VISION  [ back to Recovering from a Brain injury ]
Trauma to the head which contuses (bruises) or torques (violently rotates) the brain, can cause a variety of visual disorders. Neurologists encounter visual disorders in 20% of all cases of TBI. It is typical for a neurologist to evaluate a visual defect primarily (or exclusively) as a clue to the presence or absence of other kinds of brain damage. However, visual disorders from TBI should be assessed and treated on their own merits, because they can complicate and prolong overall recovery. Of all 5 modes of human sensory perception, vision is the most highly developed and the one upon which we are most dependent. Experts estimate that 85% of perception, cognition and learning take place primarily through seeing - as opposed to hearing, smelling, tasting or touching. Most people have a deep-seated fear of blindness. When they experience visual problems following brain trauma, they tend to be quite alarmed and frightened. Blurry vision interferes with reading and with watching TV, videos or movies - thus restricting visual learning. Loss of depth perception interferes with walking, running, cycling, driving and with physical activities requiring manual dexterity and eye-hand coordination, such as writing and drawing. Even the milder forms of visual disorders definitely merit medical attention. Visual disorders which are serious or persistent merit referral to a neuro-opthalmologist or neuro-optometrist.

Common examples of visual problems resulting from closed head trauma are photophobia, floaters, reduced peripheral vision, visual field defects, accommodation (focusing) defects, gaze stabilization defects such as nystagmus (shaking of the eye causing jittery images) and gaze shifting defects (causing blurred or doubled images with eye strain from oculo-motor palsy or convergence deficits).

Photophobia is excessive sensitivity to, and intolerance of, bright light. This tends to go away and can be mitigated by tinted glasses and staying out of bright lights while symptoms continue. The exception is for patients with post-traumatic migraine, who continue to experience photophobia whenever they have a migraine headache. Floaters are bright, scintillating specks of light. They may result from rupture of tiny capillaries in the retinal blood supply or from hyper-excitation of the occipital lobes, which may be bruised from frontal or rear impact to the head. These also tend to diminish over time. Visual field defects are blank spots or holes in one's vision which tend to result from stretch injury to the optic nerve or brain stem or from contusion to the occipital lobe. This is a very serious problem, which can be permanent, and needs to be assessed by a neuro-ophthalmologist.

Blurred vision is sometimes the result of diminution of the brain's capacity to "fuse" the separate images coming through the optic nerve from the left and right eye to the primary visual cortex in the occipital lobe. Brain injury can interfere with the coordinated targeting of gaze shifting in response to movement of the objects of vision. This can be a mechanical issue involving differential slowing of nerve impulses to the muscles swiveling both eyes or a cognitive issue. Neuro-optometrists (also called functional optometrists) will prescribe visual exercises to foster restoration of fusion and coordinated gaze tracking. One device that may help some patients with reading is the PRIMER, an electronic magnification device that looks and feels like a computer mouse, which the patient runs over the page of the book he is reading, which then displays the words on a screen many times larger and sharper. Interested persons can call Innovations, Inc. in Littleton, Colorado, at 800-854-6554 or 303-797-6554. The device costs $295.

Problems seeing can involve a cognitive element. The problem is cognitive when the brain injury diminishes the person's intuitive capacity to recognize when he is looking in the right place and when not. A hunter scanning the scene in front (from the tall grass, shrubs, rocks and trees) can rapidly switch gaze from left to right, cancel that eye movement and refocus at a distant spot to his left, as he tracks meaningful movements of the flora and fauna. In a study published by Dr. Jeffrey Schall and colleagues of Vanderbuilt in the 12/26/00 issue of Nature, this was half-humorously dubbed the "oops" response (as when we know we hit the wrong typewriter key) and the "yippee" response (as when we know we have released the bowling ball just right to get a strike). When these internal brain responses are accurately geared to our actions in the "real world" there is a good fit between cognition and control over eye movement. When TBI disrupts the connection, the visual errors we make in visual tracking mirror our cognitive disorganization.

There is also a problem known as visual neglect, seen most commonly after stroke, but sometimes following TBI. Visual neglect occurs when due to brain damage (especially to the right side of the brain), the person stops processing visual information in one or more quadrants of vision, but has no conscious awareness of the missing piece or "hole" in his visual world. The test examiner can stand in the "hole," and make funny faces, even obscene gestures, yet get no response from the test subject, who has no awareness of anything going on in that area.

