3 research outputs found

    Toxoplasmosis gondii: An Atypical Presentation of Optic Neuritis

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    Toxoplasmosis gondii is a parasite whose natural host is the cat. Ocular toxoplasmosis can be categorized into two forms of infections: congenital, where an infant is infected in utero; and acquired, where an individual is typically infected by ingesting food contaminated with T. Gondii oocytes. Although acquired infections are rare in the United States, they can occur and toxoplasmosis should be in the differential diagnosis of an infectious optic neuritis. The typical manifestation of toxoplasmosis is a retinochoroiditis, with a “headlight in the fog” appearance, due to dense inflammation of the vitreous; consequently, the diagnosis is often made clinically. This case describes a healthy 36-year-old Hispanic male who had an atypical presentation, with minimal vitritis and papillomacular involvement; thus serology was necessary for a definitive diagnosis. Treatment led to a rapid improvement in vision and ultimately a good prognosis

    Horner\u27s syndrome secondary to neuroblastoma

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    Horner’s syndrome is classically characterized by a triad of miosis, partial ptosis and anhidrosis. The etiology is due to an interruption in the sympathetic innervation to the eye. A prompt diagnosis is crucial, given that Horner’s syndrome could be a manifestation of a life-threatening condition. A thorough case history and clinical evaluation must be employed to arrive at the diagnosis. An important means for confirming Horner’s syndrome is pharmacological testing, which is also used to localize the level where the sympathetic chain is compromised. Following the diagnosis and localization of the lesion, an algorithm should be followed to determine the testing indicated, in order to ascertain the underlying cause of the condition. There is a known association between mediastinal neuroblastoma and preganglionic Horner’s syndrome. We present a case of a seven-year-old boy with a history of excision of a mediastinal neuroblastoma at age two, who soon after presented with signs and symptoms associated with a residual Horner’s syndrome
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