8.1 Introduction Show
Normal visual perception requires the proper functioning of ocular motor systems that control the position and movement of the eyes to focus the image of the object-of-interest (i.e., the visual target) on corresponding areas of the retinas of the two eyes. For example, in addition to producing adjustments in pupil size and lens refraction, accommodation involves the convergence of the two eyes to direct onto the foveae the images of near objects. Eye movements are also controlled to direct the eyes towards a visual target and to follow the movements of the visual target. Such eye movements are controlled by gaze systems. They coordinate the movement of the two eyes to ensure that the images on the two retinas fall on corresponding areas of the binocular field. When this fails, diplopia (double vision) results. 8.2 Extraocular Muscles and their Innervation The extraocular muscles execute eye movements and are innervated by three cranial nerves. The muscles are attached to the sclera of the eye at one end and are anchored to the bony orbit of the eye at their opposite ends. Contraction of the muscles produce movement of the eyes within the orbit. The cranial lower motor neurons innervate these muscles and thereby control their contractions.
A. The Extraocular Muscles For each eye, six muscles work together to control eye position and movement. Two extraocular muscles, the medial rectus and lateral rectus, work together to control horizontal eye movements (Figure 8.1, left).
The actions of these two muscles are antagonistic: one muscle must relax while the other contracts to execute horizontal eye movements. Four other extraocular muscles working together control vertical eye movements and eye rotation around the mid-orbital axis (Figure 8.1, right). Contraction of the
To direct the eye upward or downward, two muscles contract synergistically as the two antagonist muscles relax. For example, to elevate the eye while looking straight ahead, the superior rectus and inferior oblique contract together as the inferior rectus and superior oblique relax. The superior rectus and inferior oblique muscles working together pull the eye upward without rotating the eye. To depress the eye while looking straight ahead, the inferior rectus and superior oblique contract together as the superior rectus and inferior oblique relax. The inferior rectus and superior oblique working together pull the eye downward without rotating the eye. B. Extraocular Muscle Efferents Three cranial motor nuclei provide efferent control of the extraocular muscles. Activation of the motor neurons produces contraction of the innervated muscle.
C. Upper Motor Neuron Control
The motor neurons controlling synergist and antagonist muscles must coordinate their activities to produce the desired eye movements. Within the abducens nucleus are abducens interneurons, which send their axons into the contralateral medial longitudinal fasciculus (MLF). They ascend in the MLF to end on oculomotor neurons controlling the medial rectus (Figure 8.2). The abducens interneurons coordinate the activity of the
ipsilateral lateral rectus with that of the contralateral medial rectus. For example, excitation of the motor neurons in the left abducens nucleus will result in contraction of the left lateral rectus and abduction of the left eye (i.e., movement of the left eye towards the left). Excitation of the interneurons in the left abducens nucleus will excite neurons in the right oculomotor nucleus that innervate the right medial rectus. Contraction of the right medial results in adduction of the right
eye (i.e., movement of the right eye towards the left). Consequently, both the right and left eyes will be directed towards the left when the left abducens nucleus is excited. Interconnections between the trochlear nucleus and oculomotor nuclear complex coordinate their activity to allow the upward and downward movement of the eyes. These interconnecting axons appear to travel along with the fibers of the tectospinal tract (that is, they do not travel in the medial longitudinal fasciculus). 8.3 Gaze Stabilization: Eye Movements that Counter-Act Head Movement There are two functional classes of eye movements (Table I): those that stabilize the eye when the head moves or appears to move (gaze stabilization) and those that keep the image of a visual target focused on the fovea (a.k.a., foveation) when the visual target changes or moves (gaze shifting). Two gaze stabilization systems operate during head movement: the vestibulo-ocular and the optokinetic systems. Vestibulo-ocular and optokinetic movements are conjugate movements in which both eyes move in the same direction.
