Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Strabismus and Amblyopia_Wright, Spiegel, Thompson_2006
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FIGURE 2-27. Listing’s plane is shown in the center diagram, which includes the Z and X axes of Fick. Diagram shows that the eye can reach all positions of gaze by rotations around axes that are on Listing’s plane. In the center diagram, the O axes represent oblique axes that are on Listing’s plane and are oriented between the Z and X axes of Fick. Note that the oblique axes of rotation seen on the four corners of the diagram allow the eye to rotate obliquely, up and in, up and out, down and in, and down and out. Also, observe the pseudotorsion of the cornea when the eye rotates around the oblique axis.
are directly around the X axis (pure vertical movement) or directly around the Z axis (pure horizontal movement) there is no associated torsional rotation of the cornea. In contrast, oblique ocular rotations cause a torsional shift in the corneal orientation relative to the planar coordinates of Listing’s plane. This torsional shift relative to Listing’s plane is not due to true rotation around the Y axis and is therefore referred to as pseudotorsion. Active, or true, torsional rotations around the Y axis (cycloduction) are created by contraction of vertical and oblique muscles. True torsional movements normally occur to keep the eyes aligned during head tilting23 or occur pathologically when a vertical or an oblique muscle overor underacts.21
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TABLE 2-2. Agonist–Antagonist Muscle Pairs.
Medial rectus—Lateral rectus
Superior rectus—Inferior rectus
Superior oblique—Inferior oblique
Sherrington’s Law: Agonist and
Antagonist Muscles
As described in this chapter previously, ductions are monocular rotations and are clinically examined with one eye occluded to force fixation to the eye being tested. Table 2-2 lists agonist– antagonist pairs for the primary function of the muscles. This relationship between agonist (contracting muscle) and antagonist (relaxing muscle) muscles is referred to as Sherrington’s law of reciprocal innervation.
Sherrington’s law can be demonstrated by using electromyography (EMG). The EMG measures electrical potential changes within a muscle as the muscle fibers contract and indicates the degree of overall neuromuscular activity. The EMG is performed by placing a needle electrode in the muscle (extracellularly) and then recording the amplified electrical activity from the muscle. Figure 2-28 shows results of EMG for agonist and antagonist muscles that demonstrates Sherrington’s law. The needle electrode is placed in the medial and lateral rectus muscles. At the beginning of the EMG tracing, there is lowamplitude tonic activity that maintains the eye position in
FIGURE 2-28. Sherrington’s Law: Electromyographic (EMG) tracing from the lateral rectus muscle (LR) and medial rectus muscle (MR). Note that when the eye adducts, the medial rectus muscle increases EMG activity as the muscle contracts. EMG activity from the lateral rectus muscle diminishes as the antagonist lateral relaxes.
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primary position. As the eye is adducted, the medial rectus contracts, resulting in increasing EMG activity, while the lateral rectus muscle simultaneously relaxes and EMG activity is inhibited. At the end of the tracing, both muscles show tonic activity to maintain eye position. In patients with motor neuron misdirection syndromes such as Duane’s retraction syndrome, Sherrington’s law is violated. In Duane’s syndrome, the lateral rectus muscle is innervated by a branch of the third nerve that also supplies the medial rectus muscle. When the patient adducts the eye, instead of the medial rectus contracting and the lateral rectus relaxing, both the medial and lateral rectus muscles contract simultaneously. It should be remembered that Sherrington’s law of reciprocal innervation refers strictly to monocular eye movements, as does the term ductions. A trick to remember this, is the S in Sherrington stands for Single eye.
Synergist
The term synergist is used for muscles of the same eye that act to move the eye in the same direction. In other words, synergist muscles have common actions. For example, the superior oblique and the inferior rectus muscles both act as depressors; therefore, they are synergists for infraduction. These muscles are not, however, synergists for horizontal or torsional rotations, as the inferior rectus muscle is an adductor and extortor whereas the superior oblique muscle is an abductor and intortor. Table 2-3 lists synergist muscles for various duction movements. Note that synergist muscles relate to monocular rotations, not to be confused with yoke muscles involved with binocular eye movements (see Hering’s Law of Yoke Muscles, below). Like the S trick in Sherrington’s law, remember the S in Synergist stands for Single eye.
TABLE 2-3. Synergist Muscles.
