Neuroophthalmology

Chapter 16 Neuroophthalmology




Neuroophthalmology should not be a daunting study. If anatomy, physiology, and pathology of the ocular and visual innervation are understood, a diagnosis can be reached through deduction and elimination rather than from memory.


The following cranial nerves are significant in relation to ocular functions:








In addition, significant parts of the CNS are devoted to vision processing and ocular control. Therefore the workup of the neuroophthalmologic patient requires comprehensive neurologic and systemic examinations, in addition to a thorough neuroophthalmologic examination (Table 16-1). This chapter reviews the examination, clinical signs, and diseases of the neuroophthalmologic patient.


Table 16-1 Summary of the Neuroophthalmologic Examination



























TEST OR OBSERVATION NEUROLOGIC COMPONENTS
Menace response CN II, optic chiasm, optic tract, lateral geniculate nucleus, optic radiation, visual and motor cortex, facial nucleus and nerve cerebellum
Size of pupils and reaction to light CN II, optic chiasm, proximal optic tract, CN III, sympathetic nerves, diencephalon-mesencephalon (pretectal and oculomotor nuclei)
Eyelids (size of fissure) CNs III, VII, sympathetic nerves
Third eyelid Sympathetic nerves
Position of eyes CNs III, IV, VI, vestibular system, brainstem
Normal and abnormal nystagmus CN VIII—brainstem and vestibular system—CNs III, IV, VI
Palpebral reflex CNs V, VII

CN, Cranial nerve.



ASSESSING VISION AND PUPILLARY LIGHT REFLEXES



Vision and the Menace Response


Vision is initially evaluated as the patient walks into the clinic or examination room. The ability to navigate in these unfamiliar surroundings may reveal visual deficits. A more direct assessment is made by testing the animal’s response to a menacing gesture. The menace response is evoked by making a threatening gesture with the hand at each eye while the other hand covers the opposite eye. If the other eye is not covered, an alert animal that is unilaterally blind in the eye being tested may observe the threat with its normal eye and respond by blinking bilaterally, thus creating a false positive response (i.e., a blink “response” in a blind eye). It is crucial to the validity of this test that the threatening hand does not touch the patient or create enough air currents to be felt by the patient, which may also generate a false positive response (Figure 16-1).



The normal response to this threat is a rapid blink and closure of the palpebral fissure. The anatomic pathways of the afferent and efferent components are depicted in Figure 16-2. The afferent component of the response is relayed by the optic nerve, through the optic chiasm, optic tract, lateral geniculate nucleus (LGN), and optic radiation to the visual cortex located in the occipital lobe. It is assumed that the visual cortex projects to the motor cortex, which in turn projects via the internal capsule and crus cerebri to the facial nuclei in the medulla, and from there the facial nerve (CN VII) relays the efferent signal to the eyelid muscles. The complexity of this pathway implies that the resulting blinking is not a reflex but a learned response. Therefore this response may not become fully developed until 10 to 12 weeks of age in some small animals. It is usually present by 5 to 7 days in foals and calves. As a result, menace testing in young patients may result in a false negative result, as the animal does not blink even though it can see.



Crossover of optic nerve fibers occurs at the optic chiasm (Figure 16-3). Consequently, the left occipital cortex receives the axons of the lateral retina of the left eye (inputting from the right visual field) as well as the axons of the medial retina of the right eye (inputting, again, from the right visual field) (see orange pathways in Figure 16-3). The right occipital cortex inputs from the left visual fields of both eyes (see green pathways in Figure 16-3). In humans, where 50% of the axons cross over in the chiasm, the left occipital cortex inputs the right visual hemifield of both eyes, and the right occipital cortex inputs the left visual hemifield (orange and green pathways, respectively, in Figure 16-3). In animals, where a greater percentage of fibers cross over, the left occipital cortex will input a greater proportion of the right visual field of the right eye and a smaller proportion of the right visual field of the left eye. Therefore, in humans, a lesion in the left optic radiation or occipital cortex, for example, will cause a loss of the right visual hemifield, with symmetric deficits in both eyes (homonymous hemianopia). In animals, however, such a lesion will cause greater deficits in the visual field of the right eye than those of the left eye. In the dog, where 25% of the fibers remain on the ipsilateral side and 75% of the fibers cross over in the chiasm, a unilateral lesion will cause deficits of 25% and 75% in the visual fields of the ipsilateral and contralateral eye, respectively. In the cat, the respective figures are 33% and 67%. In dogs and cats such visual deficits are difficult to detect as an animal moves in its surroundings. Occasionally, the animal may bump into an object on the side opposite the lesion, but often there is no evidence of visual deficit because 25% to 33% of the visual field is relayed to the unaffected lobe. In horses, sheep, and cattle with 80% to 90% decussation of optic nerve axons there is a greater tendency to walk into objects on the side of the visual deficit, contralateral to the lesion. Theoretically, these deficits could be tested separately by threats from the lateral and medial visual fields. However, this approach is unreliable, and in all domestic animals menace reflex is poor or absent on the side contralateral to the lesion.