A. The Vestibulo-ocular Reflexes Vestibulo-ocular reflexes produce eye movements that compensate for head movements detected by the vestibular system. You have learned in earlier chapters how the vestibular system detects head movements and initiates the vestibulo-ocular responses. B. Optokinetic Nystagmus Optokinetic nystagmus is elicited
Notice that optokinetic nystagmus is a visual-ocular response - driven by visual stimuli moving across the visual field. Vestibular nystagmus is a vestibulo-ocular response - driven by a vestibular stimulus (i.e., accelerating head movement). In humans, the smooth pursuit system predominates in producing eye movements that track moving visual targets. As the optokinetic system is vestigial in humans, it will not be covered in this lecture. 8.4 Gaze Shifting: Eye Movements to Focus the Image on the Fovea Three gaze shifting systems function during foveation: smooth pursuit, which directs the eyes to follow a moving visual target; saccade, which directs the eyes toward a visual target; and vergence, which alters the angle between the two eyes to adjust for changes in distance from the visual target. We have covered the neural control of convergence during accommodation in the previous lecture. A. Voluntary Saccades Voluntary or guided saccades are eye movements initiated to bring an object-of-interest into view or initiated under direction (e.g., to the command “eyes left”). Saccades consist of short, rapid, jerky (ballistic) movements of predetermined trajectory that direct the eyes toward some visual target. The Voluntary Saccades Circuit The neurons in the frontal eye field (Figure 8.3)
The superior colliculus neurons
The vertical gaze center
The horizontal gaze center
Nuclei of the basal ganglion
The superior colliculus can initiate and control saccades independent of input from the frontal eye field. However, the motor control signals initiated by the frontal eye field and the superior colliculus differ in function.
However, when the frontal eye field is damaged, the superior colliculus will compensate for the loss following a short period of dysfunction. For example, damage to the right frontal eye field produces a transient inability to look voluntarily to the left side. Afferent Control of Voluntary Saccades Because voluntary saccades are not, in general, initiated by visual stimuli, afferent visual control occurs only after the fact. That is, the visual system (i.e., the posterior parietal visual association cortex6 in Figure 8.3) is used to determine whether the saccade was successful in bringing the desired object into view. Consequently, the saccades consists of a series of short, fast eye movement, followed by a check by the visual system as to whether the desired visual target is in view, which may be followed by another series of brief eye movements to locate the visual target. The repeated sequence of brief, rapid eye movements and image check until the visual target is in view characterizes saccades. B. Smooth Pursuit Smooth pursuit (tracking) is an eye movement elicited by a moving visual target that the eyes follow voluntarily or under direction (e.g., the request to "watch the moving pen"). Pursuit movements are described to be voluntary, smooth, continuous, conjugate eye movements with velocity and trajectory determined by the moving visual target. By tracking the movement of the visual target, the eyes maintain a focused image of the target on the fovea. Notice that a visual stimulus (the moving visual target) is required to initiate this eye movement. The Smooth Pursuit Circuit Temporal eye field neurons in the non-human primate (parts of Brodmann's areas 39 or MST- medial superior temporal gyrus & 37 or MT- middle temporal gyrus.
Frontal eye field neurons, however,
Dorsolateral pontine nucleus
The cerebellum
The vestibular nuclei
Consequently, the vestibular nuclei help coordinate the activities of antagonist muscles involved in eye movements during smooth pursuit and vestibule-ocular reflexes.10 Note that there are two decussations (double crossings) involved in the horizontal smooth pursuit pathway (i.e., the DLPN axons and the axons of the vestibular nuclei providing excitatory input to the abducens nucleus). Consequently, the command signals generated by the MST and MT cortical neurons result in an execution of smooth pursuit eye movement in a direction ipsilateral to these cortical neurons. Normally, a command generated by the left MST and MT cortical neurons results in both eyes tracking the movement of an object moving to the left.
8.5 Clinical Signs of Damage to Ocular Motor Systems Damage to the lower motor neurons that innervate an extraocular muscle results in a flaccid paralysis of the muscle, whereas damage to upper motor neurons produce deficits only in selective types of movements (e.g., smooth pursuit). A. Lower Motor Neurons Damage to an extraocular muscle’s motor neurons results in a paralysis of the muscle that is often manifested as a strabismus (a misalignment of the two eyes). At rest (while attempting to look straight ahead), the denervated eye is deviated from its normal position by the unopposed action of the muscle that is its antagonist. The strabismus may result in double vision (diplopia) because the image falling on the retina of each eye will be from non-corresponding areas in the binocular visual fields. When the patient closes one eye, the double image is replaced by a single image. Damage to the oculomotor nerve. As we have already covered this topic in the previous lecture, a brief summary of the effect of oculomotor nerve lesion on eye movements will be presented.
