[Present status of ethambutol-induced optic neuropathy].

Ethambutol is a commonly used first-line anti-tuberculosis agent, and its most important potential side-effect is ethambutol-induced optic neuropathy (EON). Understanding of the incidence,clinical characteristics, risk factors, prognosis and mechanism of EON is of practical significance in the diagnosis and treatment of this disorder. This article reviews the present status of these aspects.

Toxic optic neuropathy.

Toxic optic neuropathy (TON) is a disease entity which is not only underdiagnosed, but also often diagnosed at a stage when recovery of vision is not possible. This article gives an overview of common causes, clinical features, and management of TON.

[Acute isoniazid poisoning presenting convulsion and liver dysfunction].

A-19-year-old girl ingested 7.4 g of Isoniazid (INH) and 14.5 g of Ethambutol (EB) intentionally. She presented repetitive generalized convulsions with metabolic acidosis, treated with diazepam and 7.5 g of Pyridoxine (Vitamin B6). During day 4 and 5, liver dysfunction worsened and prothrombin time declined below 5%. She was treated with infusion of fresh frozen plasma and fully recovered on day 13. Serum concentration of INH and EB at 5 hours after ingestion was 7.6, 0.94 micrograms/ml respectively.

Neurotoxic effects of acrylamide on rat retinogeniculate fibres.

The common laboratory chemical, acrylamide, causes various clinical effects including dysfunction of the visual system. Previous electrophysiological recordings from the rat lateral geniculate nucleus (LGN) following exposure to acrylamide suggested that X-like cells were selectively disrupted by the neurotoxin. This study examines the possibility that the diameter of the optic tract fibres may underlie their differential susceptibility, but shows that fibres of all sizes are affected by acrylamide intoxication and the results suggest that the selective effect of acrylamide is not due simply to disruption of optic tract fibres.

Clinical ERG findings in ethambutol intoxication.

The human electroretinogram (ERG), evoked by white flashes of extremely short duration (10 microseconds), shows a typical dependence on flash intensity. Increasing stimulus intensity increases the amplitude of the a-wave until saturation is reached. The amplitude of the b-wave reaches a maximum value with flashes of middle intensity, then decreases at higher stimulus strengths. The values of a-wave amplitude saturation, defined as 100%, may serve as a basis for standardizing the various amplitude-intensity relationships of the a- and b-wave. The b-wave function, calculated in this way, shows different maximum values depending on whether it was determined after light adaptation or in dark adaptation and low interindividual variability. However, the difference between bmax in dark and light adaptation is markedly decreased in the case of ethambutol intoxication. ERG changes are only detected in severe cases (total central scotoma) and are below the discrimination level in cases with moderate symptoms (relative central scotoma, visual acuity greater than 0.4-0.5).