Chiasmitis caused by Mycobacterium haemophilum in an immunocompromised adult.

We report a case of chiasmitis caused by a rare nontuberculous mycobacterium in an immunocompromised patient. A 44-year-old man with a history of AIDS presented with recurrent vision loss and headache. Magnetic resonance imaging (MRI) demonstrated an enhancing mass involving the optic chiasm. Histopathologic and microbiological evaluation revealed infection with Mycobacterium haemophilum. While combination antimicrobial and steroid therapy contributed to improvement in his vision, the patient's symptoms recurred. Follow-up MRI showed extension of infection to the hypothalamus and leptomeninges, indicative of basilar meningitis. MRI is a valuable tool for early diagnosis of chiasmitis as well as for monitoring infection progression and treatment response.

Optochiasmatic tuberculomas: a vision-threatening paradoxical response in tuberculous meningitis.

The single main cause of death from infectious diseases worldwide is tuberculosis, which is more prevalent in developing countries. Tuberculous meningitis (TBM) is a severe form of TB in which morbidity and mortality depend upon the stage of presentation. Intracranial brain parenchymal tuberculomas may form paradoxically, days to months after starting antituberculous drug therapy. Tuberculomas may develop in and around he optic chiasm and optic nerves after institution of antituberculous treatment as a quite rare occurrence in TBM; this may lead to severe visual loss if not treated properly. We describe a 56-year-old man with documented TBM being treated with first line antituberculous drugs who developed visual impairment 2 months after starting the treatment. MRI after gadolinium administration revealed multiple perichiasmatic and a few parenchymal ring enhancing lesions due to tuberculomas. The patient was treated with corticosteroids and antituberculous therapy was continued after which he recovered his vision gradually. Visual impairment developing in a patient on treatment with antituberculous drugs should give rise to a suspicion of rare optochiasmatic tuberculomas; this necessitates urgent contrast-enhanced MRI of the brain and prompt treatment with steroids.

Tuberculous optochiasmatic arachnoiditis: a devastating form of tuberculous meningitis.

Tuberculous meningitis is primarily a disease of the meninges of brain and spinal cord along with adjacent brain parenchyma. The characteristic pathological changes are meningeal inflammation, basal exudates, vasculitis and hydrocephalus. Tuberculous meningitis has a strong predilection for basal parts of the brain. Exudates, if dominantly present in the interpeduncular, suprasellar and Sylvian cisterns, result in optochiasmatic arachnoiditis and tuberculoma. Optochiasmatic arachnoiditis and tuberculoma are devastating forms of tuberculous meningitis and often associated with profound vision loss. This clinical entity more frequently affects young adults. In a recent study, on the multivariate logistic regression analysis, female sex, younger age and raised cerebrospinal fluid protein content were identified as predictors for developing optochiasmatic arachnoiditis. Frequently, optochiasmatic tuberculoma and optochiasmatic arachnoiditis develop paradoxically while a patient is being treated with anti-TB drugs. MRI reveals confluent enhancing lesions that are present in the interpeduncular fossa, pontine cistern, and the perimesencephalic and suprasellar cisterns. Management of tuberculous optochiasmatic arachnoiditis and optochiasmatic arachnoiditis tuberculoma has been variable. Treatment of optochiasmatic arachnoiditis continues to be a challenge and the response is generally unsatisfactory. In isolated case reports and in small series, corticosteroids, methyl prednisolone, thalidomide and hyaluronidase have been used with variable success. The benefit from neurosurgery is controversial and deterioration may follow the initial temporary improvement. Management of paradoxical optochiasmatic arachnoiditis is also controversial. Some patients regain vision following treatment with anti-TB drugs and continued usage of corticosteroids. Neurosurgery may be considered in the patients with either treatment failure or when diagnosis is in doubt. In conclusion, presence of optochiasmatic arachnoiditis or tuberculoma has important therapeutic and prognostic implications for patients of tuberculous meningitis.

Paradoxical vision loss associated with optochiasmatic tuberculoma in tuberculous meningitis: a report of 8 patients.

BACKGROUND: Paradoxical appearance of new or expansion of existing optochiasmatic tuberculoma, leading to severe vision loss, is a devastating complication in patient with tuberculous meningitis. METHODS: We report a series of 8 cases of tuberculous meningitis that developed paradoxical vision loss associated with optochiasmatic tuberculoma. Clinical assessment and magnetic resonance imaging (MRI) done at presentation, at the time of deterioration, and at 9 months were analyzed. RESULTS: All patients had good vision acuity and normal visual field at baseline. None of them had optochiasmatic tuberculoma on magnetic resonance imaging at baseline, though 3 patients had optochiasmatic arachnoiditis. The mean interval of onset of paradoxical optochiasmatic tuberculoma was 41 days after starting antituberculosis therapy. Paradoxical optochiasmatic tuberculoma was associated with vision deterioration in all patients, 6 of whom developed severe vision loss (vision acuity

Paradoxically developed optochiasmatic tuberculoma and tuberculous lymphadenitis: a case report with 18-month follow up by MRI.

We report the first case ofextracranial tuberculous lymphadenitis which paradoxically developed during treatment of intracranial tuberculoma. Our patient, a 15-year-old girl who initially presented with meningitis and intracranial tuberculomas, developed extracranial tuberculomas during treatment for central nervous system tuberculosis. She was followed clinically with cerebrospinal fluid (CSF) studies and magnetic resonance imaging (MRI) at three monthly intervals. Within 18 months of specific antituberculous treatment, the patient had fully recovered. The course and response to therapy are discussed in light of the current literature.

Chiasmal infarction and sudden blindness caused by mucormycosis in AIDS and diabetes mellitus.

PURPOSE: To report rapidly progressive rhino-orbitocerebral mucormycosis in a 47-year-old woman with both diabetes mellitus and the acquired immunodeficiency syndrome (AIDS). METHOD: Case report including postmortem examination of the eyes, orbit, and brain of a patient with rhino-orbitocerebral mucormycosis, diabetes mellitus, and AIDS. RESULTS: Invasion by hyphae of the Rhizopus species produced an occlusive vasculitis and massive infarction of the optic chiasm. Fungal organisms were discovered in multiple granulomata of the optic nerve. CONCLUSION: Infarction at the optic chiasm probably caused sudden blindness in this patient.

Retrograde transneuronal transport of herpes simplex virus in the retina after injection in the superior colliculus, hypothalamus and optic chiasm.

Immunocytochemistry was used to identify infected cells after injection of Herpes simplex virus (HSV) into the superior colliculus, hypothalamus and optic chiasm. Ganglion cells of the retina were labeled in a pattern consistent with known projections to retinorecipient nuclei. Cells of both the inner and outer nuclear layer were labeled. If this represents retrograde transneuronal transport, then HSV may provide an important tool for studying the neuronal circuitry of the retina.