Nystagmus is usually a pendular, horizontal swinging of the eyes. Sometimes, nystagmus can have a vertical or erratic component. There are other oculomotor impairments that can be lumped under the category of "insufficiencies." These include a host of irregular eye patterns that show up when children have multiple impairments. Often there is poor control of eye muscles, an apparent lack of proprioceptive awareness of eye position, coupled with an inability to direct the eyes at will. There is often difficulty moving the eyes past the midline of the body. In some children there is also a difficulty converging or diverging the eyes to see far to near or vice versa.
If the six muscles of one eye fail to work in unison with the six muscles from the other eye, then one of two things can happen: double vision occurs if coordination of the two eyes is only slightly off; or, if the coordination is way off, the brain is presented with an intolerable situation, putting together, for example, the picture of a face coming from one eye, with an image of a wall coming from the other eye. In this scenario, the brain shuts off input coming from the non dominant eye (the "wall" eye). The wall eye will eventually become amblyopic (functionally blind), especially if the eye coordination problem is not addressed at an early age.
The mobility specialist should expect to see oculomotor problems in a large percentage of special education children, particularly students with neuromuscular impairments like cerebral palsy. There is also a high incidence of eye muscle problems in the population of mentally impaired children. Any time there is a disruption in the ability of the two sides of the body to work together, as is found often in "perceptually impaired" children, ADHD children, or learning disabled children, look for oculomotor insufficiencies, or strabismus.
Also, mobility specialists should expect to find nystagmus in most students with optic atrophy. Micronystagmus is a normal in all eyes. This micronystagmus is physiologically necessary for visual perception. When there is optic atrophy it implies that there has been damage to the macular area of the retina, which further implies that central vision is probably reduced to 20/200 acuity. When this scenario occurs, micronystagmus becomes macronystagmus, the normal pendular swing becomes exaggerated and can be seen by the naked eye of the examiner.
It is not unusual for an optometric or ophthalmological examination to report that a student (particularly a multiply impaired child) is blind. At the same time, a confused classroom teacher will report that the same student is moving in and out doors and around objects one minute and acting blind the next. This paradox is usually about the extraocular muscle system. Doctors examine children in a clinical setting. They control lighting, they control distances, and most importantly they keep the patients stationary, in a chair. They often get little information from multiply impaired students, despite their best efforts. They may get no indication under these clinical conditions that the child can see. In a classroom, while moving, the peripheral vision system, even with a dysfunctional oculomotor system, can at times signal the presence of objects or the location of doorways or landmarks. These kids have functional vision, they just can't control the eye muscles often enough to provide consistent, reliable vision. There are other reasons (discussed later) that could account for the paradox besides oculomotor damage, including peripheral, subconscious optical systems operating in the absence of central vision, and a host of parietal lobe impairments to visual spatial processing centers.
Corneas have no direct blood supply; ie. no blood vessels flow through corneal tissue. Nourishment comes from the aqueous, and from a ring of blood vessels around the corneal rim. If the cornea is cut seriously enough, blood vessels from the rim proliferate and grow into corneal tissue. These blood vessels remain even after the cut surface heals, leaving corneal scars.
The iris is the colored part of the eye. It is a sphincter muscle, meaning that when it relaxes it opens, and when it contracts it closes. The hole in the iris that can enlarge or shrink, is called the pupil. Damage to the iris results in decreased activity of the muscle; either it reacts sluggishly (opening and closing slowly), or it fails to react at all. The iris has neural connections with retinal cells as well as brain level connections (neural pathways, feedback loops). The job of the iris and pupil is to control the amount of light hitting the retina (ie. it controls brightness). The iris brightness control system is a steady state negative feedback system. The pupil shrinks in the presence of bright light, and opens in dim light. Pupil changes occur smoothly and constantly in a normally functioning iris.
The lens of the eye is made of clear protein, like the "white" of an egg. When protein is damaged (like when you heat a raw egg), the protein denatures and turns white. Damage to the lens in an eye can be from foreign chemicals, from aging, and from trauma. When the damage causes white, denatured protein to spot a lens, the doctors report that a patient has a cataract (their name for denatured protein). Cataracts, especially if they occur in the center of the lens, can interfere with the transmission of light (and visual information) through the eye. Eyes with old lenses (people over 45) or with cataracts, change focus weakly or not at all (the loss of lens function occurs gradually from age 45 to age 75, after which the lens hardens and cataracts form.)