Consequently, at rest and during an attempted right lateral gaze, the lateral strabismus will result in a diplopia. On attempting to adduct the eye (i.e., look right or during convergence), the left lateral rectus relaxes and the left eye deviates to the midline, but not past it. Damage to the trochlear nerve. When the trochlear nerve is damaged, the symptoms are mild. The downward and lateral movement of the eye may be weakened and may cause diplopia when reading or descending stairs. A patient may present with his head tilted because the damaged eye is extorted (i.e., rotated with top of the eye tilted away from the nose) and slightly elevated because of the paralysis of the superior oblique muscle. Tilting the head away from the affected eye brings the visual axis of the partially paralyzed eye into alignment with the visual axis of the normal eye. 8.6 Clinical Example #1 Symptoms. A 65 year-old male presents with a medial strabismus of his left eye (Figure 8.6, Rest) and cannot move his left eye to the left (Figure 6, Left). His right eye has normal motility and his pupillary reflexes are normal. His vision is normal in both eyes. He has normal sensation on his face and body and no other motor symptoms.
You observe that the patient
You conclude that his functional loss
Side & Level of Damage: As his symptoms
you conclude that the damage involves the
Electrophysiological tests indicate that the left lateral rectus is responsive (i.e., normal). You conclude that the left abducens nerve has been damaged. Damage to the abducens nerve. The lateral rectus will be denervated and paralyzed and the patient will be unable to abduct the eye. For example, if the left abducens nerve is damaged, the left eye will not abduct fully (move away from the nose, towards the left, laterally). While attempting to look straight ahead, the left eye will be deviated medially towards the nose (medial or nasal strabismus) due to the unopposed action of the medial rectus of the left eye. On attempting to gaze left, the left eye may deviate to the midpoint, but not past it, because the medial rectus of the left eye is relaxed. The patient may complain of double or blurred vision (diplopia) when looking towards the ipsilesional side (i.e., left) or when looking straight ahead. B. Upper Motor Neurons 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.g., voluntary saccades controlled by the frontal eye field). However, the muscle will perform reflex responses (e.g., convergence during accommodation or nystagmus during head rotation) and responses controlled by other intact ocular motor circuits. 8.7 Clinical Example #2 Symptoms. A 65 year-old male presents with a left medial strabismus and cannot move both his eyes to the left (Figure 8.7). His vision and his pupillary reflexes are normal in both eyes. He has normal sensation on his face and body and no other motor symptoms.
You observe that the patient
You conclude that his functional losses
Side & Level of Damage: As his symptoms involves
you conclude that the damage involves the
Neural imaging tests indicate a small infarct (i.e., a lacunar stroke) in the region of the left facial colliculus. 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.e., toward the damage side). As the left abducens interneurons send axons to the right oculomotor neurons innervating the medial rectus of the right eye (Figure 8.2), the failure to perform a lateral gaze to the left suggests an abducens nucleus lesion. An attempted lateral gaze in a contralesional direction (away from the damaged side) is successful. Note that as the lower motor neurons (i.e., the abducens motor neurons), as well as a motor control center (i.e., the abducens interneurons), are damaged, both reflex and voluntary eye movements in the horizontal plane are affected. An example of the effect of damage to the medial longitudinal fasciculus is presented in the Appendix. 8.8 Clinical Example #3 Symptoms. 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 8.8). 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.
You observe that the patient's eyes
You conclude that his functional loss
Side & Level of Damage: As his symptoms
you conclude that the damage involves the
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. 8.9 Clinical Example #4 Symptoms. 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 8.9). 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.
You conclude that his functional loss
Side & Level of Damage: As his symptoms
you conclude that the damage involves the
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.e., right cortex controls smooth pursuit to the right). 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. 8.10 Summary 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.e., there are no direct connections between the cerebral cortex and the extraocular motor nuclei. 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.e., the vertical and horizontal gaze centers). 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. Test Your Knowledge
The pontine paramedian reticular formation is involved in which of the following?
The pontine paramedian reticular formation is involved in which of the following?
The pontine paramedian reticular formation is involved in which of the following?
The pontine paramedian reticular formation is involved in which of the following?
The pontine paramedian reticular formation is involved in which of the following?
The pontine paramedian reticular formation is involved in which of the following?
A 57-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?
A 57-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?
A 57-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?
A 57-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?
A 57-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?
A 57-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?
APPENDIX TO OCULAR MOTOR SYSTEMS AND CONTROLThis section is included for those who wish to use further "clinical cases" to test their knowledge of ocular motor functions. Symptoms. 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. She was concerned he might have suffered a stroke. On examination, it was noted that his left pupil was much smaller than his right (Figure 8.A.1), but responded directly and consensually to light. Physical examination determines that touch, vibration, position and pain sensations are normal over the entire the body and face. There are no other motor symptoms.
