Neuro-optometric Diagnosis, Treatment and Rehabili tation Following Traumatic Brain Injuries: A Brief Overview

Traumatic brain injury (TBI) commonly impacts on the connections and interactions between signals from sensory, cognitive, motor and emotional systems and signals transmitted via both visual and non-visual retinal fiber pathways. The non-visual retinal pathways are actively involved in aspects of living, such as spatial orientation, auditory localization, circadian rhythm and motor function. Non-visual retinal signal processing and linkage dysfunctions require more than specialized neuro- ophthalmologic or traditional eye care evaluation. Neuro- optometric techniques, such as discussed herein, are necessary to test the complex, often overlooked interrelationships among these systems. As part of a multi-disciplinary approach, neuro-optometric intervention is an essential consideration for the optimal diagnosis, treatment and rehabilitation following a TBI.

“Myopia is not just a problem of vision. It is a problem of the whole body and mind… For the practitioner, it is sometimes the point at which a conclusion is reached, where one has stopped thinking.” —Dr. Albert A. Sutton, 1968

Retinal processing problems affect a majority of patients following traumatic brain injury (TBI) . Sensory, motor, emotional and cognitive systems interact and process stimuli transmitted via retinal fiber pathways ; therefore, these systems are susceptible to TBI-related retinal processing dysfunctions. Retinal processing problems can be visual, nonvisual or both . Thousands of retinal fibers are part of the visual system but not necessarily involved with eyesight . For example, the retinohypothalamic tract is a nonvisual pathway, and there is a specific mammalian nonvisual irradiance detection pathway, a complex nonvisual photoreceptive system in the inner retina and visual functions that do not require image formation on the retina . Signals transmitted through these fibers affect balance, posture, motor function, sensory integration, visualization, sleep and emotion centers in the brain and can function even with the eyelids closed .

Retinal-related symptoms are generally not visible on CT scans or MRI ; therefore, these processing problems are often overlooked during the initial phase of diagnosis and treatment. Also, many retinal processing related problems are not discernible by standard central eyesight, visual field, or eye health testing. Regardless of any visual acuity or eye health issues that might be diagnosed and treated, subtle visual and other processing or linkage problems can remain undetected and often an incorrect assumption is made that there are no other retinal system connected problems.

Because of continual stimulation to the dysfunctional nonvisual retinal pathways, patients with undiagnosed conditions may experience various symptoms, such as muscle spasms, dizziness, comprehension or attention difficulties, or they may exhibit abnormal behaviors, the causes of which are easily misdiagnosed. A frequent example is acute anxiety that can be misdiagnosed as a panic disorder . The patient might be referred for treatment for the wrong primary diagnosis while the actual underlying cause of the problem remains untreated.

Patients frequently complain that everything “looks” peculiar, yet they cannot articulate what exactly is wrong. The resultant stress and confusion can significantly alter the patient’s comfort level and lifestyle and affect the quality and duration of his or her rehabilitation. Neuro-optometric intervention can often have a significant positive impact on these retinal processing dysfunctions.

Box 1 lists examples of visual and nonvisual retinal-related symptoms that are common in patient complaints following a TBI .

Box 1

Possible visual retinal-related symptoms
Blurred vision
Intolerance to light
Double vision
Loss of visual field
Binocular vision problems
Focusing difficulties
Eye-aiming difficulties
Spatial perception difficulties
Eye movement difficulties
Visual recognition problems
Inability to distinguish colors
Inability to visually guide body movements

Possible nonvisual retinal-related symptoms
Persistent headaches
Memory problems
Comprehension and attention difficulties
Balance problems
Abnormal posture
Persistent clumsiness
Persistent motion sickness
Concentration or anxiety problems
Disorientation or disorganization
Subcortical eye-aiming difficulties (nystagmus)
Persistent dizziness and nausea
Persistent muscle tension

Courtesy of The Mind-Eye Connection Professional Corporation, Northfield, Illinois.

Examples of visual and nonvisual retinal-related symptoms common after TBI

These symptoms can, of course, reflect other stress or trauma induced physical, emotional or chemical imbalances. An added complexity in recognizing and isolating the cause of these symptoms is the fact that conscious recognition occurs through the interaction of retinal signals not only with other sensory, motor or cognitive signals but also with the limbic system , which is linked with various memories, emotions and feelings, such as anxiety, fear, pleasure, depression and anger. Sensorimotor or cognitive responses are sometimes influenced by these emotions via the limbic system and its interaction with retinal signal transmissions.