The vitreous has a small affect on the refractive status of the eye, but not enough to be significant compared to the lens and cornea. The vitreous can fill with blood when retinal vessels break. It can also get contaminated with tissue fragments, particularly in some disorders. Blood and debris can be washed from the vitreous as the fluid is refreshed, or surgical replacement can be performed in serious cases.
Congenital abnormalities can affect the structure of the eyes. Sometimes eyes are very tiny (micro-ophthalmia) and sometimes eyes are enlarged and appear to bulge (this is often related to a thyroid problem). If the structure of the eye is affected, the drainage systems for the aqueous and vitreous can get plugged resulting in glaucoma. Glaucoma is the build up of fluid in the eye that results either from a blockage of the drainage system, or from eyes that produce fluid faster than they filter-off old fluid. Structural damage can also affect the operation of the pupil or the lens. Eyes that are too long become myopic (focus too soon), and eyes that are too short become hyperopic. Colobomas are birth defects. The developing eye zips shut along the vertical axis in utero. If it fails to zip shut, a slit results. The slit zips shut from the back toward the front of the eye. Moderate colobomas affect the front structures of the eye (cornea, lens, pupil), while severe colobomas can affect even the retina.
Corneal scarring, cataracts, blood or debris in the vitreous and aqueous, all block the passage of visual information coming into the eye. If reflected light patterns do no hit the retina totally and without distortion, then visual information cannot be processed correctly.
Glaucoma causes fluid pressure to push against the back of the eye. If left untreated, retinal cells begin to die in a characteristic fashion. Visual field loses result in blind spots initially, leading to tunnel vision, and then blindness. When glaucoma is present, the mobility specialist should be looking for signs of decreased ability to function in dim light and/or for signs that the peripheral field is being neglected.
A cataract is a hard substance floating in a fluid medium. When cataracts are present, expect to find a decreased ability to focus. A cataract will block vision most when it is located directly along the axis of the eye. If it is on the edge of the lens, it will probably not affect vision significantly. The reduction in vision acuity caused by a cataract depends upon its density, spread, location, and whether or not there is a corresponding cataract in the other eye. A cataract in only one eye will cause the brain to ignore the bad image (suppress it) and use the non damaged eye for seeing.
Damage to the iris causes a disruption in the ability to regulate brightness. The visually impaired student will have difficultly adapting as light levels change in the environment. This will be most pronounced when going from a dark setting (like a movie theater) to a bright setting (coming out of the theater into bright sunlight), or vise versa. Adaptation problems can also result when there is damage to the retinal cells that are part of the iris-retina feedback loop, or to the brain level connections that regulate light adaptation.
Some disorders affect only the central processing system. Optic atrophies, which appear commonly as a congenital condition, directly affect nerve transmission from the macula. Malnutrition can selectively destroy central vision at the retinal level. Other disorders impact primarily on the peripheral processing system. Retinitis pigmentosa destroys peripheral cells initially. Conditions like retinopathy of prematurity often damage portions of the peripheral retina sparing central vision.
Damage to one system has affects in the other because of neural integrative mechanisms (feedback loops). Peripheral vision may signal the sideways approach of an object, causing central vision to swing the eyes in the direction of the approach. Damage to central vision would, however, prevent the macula from locking onto and examining the object. The purpose for the neural feedback loop is disrupted by central processing impairment (or vice versa).
When the cone system is damaged, the rod system becomes the primary detection mechanism. Expect to find degrees of color blindness, acuity reduced to 20/200 at best, inability to identify faces, words, street signs (etc.), and problems tracking, scanning and fixating (visual pattern recognition is impaired, resulting in nystagmus). Central loss also impairs the ability to find and use visual landmarks for orientation, thereby affecting the ability to navigate. There is also a shift from a conscious, focused system to the less aware, more reflexive peripheral system.
Certain diseases also affect the optic tract, most notably multiple sclerosis, which causes retrobulbar neuritis (inflammation of the optic tract behind the eyeball). The bouts of inflammation during retrobulbar neuritis can come and go as the disease goes through flare ups or remissions.
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