By John A. Thomas, M.S., O.D.
Post-Trauma vision syndrome (PTVS) describes a constellation of symptoms that evolves as secondary injury in traumatic brain injury. This syndrome includes binocular coordination dysfunctions, disorientation, loss of equilibrium, memory problems, cognitive dysfunction, loss of executive function (including reading), an inability to follow sequential instructions, fatigue, irritability, and sensitivity to light to name the most frequent symptoms. Electrophysiological research suggests that these symptoms are the result of a breakdown in the cellular systems that form the basis of our ambient-focal visual systems (the ambient visual system lets you know where you are in space, and provides the information needed for balance, movement, coordination, and posture. The focal system identifies what you are seeing around you. If the ambient system breaks down, it, in turn, destabilizes the focal system and you cannot maintain a focus on, and properly identify, what you are seeing).
Studies involving brain trauma on animals identifies the molecular basis of neuro disruption resulting in delayed and progressive secondary injury. The molecular mechanism is a breakdown of the intimate association between cerebral blood flow (CBF) and cerebral glucose metabolism (CMGL) causing ischemia (a deficient blood supply) and hypoxia (deficient oxygen supply), which results in metabolic imbalances that change neuronal cell membrane (neurolemma) permeability. Changes in cell membrane permeability immediately result in a cascade of cellular changes that lead to cell toxicity. It is this degenerative neuro-biochemical cascade that results in a delayed and progressive loss of injured-neuron function and is classified as secondary injury. The degree of secondary injury and the rate and extent of progress varies with each individual.
The Visual Operating System
Vision is universally recognized among bioscientists as the dominant ranking sensory perceptual construct of man. Efficient binocular visual perception is the Holy Grail of information processing for Homo Sapiens. Vision is the operating system of the brain. Analogy: Vision is to the brain (visual information processing) as DOS is to the computer, the operating system. Any disturbance in precision visual sensory motor integration or sensory ambient-focal integration results in decompensation and a breakdown of the visual processing systems, resulting in multiple dysfunctions.
It is essential to recognize that cerebral trauma comes in all degrees. No two victims of injury have the same tolerance to the physical forces imposed on the incredibly complex and sensitive central nervous system structure. Like other biological functions, traumatic brain injury comes in all degrees. Existing clinical rating systems, such as the Glasgow Coma Scale, the Ranchos Amigos Scale, presence or absence of consciousness, or velocity statements in police accident reports cannot relate, predict, or correlate the degree of resulting post-trauma vision syndrome. The extent of all secondary injury is not only related to the degree of trauma but is complexly related to victim robustness.
The mild closed head trauma patient is the most frequently under-diagnosed category of traumatic brain injury with secondary injury. Generally, the diagnostic community relies upon loss of consciousness, length of coma, radiological imaging and on occasion neuro-psychological evaluation in the assessment of traumatic brain injury. The noncomatose patient with a negative CT or MRI scan is the classical case. Their symptoms are frequently dismissed as both exaggerated and psychosomatic in origin. This is often disastrous for a mild closed head injury patient and often results in denial of appropriate and necessary rehabilitative services and contributes to the army of walking wounded who look and seem normal but live with generalized cognitive dysfunction.
Drs. William Padula and Stephanie Argyris, in Parts I and II of the Post-Trauma Vision Syndrome series aptly described the primary symptoms of post-trauma vision syndrome to include visual midline shift syndrome (VMLSS). To their list I would add such eye alignment malfunctions as increased esophoria (a tendency to cross eyes) and esotropia (permanently crossed eyes), hyperphoria/hypertropia (one eye up and one eye down), cyclophoria/cyclotropia (rotational misalignment), suppression, photophobia (sensitivity to light), headache, memory deficits, comprehension dysfunction, cognitive dysfunction, compromised reading and writing ability, and the inability to follow sequential instructions. The last seven deficits are classified as executive function disorder. Initial history of the patient, at the scene of the accident and in the emergency room, frequently will not include any comments regarding vision or information processing disturbances. In the absence of obvious facial or eye trauma, or reports of immediate diplopia (double vision), later evolving visual dysfunction symptoms are most frequently dismissed as exaggerated or the result of psychosomatic conversion. This is the result of a lack of appreciation of progressive secondary injury, neuro-biochemical in origin and below the sensitivity of radiological imaging.
The traumatic forces imposed upon the central nervous system, whether by blunt trauma or whiplash trauma (hyperextension/hyperflexion), cause massive nerve conduction disruptions due to electrical charge changes in cells (depolarization). A breakdown of the connection between CBF and CMGL and membrane permeability changes cause potassium ion losses and an influx of calcium ions. The result is an activation of cellular protease enzymes, which triggers cellular skeletal disruption and simultaneous, excessive neurotransmitter activity. All these factors combine to create an abnormal neuro-biochemical milieu that is degenerative, progressive, and contributes to the degenerative process that erodes the memory imprints controlling the precision of binocular coordination, ambient-focal functioning, and efficient integrated information processing. Thus, the learned and life-long established memory imprints that provided the automatic controls of the very complex sensory motor components of the visual process become eroded. The result is degradation of our dominant sensory perception, our dominant guidance system: visual information.
Aggressive neuro-biological and pharmacological research yields agents that can control excess neurotransmitter activity by blocking certain receptor sites, blocking production of endogenous opioids (such as endorphins), blocking enzymatic activity, causing selective enzymatic activity, stabilizing cell membranes, and neutralizing free radicals, thus providing a degree of control over progressive secondary injury. However, controlled studies of these substances and their utilization have been restricted to animals. No approved pharmacological interventions exist for human use.
Multiple advanced technologies have confirmed that the cell-toxic neuro-biochemical milieu that results in cell structure collapse and progressive secondary injury, also results in decreased cerebral competence such as: post-trauma vision syndrome, compromised executive function (including cognitive skills loss), reading dysfunction, and general degradation of cognitive function. Extensive research has provided a sound neuro-biochemical basis to include the elements of post-trauma vision syndrome in explaining the previously unexplainable symptoms, with late onset and progression, of secondary injury.
Neuro-biologists are working aggressively to establish pharmacological interventions to minimize the progressive neurological insult described above. Present pharmacological intervention is primarily relegated to severe traumatic brain injury and includes a handful of old standbys, which include naloxone, dextromethorphan, methylprednisone, furosemide, and the antioxidant family. Only the family of antioxidants is clinically applicable to a mild closed head injury case.
As described in the previous segments of this series, neuro-optometric rehabilitative treatment has been enormously successful in contributing to the reordering of the visual information processing coordinant systems essential to reestablishing the visual guidance faculty. I confirm Drs. Argyris? and Padula?s statement that neuro-optometric rehabilitation needs to be concurrent with, or preceding, other rehabilitative strategies. This is essential and prerequisite to any cognitive rehabilitative therapy. Attempts to provide cognitive rehabilitation in the presence of post-trauma vision syndrome is equivalent to throwing back the ocean with a bottomless bucket. Without an intact, coordinated, and integrated binocular vision processing faculty, cognitive rehabilitation is futile, frustrating, and frequently results in a premature pronouncement of maximum medical achievement. Neuro-optometric rehabilitation is an essential component of the transdisciplinary rehabilitative team essential to the restoration of integrated function.
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