Dear Editor,In the article titled “Isolated traumatic chiasmal syndrome with hemifield slide phenomenon: A case report”, the authors have mentioned the sequelae of chiasmal trauma following head injury (HI).[1] We would like to highlight a few points regarding the difficulty in diagnosing nutritional optic neuropathy (NON) in HI patients. In critically ill patients, pre-existing malnutrition, the severity of current illness, and side effects of therapeutic regimens are responsible for micronutrient deficiency.[2] In our neuro-ophthalmic clinical practice, we observed bilateral defective vision and optic disk pallor in a few patients who have undergone intensive care treatment and surgical intervention following HI. The patients were not aware of the exact point of onset of defective vision in the timeline of events, i.e., before HI or following HI (acute/recovery phase). The patients were aware of the cessation of visual acuity loss during the recovery phase. Probably tobacco-alcohol abuse caused NON. Vitamin supplementation during neurointensive care and abstinence during the recovery phase of HI prevented the worsening of NON. We explained the significance of abstinence/de-addiction therapy to these patients. In alcohol dependence syndrome, sudden blurring of vision may develop in the background of excess alcohol consumption following a period of abstinence.[3]Alcohol abuse is a common problem in our society. Chakrabarty et al.’s[1] case report mentioned the role of steroids in HI patients. There is evidence to suggest that steroid use in HI may cause harm in certain situations.[4] Our assumption is that NON has to be considered if there is a history of chronic alcohol consumption, gastrointestinal surgery, or proton pump inhibitor therapy in the above-mentioned chiasmal injury (CI) patient. Nutritional deficiency may involve chiasma.[5] Nutritional chiasmopathy in HI patients might be attributed to the CI. To conclude, CI may conceal concurrent NON, thus, a treatable condition might be overlooked.