Floaters and visual field defects, as well as blurry vision, may also result from post-traumatic migraine headaches. Such headaches involve hyper-excitation of the trigeminal nerve (which has branches to the forehead and eyes) and reduced bloodflow to various parts of the head including the retina and the muscles of accommodation which help us focus our vision. Not all patients with post-traumatic migraine (intense, throbbing headache with sensitivity to light, sound and/or odors, often accompanied by nausea) experience the hallucinatory lightshow called migrainous aura. Some experience no aura, but instead "migraine equivalents" which include visual disturbances, mental confusion, dizziness and the like. It is common for such patients to be treated as hysterics or fakers by ophthalmologists, since their eye structures, extra-occular muscles and optic nerve look normal. Our office had one client who complained of throbbing headache, dizziness and blurry vision and vomited all over the eye doctor's floor while trying to read the eye chart. Instead of referring her to a headache specialist, he suggested she was malingering because she could read the chart.

The eyes on the human face are designed to work together so the brain can smoothly fuse their separate images into one clear and stable visual perception of an object. Double vision is highly disorienting and disturbing to people, who will cover one eye or turn their heads at odd angles to stop it. Vision deficits from a brain injury can significantly interfere with and restrict driving, reading, computer keyboard use, food preparation, craft making, sports participation and many other activities. They can partially or completely disable someone from work, especially if no compensatory techniques exist to substitute for poor vision skills on the job. In the April 2000 edition of Brain (Vol. 123:28-35) researchers reported finding abnormalities in involuntary saccades of whiplash patients who complained of dizziness, poor concentration and headache, which they attributed to traumatic frontal lobe dysfunction. The abnormalities included delay in involuntary tracking and inability to inhibit unwanted eye tracking. Patient groups without head trauma and those with head trauma who were non-symptomatic, did not show these abnormalities.

The visual system consists of hardware and software. The hardware consists of the eyes (including cornea, lense, pupil, iris, retina and macula), eyelids, eye sockets and the 6 extra-occular muscles which move the eyes. Ophthalmologists are trained to diagnosis and treat disease and injury involving the hardware of the visual system. Their treatment often involves surgery, such as lense transplants for glaucoma, sewing detached retinas or shortening the rectus muscles to correct strabismus problems like crossed-eyes or wall-eyes. They are very comfortable dealing with the hardware, because it is easily visible and accessible, and surgically correctable when malfunctioning. Opthalmologists will readily support a patient's claim of visual damage secondary to a brain injury when they find "strabismus," which is the inability of a patient to direct both her eyes to the same target. A patient who develops an inward deviation of one eye (esotropia) within 24-48 hours a head injury is believed to have suffered a traumatic stretch injury to the 6th cranial nerve (the Abducens) with lateral rectus muscle palsy rendering him unable to abduct the eye. A patient who develops outward deviation of one eye (exotropia) in the same time frame following a head injury is believed to have suffered traumatic stretch injury to the 3rd cranial nerve (the Occulomotor) with medial rectus muscle palsy rendering him unable to adduct the eye. 3rd cranial nerve damage may cause a patient to lose automatic pupillary constriction in the affected eye when a light is shone directly in it. Such a patient's other eye (the one in which no light is shone) will reflexively constrict, because the pre-tectal area of his brain which controls that response is still working. A patient who develops hyperopia (inability to move one eye vertically up) right after a head injury is believed to have suffered traumatic damage to his trochlear nerve with palsy of the superior oblique muscle, causing the eye to look down. The visual disorders cause diplopia (double vision) which can be corrected with prisms fitted to one's glasses. They can be treated by an ophthalmologist by weakening of the the opposite eye muscle which is not palsied, either by injection of Botox (botulinum toxin) or surgical shortening.

The software of the visual system consists of the neural wiring of the optic nerve, the optic chiasm, the optic tracts and their offshoots, the lateral geniculate nucleus (LGN) of the thalamus, the optic radiations from the LGN and the visual cortex located at the back of the brain in the occipital lobe. The wiring is made up of thin, delicate axons and the visual processing units in the LGN and visual cortex consist of tiny living cells with fragile membranes. The axons are vulnerable to stretch/strain damage and the cells are vulnerable to shaking or perturbation which can damage or kill them. Closed head trauma causing "mild TBI" (with minimal or no loss of consciousness) frequently traumatizes the software of the visual system with disruption of binocular vision such as blurry or double vision. However, closed head brain trauma which damages the vision software causes no detectable mechanical damage to eye structures and no cranial nerve damage with easily detectible strabismus or hyperopia. The patient's eyes look fine. He can still read an eye chart. His brain shows no bleeding on CT or swelling/compression on MRI. In such cases, and there are many thousands every year, the typical ophthalmologist chalks up the patient's complaints of double vision to "hysteria" or "malingering," especially when they learn a claim has been filed. This not only wounds the feelings of the patients (who know they are telling the truth, their vision really is double) but deprives them of necessary treatment and may ruin their personal injury lawsuit or workers compensation claim without good reason.

