The overall shape of the curves is the same. Point A indicates the slack length; point B, the primary length for the contractured muscle. For the contractured muscle, the curve is shifted to the left along the horizontal axis and hence slack length is shorter.
For the stretched muscle, the curve is shifted to the right, denoting a longer slack length. In the primary position, the normal and stretched muscles exert no elastic force. All curves are from human medial rectus muscles modified from Collins and Jampolsky Patient with a left superior oblique SO palsy with a chronic head tilt to the right. The left inferior oblique IO and inferior rectus IR muscles are chronically stimulated, and the left SO and superior rectus SR muscles are chronically inhibited.
Also note that the superior muscles in the right eye are stimulated and the inferior muscles inhibited. Kushner BJ. Arch Ophthalmol. Methods By extrapolating from known principles of striated muscle physiology, a cohesive theory about extraocular muscle behavior is derived. Results The key to understanding apparent extraocular muscle overaction is to differentiate between a muscle that has decreased elasticity and one that is strengthened.
Many motility patterns that appear to be due to an overacting muscle may in fact be caused by other muscles than the suspected one. Conclusion Apparent extraocular muscle overaction can be caused by many different factors. When an eye moves excessively into the field of action of an extraocular muscle on version testing, that muscle is typically described as being overacting.
Because terminology influences understanding, the use of the term overacting can be misleading for several reasons. In many circumstances, an excessive movement of an eye may in fact be in the field of action of a muscle that is not actually responsible for the abnormal movement. For example, overelevation in adduction can be due to one of multiple different causes, many of which are not related to the inferior oblique IO muscle in the adducting eye.
However, the aforementioned definition would categorize this as IO overaction. Common examples of clinical scenarios that all might be incorrectly thought of as being due to an overacting IO are described in the Table. They include the following: Duane syndrome, 1 , 2 dissociated vertical divergence, 3 craniofacial syndromes, 4 - 6 the antielevation syndrome that can occur after anterior transposition of the IO, 7 mechanical restriction of the contralateral inferior rectus IR , 3 pseudo IO overaction associated with a Y or V pattern, 8 and pulley heterotopia or instability according to Oh et al 9 and Demer There are numerous other clinical situations in which an excessive movement of an eye is in fact caused by the muscle in whose field of action the movement occurs.
As is described later in this article, an increase in a muscle's contractile or elastic force may cause an eye to rotate excessively into its field of action on version testing, yet these represent very different pathophysiologic processes.
In addition, multiple different scenarios can lead to an increase in contractile force. These include an increase in innervation, increase in muscle bulk cross-sectional area , and changes in the types of muscle fibers within the muscle. Consequently, the use of the term overaction to describe heterogeneous situations may be misleading and can confuse our understanding of why particular motility patterns develop in different strabismic disorders because it implies an etiology for the observed motility based solely on the relative position of the 2 eyes.
In addition, characterizing differing clinical situations as having muscle overaction leads to several inconsistencies with observed findings, particularly if one incorrectly assumes that overacting implies the muscle is strengthened.
For example, IO-OA that is secondary to SO palsy is characterized by an abnormal elevation in adduction and is typically associated with a positive Bielschowsky head tilt test; the hypertropia increases with head tilt toward the affected side.
Putting it succinctly, the term overaction is misleading because it assumes that clinical observation implies etiology. The purpose of this article is to assign more specific pathophysiologic processes to the protean patterns of extraocular muscle overaction that we see in clinical practice. This article is a derivation of a unifying hypothesis to explain many of the different mechanisms responsible for apparent extraocular muscle overaction that reconciles clinical observations with known concepts.
It consists of a review of established principles of striated muscle physiology and the application of those principles to accepted observations about various abnormal patterns of ocular motility.
A muscle is made up of multinucleated cells called muscle fibers, each of which contains many myofibrils that run longitudinally within the muscle. The basic contractile unit within the myofibrils is the sarcomere. It consists of overlapping thin filaments actin and thicker filaments myosin as shown in Figure 1 A. The actin filaments insert on an electron dense structure called the Z line, which delineates the end of the sarcomere. The myosin filaments lie between parallel filaments of actin and bridge the gap between actin filaments that are adjacent serially end toward end.
Myosin filaments have knob-like heads that interact chemically with actin filaments, causing them to move along the adjacent actin filament resulting in muscle contraction Figure 1 B.
