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Byline: Vinny. Wilson, Prabhjit. Kaur, Sofia. Singh, Radhika. Ramachandran, Vislavath. Jyothi, Karthik. Mahesh, Aastha. Takkar, Giriraj. Chandak, Ramandeep. Singh Background: Leber hereditary optic neuropathy (LHON) is a maternally inherited disease [...]

Byline: Vivek. Lal, Aastha. Takkar, Sucharita. Ray, Karthik. Mahesh When we were asked by the Indian Academy of Neurology to do a supplement on neuroophthalmology, we had mixed feelings. It [...]

The contributions of the present Continuing Nutrition Education (CNE) Conference on "Nutrition and Brain Health" provide a representative overview of gut-brain interactions and their role in acute and chronic brain diseases. Nutrition plays a crucial and lifelong role in brain health. A well-balanced diet can significantly impact cognitive function, mood and overall brain health by influencing brain development and neuroplasticity. Advances in fields like nutrigenomics (the study of how genetics and nutrition interact) and the microbiome are shedding light on the complex relationships between nutrition and brain health. As our understanding deepens, more precise dietary recommendations and personalized approaches to support brain health may emerge. However, there are still some areas where the role of nutrition in brain health remains unclear. These include individual variability, the long-term effects of nutrition, nutrient interactions, the influence of complex dietary patterns, the gut-brain connection and the effects of aging on brain plasticity. The aim of this proceeding is to delve into some of these issues to lay out a comprehensive rundown of the existing knowledge in the field. [ABSTRACT FROM AUTHOR]

Tuberculosis (TB) is a global health concern and central nervous system (CNS) TB leads to high mortality and morbidity. CNS TB can manifest as tubercular meningitis, tuberculoma, myelitis, and arachnoiditis. Neuro-ophthalmological involvement by TB can lead to permanent blindness, ocular nerve palsies and gaze restriction. Visual impairment is a dreaded complication of tubercular meningitis (TBM), which can result from visual pathway involvement at different levels with varying pathogenesis. Efferent pathway involvement includes cranial nerve palsies and disorders of gaze. The purpose of this review is to outline the various neuro-ophthalmological manifestations of TB along with a description of their unique pathogenesis and management. Optochiasmatic arachnoiditis and tuberculomas are the most common causes of vision loss followed by chronic papilloedema. Abducens nerve palsy is the most commonly seen ocular nerve palsy in TBM. Gaze palsies with deficits in saccades and pursuits can occur due to brainstem tuberculomas. Corticosteroids are the cornerstone in the management of paradoxical reactions, but other immunomodulators such as thalidomide and infliximab are being explored. Toxic optic neuropathy caused by ethambutol necessitates careful monitoring and immediate drug discontinuation. Cerebrospinal fluid diversion through ventriculo-peritoneal shunting may be required in patients with hydrocephalus in stage I and II of TBM to prevent visual impairment. Early diagnosis and prompt management are crucial to prevent permanent disability. Prevention strategies, public health initiatives, regular follow-up and timely intervention are essential in reducing the burden of CNS TB and its neuro-ophthalmological complications. [ABSTRACT FROM AUTHOR]

Byline: Sucharita. Ray, Aastha. Takkar, Vivek. Lal Idiopathic Intracranial Hypertension (IIH), also known as primary pseudotumor cerebri is an important neurological cause of reversible visual loss. IIH was originally considered [...]

Byline: Rekha. Hans, Satya. Prakash, Ratti. Sharma, Naveen. Sankhyan, Aastha. Takkar, Manoj. Goyal, Biman. Saikia, Vivek. Lal, Neelam. Marwaha Background: Therapeutic plasma exchange (TPE) is indicated in the acute presentation [...]

Supplemental Digital Content is Available in the Text. [ABSTRACT FROM AUTHOR]

Byline: Madhivanan. Karthigeyan, Pravin. Salunke, Aastha. Takkar Sir, A 55-year-old man with ruptured distal anterior cerebral artery aneurysm [Figure 1]a underwent clipping through the basal interhemispheric approach. Despite sufficient maneuvers [...]