The focus of this article is on neuro-optometry, not neuro-ophthalmology. The neuro- ophthalmologist specializes in locating a disease or disruption of a structure in the visual pathways. Once it is located many treatment options are available. For example, medication might be prescribed, surgery might be performed to repair the damage or lenses may be prescribed to maximize central eyesight. The neuro- optometrist works with brain functions , such as sensory, motor and information processing, and specifically, with the perception of external and internal stimuli. Both structure and function can have a role in rehabilitation following TBI.

Neuro-optometric tests can be used to diagnose and treat visual and nonvisual retinal signal processing dysfunctions following TBI. These tests, separately and, more importantly, in the aggregate, can provide information not otherwise available from standard examinations. Four of these tests are discussed herein:

The Yoked Prism Walk evaluates gross body movements at a reflexive level and spatial orientation while the patient is moving. It can demonstrate how poor stability may impair higher level perception such as spatial organization.
The Padula Visual Midline Shift Test measures spatial perception and shows how the patient is organizing space while he or she is stationary and there is an object moving in front of him or her.
The Super Fixation Disparity Test© identifies and quantifies sensory misalignment of the visual axes in the presence of binocular vision. It measures the disparity of foveal alignment at both near and far distances and therefore within the operations of both central and limited peripheral systems and central and expansive peripheral systems.
The Z-Bell© Test evaluates the interaction between auditory localization ability and visual input , helps to identify dysfunctional integration of information processing systems, and can determine the kind and amount of intervention necessary through the use of lenses, prisms, filters, and/or occluders.

Neuro-optometric intervention can affect changes to brain processing via the autonomic and central nervous systems, for example, by using lenses, filters, prisms, and occluders to alter light and thereby sensory systems integration. By controlling the amount and direction of light input, the patient’s reactions to new environmental stimuli can be measured to determine how well, and in what areas, the visual and nonvisual retinal systems are interacting . Information processing, perception and motor disorders can thereby be identified and modified. As an aid to rehabilitation, lenses can be designed to eliminate or reduce some of the systemic stress deriving from the TBI.

Visual and nonvisual processing affects many sensory, motor, cognitive and emotional systems. Dysfunctional processing or linkages can cause a distortion in spatial or temporal orientation and an overall diminution in the patient’s ability to perform even simple everyday tasks.

More than 30% of the human cortex is devoted to vision and visual processing connections with nonvisual systems . Even without eyesight, this capacity is used in other aspects of information processing. Recent research indicates that some segments of the blind population show an improvement in auditory processing when compared with sighted individuals that may derive from the ability to use the occipital cortex for non-visual tasks . An integrated approach to patient testing should include all dimensions of neurologic, endocrinal and emotional possibilities to reveal previously undetected processing dysfunctions. Because effective visual processing and sensory integration are such important elements in patient rehabilitation following most TBIs, a multidisciplinary team that includes a neuro-optometrist is essential for the best possible diagnostic and rehabilitation patient outcome.

Retinal processing

All sensory systems have receptive fields, many of which overlap. The more nerve endings, the more the sensory overlap. The visual system is most notable for sensory receptivity and overlap because each retina has more than 100 million receptor cells in a relatively small area. The size is such that even a 0.1-mm dot of light covers the receptive field of many retinal output ganglion cells, some of which are excited and others inhibited by the light. Additionally, each point on the retina sends signals through parallel channels from each type of receptive field .

The retina has two types of receptive fields, each with two concentric and opposite zones. In one field, light striking the inner circle causes an output signal; in the outer circle, light suppresses output. In the opposite field, light striking the periphery triggers an output signal while the inner circle suppresses output.

Receptive fields on each retina combine their information at subcortical and cortical levels to determine eye aiming and fusion, which is measured within the tolerance range of fixation disparity, that is, the range within which a patient can maintain coordinated eye aiming. A normal range of fixation disparity is achieved by a two-speed mechanism . There is a faster response to retinal image disparity and then a slower response for binocular alignment. The timing and balance of this sequencing is dependent on retinal signal information that is processed by the brain, also within a two-speed sequence. The brain processes subcortical information more quickly than it does cortical information; therefore, subcortical signals, which are most likely to be distorted following a TBI, first affect retinal image disparity. In this situation, the patient might not be able to achieve a normal range of fixation disparity. If the amount of fixation disparity between the eyes is past the tolerance range, the image for central eyesight will not be comfortable, single or clear unless binocular vision is suppressed. Even a mild concussion or stroke for example, can easily disrupt the interaction of these fragile fields and their integration with other sensory systems, causing a sensory integration imbalance.

