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Idiopathic intracranial hypertension (previously known as pseudotumor cerebri or benign intracranial hypertension) is a syndrome of increased intracranial pressure of unclear etiology that most often occurs in women of childbearing age, although it can also occur in men, children, and older adults. Most patients are overweight or obese with a history of recent weight gain. Papilledema is the hallmark clinical sign and, if severe and untreated, can result in irreversible vision loss. Recent population studies in the USA have found that the annual incidence of idiopathic intracranial hypertension is increasing in association with obesity rates, while recent scientific studies indicate a possible role for androgen sex hormones and adipose tissue in the pathogenesis of the disease. The main goals of treatment are to preserve vision and alleviate symptoms, which can usually be achieved using a combination of weight loss, medical therapies, and surgical interventions. Prospective clinical trials have found benefit from weight loss, acetazolamide, and topiramate in the management of mild to moderate severity disease. However, the indications for surgical intervention, optimal timing and choice of intervention, and their long-term outcomes remain unclear due to a lack of prospective and controlled clinical trials evaluating surgical interventions for idiopathic intracranial hypertension.

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An organized clinical approach in the diagnosis and management of demyelinating optic neuropathies is important for holistic management of patients.

Demyelinating Optic neuropathies are of three different types –a) Optic Neuritis (ON), b) Neuromyelitis Optica and c) Optic neuropathies associated with Myelin Oligodendrocyte Glycoprotein. The later two are often grouped under Neuromyelitis optica spectrum disorders (NMOSD). All three are characterized by the triad of sub-acute vision loss, dys-chromatopsia and peri-ocular pain. From anatomical point of view, ON has also been divided into papillitis, retrobulbar neuritis, optic peri-neuritis and neuro-retinitis.

Clinically, ON associated with Multiple sclerosis (ON-MS) is mild in severity, often unilateral and associated with demyelination without axonal loss. Evidence of additional axonal loss is seen in patients with ON associated with NMOSD.

The differential diagnoses of ON include infectious, and post-infectious autoimmune conditions, neoplastic, toxic, and hereditary causes. Recognizing red flags is important in wake of long-term implications. Clinico- radiological correlation is another important aspect in management of patients. Importance of a multidisciplinary team cannot be underscored when dealing with specific causes of ON like infectious, neoplastic or certain paraneoplastic causes.

Conclusion: A careful and meticulous approach helps in determination of demyelinating ON. Recognition of red flags suggesting atypical causes is equally important for prompt and adequate management.

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Ischemic optic neuropathy (ION) is the sudden loss of vision due to a decrease or interruption of blood flow to the optic nerve. These conditions can be classified according to a) the location of the damage and b) the etiological factors leading to the ischemia. If the optic nerve head is involved with associated optic disc edema, this is classified as anterior ischemic optic neuropathy (AION). If the ischemia involves the intra-orbital optic nerve or portions more posterior, then no disc edema is seen and the condition is classified as posterior ischemic optic neuropathy (PION). Outside of the peri-anaesthetic setting or in cases of giant cell arteritis (GCA), PION is rare. However, AION is the most common cause of disc swelling and optic neuropathy in patients over the age of 50. Giant cell arteritis is the most critical cause of AION, as the initial management is crucial to protecting further vision loss. Therefore AION is typically classified as either arteritic (due to GCA) and non-arteritic.

In this talk we will discuss the different presentations of these types of ION, and how to best distinguish them clinically and on investigation. The management strategies for each will be addressed based on current evidence-based medicine. Prevention and risk factor modification will also be reviewed.