The increase in force that results from this active contraction is referred to as the muscle's active contractile force generation. If a muscle is given a single maximum stimulation, the resultant contractile force is called the muscle's twitch. The magnitude of the twitch that a muscle can generate is proportional to the sum of the contractile force of each of the parallel contractile elements sarcomeres in the muscle. Thus, a muscle with a stronger twitch than normal may have a somewhat larger cross-sectional diameter because it may have more sarcomeres in parallel.
This increase in muscle strength can be due to each muscle fiber having a larger diameter muscle hypertrophy or due to a greater total number of parallel fibers muscle hyperplasia. A muscle's tetanic tension is that force it develops in response to a constant stimulus. A muscle with a higher peak tetanic tension may have a greater cross-sectional diameter than one with a lower tetanic tension if hyperplasia or hypertrophy were responsible for the increased tetanic tension.
Conversely, a muscle that has lost elasticity but has not developed a change in its twitch or tetanic tension contractile force has only undergone a change in the number of sarcomeres in series end to end. Consequently it should have a normal cross-sectional diameter because there is no change in the number of sarcomeres in parallel. Muscles with either an increased twitch or tetanic tension can be thought of as being stronger than muscles with a lower twitch or tetanic tension. The number of sarcomeres in series end to end does not affect muscle contractile force 27 , 28 ; however, acute changes in muscle length do.
If a muscle is stretched substantially beyond its resting length, there is insufficient overlap of the actin and myosin to generate as effective a contractile force Figure 1 C. If the muscle is passively shortened considerably, there is insufficient room for the myosin to move along the adjacent actin filament before it collides with the dense Z band Figure 1 B.
In either circumstance, lengthening or shortening from the optimum length will decrease the contractile force a muscle can generate. For skeletal muscles, the contractile force is at its peak when the length of the muscle provides optimum overlap of the actin and myosin filaments. For most skeletal muscles, this is typically around its resting length Figure 2.
Other factors that can increase the contractile force of a muscle include an increase in its innervation, a change in the proportion of different types of fibers within the muscle eg, twitch or singly innervated fibers vs nontwitch or multiply innervated fibers; or high oxidative vs low oxidative fast twitch fibers.
In addition to a muscle's force that results from active contraction, a muscle has an elastic resistance to stretch much like a rubber band or spring. Each myosin filament is anchored to the adjacent Z line by an elastic protein called titan , which is responsible for most of the muscle's elastic resistance to stretch Figure 1 A.
A muscle's slack length is that length below which the muscle exerts no elastic force. In this latter position, the muscle is said to be at its primary length. As a muscle is passively stretched beyond its slack length, the elastic tension rises rapidly Figure 2. The tether length of a muscle is the length beyond which the muscle will tear. Throughout this article, I refer to a muscle that has increased resistance to passive stretch is stiffer than normal and with a shorter than normal tether length as having decreased elasticity or being relatively inelastic.
I refer to a muscle that generates a greater twitch active contraction to a single maximum stimulus or tetanic tension as being stronger than normal or strengthened.
The total force of a muscle is the sum of the contractile force it can generate and the elastic forces. Because both contractile and elastic forces are a function of a muscle's length, the relationship between muscle length and total force contractile plus elastic is biphasic as depicted in Figure 2.
Studies of animal skeletal muscles have shown great plasticity in muscle structure as a response to chronic stretching or shortening. However, if that stretch is maintained for a period of several weeks, new sarcomeres are laid down in series end to end , thus allowing each sarcomere to return to its initial optimum length Figure 3.
If a muscle is passively shortened, each sarcomere is initially shortened as shown in Figure 1 B, also resulting in a suboptimal actin-myosin relationship. However, if the shortened position of the muscle is maintained for several weeks, sarcomeres drop out serially end to end. When the muscle loses sarcomeres in this manner, the remaining sarcomeres are able to resume their original optimum length Figure 4.
A muscle taking up its slack in this manner is the physiologic basis for a muscle losing elasticity, which results in increased stiffness. This is also described as a muscle being contractured.
When a muscle loses elasticity in this manner, there typically is not an increase in its cross-sectional area. There is substantial evidence these observations hold true for extraocular muscles. Collins and Jampolsky 35 have observed that when human rectus muscles lose elasticity as a result of maintaining a chronically shortened length, their length-elastic tension curve retains its normal shape; however, the curve is merely shifted to the left on the length axis Figure 5.
The slack length is shorter, and elastic forces begin to develop at a shorter length than in a normal muscle. This would mean that the total force produced by stimulation of a relatively inelastic muscle at any given length as long as it exceeds its slack length would be greater than normal because the total force is the sum of the contractile and elastic forces.