If the menace response does not occur, the examiner should rule out another potential cause of false negative responses by checking the facial nerve innervation of the orbicularis oculi. It is possible that the patient is visual but cannot blink due to facial nerve paralysis. This is checked by touching the lateral and medial canthi of the eyelids to test the palpebral reflex, which is expressed as a blink in response to the tactile stimulation. Another way to rule out a false negative response caused by facial nerve paralysis is to carefully watch the eye while performing the menace test. If a facial nerve paralysis exists, forehead or eye retraction is observed when that eye is threatened, but no blinking is observed. With slight retraction of the eye, the third eyelid passively protrudes. A patient with a facial nerve paralysis may therefore have “flashing third eyelid,” which is an indication that vision is intact. If there is no facial nerve paralysis and no menace response occurs, the animal should be lightly struck two or three times with the threatening hand, and then the threat should be repeated without touching the patient. This procedure often arouses and directs the attention of the patient and is then followed by a normal response. Significant cerebellar disease may also cause lack of menace response in a visual animal, as pathways from the visual cortex to the facial nucleus likely run through the cerebellum (see Figure 16-2).


In patients in which results of the menace testing are equivocal, vision can be assessed using any of the three following tests:






Pupillary Light Reflex



The Anatomic Basis of the Pupillary Light Reflex


The afferent and efferent pathways controlling pupil size and reaction are depicted in Figure 16-5. The size of the pupil at rest represents a balance between two anatagonistic forces: (1) the amount of incident light stimulating the retina and influencing the oculomotor neurons to constrict the pupil (parasympathetic innervation through CN III), and (2) the emotional status of the patient (e.g., fear, anger, or excitement), which influences the sympathetic system and causes pupillary dilation. In the resting pupil, both pupillary dilator (sympathetic) and the antagonistic pupillary sphincter (parasympathetic) muscles are active. The relative resting parasympathetic and sympathetic innervation and resulting muscle tone determine the size of the pupil (see Figure 16-5, efferent pathways A and B, respectively). The pupillary sphincter (or constrictor) is the more powerful of the two muscles.


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Figure 16-5 Neuroanatomic tracts controlling the pupil size and response include parasympathetic (A) and sympathetic (B) pathways. The afferent pathway to the parasympathetic oculomotor nucleus is via the optic nerve to the optic chiasm (where some crossing occurs), through both optic tracts, over the lateral geniculate nucleus (without forming a synapse) to synapse in the pretectal nuclei in the mesencephalon. Note that fibers inputting to the lateral geniculate nucleus and visual cortex diverge in the middle of the optic tract; these are depicted in darker shades of green and orange. Crossing of the afferent PLR fibers between sides occurs between the pretectal nuclei via the caudal commissure. Axons of the pretectal cell bodies pass to the Edinger-Westphal (parasympathetic oculomotor) nucleus of both sides. The parasympathetic axons leave the mesencephalon with the motor axons of cranial nerve III, enter the orbit through the orbital fissure, and synapse in the ciliary ganglion. The postganglionic axons pass via short ciliary nerves, enter the globe adjacent to the optic nerve, and innervate the pupillary constrictor muscles. Preganglionic sympathetic cell bodies are located in the first three segments of the thoracic spinal cord (T1-T3). These preganglionic axons join the thoracic sympathetic trunk inside the thorax and terminate in the cranial cervical ganglion. The postganglionic fibers pass between the tympanic bulla and the petrosal bone into the middle ear cavity and continue to the eye, where they innervate the iris dilator muscle.


(Modified from de Lahunta A [1983]: Veterinary Neuroanatomy and Clinical Neurology, 2nd ed. Saunders, Philadelphia.)


As noted, pupillary constriction and pupillary light reflex (PLR) are controlled by the parasympathetic system. The afferent pathway to the parasympathetic oculomotor nucleus is via the optic nerve to the optic chiasm (where some crossing occurs), through both optic tracts, over the LGNs without forming a synapse, and ventrally into the region between the thalamus and the rostral colliculus, called the pretectal area. Synapse takes place in the pretectal nuclei in the mesencephalon (see Figure 16-5). Crossing between sides occurs between the pretectal nuclei via the caudal commissure. Axons of the pretectal cell bodies pass to the Edinger-Westphal (parasympathetic oculomotor) nucleus of both sides. The parasympathetic axons leave the mesencephalon with the motor axons of CN III (that control four of the extraocular muscles and the levator palpebral muscle), and enter the orbit through the orbital fissure. The ciliary ganglion is located at the rostral end of the oculomotor nerve, ventral to the optic nerve (see figure 16-5 and 16-6). Preganglionic parasympathetic axons of the oculomotor nerve synapse here with the cell bodies of the postganglionic axons. The postganglionic axons pass via short ciliary nerves, enter the globe adjacent to the optic nerve, and innervate the ciliary body and pupillary constrictor muscles. The feline eye has only two short ciliary nerves, each serving half of the iris. A partial parasympathetic lesion may therefore cause a hemidilated pupil (partial internal ophthalmoplegia) in the cat.