Of approximately 1 million retinal ganglion fibers per eye that are involved in processing light, more than 80% travel to the visual cortex to be used in eyesight . The signals are specifically bundled or grouped. Signals representing details and color travel from the visual cortex to the inferior temporal lobes, whereas others, signals of position, speed and size, travel from the visual cortex to the superior and middle temporal lobes. The retinal signals from the remaining 20% (approximately 200,000 fibers) of the 1 million retinal ganglion fibers branch off to nonvisual structures such as the hypothalamus and to atypical visual structures, such as the superior colliculus, where a majority of visually responsive neurons receive nonvisual sensory signals. These multisensory neurons are cross-modal and their nonvisual inputs can have a significant impact on visual as well as nonvisual responses (at a conscious cortical level), reactions (at a subconscious cortical level) or reflexes (at an unconscious subcortical level) . The superior colliculus processes retinal signals at reflexive subcortical and subconscious and conscious cortical levels . It functions independent of and parallel with the visual cortex. The superior colliculus links incoming sensory information with motor output. For example, it is integral to head and eye orientation toward an object or sound being seen or heard.

The retina and its connecting systems are also directly involved in the body’s chemical functions. For example, the melatonin chemical receptor has a significant role in vision and is involved in rapid eye movement. Melatonin is linked with thyroid development, and the thyroid hormone receptor is involved in retinal cell proliferation . Retinal signals can directly affect mood, posture, hearing, memory and body chemistry. Thus, in addition to attention and consciousness affecting what the patient sees, equally important is the fact that what the patient sees, and how it is processed, can affect his or her attention and consciousness .

In summary, there are roughly 1 million retinal ganglion fibers per eye, approximately 200,000 of which are from the peripheral retina and used mostly for nonvisual functions. All cortical areas have significant nonvisual inputs and major feedforward and feedback connections to numerous nonvisual (subcortical) structures in the thalamus, midbrain and brainstem, including the lateral geniculate nucleus, superior colliculus, pulvinar, basal ganglia and pons . These remaining peripheral retinal fibers in each eye affect balance, posture, reflexes, emotions, muscles (especially neck muscles), sleep and auditory processing. They function with minimal light and even with the eyelids closed.

Retinal signals

The retina is an extension of brain tissue and has cortical and subcortical feedback and feedforward loops. It converts light energy into electrical signals that are transmitted to precisely mapped sections in the various regions of the brain . Retinal sensors transmit information to visual and nonvisual centers and connect with the other sensory systems. As is true for the peripheral retinal fibers discussed previously, they function even when the eyelids are closed.

Retinal signals can be classified according to their processing level in the brain. Unconscious (non-planned) reflexes are processed subcortically; subconscious (learned) reactions and conscious responses are processed in the cortex.

Specifically, peripheral retinal signals are processed at both cortical and subcortical levels. The peripheral information that is processed subcortically determines unconscious reflexes; those signals processed in the cortex influence decisions about speed, location, size and shape.

There are three levels in the hierarchy of visual processing. First, the brain processes unconscious subcortical brainstem, cerebellar, proprioceptive and vestibular reflexes. Second, it processes subconscious cortical reactions for peripheral awareness and organization. Third, it processes conscious central cortical responses for attention, identification, and interpretation.

As our environment continues to cause more stress, with the concomitant necessity to organize more and more sensory input, the demand for a stable linkage between peripheral and central eyesight becomes more critical. Also, the interaction of the subcortical and cortical systems becomes more important, yet, the hierarchy of visual processing does not change. It remains the same as when our requirements for basic survival were more primitive and humans relied primarily on subcortical reflexes and subconscious cortical reactions.

A TBI usually results in retinal processing problems that cause a sensory mismatch at subcortical and subconscious cortical levels. Signals from these now dysfunctional levels are naturally processed at a much faster rate than are signals received by central eyesight (at a higher conscious cortical level). The resultant immediate and continual stimulation to the peripheral pathways interferes with the patient’s ability to concentrate on central cortical inputs, causing problems with central attention and overall awareness. For example, the peripheral nonvisual retinal signals that are linked with body posture at a reflexive level trigger eye and head movement. The head and eye position determines the volume of space available within which a person can select where to place his or her attention and, finally, where to aim and focus his or her eyes. The symptoms of visual and nonvisual system dysfunction following TBI often derive from subcortical or subconscious pathways dysfunctions that can be, by standard central eyesight testing or prescriptions, neither properly diagnosed nor treated.

