Leber hereditary optic neuropathy (LHON) is a maternally inherited, bilateral, sequential optic neuropathy that usually affects young males. LHON arises from a defect in complex I of the oxidative phosphorylation chain that generates increased reactive oxygen species and causes a decline in cellular ATP production. There exists no cure at present for LHON.
View Article and Find Full Text PDFMult Scler Int
February 2016
Until recently, multiple sclerosis has been viewed as an entirely inflammatory disease without acknowledgment of the significant neurodegenerative component responsible for disease progression and disability. This perspective is being challenged by observations of a dissociation between inflammation and neurodegeneration where the neurodegenerative component may play a more significant role in disease progression. In this review, we explore the relationship between mitochondrial dysfunction and neurodegeneration in multiple sclerosis.
View Article and Find Full Text PDFBackground: The management of acute optic neuritis differs according to the underlying etiology and techniques which may help with early differential diagnosis are therefore of considerable value.
Objective: We wanted to determine if multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) could be differentiated on the basis of neuroimaging abnormalities of the anterior visual pathways following an episode of optic neuritis.
Methods: Magnetic resonance imaging (MRI) findings of 27 patients diagnosed with MS (n = 15) or NMOSD (n = 12), who presented with acute isolated optic neuritis over a 3-year period, were reviewed retrospectively.
Asia Pac J Ophthalmol (Phila)
June 2015
Although nonarteritic anterior ischemic optic neuropathy (NAION) is known to occur as a result of ischemic insult to the anterior portion of the optic nerve, its etiology and pathogenesis remain elusive. Because NAION is a nonfatal condition, acute, postmortem histopathologic analysis has never been undertaken. Animal models of NAION have been created with the use of an iodinated derivative of fluorescein, rose bengal.
View Article and Find Full Text PDFBackground: Complement mediated autoimmunity against aquaporin-4 results in astrocytic damage in neuromyelitis optica (NMO). There is evidence for increased CSF glial fibrillary acidic protein (GFAP) and S100B levels in acute NMO. Here we tested whether the CSF finding also holds true for the diagnostic value of serum GFAP and S100B levels in NMO.
View Article and Find Full Text PDFPurpose: To investigate the presence of an ethnicity bias within patients presenting with optic neuritis in London.
Design: Observational cross-sectional study.
Methods: The ethnicity profile of all patients attending a neuro-ophthalmology clinic in central London with acute optic neuritis over a 16month period (n=86) was studied.
Background: Glial fibrillary acidic protein (GFAP) is a specific intermediate filament of the cytoskeleton of the astrocyte and may be used as a specific marker for astrocytic damage. It is detectable in the cerebrospinal fluid following a relapse caused by Multiple Sclerosis (MS) and Neuromyelitis Optica (NMO) spectrum disease. Higher levels are found following an NMO-related relapse.
View Article and Find Full Text PDFWe compared the appearance of a line passing through the optic-disc blind spot with that of lines passing just medial or just lateral to the blind spot. Though there is no well-defined gap in the line, we see a consistent difference, which is hard to describe. On the other hand, during a migraine aura experienced by one of us, lines passing through scintillating scotomas showed clear sharply defined gaps.
View Article and Find Full Text PDFBinocular vision provides important advantages for controlling reach-to-grasp movements. We examined the possible source(s) of these advantages by comparing prehension proficiency under four different binocular viewing conditions, created by randomly placing a neutral lens (control), an eight dioptre prism (Base In or Base Out) or a low-power (2.00-3.
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