What can be done when you have vision problems consequent to a mild TBI, where the damage is to the visual system software, consisting of tiny structures lying inaccessible to inspection deep within the brain? There is a specialty group of optometrists, sometimes called "functional optometrists" and sometimes"neuro-optometrists" who are trained in the neuro-physiology of human vision, how to test for traumatic damage to the visual software and how to treat the resulting impairments of vision through vision restoration therapy. Neuro-optometrists are respected professionals who work at hospitals and clinics all over the country and who are reimbursed by big HMOs. However, when litigation ensues over a brain injury and the forensic "experts" get involved, you can be sure an ophthalmologist working for the liability, disability or worker's compensation insurance carrier will say that neuro-optometrists are quacks and their findings and opinions have no validity. This is a situation which needs to change, which is reminiscent of the old battles between orthopedic surgeons and chiropractors. Meanwhile, a person with a TBI who is experiencing visual disturbance, but who has been declared "normal" by the eye doctor, should consults an experienced neuro-optometrist and give visual restoration therapy a try. Neuro-optometrists are not quacks. They are duly licensed optometrists (ODs) who have not only become Fellows of the American Academy of Optometry (FAAOs), but have gone on to become Fellows of the College of Optometrists in Vision Development (FCOVD). Many of them are members of NORA (the Neuro-Optometric Rehabilitative Organization). Their interest lies in traumatically induced disturbances of vision from damage to the software of the brain. They do not prescribe drugs or surgery. They work to restore normal visual function by means of a structured program of visual exercises.

For those interested in the fine points of neuro-anatomy, I have included a detailed description of the visual software system at the very end of this section on vision. Here I want to give a more generalized description of vision problems one typically sees after a TBI. Photophobia is hypersensitivity to and intolerance of light and is often the result of post-traumatic headache, including migraine and cluster. It can also result traumatic damage to the occipital lobes. Floaters s are tiny spots before the eyes which can be black or silvery and shimmering. They can result from a partially detached retina or from rupture of tiny blood vessels in the retina which leak blood into the vitreous humor of the globe. They can also occur with occipital lobe damage. A visual field defect is a discrete hole in one's visual field, in which nothing is visible. It is caused by traumatic damage to the optic nerve, the lateral geniculate nucleus or the visual cortex in the occipital lobes. The site of damage can be localized depending on where the hole sits in the 4 quadrants of vision (left upper/lower or right upper/lower). People with visual field defects tend to tilt their head so they can look around the blank spot. Optometrists can detect visual field defects using visual confrontation testing. This involves placing the patient's head on chin bar, having him watch a blank screen in a darkened box, and click a counter the instant he notices tiny spots of light appear at the edges. Results are computer scored and can be printed out in the form of a map of visual strengths, weaknesses and blind spots.

Gaze stabilization defect (nystagmus) occurs when the automatic reset movement of the eyes to adjust for turning of the head are off the mark, creating an unstable,blurry and jittery looking world. Nystagmus is a result of brain stem or cerebellar damage, which affects the vestibulo-ocular reflex (to compensate for rapid head movement) or the optokinetic reflex (to compensate for slow, sustained head turn). This can be verified by an electro-diagnostic vision test known as an ENG (electronystagnogram). Gaze shifting defect means our eyes have became poor at tracking moving objects or re-orienting to new objects of interest without turning our head. Gaze shifting is only partly subconscious and reflexive (i.e. under control of brainstem and cerebellum). Due to circuits in the frontal lobes, we can override reflexes and control gaze direction voluntarily. Voluntary gaze shifting can be tested by the examiner moving his finger or a pencil across the patient's eyes.

