theoretical and experimental nuclear mass tables. Next we deal with nuclei in the inner crust. Nuclei which are arranged in a lattice, are immersed in a nucleonic gas as well as a uniform background of electrons in the inner crust. The Wigner-Seitz approximation is adopted in this calculation and each lattice volume is replaced by a spherical cell. The coexistence of two phases of nuclear matter - liquid and gas, is considered in this case. We obtain the equilibrium nucleus corresponding to each baryon density by minimizing the free energy of the cell. We perform this calculation using Skyrme nucleon-nucleon interaction with different parameter sets. We find nuclei with larger mass and charge numbers in the inner crust in the presence of strong magnetic fields than those of the zero field case for all nucleon-nucleon interactions considered here. However, SLy4 interaction has dramatic effects on the proton fraction as well as masses and charges of nuclei. This may be attributed to the behaviour of symmetry energy with density in the sub-saturation density regime. Further we discuss the implications of our results to shear mode oscillations of magnetars.Comment: presented in "Exciting Physics Symposium" held in Makutsi, South Africa in November, 2011 and to be published in a book by Springer Verla

    Changes in synaptic transmission and protein expression in the brains of adult offspring after prenatal inhibition of the kynurenine pathway

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    During early brain development, N-methyl-d-aspartate (NMDA) receptors are involved in cell migration, neuritogenesis, axon guidance and synapse formation, but the mechanisms which regulate NMDA receptor density and function remain unclear. The kynurenine pathway of tryptophan metabolism includes an agonist (quinolinic acid) and an antagonist (kynurenic acid) at NMDA receptors and we have previously shown that inhibition of the pathway using the kynurenine-3-monoxygenase inhibitor Ro61-8048 in late gestation produces rapid changes in protein expression in the embryos and effects on synaptic transmission lasting until postnatal day 21 (P21). The present study sought to determine whether any of these effects are maintained into adulthood. After prenatal injections of Ro61-8048 the litter was allowed to develop to P60 when some offspring were euthanized and the brains removed for examination. Analysis of protein expression by Western blotting revealed significantly reduced expression of the GluN2A subunit (32%) and the morphogenetic protein sonic hedgehog (31%), with a 29% increase in the expression of doublecortin, a protein associated with neurogenesis. No changes were seen in mRNA abundance using quantitative real-time polymerase chain reaction. Neuronal excitability was normal in the CA1 region of hippocampal slices but paired-pulse stimulation revealed less inhibition at short interpulse intervals. The amount of long-term potentiation was decreased by 49% in treated pups and recovery after low-frequency stimulation was delayed. The results not only strengthen the view that basal, constitutive kynurenine metabolism is involved in normal brain development, but also show that changes induced prenatally can affect the brains of adult offspring and those changes are quite different from those seen previously at weaning (P21). Those changes may be mediated by altered expression of NMDAR subunits and sonic hedgehog
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