Normal vision depends on a multi-faceted, compound development. Light passes into the eye through the cornea and lens, with the iris helping to focus the image (Post, 1934). Then light is projected onto the back wall of the eye, where it is perceived by zillions of tiny nerve endings that make up the retina. From here, the retina translates the images into nerve impulses that are transmitted to the brain through the optic nerve (Post, 1934). Blindness: People who are going blind often first deal with vision impairment, which then progresses into blindness. Blindness can affect one or both eyes, and doesn't necessarily cause total darkness. Various people who are considered blind can still see some light or shadows, but cannot perceive anything clearly (Simon & Levin, 1997). When one is legally blind it does not mean that a person cannot see anything, but that their vision is so impaired that they need a lot of help perceiving images (Tielsch, Sommer, Witt, Katz, & Royall, 1990).

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Nearly all cases of blindness in the United States are caused by eye diseases, with less than 4 percent of blindness caused by eye injury or trauma. About 77 percent of people who have eye injuries fully recover, while another 11 percent have mild impairment (Foster & Johnson, 1990).

There are many eye diseases which are looked at as common causes of blindness such as:

Congenital blindness is blindness that happens at birth.

Cataracts which occurs when the normally crystal clear lens of the eye becomes cloudy. This causes blurry vision, faded colors, and problems seeing through glare. Cataracts is known as the number one cause of blindness. (Munoz, West, Rubin, Schein, Quigley, Bressler, & Bandeen-Roche, 2000).

Glaucoma which usually occurs when the fluid pressure inside one or both eyes slowly begins to increase. This pressure damages the optic nerve and the retina, causing a gradual decrease in peripheral vision (Foster & Johnson, 1990).

Macular degeneration involves the gradual deterioration of the macula, or the nerve endings in the retina that are crucial for sharp central vision. People with this condition deal with blurring and blind spots in their central vision (Foster & Johnson, 1990).

Diabetic retinopathy occurs when the systemic damage caused by diabetes begins to affect the retina. Specifically, the blood vessels that nourish the retina can be negatively affected by diabetes, causing vision loss through bleeding and damage to the retina (Foster & Johnson, 1990).

what causes blindness


One third of the brain is dedicated to vision. The whole back section of the brain contains the visual cortex. With blindness there are deficits in the primary and secondary visual cortices. The regions outside the occipital lobe can show significant hypertrophy (Green, Chapman, Kalaska, & Lepore, 2011). Next, the brain’s corpus callosum which aids in the transmission of visual information between the two hemispheres of the brain can be affected. This may be due to the fact that there is a reduced amount of myelination in the absence of visual input. Myelin, the fatty sheaf that surrounds nerves and allows for fast communication, develops rapidly in the very young. Gains in the isthmus and non-occipital white matter can be more widespread. When the onset of blindness occurs in adolescence or later, the growth of myelin is already relatively complete, so the structure of the corpus callosum may not be strongly influenced by the loss of visual input(University of California, 2009). Individuals who are blind show significant volume deficits in dorsal visual cortices, spanning in both the main and minor visual areas in the brain. Volumes can be lower in occipital regions in both hemispheres, with more widespread shortages in the left hemisphere. Occipital regions can have large volume reductions, but these differences can also be seen in other areas blindness (Lepore, Voss, Lepore, Chou, Fortin, Gougoux, & Toga, 2010). Most particularly, the cingulate region presents significant volume decreases, in both anterior and posterior regions. The frontal lobes, the left supplementary motor area and the premotor area can show a decrease in volume also. Subcortical prefrontal and frontal white matter tend to be larger in the blind subjects blindness (Lepore, Voss, Lepore, Chou, Fortin, Gougoux, & Toga, 2010). Additionally, in the parietal lobes, substantial declines are seen in the superior parietal lobule while the parietal subcortical white matter is amplified. In addition, volume excesses may also occur in the volume of the cerebellum which can be an effect of blindness (Lepore, Voss, Lepore, Chou, Fortin, Gougoux, & Toga, 2010) Finally, there is a substantial amplification in areas of the brain not accountable for vision. An example is that the frontal lobes, which are involved with working memory can be found to be abnormally enlarged, perhaps offering an anatomical foundation for some of blind individuals' enhanced skills. (University of California, 2009). The method in which the brain processes visual information undergoes remarkable change in reaction to blindness. First, there are neuroplastic changes that implicate not only processing being carried out by remaining senses, but there is a higher cognitive functions in relation to language and memory (Green, Chapman, Kalaska, & Lepore, 2011).
Understanding Blindness and the Brain (Brian Wandell, Stanford University)


