Homonymous hemi-macular atrophy in multiple sclerosis.

Background: Retrograde trans-synaptic degeneration (TSD) following retro-chiasmal pathology, typically retro-geniculate in multiple sclerosis (MS), may manifest as homonymous hemi-macular atrophy (HHMA) of the ganglion cell/inner plexiform layer (GCIPL).

Objective: To determine the frequency, association with clinical outcomes, and retinal and radiological features of HHMA in people with MS (PwMS).

Methods: In this cross-sectional study, healthy controls (HC) and PwMS underwent retinal optical coherence tomography scanning.

Synaptic Protein Loss in Extracellular Vesicles Reflects Brain and Retinal Atrophy in People With Multiple Sclerosis.

Objectives: To assess whether the rate of change in synaptic proteins isolated from neuronally enriched extracellular vesicles (NEVs) is associated with brain and retinal atrophy in people with multiple sclerosis (MS).

Methods: People with MS were followed with serial blood draws, MRI (MRI), and optical coherence tomography (OCT) scans. NEVs were immunocaptured from plasma, and synaptopodin and synaptophysin proteins were measured using ELISA.

Effects of Ibudilast on Retinal Atrophy in Progressive Multiple Sclerosis Subtypes: Post Hoc Analyses of the SPRINT-MS Trial.

Background And Objectives: Ganglion cell + inner plexiform layer (GCIPL) thinning, measured by optical coherence tomography (OCT), reflects global neurodegeneration in multiple sclerosis (MS). Atrophy of the inner (INL) and outer nuclear layer (ONL) may also be prominent in progressive MS (PMS). The phase 2, SPRINT-MS trial found reduced brain atrophy with ibudilast therapy in PMS.

Effects of Myopia on Rates of Change in Optical Coherence Tomography Measured Retinal Layer Thicknesses in People with Multiple Sclerosis and Healthy Controls.

Purpose: To quantify the associations of myopia with longitudinal changes in retinal layer thicknesses in people with multiple sclerosis (PwMS) and healthy controls (HC).

Methods: A cohort of PwMS and HC with recorded refractive error (RE) prospectively scanned on Cirrus HD-OCT at the Johns Hopkins MS Center was assessed for inclusion. Exclusion criteria included OCT follow-up < 6 months, ocular comorbidities, incidental OCT pathologies, and inadequate scan quality.

Use of retinal optical coherence tomography to differentiate suspected neuromyelitis optica spectrum disorder from multiple sclerosis: A cross-sectional study.

Background: Retinal optical coherence tomography (OCT) can differentiate definite NMOSD (dNMOSD) from multiple sclerosis (MS), but has not been evaluated in patients with a high clinical suspicion of NMOSD and not fulfilling the current consensus diagnostic criteria, referred in this paper as "potential" NMOSD (pNMOSD).

Aim: To compare the retinal OCT measurements between patients with pNMOSD, dNMOSD, MS, and reference healthy controls (HC).

Material And Methods: In this cross-sectional study, clinical and demographic characteristics, as well as OCT measurements of peripapillary retinal nerve fiber layer (pRNFL), inner nuclear layer (INL), macular retinal nerve fiber layer (mRNFL), outer nuclear layer (ONL) ganglion cell/inner plexiform layer (GCIPL), and macular volume (MV) were compared between groups.

Visual Pathway Involvement in NMDA Receptor Encephalitis: A Clinical, Optical Coherence Tomography, and 18-Fluorodeoxyglucose PET/CT Approach.

Background: Anti-NMDA receptor (NMDAR) encephalitis patients have been reported to exhibit visual dysfunction without retinal thinning. The objective of our study was to examine the involvement of the visual pathway structure and function in anti-NMDAR encephalitis by assessing postrecovery visual function and retinal structure, and acute-phase occipital cortex function.

Methods: In this cross-sectional study, patients diagnosed with anti-NMDAR encephalitis per consensus criteria underwent postrecovery visual acuity (VA) testing and optical coherence tomography (OCT) with automated retinal layer segmentation.

Central vein sign: A putative diagnostic marker for multiple sclerosis.

The presence of a "central vein sign" (CVS) has been introduced as a biomarker for the diagnosis of multiple sclerosis (MS) and shown to have the ability to accurately differentiate MS from other white matter diseases (MS mimics). Following the development of susceptibility-based magnetic resonance venography that allowed the in vivo detection of CVS, a standard CVS definition was established by introducing the "40% rule" that assesses the number of MS lesions with CVS as a fraction of the total number of lesions to differentiate MS lesions from other types of lesions. The "50% rule," the "three-lesion criteria," and the "six-lesion criteria" were later introduced and defined.

Rituximab Treatment for Chronic Idiopathic Axonal Polyneuropathy.

Chronic idiopathic axonal polyneuropathy is a disorder of unknown etiology resulting in progressive weakness and sensory disturbances predominantly in the hands and feet. Nerve conduction studies and electromyography confirm axonal damage in the nerves of the upper and lower extremities. The pathology is symmetrical with a distal predilection.

Correlation of Pattern Reversal and Flash Visual Evoked Potential Latencies With Optical Coherence Tomography Measures in Patients With Optic Neuropathy and Patients With Multiple Sclerosis Without Optic Neuropathy.

Purpose: The object of the study is to relate the pattern reversal visual evoked potential (PRVEP) and flash VEP (f-VEP) latencies with retinal neurons and their fibers.

Methods: We studied 104 eyes. Forty-two eyes from patients with optic neuritis (ON), 28 eyes from patients with multiple sclerosis without involvement of the optic nerves (MS-non-ON), and 34 eyes of normal controls.

Spinal cord infarction in a young adult: What is the culprit?

Non-traumatic spinal cord infarction in the young adult is usually associated with a single or multiple genetic mutations. There are certain gene mutations that are more commonly associated with spinal cord infarctions. Homozygous or heterozygous mutations, and single mutations or polymorphism, do not seem to determine the probability of spinal cord infarction.