The visual system is one of the most energetically demanding systems in the brain. The currency of energy is ATP, which is generated most efficiently from oxidative metabolism in the mitochondria. ATP supports multiple n...The visual system is one of the most energetically demanding systems in the brain. The currency of energy is ATP, which is generated most efficiently from oxidative metabolism in the mitochondria. ATP supports multiple neuronal functions. Foremost is repolarization of the membrane potential after depolarization. Neuronal activity, ATP generation, blood flow, oxygen consumption, glucose utilization, and mitochondrial oxidative metabolism are all interrelated. In the retina, phototransduction, neurotransmitter utilization, and protein/organelle transport are energy-dependent, yet repolarization-after-depolarization consumes the bulk of the energy. Repolarization in photoreceptor inner segments maintains the dark current. Repolarization by all neurons along the visual pathway following depolarizing excitatory glutamatergic neurotransmission preserves cellular integrity and permits reactivation. The higher metabolic activity in the magno- versus the parvo-cellular pathway, the ON- versus the OFF-pathway in some (and the reverse in other) species, and in specialized functional representations in the visual cortex all reflect a greater emphasis on the processing of specific visual attributes. Neuronal activity and energy metabolism are tightly coupled processes at the cellular and even at the molecular levels. Deficiencies in energy metabolism, such as in diabetes, mitochondrial DNA mutation, mitochondrial protein malfunction, and oxidative stress can lead to retinopathy, visual deficits, neuronal degeneration, and eventual blindness.
A 36-year-old woman with a 3-month history of progressive visual loss had papilledema, dilatation of the optic nerve sheaths and normal cerebrospinal fluid pressures. She was diagnosed as dural ectasia of the optic nerve...A 36-year-old woman with a 3-month history of progressive visual loss had papilledema, dilatation of the optic nerve sheaths and normal cerebrospinal fluid pressures. She was diagnosed as dural ectasia of the optic nerve sheaths and surgical decompression was performed. In this case report, severe visual loss is described as a serious complication of this rare disease and the importance of early surgical intervention is emphasized.
INTRODUCTION: Neurotrophic keratitis, a degenerative corneal disease caused by trigeminal nerve impairment, has many etiologies and remains very difficult to treat. METHODS: Case report of a 23-year-old male with a right...INTRODUCTION: Neurotrophic keratitis, a degenerative corneal disease caused by trigeminal nerve impairment, has many etiologies and remains very difficult to treat. METHODS: Case report of a 23-year-old male with a right corneal ulcer that failed to improve despite broad-spectrum antimicrobials. RESULTS: Prior diagnosis of disseminated lymphangiomatosis with a lesion in the right petrous apex effacing Meckel's (trigeminal) cave in conjunction with a history of nonhealing corneal abrasions suggested a neurotrophic etiology. Drawstring temporary tarsorrhaphy, in addition to antibiotics and autologous serum, lead to successful clearing of the infection and resolution of the corneal ulcer. Visual acuity improved from light perception (LP) at the peak of infection to 20/40 six weeks after treatment. CONCLUSIONS: To our knowledge, we report the first case of neurotrophic keratitis in a patient with disseminated lymphangiomatosis that caused a mass effect in Meckel's (trigeminal) cave leading to compression of the trigeminal nerve. The antibiotic-resistant corneal ulcer was successfully treated with drawstring tarsorrhaphy, confirming the utility of this therapeutic measure in treating neurotrophic keratitis.