Neuro-optometry is concerned fundamentally with tracking, alignment, focusing and stereopsis. Our visual system has components or sub-systems, one of which is called the vergence system. Convergent or conjugate vision refers to the uniform horizontal or vertical movement of the eyes with the visual axes of both eyes remaining precisely aligned, so that we only see clear, distinct images of the objects around us. Maintenance of alignment assures that the stream of visual information falls on exactly the same spot of the retina in each eye, a place called the fovea (bull's eye of the retina where the density of retinal photoreceptors is at its very maximum).When our visual axes meet in space at a central point of the same visual target, our brain is enabled to fuse the two images of the object into a seamless whole, so we see just one object. A traumatically induced defect in tracking in one or both eyes throws off alignment and prevents proper fusion, leaving the image blurred or even double. To have true stereoscopic vision with depth perception (3D vision) we need those visual systems to be intact and operating properly. Traumatic visual disorders produce divergent or disconjugate vision with incomplete fusion.

In the normal individual if you bring an object close to the nose, it begins to split visually. While the double image is partially fused (so it still appears to one, partially split object) we are in Panum's area. Once the object splits completely into two clearly separate copies of itself, we have true diplopia or double vision. Diplopia is a failure of sensory integration or fusion of the separate images from each eye. It is very disturbing. People with visual disorders of fusion (also called defective tonic vergence), can have the problem only with near object, only with far objects or both. Disorders of fusion can be the result of traumatic damage to the superior colliculus or other parts of the brain. People with double vision can temporarily restore a single image by covering up one eye, but no one wants to go through life covering their eye or wearing a patch, if they have a better alternative. In fact, the brain is so intolerant of poorly fused or unfused images of the same object, that it automatically suppresses vision in one eye to restore a single image, when a person with a fusion disorder struggles to see clearly. Suppressing vision in one eye (temporarily shutting off its input to the visual processing center in the occipital lobe) takes a great amount of brain energy. This is why TBI patients with a fusion disorder, get so tired and worn out so quickly while trying to read. They keep alternating from disconjugate vision to suppression and it can produce dizziness, nausea or headache as well as fatigue.

Where the cause of the diplopia is partial paralysis of an oculomotor nerve resulting in an outward or inward deviation of one eye, neuro-ophthalmologists may attempt restoration of fused vision by a variety of means. One way is to relax the contracted muscle with an injection of botulinum toxin (Botox). If that does not work, or the patient cannot tolerate such injections, they will try to surgically weaken the healthy muscle on the opposite side of the eye to restore balance in muscle tension. These techniques may or may not work. Unfortunately such techniques have no application to the many TBI patients with normal visual alignment who have a brain problem involving incomplete fusion. This is where vision restoration training by a neuro-optometrist can help. The objective of the training is to stimulate the damaged fusion mechanism in the brain to rebuild and strengthen itself. We have had clients go for years with severe limitations on their ability to read, ride a bike, stitch and sew, fix machines, etc. who substantially recovered their abilities due to customized vision therapy. Because ophthalmologists care only about damage, or lack thereof, to the hardware of the visual system, they tend to react to the same patients very differently than functional optometrists, who act as clinicians working to fix the damaged software of the visual system.

For those interested in neuro-anatomy, here follows a description the visual software system. The image of an object in the external world is presented to the eyes as a wave pattern of photons or light energy. Specialized photo-receptor cells in the retina at the back of each eye convert light energy to an electric nerve signal. The signal is sent from the retinal ganglion cells (the optic disc) into the branches of the optic nerve which come off each eye. Each branch has a nasal side (near the nose) and a temporal side (near the ear). The inner, nasal portion of each branch crosses or "decussates" at the optic chiasm which lies in the floor of the 3rd ventricle under the hypothalamus and in between the carotid arteries. The outer, temporal portion of each branch remains at the edge of the X-shape, always remaining within its brain hemisphere of origin. In practice, the way this works is that if person sees a stop sign to his right, the image of the sign will fall on the nasal side of his right eye and temporal side of his left eye. The nasal portion of the optic nerve branch from the right eye and the temporal portion of the optic nerve branch from the left eye will both transmit their visual data to the occipital lobe at the back of the left hemisphere of the brain, which will create a complete image of what lies within the viewer's right visual field.