In the brain of an individual that is blind, there visual regions are smaller in volume than in an individual that can see. Another difference is that the non-visual regions are larger in individuals who are blind. The brains in individual who are blind make up for the concentrated volume in areas that are dedicated normally to vision. There is a major difference in the brain’s corpus callosum which helps in the transmission of visual information between the two hemispheres on the brain (Pascual-Leone, Amedi, Fregni, & Merabet, 2005). In an individual that can see, the sight process is where focused light lands on the retina causing neuronal signals to leave the eye through the optic nerve. Then those signals are sent via the lateral geniculate nucleus of the thalamus to the occipital cortex, where the majority of visual processing actually takes place (Amedi, Merabet, Bermpohl, & Pascual-Leone, 2005). In a sighted person they read through visual recognition of words, involving a complex network of language-processing areas intimately related with spatial information processed by the visual system while, a blind individual uses braille to recognize words and interpret meaning patterns (Amedi, Merabet, Bermpohl, & Pascual-Leone, 2005). Braille is an array of raised dots are scanned and spatial information is extracted and interpreted into meaningful patterns that encode semantic and lexical properties. Furthermore, a blind subject also learns to rely on verbal descriptions and verbal memory, in place of visual perception as practiced by sighted subjects (Amedi, Merabet, Bermpohl, & Pascual-Leone, 2005). Finally, another difference looks at the idea of the increasing specialization of the language system in both the sighted and the blind. Language that is normally observed during development may not take place to the same degree in a blind individual since the posterior visual areas do not receive adequate input. In saying that, it is perceived that blind individuals, due to their greater reliance on auditory language signal, may process speech faster than the sighted. Due to the ability to process language that is heard faster, language function may go through the process of reorganization in a blind individual (Roder, Rosler, & Neville, 2000).

Although there are many differences, there are similarities between a blind individual and a sighted such as both a blind and sighted individual can judge materials similarly. Next, their categorization performance is equal. Finally, both the blind and the sighted develop similar haptic representations of materials (Baumgartner, Wiebel, & Gegenfurtner, 2015).

Zvi Zobin: Talk on Reading, Vision & the Brain
The Braille Trail: Inside the Push to Restore Literacy for the Blind​


Amedi, A., Merabet, L. B., Bermpohl, F., & Pascual-Leone, A. (2005). The occipital cortex in the blind lessons about plasticity and vision. Current Directions in Psychological Science, 14(6), 306-311.

Baumgartner, E., Wiebel, C. B., & Gegenfurtner, K. R. (2015). A comparison of haptic material perception in blind and sighted individuals. Vision research, 115, 238-245.

Foster, A., & Johnson, G. J. (1990). Magnitude and causes of blindness in the developing world. International Ophthalmology, 14(3), 135-140.

Green, A. M., Chapman, C. E., Kalaska, J. F., & Lepore, F. (2011). Insights from darkness: what the study of blindness has taught us about brain structure and function. Enhancing Performance for Action and Perception: Multisensory Integration, Neuroplasticity and Neuroprosthetics, 17.

Munoz, B., West, S. K., Rubin, G. S., Schein, O. D., Quigley, H. A., Bressler, S. B., & Bandeen-Roche, K. (2000). Causes of blindness and visual impairment in a population of older Americans: The Salisbury Eye Evaluation Study. Archives of Ophthalmology, 118(6), 819-825.

Pascual-Leone, A., Amedi, A., Fregni, F., & Merabet, L. B. (2005). The plastic human brain cortex. Annu. Rev. Neurosci., 28, 377-401.

Post, L. T. (1934). Definition of blindness. American Journal of Ophthalmology, 17(12), 1167-1168.

Röder, B., Rösler, F., & Neville, H. J. (2000). Event-related potentials during auditory language processing in congenitally blind and sighted people. Neuropsychologia, 38(11), 1482-1502.

Simons, D. J., & Levin, D. T. (1997). Change blindness. Trends in cognitive sciences, 1(7), 261-267.

Tielsch, J. M., Sommer, A., Witt, K., Katz, J., & Royall, R. M. (1990). Blindness and visual impairment in an American urban population: the Baltimore Eye Survey. Archives of Ophthalmology, 108(2), 286-290.

University of California - Los Angeles. (2009). Blindness causes structural brain changes, implying brain can re-organize itself to adapt. Science Daily. Retrieved from: