Search

Tuberculosis (TB) is a global health problem with the major brunt of disease occurring in developing countries. The cornerstone of treatment of TB is anti-tubercular therapy (ATT), which includes rifampicin, isoniazid, pyrazinamide and ethambutol. Because of emerging drug resistance, treatment failures, defaulters and increasing incidence of disseminated and extrapulmonary TB, the guidelines have been modified in some countries. Ethambutol is prescribed for longer times (in some cases8 months) and hence the incidence of ethambutol-induced optic neuropathy (EtON) is expected to rise. The fundamental question which needs explanation is why only a small subset of patients on ethambutol are prone to develop loss of vision. This review focuses on available genetic studies which provide evidence that mitochondria are the likely substrates involved in the final pathway of reactive oxidative damage of the papillo-macular bundle. Genetic analysis of mitochondrial mutations encoding genes involved in oxidative phosphorylation pathways may help in isolating the subset of patients who are genetically susceptible. If the groups having high risk of developing EtON are recognised then prolonged duration of ethambutol treatment can be avoided in these susceptible individuals. A better understanding of the pathophysiology will also pave the way for the development of management strategies in this condition.

We prospectively evaluated 22 consecutive patients (24 eyes) suffering from non-arteritic anterior ischaemic optic neuropathy (NAION) at a tertiary care centre in Northern India. The mean age was 51.7 years. Visual loss on awakening was noticed only in three (12.5%) eyes. Six (27.3%) patients had headache while three (9.7%) patients had retro-orbital pain at the onset of visual loss. Peripapillary haemorrhages were seen in two (8.3%) eyes. At follow up, only one eye showed improvement in visual acuity. The results of our study suggest that NAION may not always present with the classic clinical picture. Accordingly, a high index of suspicion remains the key to correct diagnosis.

The importance of ovarian teratoma as a cause of opsoclonus myoclonus ataxia syndrome (OMAS) and other paraneoplastic syndromes continues to be underestimated. A strong suspicion and appropriate diagnosis remain keys to successful outcome of paraneoplastic OMAS with ovarian teratoma. We report a 14-year-old girl with paraneoplastic OMAS in association with an ovarian teratoma who improved completely following resection of tumour as well as immunotherapy and review the literature briefly.

Despite the potential of Idiopathic Intracranial Hypertension (IIH) to cause visual morbidity, limited literature is available focussing on predictors of visual outcome in IIH. This study was planned to assess visual morbidity in patients of IIH in terms of clinical and neuro-ophthalmo- logical parameters. In this prospective study of 40 patients of IIH, neuro-ophthalmological parameters were noted in the form of visual acuity, visual field, contrast sensitivity, Retinal Nerve Fibre Layer thickness, and visual evoked potential. Visual outcome was defined in using specific criteria. Final visual outcome of patients was compared with clinical and neuro-ophthalmologic para- meters to determine any correlation. The most common presenting clinical symptoms were headache (85%) and Transient visual obscurations (TVOs) (52.5%). In univariate analysis severity of visual loss, Cerebro Spinal Fluid (CSF) pressures and abnormal Visual evoked potential (VEP) were associated with worse visual outcome or need of aggressive management. When adjusted for severity of visual loss no independent clinical/neuroophthalmic predictor could be established. High CSF opening pressure, worsening vision/papilledema, greater Retinal Nerve Fiber Layer (RNFL) thickness and abnormal VEPs may be some of the alarming signs for physicians, but none of these parameters can be used as an independent predictor for visual outcome in isolation. Visual loss at presentation is probably the most important predictor of the final visual outcome in these patients. This may also suggest that patients presenting in an advanced disease course (with worse visual status) fair badly despite best medical/surgical management. Early diagnosis and prompt management is the cornerstone of management.

Optic disc edema may be caused by a number of conditions. A commonly ignored but important aspect is the presence of “infiltration” of disc; that may closely mimic disc edema. Disc edema, optic nerve dysfunction and a normal appearing disc in any combination may occur in infiltrative optic neuropathies. Identifying disc infiltration can aid in diagnosis of many sinister pathologies even in the absence of other specific clinical features. We describe two patients presenting with optic nerve dysfunction and infiltrated disc appearance, which on investigations were found to have underlying malignancies thereby underscoring the importance of detecting infiltrative optic neurpathies.

A young male with acute blurring of vision (6/9) complained of an inferior altitudinal field defect in right eye. Clinical ophthalmological examination was normal. Magnetic resonance imaging (MRI) of the brain revealed the expansion and mucosal thickening of right posterior ethmoid and sphenoid sinuses and opacified right maxillary sinus. Surgical intervention (transethmoidal sphenoidotomy) and histopathological examination revealed chronic invasive granulomatous fungal sinusitis. Anti-fungal therapy led to resolution of visual complaints and restoration of visual field defects.

Tuberculosis never stops fascinating physicians. The burden of tuberculosis is a major cause of disability. While drugs are often blamed when patients develop new focal deficits on treatment, the deterioration in these patients can have a myriad of causes including the development of new tuberculomas. Recognizing the critically located tuberculomas as potential causes of vision loss is indispensable. Here, we report two patients with strategic tuberculomas leading to vision loss. In one patient, the cause of visual morbidity was compression of the optic pathways; in the other patient, cortical vision loss was noted due to strategic location of tuberculomas.