From the eyes to the optic chiasm the optic nerve contains 1,000,000 narrow, delicate axon tubes. After leaving the chiasm it becomes the optic tracts passing around the pituitary stalk and the cerebral peduncles, through the lateral geniculate nucleus (LGN) and through the retro-lenticular portion of the internal capsule, where they become the fan shaped "optic radiations." Prior to the optic tracts reaching the LGN, about 10% of the optic tract fibers branch off. Some go to the pretectal area which mediates constriction of the pupils in response to light. Some go to the superior colliculus which controls reflex saccadic eye movements, such as rapid automatic eye movement towards a flash of light. The rest go to the light sensitive suprachiasmatic nucleus (SCN) of the hypothalamus, which controls the 24 hour circadian rhythm of waking, slow wave sleep and REM sleep. The other 90% of the fibers in the optic tracts pass through the LGN where they become the optic radiations. These loop in two directions before terminating at the visual cortex in the occipital lobes. They move upward, above the calcarine sulcus, into the posterior parietal area where automatic visuo-motor responses are generated, and downward, below the calcarine sulcus, to the inferior-posterior temporal lobe where objects and faces get recognized through pattern discrimination.

The LGN is the relay station between the retinas and the visual cortex at the back of the brain. It has a highly complex structure. The LGN consists of 6 distinct layers folded around a central "hilum" in a 3 dimensional horseshoe shape. Two layers are composed of large "magnocellular" ganglion neurons which respond to movement. The other four layers are composed of smaller "parvocellular" ganglion neurons which respond to form and color. The LGN contains a point by point map of the macular portion of the retina which surrounds the fovea, the bull's eye of the retina where vision is clearest. Cells in the LGN can discriminate and transmit visual information, in the form of spatial and temporal changes in light intensity, with remarkable temporal precision. A recent study measured the firing rate of LGN cells at 15 - 102 bits/second, see J. Neuroscience 7/15/2000. 20(14):5392. Damage between the LGN and occipital lobes is associated with loss of visual field. The loss can be of half of the visual field or occur in quadrants, like upper right or lower left, with subtotal damage. A number of specific tests exist for checking vision loss, including the VOSP or Visual Object and Space Perception test devised by Warrington and James in 1991. Apart from asking the patient to tell the examiner what he sees when presented with this type of "confrontation test," doctors can use VEP or visual evoked potential studies. VEP consists of a stimulus, such as a flash of light, with electronic measurement of the time it takes visual processing cells to register the stimulus (latency) and the strength of the signal in response to the stimulus.

The retinal conversion of light waves to electric signals and the transmission of electric signals through the optic nerve, chiasm, optic tracts and optic radiations to the back of the brain initiates a complex process by which those signals are reconstituted into the clear, crisp color image of an object in our visual field. The first processing of the raw visual data is done in the "primary visual cortex" which lies in the walls and depths of the calcarine sulcus. Bilateral damage to the PVC causes blindness, although a patient with sub-total damage may have a certain amount of "blind sight," which is a knowledge of where objects are located around him, which apparently comes from the work done by the small number of survivor cells in the PVC. Binocular fusion of the separate images beamed back from the left and right eye occurs first, on a primitive level, in the PVC. Images landing upon the upper portion of the retina are sent to the lower portion of the PVC below the calcarine sulcus. Images landing upon the lower portion of the retains are sent to the upper portion of the PVC above the calcarine sulcus.

In addition to the primary visual cortex, the occipital lobes contain the "visual association cortex" or VAC. This is where separate layers of highly specialized cells identify the separate components of visual objects into such categories as color, shape, edge, vertical orientation or horizontal orientation. Traumatic damage to a part of the VAC can leave someone with a narrow incapacity to recognize some highly specific aspect of our entire visual world, such as inability to identify particular faces, fruits, minerals, cars, farm equipment, etc. Damage to the neural connections between the occipital cortex and Wernicke's area in the superior temporal gyrus of the temporal lobe (where we process our comprehension of language) can cause inability to understand what we read. Patients with that damage can see the words but cannot figure out what they mean.

When describing the neuro-physiology of the human visual system, neuro-scientists speak of the dorsal and vental "visual streams." The dorsal stream (called the how system) integrates motoric response with visual perception. It controls eye movements along with reaching, grasping and manipulating objects. The dorsal stream is located in the posterior parietal lobe. It is a fast, action stream largely automatic, and based upon unconscious visuo-motor action programs grooved from experience during development. When we reach for a glass of milk, accidentally knock it off the table and grab it in a flash before it hits the floor, without time to even think about what we are doing, we are using the dorsal visual stream.The ventral stream (called the what and who system) identifies what and who we are looking at, and is concerned with object and facial recognition based upon pattern discrimination. The ventral stream is located in the inferior-posterior temporal lobe. It is a slower, perceptual stream associated with conscious awareness of what we are doing, and hooked into our memory system for visual comparison. Both vision streams have connections with the basal ganglia, and some researchers believe that integration of the motor aspect of the two streams occurs in the basal ganglia.