Duction |
Primary mover |
Secondary mover |
Supraduction |
Superior rectus |
Inferior oblique |
Infraduction |
Inferior rectus |
Superior oblique |
Adduction |
Medial rectus |
Superior rectus/inferior rectus |
Abduction |
Lateral rectus |
Superior oblique/inferior oblique |
Extorsion |
Inferior oblique |
Inferior rectus |
Intorsion |
Superior oblique |
Superior rectus |
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Oculomotor Reflexes
Two important oculomotor reflexes are the vestibulo-ocular reflex (VOR) and optokinetic nystagmus (OKN). The vestibuloocular reflex functions to keep the eyes steady when the head moves. Vestibular stimulation, induced by turning the head, results in a compensatory movement of the eyes to maintain the position of gaze. If the head is rapidly turned to the left, the eyes move to the right with the same velocity. A similar reflex, the orthostatic reflex, is responsible for keeping the eyes torsionally aligned when the head is tilted. This reflex is the basis of the Bielschowsky head tilt test for vertical muscle palsies. Optokinetic nystagmus is a visually mediated reflex consisting of smooth pursuit alternating with saccadic refixation as a series of objects cross the visual field. The eyes follow a moving object with smooth pursuit, then use a saccadic movement in the opposite direction to refixate on the next approaching target. The stimulus most commonly used to produce OKN is a pattern of black and white stripes presented on a rotating drum or moving tape. The best OKN stimulus fills the visual field so there are no stationary objects for the subject to fixate.
Hering’s Law of Yoke Muscles
Normally, our two eyes move together in the same direction; this is termed a version movement. Coordinated binocular eye movements require symmetrical innervation of each eye. For example, when one looks to the left, the left lateral rectus and right medial rectus muscles simultaneously contract as the left medial and right lateral rectus muscles relax (Fig. 2-29). The paired agonist muscles from each eye are referred to as yoke muscles. In Figure 2-29, the left lateral and right medial rectus muscles are yoke agonist muscles whereas the left medial and right lateral are yoke antagonists. Hering’s law states that yoke muscles receive equal innervation. Remember, Hering’s law relates to yoke muscles and binocular eye movements (versions), whereas Sherrington’s law explains agonist–antagonist relationships and monocular eye movements (ductions). Figure 2-30 shows the yoke agonist muscles responsible for various fields of gaze. In most situations, the term yoke muscles refers to yoke agonist muscles.
FIGURE 2-29. Hering’s Law: Diagram of version movements to the left. As the left lateral rectus (LR) contracts ( ), the contralateral medial rectus (MR) simultaneously contracts ( ). Also note that the left medial rectus relaxes ( ) and the right lateral rectus also relaxes ( ).
FIGURE 2-30. Yoke muscles are shown for specific field of gaze. Top: gaze up and to the side with yoke muscles being the superior rectus (SR) and inferior oblique (IO) muscles. Middle: straight sidegaze with the yoke muscles being lateral rectus (LR) and medial rectus (MR). Bottom: gaze down and to the side with yoke muscles being the inferior rectus (IR) and superior oblique (SO).
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Versions
Versions can be classified as follows: dextroversion for rightgaze, levoversion for leftgaze, supraversion for upgaze, and infraversion for downgaze. In contrast to ductions, versions are performed with both eyes open and compare how well the eyes move together in synchrony. Versions will identify a subtle restriction or paresis and muscle overaction that results in asymmetrical eye movements.
References
1.Atkinson J. Development of optokinetic nystagmus in the human infant and monkey infant: an analogue to the development in kitten. In: Freeman RD (ed) Developmental neurobiology of vision. New York: Plenum Press, 1979.
2.Bartini C, Horcholle-Bossavit G. Extraocular muscle afferents and visual input interactions in the superior colliculus of the cat. Prog Brain Res 1979;50:335.
3.Beisner DH. Reduction of ocular torque by medial rectus recession. Arch Ophthalmol 1971;85:13.
4.Bloom JN, Graviss ER, Mardelli PG. A magnetic resonance imaging study of the upshoot-downshoot phenomenon of Duane’s retraction syndrome. Am J Ophthalmol 1991;111:548–554.
5.Bremer DL, Rogers GL, Quick LD. Primary-position hypotropia after anterior transposition of the inferior oblique. Arch Ophthalmol 1986;104:229–232.