The brainstem deals with low-level, unconscious life-sustaining functions. When any of these functions are out of control owing to a TBI, the lack of stability may force the conscious level to take attention away from higher level needs and to focus on these low-level functions. For example, if a patient’s lower level motor system is unable to keep him or her balanced, his or her conscious attention will be pulled away from other information inputs to reorient his or her body in space. This need for reorientation will detract from the patient’s ability to concentrate on other stimuli or to maintain a smooth stream of information, affecting everyday life as well as the increased demands of TBI rehabilitation.

The unconscious peripheral nonvisual retinal signals that are processed in subcortical structures account for a significant majority of the total peripheral retinal fibers. They provide information for spatial orientation, balance and integration with other sensory signals, including, cerebellar functions that involve coordination of balance, movements, and thoughts. Functionally, the fundamental senses (vision, olfactory, auditory, tactile, gustatory, vestibular, proprioceptive, and the other parts of the somatosensory systems) are not separate. The sensory totality links within the brain and there are myriad interconnections and interactions. TBI usually impacts on this signal interdependence and integration.

When a TBI disrupts normal unconscious automatic functions, such as muscle tone, reflexes, balance, gait or postural alignment, these functions are often replaced with new and frequently maladaptive patterns. One of the manifestations of these changes is increased or decreased subcortical sensitivity as a result of processing dysfunctions, such as nausea during normal head movement or midline posture shifts in an attempt at spatial reorientation. If the maladaptive behavior occurs at this reflexive brainstem level it can cause unconscious alterations of postural alignment or balance. This complex integration of information ultimately governs reflexive motor control and the effects are circular. Because the eyes interact with the neck muscles, eye movement causes the neck muscles to tighten and loosen. As neck muscles move to maintain balance and head position, the eyes move. The retinal signal dysfunction that usually follows TBI affects the entire gamut of sensory integration and impacts negatively on the patient’s lifestyle in general and specifically on his or her rehabilitation process.

Subconscious peripheral visual retinal signals are processed in the visual cortex. This process is commonly called “peripheral eyesight” and includes information not being attended to but occurring in the periphery. These signals lead to eye aiming. They aid a person in organizing his or her environment and enable him or her to judge object location. What is commonly known as “eyesight” is the conscious central retinal signals that are also processed in the visual cortex. These signals are stimulated after attention is shifted and aiming is completed.

Approximately 80% of the retinal ganglion fibers transmit signals to the visual cortex; approximately 20% transmit signals to subcortical structures where visual processing integrates with nonvisual signals. Cortical and subcortical retinal signals are linked through the pathways listed in Box 2 via the reticular system , which affects muscle control, postural alignment, and arousal and suppression of cortical activity, and have multiple feedback and feedforward connections .

Box 2

SUBCORTICAL

Retino-tectal (collicular) pathway

SPATIAL ORIENTATION

Neuromuscular (balance and posture)

Retino-hypothalamic pathway

CIRCADIAN RHYTHMS

Biochemistry (emotional behavior and sleep patterns)

Accessory optic system

SPATIAL VISUALIZATION

Internal organization (memory and emotions)

Retino-pretectal pathway

VISUAL-MOTOR REFLEXES

Instinct (avoidance and attraction behaviors)

CORTICAL

Retino-geniculo-striate pathway for peripheral eyesight

LOCALIZATION

External organization (speed, location, size and shape)

Retino-geniculo-striate pathway for central eyesight

IDENTIFICATION

Attention (detail and color awareness)

Adapted from Retinal pathways chart, courtesy of The Mind-Eye Connection Professional Corporation, Northfield, Illinois, 2006.

Retinal signal pathways

Light entering the retina stimulates the brain at a reflexive subcortical level and a reactive or responsive cortical level. It is the relationship between the faster subcortical and the slower cortical processing that is often disturbed as a result of TBI and neither these unconscious pathways nor the interaction between sensory inputs is evaluated during a standard neuro-ophthalmologic, ophthalmologic or optometric examination.