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Chlorpromazine is known to cause ocular pigmentary deposits. However, delayed presentation after cessation of chlorpromazine has not been reported. There are also no reports on whether newer generation of anti-psychotic agents contribute to ocular toxicity. We describe a case of ocular toxicity related to anti-psychotic agents. To the best of our knowledge, this is the first reported case of anterior segment pigmentary deposits associated with olanzapine use, 2 years after the cessation of chlorpromazine. We report a case of ocular toxicity in a patient with history of chlorpromazine usage of 100 mg per day for 13 years and subsequently switched to olanzapine 5 mg for 2 years. There were no signs of ocular toxicity while the patient was on chlorpromazine. However, when the patient switched to olanzapine, she developed the ocular side effect as described for chlorpromazine-induced ocular toxicity, with pigmentary depositions on both corneas and the anterior lens surface and decrease in vision. Olanzapine, a newer anti-psychotic agent, may play a role in the ocular pigmentary deposition, either directly causing pigmentary deposition itself or accentuating the effect of chlorpromazine as the 2 drugs act on the same receptors, although further studies are required to support this hypothesis. As patients with psychiatric conditions may not voluntarily complain of visual symptoms, ocular screening could be considered in these patients receiving chronic anti-psychotic treatment, so that any ocular toxicity could be diagnosed in a timely manner.

Optic nerve regeneration is an important area of research. It can be used to treat patients suffering from optic neuropathy and provides insights into the treatment of numerous neurodegenerative diseases. There are many hurdles impeding optic regeneration in mammals. The mammalian central nervous system is non-permissive to regeneration and intrinsically lacks the capacity for axonal regrowth. Any axonal injury also triggers a vicious cycle of apoptosis. Understanding these hurdles provides us with a rough framework to appreciate the essential steps to bring about optic nerve regeneration: enhancing neuronal survival, axon regeneration, remyelination and establishing functional synapses to the original neuronal targets. In this review article, we will go through current potential treatments for optic nerve regeneration, which includes neurotrophic factor provision, inflammatory stimulation, growth inhibition suppression, intracellular signaling modification and modeling of bridging substrates.