Background: There is ongoing debate about whether the oculomotor (III), trochlear (IV), or abducens (VI) nerve paresis in patients with migraine is directly attributable to migraine (ophthalmoplegic migraine [OM]) or is due to an inflammatory neuropathy (recurrent painful ophthalmoplegic neuropathy [RPON]). As migraine is associated with elevated serum calcitonin gene-related peptide (CGRP) levels, we studied serum CGRP levels among patients with OM/ RPON to determine whether they are elevated during and between attacks. This is the first study assessing CGRP levels in the serum of patients with OM/RPON. Methods: The aim of this case–control study was to assess serum CGRP levels in patients with ophthalmoplegia and a headache consistent with migraine according to ICHD-3 criteria. Serum CGRP levels were measured during the ictal and interictal phases in 15 patients with OM/RPON and compared with age-matched and sex-matched controls without migraine (12 patients). Results: The median serum CGRP levels were significantly elevated (P = 0.021) during the ictal phase (37.2 [36.4, 43.6] ng/L) compared with controls (32.5 [30.1, 37.3] ng/L). Serum CGRP levels during the attack correlated with the total duration of ophthalmoplegia. A CGRP level of 35.5 ng/L in the ictal phase of the attack had a sensitivity of 86.7% and specificity of 75.0% in diagnosing a patient with OM/RPON. Conclusions: Elevated serum CGRP levels during the ictal phase of OM/RPON favor migraine as the underlying cause of episodic headache with ophthalmoplegia. [ABSTRACT FROM AUTHOR]

Byline: Pravin. Salunke, Madhivanan. Karthigeyan, Kokkula. Praneeth, Savleen. Kaur, Aastha. Takkar Background: The pathway underlying ocular convergence is less clear. Convergence weakness is usually a clinical sign of dorsal midbrain [...]

Byline: Saurabh. Bansal, Ramandeep. Bansal, Manoj. Goyal, Aastha. Takkar, Ramandeep. Singh, Paramjeet. Singh, Vivek. Lal Background: Although first described more than two decades ago, posterior reversible encephalopathy syndrome (PRES) continues [...]

Byline: Aastha. Takkar, Vivek. Lal Idiopathic intracranial hypertension (IIH) is defined as a syndrome of raised intracranial pressure with normal imaging of the brain and cerebrospinal fluid (CSF) composition. There [...]

A patient with idiopathic intracranial hypertension and transverse sinus stenosis developed venous overload choroidopathy and bilateral serous macular detachments. Increased venous back pressure seemed to have overloaded the choroid that showed vortex vein anastomoses, choroidal vascular hyperpermeability, retinal pigment epithelium leaks, and serous detachments in both eyes. Purpose: To report a case of venous overload choroidopathy associated with idiopathic intracranial hypertension in a 41-year-old man. Methods: History and clinical examination, fluorescein angiography, ultra-widefield indocyanine green angiography, swept-source optical coherence tomography, and contrast-enhanced magnetic resonance imaging. Results: The patient was diagnosed as having idiopathic intracranial hypertension 2 years ago, was being managed on oral acetazolamide, and retained 20/20 visual acuity in both eyes until now when he presented with a complaint of visual loss in the right eye. Ophthalmoscopy revealed serous detachment in the fovea of the right eye. Swept-source optical coherence tomography showed the presence of subretinal fluid and detachments of the retinal pigment epithelium in both eyes. Fundus fluorescein angiography showed multiple dot leaks at the level of the retinal pigment epithelium in both eyes. Indocyanine green angiography revealed vortex vein anastomoses and choroidal vascular hyperpermeability in both eyes. Contrast-enhanced magnetic resonance imaging revealed dilated optic nerve sheath diameter and a partial empty sella and magnetic resonance venography showed bilateral stenosis of the transverse sinus. Conclusion: Transverse sinus stenosis is a common finding in "idiopathic" intracranial hypertension and contributes to the intracranial pressure through intracranial venous hypertension. Increased venous back pressure seemed to have overloaded the choroid resulting in choroidal vascular congestion and hyperpermeability, leaks from the level of the retinal pigment epithelium, and accumulation of subretinal fluid. [ABSTRACT FROM AUTHOR]

Byline: Mazda. Turel, Manjul. Tripathi, Ashish. Aggarwal, Navneet. Singla, Chirag. Ahuja, Aastha. Takkar, Sahil. Mehta, Kanwaljeet. Garg, Ravi. Yadav, Anant. Mehrotra, Kuntal. Das Li S, et al . Mannitol improves [...]

Byline: Mazda. Turel, Manjul. Tripathi, Ashish. Aggarwal, Navneet. Singla, Chirag. Ahuja, Aastha. Takkar, Sahil. Mehta, Kanwaljeet. Garg, Ravi. Yadav, Anant. Mehrotra, Kuntal. DasZiai H, et al . Impact of dural [...]