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At this event, the Name lectures session was under the spotlight. The lectures highlighted some interesting and most forthcoming challenges of eight different specialties in ophthalmology. Robert Ritch provided us with exciting insight of glaucoma treatment beyond lowering intraocular pressure (IOP); namely, the controversial topics of neuroprotection and ‘non-pharmaceutical therapy’, how we should interpret the currently available evidence and the problems that we are facing for the development of these alternative therapies.
Another eye-catching feature were the keynote/Plenary/Ward lectures. Robert Weinreb discussed about another hot topic – 24-hour IOP measurement. He talked about personalising the management of IOP; how measurement of IOP at different times of the day and 24-hour IOP monitoring might help us to appropriately select personalised therapy for our patients. Gene transfer via viral or non-viral vectors for the treatment of ocular diseases such as Stargardt’s disease and wet AMD are already underway for clinical trials. Paul Kaufman’s lecture took a step further and discussed the strategies for glaucoma gene therapy, which include increasing conventional and/or uveoscleral outflow, decreasing aqueous humour production and neuroprotection. The future is challenging but equally exciting.
There were also numerous Instruction courses and skill transfer sessions. I was very inspired by Paul Palmberg’s session on Tran-corneal needling at the slit lamp. One would be amazed how much a 30-gauge needle that ‘bent like Zorro’ could achieve when needling a failing bleb, without upsetting the conjunctiva. Also, the dramatic change one could make out of a needle for patient with acute primary angle closure.
There were also numerous exciting free papers. Vinay Nangia shared his study on translamina cribrosa pressure (TLCPD) difference and open-angle glaucoma (OAG). In the Central India Eye and Medical Study that involves more than 4000 subjects, Dr Nangia demonstrated that TLCPD calculation was better associated with glaucoma presence and amount of glaucoma optic neuropathy when compared to IOP measurement. This supports the potential role of low cerebrospinal fluid pressure in the pathogenesis of OAG.