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• W4292854992 abstract "An approximately 30-year-old woman presented to the emergency department (ED) with a 1-month history of headaches, blurred right eye vision, and loss of left eye vision. She denied any head or ocular trauma. On examination, she exhibited 20/30 right eye vision and was unable to count fingers with the left eye. Cranial nerves were intact, and there was no temporal or scalp tenderness. The patient underwent camera ophthalmoscopy and magnetic resonance imaging (MRI) of the orbits (Figure 1, Figure 2 to 3).Figure 2T2-weighted magnetic resonance imaging scan of orbits indicating optic nerve tortuosity and tram-track fluid around the optic nerve (1), consistent with papilledema.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Figure 3T1-weighted magnetic resonance imaging scan of orbits indicating hyperenhancement of the optic nerve (1) and optic disc (2), consistent with papilledema.View Large Image Figure ViewerDownload Hi-res image Download (PPT)DiagnosisPapilledema associated with idiopathic intracranial hypertension. Ophthalmoscopy revealed vascular congestion, optic disc hyperemia, and blurred disc margins, suggestive of papilledema. MRI indicated optic nerve abnormalities consistent with papilledema, including optic nerve tortuosity, tram-track fluid around the optic nerve, and hyperenhancement of the optic disc. Lumbar puncture revealed an increased opening cerebrospinal fluid pressure of 68 mm Hg, confirming the diagnosis of idiopathic intracranial hypertension. The patient subsequently underwent lumboperitoneal shunt placement.The disorder of increased intracranial pressure of unknown etiology, idiopathic intracranial hypertension, is most prevalent in women and the obese and may result from an interruption of axoplasmic transport.1Wall M. Idiopathic intracranial hypertension.Neurol Clin. 2010; 28: 593-617Abstract Full Text Full Text PDF PubMed Scopus (238) Google Scholar,2Cogan D.G. Kuwabara T. Papilledema. Exp Eye Res. 1977; 25: 419-433Crossref PubMed Scopus (6) Google Scholar Key elements of the workup include MRI to rule out structural and vascular lesions and lumbar puncture to confirm increased cerebrospinal fluid pressure (of >20 mm Hg). Definitive treatment includes decompression of intracranial pressure, typically through a lumboperitoneal or ventriculoperitoneal shunt.3Friedman D.I. Contemporary management of the pseudotumor cerebri syndrome.Expert review of neurotherapeutics. 2019; 19: 881-893Crossref PubMed Scopus (9) Google Scholar,4Thurtell M.J. Idiopathic intracranial hypertension.Continuum: Lifelong Learning in Neurology. 2019; 25: 1289-1309Crossref Scopus (18) Google Scholar Early diagnosis and treatment are important to avert permanent vision loss. Although not widely available in EDs, our use of camera ophthalmoscopy facilitated the prompt identification of papilledema and idiopathic intracranial hypertension. An approximately 30-year-old woman presented to the emergency department (ED) with a 1-month history of headaches, blurred right eye vision, and loss of left eye vision. She denied any head or ocular trauma. On examination, she exhibited 20/30 right eye vision and was unable to count fingers with the left eye. Cranial nerves were intact, and there was no temporal or scalp tenderness. The patient underwent camera ophthalmoscopy and magnetic resonance imaging (MRI) of the orbits (Figure 1, Figure 2 to 3). DiagnosisPapilledema associated with idiopathic intracranial hypertension. Ophthalmoscopy revealed vascular congestion, optic disc hyperemia, and blurred disc margins, suggestive of papilledema. MRI indicated optic nerve abnormalities consistent with papilledema, including optic nerve tortuosity, tram-track fluid around the optic nerve, and hyperenhancement of the optic disc. Lumbar puncture revealed an increased opening cerebrospinal fluid pressure of 68 mm Hg, confirming the diagnosis of idiopathic intracranial hypertension. The patient subsequently underwent lumboperitoneal shunt placement.The disorder of increased intracranial pressure of unknown etiology, idiopathic intracranial hypertension, is most prevalent in women and the obese and may result from an interruption of axoplasmic transport.1Wall M. Idiopathic intracranial hypertension.Neurol Clin. 2010; 28: 593-617Abstract Full Text Full Text PDF PubMed Scopus (238) Google Scholar,2Cogan D.G. Kuwabara T. Papilledema. Exp Eye Res. 1977; 25: 419-433Crossref PubMed Scopus (6) Google Scholar Key elements of the workup include MRI to rule out structural and vascular lesions and lumbar puncture to confirm increased cerebrospinal fluid pressure (of >20 mm Hg). Definitive treatment includes decompression of intracranial pressure, typically through a lumboperitoneal or ventriculoperitoneal shunt.3Friedman D.I. Contemporary management of the pseudotumor cerebri syndrome.Expert review of neurotherapeutics. 2019; 19: 881-893Crossref PubMed Scopus (9) Google Scholar,4Thurtell M.J. Idiopathic intracranial hypertension.Continuum: Lifelong Learning in Neurology. 2019; 25: 1289-1309Crossref Scopus (18) Google Scholar Early diagnosis and treatment are important to avert permanent vision loss. Although not widely available in EDs, our use of camera ophthalmoscopy facilitated the prompt identification of papilledema and idiopathic intracranial hypertension. Papilledema associated with idiopathic intracranial hypertension. Ophthalmoscopy revealed vascular congestion, optic disc hyperemia, and blurred disc margins, suggestive of papilledema. MRI indicated optic nerve abnormalities consistent with papilledema, including optic nerve tortuosity, tram-track fluid around the optic nerve, and hyperenhancement of the optic disc. Lumbar puncture revealed an increased opening cerebrospinal fluid pressure of 68 mm Hg, confirming the diagnosis of idiopathic intracranial hypertension. The patient subsequently underwent lumboperitoneal shunt placement. The disorder of increased intracranial pressure of unknown etiology, idiopathic intracranial hypertension, is most prevalent in women and the obese and may result from an interruption of axoplasmic transport.1Wall M. Idiopathic intracranial hypertension.Neurol Clin. 2010; 28: 593-617Abstract Full Text Full Text PDF PubMed Scopus (238) Google Scholar,2Cogan D.G. Kuwabara T. Papilledema. Exp Eye Res. 1977; 25: 419-433Crossref PubMed Scopus (6) Google Scholar Key elements of the workup include MRI to rule out structural and vascular lesions and lumbar puncture to confirm increased cerebrospinal fluid pressure (of >20 mm Hg). Definitive treatment includes decompression of intracranial pressure, typically through a lumboperitoneal or ventriculoperitoneal shunt.3Friedman D.I. Contemporary management of the pseudotumor cerebri syndrome.Expert review of neurotherapeutics. 2019; 19: 881-893Crossref PubMed Scopus (9) Google Scholar,4Thurtell M.J. Idiopathic intracranial hypertension.Continuum: Lifelong Learning in Neurology. 2019; 25: 1289-1309Crossref Scopus (18) Google Scholar Early diagnosis and treatment are important to avert permanent vision loss. Although not widely available in EDs, our use of camera ophthalmoscopy facilitated the prompt identification of papilledema and idiopathic intracranial hypertension." @default.
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• W4292854992 title "Patient with Blurred Vision" @default.
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• W4292854992 doi "https://doi.org/10.1016/j.annemergmed.2022.02.003" @default.
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