The anatomy of the sympathetic pathway, responsible for pupil dilatation, is discussed later in this chapter (see Sympathetic Lower Motor Neuron Innervation).



Testing the Pupillary Light Reflex


The size and response of pupils to light are assessed after the menace test. If there is a visual deficit, localization of the lesion depends on a careful examination of the eyes and the pupils.


First, the size of the pupils at rest (without stimulation) should be evaluated both in normal room light and in dim light. If the pupils cannot be seen without extra light, a dim penlight is held in front of the nose of the patient and at a distance that will just allow the pupillary margins to be seen, without stimulating them. The size of the pupils is assessed and compared with each other to determine if there is anisocoria (unequal pupils).


Next, the reaction to strong light is tested. Because of the crossover in the optic chiasm and mesencephalon (see Figure 16-5), stimulation of the retina of one eye with a bright source of light causes constriction of both pupils. First the examiner evaluates the direct PLR by shining a bright light into one eye while observing the reaction of its pupil. To evaluate the indirect PLR, the examiner shines a bright light into one eye while observing the reaction of the contralateral pupil. The patient should be relaxed for this part of the examination, because circulating epinephrines and sympathetic stimulation may interfere with the PLR.


It is important to remember that PLR, as well as the following four tests described next, evaluate subcortical reflexes. Therefore they are not indicators of vision and may be normal in a blind animal (e.g., in cases of cortical disease). Furthermore, the PLR is remarkably resistant to serious ocular diseases that substantially reduce its afferent input. Animals with extensive retinal disease (e.g., progressive rod-cone degeneration) or mature cataracts can be functionally blind and yet their pupils may still respond to bright light. However, these animals have pupils that are dilated more than normal in the room light because they do not react to incident light in the room. This helps distinguish them from cases of central blindness, where pupils constrict in response to incident light. If the clinician is not aware of this possibility, he or she may erroneously diagnose a lesion in the central visual pathways in that patient (based on the presence of PLR in a blind animal).






Electrophysiology


Retinal function can also be evaluated electrophysiologically, using electroretinography to record the responses of the retina to light stimulation. The test is described in detail in Chapter 15. It may be used to determine whether blindness is caused by retinal or postretinal disease. Placing the active electrode over the visual cortex, rather than on the cornea, allows for the recording of visual evoked potentials, which are useful in determining cortical function and vision.



LESIONS IN PATIENTS WITH VISUAL AND PUPILLARY LIGHT REFLEX DEFICITS


Based on the results of the visual performance and PLR tests, patients with deficits may be divided into one of three categories:





This simple categorization is the first step in localizing the pathologic lesion(Table 16-2 and Figures 16-8 to 16-12). It assumes that ophthalmic examination did not reveal any pathology that would prevent light from reaching the retina (e.g., hyphema, cataract).









Lesions in Blind Patients with Normal Pupillary Light Reflexes


Based on the anatomy of the PLR pathway, the size of the pupils and their response to light are normal in blind animals with disease limited to the distal optic tract (after the afferent PLR fibers have diverged), LGN, optic radiations, and/or visual cortex (see dark green and dark orange pathways, Figures 16-2 and 16-3).


Bilateral cerebral lesions that cause blindness include prosencephalic hypoplasia with no cerebral hemispheres (calves), hydranencephaly (calves, lambs), cerebral contusion, cerebral edema (following trauma, postictal, or due to space-occupying lesions), viral encephalitis, thrombotic meningoencephalitis (Haemophilus somnus in cattle), inflammatory diseases such as granulomatous meningoencephalitis (GME) in dogs and horses, metabolic disorders (hypoglycemia, hepatic encephalopathy), poisonings, and nutritional and storage diseases. These diseases are discussed at the end of the chapter (see Diseases of the Central Visual Pathways).


The most common causes of a unilateral cerebral lesion with contralateral visual deficit are neoplasms in small animals and abscesses in large animals. Others are cerebral infarction (most common in cats), protozoan encephalitis in horses, chronic canine distemper encephalitis, Toxoplasma granulomas, GME in dogs, thrombotic meningoencephalitis in cattle, and parasitic cysts (coenurosis in sheep) or migrations. These diseases are discussed at the end of this chapter (see Diseases of the Central Visual Pathways).



