China
Africa
Explore chapters and articles related to this topic
Infectious Optic Neuropathies
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Imran Rizvi, Ravindra Kumar Garg
Ophthalmological manifestations are common in syphilis. Common eye complications are scleritis, panuveitis, dacyroadenitis, chorioretinitis, vitritis, keratitis, oculomotor palsies and optic neuropathy.33 Ocular involvement is generally part of central nervous system involvement. The optic nerve in syphilis is involved in secondary or tertiary stages.2 The syphilitic optic neuropathy can be unilateral or bilateral, often without involvement of the anterior segment.2 Syphilitic optic neuropathy presents either as papillitis, chiasmal syndrome, neuroretinitis, optic nerve gumma or optic nerve perineuritis.34–36 There can also be cortical vision loss. Appropriate tests for the diagnosis of ocular syphilis are fluorescent treponemal antibody absorption assay or the Treponema pallidum particle agglutination assay. The non-treponemal tests, like venereal disease research laboratory (VDRL), fail to diagnose late stages of syphilis.37 Intravenous penicillin G is the drug of choice for all forms of syphilis. Intramuscular benzathine penicillin along with oral probenecid is another option. Newer treatment options include drugs with good cerebrospinal fluid penetration, like ceftriaxone and azithromycin.38
Hemifield-slide diplopia successfully managed with botulinum toxin injection in a patient with traumatic chiasmal disruption
Published in Clinical and Experimental Optometry, 2022
Kaveh Abri Aghdam, Ali Aghajani, Faeze Hashemi Rahbarian, Mostafa Soltan Sanjari
Traumatic chiasmal syndrome can be accompanied by various ocular and non-ocular complications, including cranial nerve palsies, various degrees of visual disturbances, carotid-cavernous fistula, and pituitary hormone imbalances.3 One suggested mechanism for chiasmal injury is the shearing forces applied to the optic chiasm that cause selective stretching and tearing of crossing axons of this structure. Another proposed mechanism is chiasmal ischaemia due to traumatic arterial disruption. Contusion necrosis or compression necrosis of the herniated gyrus rectus are other suggested mechanisms for chiasmal injury after trauma.4
Coexistence of Papillitis and Posterior Placoid Chorioretinopathy as the Presenting Symptoms of Syphilis-Human Immunodeficiency Virus Coinfection
Published in Neuro-Ophthalmology, 2019
Omer Karti, Dilek Top Karti, Hulya Ozkan Ozdemir, Neslihan Eskut, Mehmet Ozgur Zengin, Tuncay Kusbeci, Ali Osman Saatci
Syphilis is considered to have four disease stages: primary, secondary, latent, and tertiary stages. Ocular syphilis, a rare manifestation of syphilis, usually occurs in the secondary or latent stages. It is more common in males and often affects both eyes.13,14 Uveitis is the most common ocular manifestation of syphilis that may affect both the anterior and posterior segments of the eye.15 While anterior uveitis is more common in immunocompetent patients, posterior uveitis is more common in HIV-infected patients. Shalaby et al.16 reported that the rate of posterior uveitis was 38%, and that of anterior uveitis was 31%, in patients with ocular syphilis and HIV coinfection. Anterior uveitis can be nongranulomatous or granulomatous, mimicking ocular sarcoidosis and tuberculosis. Posterior uveitis most often presents as a chorioretinitis but can also occur with retinitis alone. Acute syphilitic posterior placoid chorioretinitis (ASPPC) refers to the presence of one or more placoid, yellowish, outer retinal lesions, typically in the macula, and was first used by Gass et al.10 Besides typical lesions, cases of ASPPC may also be characterized by focal, yellow, and deep retinal lesions. FAF, FA, indocyanine green angiography (ICGA), and OCT provide additional useful information about pathological processes. FAF patterns of ASPPC have been described in detail and the active placoid lesion is hyperautofluorescent. This may suggest lipofuscin accumulation at the level of the RPE-photoreceptor complex and is the most typical presentation of placoid syphilis.17 Unlike most previous studies, our case was presented with mottling hypoautofluorescence and hyperautofluorescence. This pattern is uncommon in ASPPC, but has been described previously.17 Early phase FA exhibits either hypofluorescence or faint hyperfluorescence. Scattered hypofluorescent spots are often observed in the area corresponding to the yellowish opacification; this pattern is sometimes called “leopard spotting.” However, progressive hyperfluorescence is observed in the mid- and late-phase FA. ICGA characteristics of ASPPC reveal early phase hypofluorescent areas corresponding to lesions that persist into later phases of angiography. 10,18–20 In some patients, late-phase ICGA hyperfluorescence in affected areas has also been described.20,21 Burkholder et al.22 reported OCT findings including thickening and hyperreflective nodularity of the choroid-RPE complex, with disruption of the overlying photoreceptor IS/OS bands and ELM in the areas corresponding to retinal lesions in patients with ASPPC. Optic nerve involvement, one of the causes of vision loss in syphilis, usually occurs in secondary and tertiary stages of syphilis. Optic nerve involvement may occur as neuroretinitis, gumma of the optic disc, papillitis, optic disc cupping, optic atrophy, perineuritis or chiasmal syndrome.23–29