It has been hypothesized that the retina is a site of functional and structural changes in neuropsychiatric disorders, including Parkinson’s Disease (PD), Alzheimer’s Disease (AD) and schizophrenia (Silverstein 2015). The RNFL thickness which mirrors the structural ganglion cell damage is said to be a speculum of brain neurodegeneration, progression of RNFL thinning parallels disease progression in PD (Satue et al., 2014), Multiple Sclerosis (Ratchford et al., 2014), AD (Parisi et al., 2001) and Schizophrenia (Silverstein et al., 2015). As functional alterations in the retina precede structural damage, electroretinography is ideally suited to reveal these subtle losses. Loss in contrast sensitivity and changes in pERG signals have been observed in PD, (Wollner et al., 1987; Gottlob et al., 1987; Tagliati et al., 1994; Tagliati et al., 1996; Peppe et al., 1998; Sartucci et al., 2006) AD, (Katz et al., 1989; Gary L. Trick, Principles and Practice of Clinical Electrophysiology of Vision; Karsodomska et al., 2010), with suggestive evidence being found in Schizophrenia (Silverstein et al., 2015). The functional and structural accessibility of retinal health through electroretinography provides a clinically advantageous platform to study the extent to which these alterations can act as biomarkers to changes in the brain. A diagnostic tool more sensitive to peripheral ganglion cell activity can prove useful in early assessment of functional damage and may ultimately aid in monitoring at-risk individuals or those currently undergoing treatment for neuropsychiatric disorders.