1. Articles 9 min read

    Ten Pearls in Interpreting Humphrey Visual Field

    A visual field encompasses the area of space or area of the external environment that is seen by a steadily fixating eye. Advances in the technology of visual field testing have changed our clinical perception of normal and abnormal fields of vision. It is of great importance to diagnose and monitor optic nerve diseases, notably glaucoma. Automated perimetry is now the current gold standard for both diagnosis and follow-up of glaucoma. The Humphreys visual field analyzer by Zeiss technology is the most widely used machine for visual field assessment. In this write-up, we will illustrate ten pearls to interpret a Humphrey’s Automated visual field printout. 1. Pre-requisites For a reliable visual field test, a good understanding between the operator (usually an ophthalmic technician) and the patient is important. It is a good practice for the technicians to undergo self-testing in order to get an idea about the procedure and would help in explaining the procedure better. The patient need

  2. Articles 6 min read

    Monocular elevation Deficit/ Double elevator palsy

    Definition: Double elevator palsy is classically defined as a congenital inability to elevate one eye, with the limitation more in abduction than adduction.1 MED is most often associated with ptosis/pseudoptosis. The word Double elevator palsy was coined by Dunlap to describe the weakness affecting both muscles of elevation i.e. superior rectus and inferior oblique. Pathogenesis/Theories: 2 Superior Rectus palsy: Superior rectus is the main elevator in abduction, adduction, or primary position. Thus, the defective elevation can be explained by the presence of superior rectus palsy alone. Inferior rectus restriction: Subsequently it was found that inferior rectus restriction can also cause such a limitation. The word double elevator palsy is a misnomer, Nearly 70% of cases, the cause for limitation was found to be IR restriction and not palsy. This was confirmed in several studies using saccadic velocity measurement and forced duction test. Supranuclear palsy: The nucleus for upgaze is

  3. Articles 8 min read

    Down's Syndrome: Ten Points All Ophthalmologists Should Know

    Down’s syndrome is a trisomy caused by an extra copy of chromosome 211. The extrachromosomal material is transmitted either by non-disjunction, unbalanced translocation, or mosaicism. It is the most common chromosomal anomaly seen in live births2. As an ophthalmologist, it is important to screen for ocular abnormalities since the incidence of ophthalmic disorders is between 46-100%3. One study found 97 % of children with Down’s syndrome with at least one ocular abnormality4. This proves the necessity to carefully screen these children for any disorders and their prompt treatment. It is recommended that all children diagnosed with Down’s syndrome must undergo evaluation by a Pediatric ophthalmologist before the age of 6 months and then annually thereafter if no abnormalities are found at the first visit 5 Although there are many ophthalmological anomalies seen in Down’s syndrome, we will be discussing only the ten most clinically significant ones below. 1. Refractive Error and Visual ac

  4. Articles 4 min read

    Ten Things You Should Know about Brolucizumab

    1. Brolucizumab is a humanized, single-chain variable fragment (scFv) antibody with a molecular mass of approximately 26 kDa that inhibits VEGF-A.[1] (An scFv is an autonomous binding agent that is no longer dependent on a heavy molecular support structure but still retains the full binding capacity to its target). Mechanism of Action of Brolucizumab Unique Properties of Brolucizumab 2. The pharmacokinetics of a single intravitreal (IVT) injection of Brolucizumab in cynomolgus monkeys revealed a mean terminal half-life of 2.4 ± 0.3 days in all ocular compartments. It was cleared from the serum with a mean half-life of 51 hours (approximately 2 days).[2] Brolucizumab Bevacizumab Ranibizumab Aflibercept Molecule Short-chain variable fragment Full antibody (IgG) Monoclonal humanized antibody format Fusion protein Clinical dose in neovascular ARMD 6 mg 1.25 mg* 0.5 mg 2 mg Equivalent Molar dose 11.2-13.3 0.4-0.5 0.5-0.6 1.0 Table: Molecular properties of anti-VEGF agents (ARMD= Age-related

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