6.Clark RA, Miller JM, Demer JL. Three-dimensional location of human rectus pulleys by path inflections in secondary gaze positions. Investig Ophthalmol Vis Sci 2000;41:3787–3797.
7.Collins CC. The human oculomotor control system. In: Lennerstrand G, Bach–y-Rita P (eds) Basic mechanism of ocular motility and their clinical implications. New York: Pergamon, 1975:145–180
8.Cynader M, Berman N, Hein A. Recovery of function in cat visual cortex following prolonged deprivation. Exp Brain Res 1975;25:139– 156.
9.Daniel P. Spiral nerve endings in the extrinsic eye muscles of man. J Anat 1946;80:189.
10.Demer JL, Poulkens V, Miller JM, Micevych P. Innervation of extraocular pulley smooth muscle in monkeys and humans. Investig Ophthalmol Vis Sci 1997;38:1774–1785.
11.Demer JL, Oh SY, Poulkens V. Evidence for an active control of rectus extraocular muscle pulleys. Investig Ophthalmol Vis Sci 2000;41: 1280–1290.
12.Fells P, March RJ. Anterior segment ischemia following surgery on two rectus muscles. In: Reinecke RD (ed) Strabismus: proceedings of
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the third meeting of the International Strabismological Association, May 10–12, 1978, Kyoto, Japan. New York: Grune & Stratton, 1978: 375–380.
13.Fink WH. Surgery of the oblique muscles of the eye. St. Louis: Mosby, 1951:92–95.
14.Fishman PH, Repka MX, et al. A primate model of anterior segment ischemia after strabismus surgery. Ophthalmology 1990;97(4):456–461.
15.France TD, Simon JW. Anterior segment ischemia syndrome following muscle surgery. The AAPO&S experience. J Pediatr Ophthalmol Strabismus 1986;23:87–91.
16.Guemes A, Wright KW. Effect of graded anterior transposition of the inferior oblique muscle on versions and vertical deviation in primary position. JAAPOS 1998;201–206.
17.Hawes MJ, Dortzbach RK. The microscopic anatomy of the lower eyelid retractors. Arch Ophthalmol 1982;100(8):1313–1318.
18.Hayreh SS, Scott WE. Fluorescein iris angiography. Arch Ophthalmol 1978;96:1390–1400.
19.Helveston EM, Merriam WW, Ellis FD, et al. The trochlea: a study of the anatomy and physiology. Ophthalmology 1982;89:124–133.
20.Hiatt RL. Production of anterior segment ischemia. Trans Am Ophthalmol Soc 1977;75:87–102.
21.Jampel RS. The fundamental principle of the action of the oblique ocular muscles. Am J Ophthalmol 1970;69:623.
22.Koornneef L. Orbital septa: anatomy and function. Ophthalmology 1979;86:876–880.
23.Linwong M, Herman SJ. Cycloduction of the eyes with head tilt. Arch Ophthalmol 1971;85:570.
24.McKeown CA, Lambert HM, et al. Preservation of the anterior ciliary vessels during extraocular muscle surgery. Ophthalmology 1989;96: 498–507.
25.Mims JL, Wood RC. Bilateral anterior transposition of the inferior obliques. Arch Ophthalmol 1989;107:41–44.
26.Mims JL, Wood RC. Anti-elevation syndrome after bilateral anterior transposition of the inferior oblique muscles: incidence and prevention. J Am Assoc Pediatr Ophthalmol Strabismus 1999;3(6):333–336.
27.Morrison JC, van Buskirk EM. Anterior collateral circulation in the primate eye. Ophthalmology 1983;90:707–715.
28.Oh SY, Poulkens V, Demer J. Quantitative analysis of rectus extraocular muscle layers in the monkey and humans. Investig Ophthalmol Vis Sci 2001;42(1):10–17.
29.Parks MM, Bloom JN. The “slipped muscle.” In: Symposium on strabismus. Transactions of the New Orleans Academy of Ophthalmology. St. Louis: Mosby, 1978:1389–1396.
30.Parks MM. Atlas of strabismus surgery. Philadelphia: Harper & Row, 1983.
31.Parks MM. Causes of the adhesive syndrome. In: Symposium on strabismus. Transactions of the New Orleans Academy of Ophthalmology. St. Louis: Mosby, 1978:269–279.
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32.Plager DA, Parks MM. Recognition and repair of the “lost” rectus muscle. Ophthalmology 1990;97:131.