Only the elastic force, however, would be responsible for the increase seen in total force. Below the slack length there would be no contribution from contractile forces by definition, and consequently this statement would not hold true. This can either result in an isometric contraction eg, one that is not accompanied by a change in muscle length or an isotonic contraction eg, one that is accompanied by muscle movement. Studies done on animal skeletal muscle show that increased innervation is often accompanied by a change of many of the fast twitch fibers to slow twitch; however, this has not been observed in humans.
Results in other species have been conflicting. There are 6 important principles for understanding why human extraocular muscles may appear to overact. Five relate to general principals of muscle physiology and one involves understanding Hering's law. This may not necessarily result in an increase in cross-sectional area, depending on the type of cellular changes that occur. The importance of this is outlined later in the article; however, the reasoning can be understood by considering the right eye of a normal subject tilting his head to the right.
It is classically held that there would be stimulation to the right SR and right SO muscles to provide some degree of static countertorsion. However, the SR muscle can normally create a much greater vertical force vector in the primary position than can the SO muscle.
In brief, my hypothesis states that strengthened extraocular muscles overact and inelastic extraocular muscles represent a form of pseudo-overaction. A key observation for understanding primary IO-OA is that objective fundus extorsion typically precedes the development of the clinical picture of IO-OA eg, overelevation in adduction , often by many months to several years. I reported this observation in my discussion of the article by Guyton and Weingarten 49 on sensory torsion at the 21st Annual Scientific Meeting of the American Association for Pediatric Ophthalmology and Strabismus unpublished oral presentation, , and I have found it to be valid for more than 20 years.
Subsequently, Eustis and Nussdorf 50 confirmed this observation in a prospective study. Any substantial extorsional drift must either come from increased stimulation to the IOs or decreased stimulation to the SOs because the vertical rectus muscles have weak torsional vectors.
It is also called the second cranial nerve or cranial nerve II. It is the second of several pairs…. The orbicularis oculi muscle is one of the two major components that form the core of the eyelid, the other being the tarsal plate. The orbicularis…. The jejunum is one of three sections that make up the small intestine.
Learn about its function and anatomy, as well as the conditions that can affect…. The vagus nerve is the longest of the 12 cranial nerves. Here, learn about its anatomy, functions, and the kinds of health problems that can occur. The fimbriae of the uterine tube, also known as fimbriae tubae, are small, fingerlike projections at the end of the fallopian tubes, through which…. The bladder, like the stomach, is an expandable saclike organ that contracts when it is empty.
The inner lining of the bladder tucks into the folds…. Health Conditions Discover Plan Connect. Read this next. The patient may complain of double or blurred vision diplopia when looking towards the ipsilesional side i. Damage of upper motor neurons does not result in a flaccid paralysis. However, the muscle will not be activated into the response normally controlled by the upper motor neuron e. However, the muscle will perform reflex responses e.
A 65 year-old male presents with a left medial strabismus and cannot move both his eyes to the left Figure 8. His vision and his pupillary reflexes are normal in both eyes. Neural imaging tests indicate a small infarct i. You conclude that the damaged area includes the left abducens nucleus. Damage to the abducens nucleus. The result is an abnormality of conjugate horizontal eye movements called lateral gaze paralysis. With the eyes at rest, there is a medial strabismus in the eye ipsilateral to the damage indicating abducens motor neuron damage.
During an attempted lateral gaze, both eyes cannot be moved beyond the midline in an ipsilesional direction i. As the left abducens interneurons send axons to the right oculomotor neurons innervating the medial rectus of the right eye Figure 8. An attempted lateral gaze in a contralesional direction away from the damaged side is successful. Note that as the lower motor neurons i. An example of the effect of damage to the medial longitudinal fasciculus is presented in the Appendix.
A 65 year-old male was brought to the emergency room because he suddenly lost the ability to speak and could not move the right side of his body or face. He was described to be right handed and on antihypertensive medications. Examination revealed weakness in his right face, no movement in his right arm and weakness in his right leg with Babinski's sign.
His speech was nonfluent. He could not move his eyes to the right when asked to "look right" Figure 8. He was able to move his eyes in other directions. Sensation over the body and face was decreased on the right side. His vision and hearing appeared within the normal range. Notice at the "look straight" command, this patient exhibits a "left gaze preference" when the eyes are at rest.
Neural imaging tests indicate infarction of branches of the medial cerebral artery supplying the lateral surface of the left frontal cortex. Damage to the voluntary saccades circuit. Damage to the frontal cortical eye field and the midbrain superior colliculus effect voluntary and reflex saccades, particularly those in the horizontal plane.