You observe that the patient exhibits
You conclude that his left eye's functional loss is
Pathway(s) affected: You conclude that structures in the following motor pathway have been affected is
Side & Level of Damage: As these symptoms
you conclude that the damage
Sympathetic Innervation of the Eye. Horner's syndrome is a constellation of symptoms that includes miosis, pseudoptosis and enopthalmosis (sunken eyeball). It is characteristic of damage to the sympathetic innervation of the face provided by the superior cervical ganglion. This syndrome also occurs when the hypothalamic output to the sympathetic preganglionic neurons in the lateral horn at T1 to T3 is interrupted or when the T1 to T3 anterior roots are damaged. Symptoms. A 35 year-old female complains that she has double vision when she attempts to look to the right. When looking straight ahead, both her eyes assume normal positions (Figure 8.A.2). She is able to look up and down and to the left with both eyes. However, she cannot adduct her left eye (i.e., move it to the right). Both her eyes converge when a visual target is brought close to her eyes. Her vision and pupillary reflexes are normal in both eyes. She has normal sensation on her face and body and no other motor symptoms.
You observe that the patient's eyes
You conclude that her functional loss
Side & Level of Damage: As her symptoms
you conclude that the damage involves the
Neural imaging tests indicate demyelination of the medial longitudinal fasciculus on the left side. Damage to the medial longitudinal fasciculus. The medial longitudinal fasciculus (MLF) is a fiber tract that contains, in part, axons of the vestibular nuclei and of the contralateral abducens interneurons. Lesions in the MLF results in an abnormality of conjugate horizontal eye movements called an internuclear ophthalmoplegia. The medial rectus ipsilateral to the damaged MLF does not function during a lateral gaze in a contralesional direction. With the eyes at rest, both eyes are directed forward in the “normal” position. If the damage is unilateral, both eyes can be moved in an ipsilesional direction during an attempted lateral gaze (i.e., towards the left if the left medial longitudinal fasciculus is damaged). In contrast, the ipsilesional eye (i.e., the left eye ipsilateral to the severed left tract) cannot be moved beyond the midline during an attempted contralesional (right) lateral gaze.
Recall the left MLF carries the axons of the right abducens interneurons to the left oculomotor neurons, which control the medial rectus of the left eye (Figure 8.A.3). Also recall that contraction of the medial rectus of the left eye directs the left eye nasally (i.e., contralaterally to the right). Both eyes are adducted on convergence as the axons from the supraoculomotor area to the oculomotor neurons controlling the medial rectus muscles of the two eyes are not affected by MLF lesions.
[1] Note that each oculomotor nerve controls the extraocular muscles of its ipsilateral eye, i.e., the right nerve controls the superior and inferior oblique and superior and inferior rectus of the right eye.[2] For the curious, the vertical gaze center is located in the rostral interstitial nucleus of the medial longitudinal fasciculus and, according to some, also in the interstitial nucleus of Cajal.[3] This is all you need to know about the role of the basal ganglion for ocular motor tasks.[4] No need to memorize this.[5] See footnotes 3 and 4 above.[6] Recall the posterior parietal cortex is part of the dorsal visual stream that determines the "where" of the visual scene (i.e., the location and movement of the visual target).[7]Please note this is in disagreement with Nolte, pg. 521, Figure 21-15, which identifies the extrastriate cortex as the course o the cortical neurons controlling smooth pursuit.[8]Recall from the lectures on the visual system that these cortical areas, MST and MT, are part of the visual sensory circuit involved with detecting the "where" of a visual stimulus.[9]For the curious, the DLPN axons end in the flocculus, paraflocculus & vermis of the cerebellum.[10] the paramedian pontine reticular formation and abducens interneurons coordinate the activities of antagonistic muscles involved in horizontal eye movements during saccades.When a patient moves his arm away from the midline This movement is called?Abduction moves the limb laterally away from the midline of the body, while adduction is the opposing movement that brings the limb toward the body or across the midline.
What means to move away from the midline of the body?Abduction/Adduction
A movement of a body part away from the midline, either of the body as a whole or that of the hand or foot, is termed abduction (L., to carry away).
Which of the following is the movement of a limb away from the midline of the body quizlet?Extension. Moving a limb toward the midline of the body is called adduction; moving a limb away from the midline of the body is called abduction. Flexion is bending a limb at a joint; and extension is straightening a limb at a joint.
What are the different types of movement in joints?Types of joint movement. Flexion – bending a joint. ... . Extension – straightening a joint. ... . Abduction – movement away from the midline of the body. ... . Rotation – this is where the limb moves in a circular movement around a fixed joint towards or away from the midline of the body.. |
A client moves their arm out away from their body. what is type of movement called?
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