This is part one of a three-part article published to health.mil.
Vision Problems After Brain Injury
Visual problems following brain trauma are frequent and often complex. It is probably easiest to define the problems based upon how they affect incoming visual information (i.e., the afferent visual pathways) or the outflow of information to the visual organs (i.e., efferent visual pathways). Afferent defects include reduction in visual acuity, visual field, color vision, contrast sensitivity, comfort (usually as it relates to glare), and higher level visual processing, including recording of visual memory and comprehension of visual stimuli. Efferent defects include reduction of the ability to visually pursue a target, focus the lens inside the eye, train the two eyes onto a single target, maintain gaze once a visual target is obtained, and open and close the eyelids. In this three part series, we will describe 1) damage to the afferent visual pathways, 2) damage to the efferent visual pathways, and 3) the role of the neuro-ophthalmologist in visual restoration and rehabilitation.
The Afferent Visual Pathway and How Brain Injury Can Affect It
Light enters the eye through the cornea, the clear window of the eye. The cornea provides the majority of the focusing power of the eye, and is an extremely poor refractive surface, but with a healthy tear film it becomes nearly perfect. Brain injury often causes dry eye thereby reducing visual acuity. Furthermore, brain injury patients often lose an adequate blink response or develop lagophthalmos, the inability to completely close the eye. Dry, unprotected corneas are subject to scarring and infection.
Trauma to the brain often entails injury that can also shake or directly damage the eye along with the rest of the body. Patients suffering a blast injury can experience rapid elevation of pressure in the chest, which is then transmitted by the blood vessels to the retina, the neural tissue lining the inner wall of the eye. This is the tissue which converts light rays into the electrical impulses that are sent to the brain. The retinal blood vessels can rupture from the sudden increase in pressure and cause bleeding within the retina, a condition called Purtscher's retinopathy. The free blood inside the eye can cause significant scarring and loss of vision.
Direct head trauma can also cause the eye to move too quickly and/or too far relative to the fixed structures in the eye socket. This can cause stretching or shearing of the optic nerve, the nerve that carries visual information to the brain. This traumatic optic neuropathy often can result in permanent visual impairment. Multiple direct head traumas also are a risk factor for problems within the eye itself, such as detachment of the retina from the back of the eye, or formation of a cataract, a clouding of the natural lens.
Trauma to the head invariably is associated with some degree of trauma to the neck, a risk factor for damage to the blood vessels of the neck. Injury to the wall of an artery can cause it to bulge (i.e., form an aneurysm) or separate from its inner lining (i.e., arterial dissection). Either situation can lead to abnormal blood flow to the visual pathways of the brain. Furthermore, either condition can cause the vessels to physically compress portions of the visual pathways, such as the nerves that control the eye muscles or the nerves that bring visual information to the brain. This could result in double vision or in reduction of visual acuity and visual field, respectively.
It has been demonstrated that the world we see is formed into a map upon our brain, specifically onto an area called the visual cortex. This map is organized such that the image of the world is inverted and reversed; the left side of our brain sees what is to the right of where we look and the right side of the brain sees light from the left of where we gaze. Furthermore, visual information emanating from above our visual point of interest is transmitted to the lower portion of the visual cortex while the upper portion of the visual cortex maps the visual world below the object of regard. It is for this reason that damage to the visual cortex causes loss of peripheral vision rather than simply loss of visual clarity.
While we do not know how visual memories are created or stored in our brains, it is known that brain injury slows the acquisition and processing of visual information and impairs the formation of visual memory. Recent research has suggested that these impairments may result from stretching or shearing of nerve fiber bundles after head injury. Sadly, higher level visual processing failure is often particularly difficult for a patient to express. Neuropsychologists have proven to be critically important for the diagnosis of these problems and for guidance in directing rehabilitation efforts.