33.Porter JD, Baker RS, Ragusa RJ, Brueckner JK. Extraocular muscles: basic and clinical aspects of structure and functions. Surv Ophthalmol 1995;39:451–484.
34.Saunders RA, Sandall GS. Anterior segment ischemia syndrome following rectus muscle transposition. Am J Ophthalmol 1982;93: 34–38.
35.Saunders RA, Phillips MS. Anterior segment ischemia after three rectus muscle surgery. Ophthalmology 1988;95:533–537.
36.Simon JW, Price EC, et al. Anterior segment ischemia following strabismus surgery. J Pediatr Ophthalmol Strabismus 1984;21:179–184.
37.Spencer RF, Porter J. Structural organization of the extraocular muscles. In: Buttner-Ennever J (ed) Neuroanatomy of the oculomotor system. Amsterdam: Elsevier, 1988:33–79.
38.Stager DR, Weakley DR, Stager D. Anterior transposition of the inferior oblique: anatomic assessment of the neurovascular bundle. Arch Ophthalmol 1992;110:360–362.
39.Stager DR, Porter J, Weakley DR, Stidham DB. A comparative microscopic analysis of the capsule of the nerve to the inferior oblique muscle. Trans Am Ophthalmol Soc 1997;95:453–462; discussion 463–465.
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41.Virdi PS, Hayreh SS. Normal fluorescein iris angiographic pattern in subhuman primates. Investig Ophthalmol Vis Sci 1983;24:790–793.
42.von Noorden GK. Anterior segment ischemia following the Jensen procedure. Arch Ophthalmol 1976;94:845–847.
43.von Noorden GK. Letter to the Editor. A magnetic resonance imaging study of the upshoot downshoot phenomenon of Duane’s retraction syndrome. Am J Ophthalmol 1991;112:358–359.
44.Wilcox LM Jr, Keough EM, et al. The contribution of blood flow by the anterior ciliary arteries to the anterior segment in the primate eye. Exp Eye Res 1980;30:167–174.
45.Wright KW, Lanier AB. Effect of a modified rectus tuck on anterior segment circulation in monkeys. J Pediatr Ophthalmol Strabismus 1991;28:77–81.
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3
Binocular Vision and Introduction to Strabismus
Kenneth W. Wright
In normal vision, both eyes are precisely aligned on an object of regard, so the images from that object fall on the fovea of each eye. Precise image orientation on corresponding retinal areas of each eye permits cortical processing, which results in the merging or fusion of the two images. This process is termed binocular fusion. There are two important aspects of binocular fusion: sensory fusion and motor fusion. This chapter discusses the process of binocular vision and provides an introduction to
strabismus.
SENSORY FUSION
Sensory fusion is the cortical process of blending the images from each eye into a single binocular stereoscopic image. This fusing occurs as optic nerve fibers from the nasal retina cross in the chiasm to join the uncrossed temporal retinal nerve fibers from the fellow eye. Together, ipsilateral temporal fibers and contralateral nasal fibers project to the lateral geniculate nucleus and then on to the striate cortex. This division of hemifields does not totally respect the midline. There is significant overlap in the foveal area with some of the nasal foveal fibers projecting to the ipsilateral cortex and some of the temporal foveal fibers crossing to the contralateral cortex. Within the striate cortex, afferent pathways connect to binocular cortical cells that respond to stimulation of either eye. Retinal areas from each eye that project to the same cortical binocular cells are called corresponding retinal points. In Figure 3-1, points “A” left eye and “A” right eye, and points “B” left eye and “B” right eye, are cor-
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FIGURE 3-1. Vieth–Müller circle and the empirical horopter. By mathematical theorems, points on the Vieth–Müller circle should project to corresponding retinal points. Point A stimulates the nasal retina of the left eye and the temporal retina of the right eye, and these retinal areas should mathematically correspond. Psychophysical experiments, however, show that the retinal architecture does not follow the mathematical circle of Vieth–Müller and that points on the empirical horopter stimulate corresponding retinal points. The bottom of the figure shows the fusion of the images from each eye into a binocular perception.
responding retinal points. In humans, approximately 70% of the cells in the striate cortex are binocular cells whereas the minority are monocular cells. Binocular cortical cells, along with neurons in visual association areas of the brain, produce single binocular vision with stereoscopic vision.