Immediately following unilateral damage of the frontal cortical eye field, there is an inability to voluntarily initiate a horizontal eye movement in a direction contralateral to away from the side of the lesion. That is, immediately following a right frontal lobe lesion, both eyes cannot be moved voluntarily to the left beyond the midline. However, both eyes will move to the left beyond the midline to vestibular stimulation.
Both eyes can also be directed to the side ipsilateral to the lesion and may tend to deviate toward the lesion when the eyes are at rest. The deficits disappear with time if the damage is localized to the frontal cortical eye field and does not involve the superior colliculus. A 55 year-old male was brought to the emergency room.
He was overweight and reportedly normally right-handed, a heavy smoker and drinker. He had lost consciousness during a game of basketball and when he awoke, appeared confused. When examined in the ER, he was conscious but followed no commands and could not repeat. He could mimic gestures and was able to voluntarily look to the left and right Figure 8.
His eyes followed a pen moving to his right with a smooth pursuit movement. However, his eye movements became jerky and ballistic at midpoint in the attempt to follow the pen as it moved to his left. Notice at the "look straight" command, the patient's eyes tend to wander when at rest. Also notice at the "look left" command, the patient's eyes tend to move in a jerky, step-like manner. Neural imaging tests indicate infarction of branches of the left medial cerebral artery supplying the caudal superior temporal gyrus and inferior parietal gyrus.
Damage to the smooth pursuit circuit: Damage to the temporal eye field causes deficits in the ability to fixate on objects and to track them. Attempts to fixate on a target will be undermined by severe instability and wandering of the eyes.
Tracking movements are jerky rather than smooth when attempting to follow an object moving in a direction toward ipsilateral to the side of the lesion. Note that the smooth pursuit circuit includes a double crossing and the temporal eye field controls ipsilateral eye movements i. When the temporal eye field is damaged, the two eyes may follow a visual target in an ipsilesional direction; but does so using the voluntary saccades circuit. That is, if the frontal cortical eye fields are intact, the eyes may be moved voluntarily guided saccade toward an object of interest ipsilateral to the impairment.
However, in this case, the movements will be jerky unlike the eye movements in smooth pursuit. Tracking of visual targets contralateral to the lesion will be smooth. This chapter reviews the ways in which voluntary eye movements are initiated by cerebral cortical activity and involve more ocular motor control structures than the simple ocular reflexes. The cortical areas initiate eye movements and work through brainstem ocular motor centers to produce a response, i.
The smooth pursuit system utilizes a pontine nucleus, the cerebellum, and the vestibulo-ocular reflex pathway to execute eye movements to tract visual targets.
The voluntary saccades system is similar to other voluntary motor systems in engaging areas in the frontal cortex to initiate the response and in influencing the motor neurons indirectly through lower motor control structures i. The gaze centers function to coordinate and control the activity of motor neurons to insure that the extraocular muscles act synergistically to produce conjugate saccades.
Vestibular nystagmus is elicited by stimulation of the vestibular receptors and involves structures in the vestibulo-ocular response pathway. The frontal eye field neurons send control signals to the pontine paramedial reticular formation for voluntary horizontal eye movements i. The pontine paramedial reticular formation is not part of the smooth pursuit pathway, which involves the dorsal pontine nuclei, cerebellum and structures in the vestibulo-ocular pathway.
The pontine paramedial reticular formation is not part of the accommodation neural circuitry. For example, it is not involved in the convergence of the two eyes. A year old male with a past history of high blood pressure awakens with a terrible headache.
His eyes tend to drift about and when he is asked to track a pen moving to his left, both eyes move in short, jerky steps. In contrast, both eyes move smoothly when his eyes track a pen moving to his right.
Given the patient's history, a radiological study is scheduled to determine whether a stroke had occurred. The study determines the area of infarction to include which of the following? If it had been damaged, the left eye would not have moved to the right while attempting to track an object moving to the right. If it were damaged, it would not interfere with smooth pursuit as it controls saccades toward the left.
Neurons in the left temporal lobe middle superior and middle temporal gyri are involved in detecting movement of objects in space and in guiding tracking eye movements during smooth pursuit. The left tracking movement is jerky because the frontal eye field is being used to guide the eye movement in saccades. The two eyes move to the left and if the object isn't in view, the eyes make another saccade to direct them towards the expected position of the moving object.
This section is included for those who wish to use further "clinical cases" to test their knowledge of ocular motor functions. A patient visits his primary care physician at the urging of his wife. She noticed that his left eye lid was drooping slightly and that his face appeared flushed.
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