Lesions in Blind Patients with Abnormal Pupillary Light Reflexes


As can be seen in Figures 16-2, 16-3, and 16-5, the afferent fibers of the PLR and visual signal run together from the retina through the optic nerve, optic chiasm, and proximal optic tract, diverging just before the LGN (see light green and light orange pathways in these figures). Minor lesions in this common pathway (e.g., early retinal degeneration) may cause visual deficits without affecting the PLR. This is because, as noted earlier, the PLR is resistant to deficits in afferent input. Therefore if a lesion in this common pathway is significant enough to cause a pupillary abnormality, it usually also causes blindness. Converesely, if the eye is blind due to an afferent lesion, the PLR is almost always abnormal (though not necessarily absent). As a rule, afferent lesions that interrupt this pathway occur in the retina, optic nerve, or optic chiasm (see Figures 16-8 and 16-9). Rarely both proximal optic tracts are affected sufficiently to cause pupillary abnormalities, because the tracts are spread out over a relatively large area. A single optic tract lesion is rare and may cause no PLR abnormality (due to the crossover in the pretectal and oculomotor nuclei) (see Figure 16-10).


A patient with a unilateral lesion in the retina or optic nerve has no menace response in that eye. The pupil in that eye may be slightly larger (because it receives no direct parasympathetic stimulation from incident light), although it is not fully dilated (due to the indirect stimulation from the unaffected eye) (Figure 16-13). Light directed into the affected eye causes no response in either eye. Light directed into the unaffected eye elicits a bilateral response (see Figure 16-8). To assess direct and indirect responses, the examiner moves the light back and forth between the eyes. In an animal with a unilateral lesion, as the light is directed from the unaffected eye to the affected eye, the pupil in the affected eye dilates back to the resting state created by the room light (indirectly, through the unaffected eye). This is because the strong light source was taken away from the unaffected eye (thereby removing the indirect stimulation) and the lesion in the affected eye has interrupted the direct afferent pathway for this reflex. This phenomenon is readily apparent as the light is repeatedly moved between the eyes. Further confirmation of a unilateral lesion is made by covering the normal eye and observing further dilation of the pupil in the affected eye which is no longer stimulated indirectly by room light through the normal, covered eye.



Common causes of unilateral lesions resulting in PLR and visual deficits include retinal detachment, glaucoma, and retrobulbar abscess or neoplasia. Trauma to the optic nerve is another common cause of unilateral lesions. The trauma may cause direct avulsion of the axons at the level of the optic canals or interference with the vascular supply of the intracanalicular part of the optic nerve. This problem may be more common in horses and in brachycephalic dogs. Ophthalmoscopic examination often shows optic disc atrophy, with secondary retinal degeneration.


Severe bilateral retinal, optic nerve, or optic chiasm lesions cause blindness with dilated pupils that are unresponsive to light (see Figure 16-9). Bilateral retinal diseases include retinal detachment, end-stage retinal degeneration, SARD, and glaucoma. The most common optic nerve disease to affect vision and PLR is optic neuritis. The disease may be infective (e.g., distemper, cryptococcosis, toxoplasmosis) or inflammatory (GME) though it is frequently idiopathic in nature. It can affect both optic nerves and the optic chiasm, and the patient presents with blindness and fixed, dilated pupils (optic neuritis is discussed under Diseases of the Optic Nerve). In young cattle, vitamin A deficiency may cause optic nerve compression from stenosis of the optic canals. Rarely in cats does ischemic encephalopathy syndrome result in infarction of the optic chiasm.


The optic chiasm may be compressed by extramedullary space-occupying lesions near the hypophyseal fossa. Pituitary neoplasms are the most common tumor in this site, although meningiomas and germ cell neoplasms (teratomas) have also been reported. The latter are more common in dogs younger than 5 years. Diseases of the optic nerve and chiasm are discussed further at the end of the chapter (see Diseases of the Central Visual Pathways).


A retrobulbar or intracranial lesion that affects both the optic nerve and the parasympathetic part of the oculomotor nerve causes a widely dilated pupil in the ipsilateral eye at rest (see Figures 16-8 and 16-11). Because of CN II involvement there is no menace response from this affected eye, and light directed into the affected eye elicits no response in either eye. Light directed into the unaffected eye causes pupillary constriction only in that eye (due to CN III lesion in the affected eye). In addition to loss of PLR, a complete oculomotor nerve deficit will also cause ventrolateral strabismus and ptosis due to denervation of four extraocular muscles and the levator palpebral muscle. However, lesions that involve only the oculomotor nerve, and do not affect vision, may also occur. These are discussed later (see Lesions Causing Pupillary Light Reflex Abnormalities in Visual Patients).



Pupils in Patients with Intracranial Injury


Pupillary abnormalities are common after intracranial trauma. They may also accompany severe acute brain lesions such as those found in polioencephalomalacia and lead poisoning in ruminants. Evaluation of the size of the pupils is important to the assessment both of the location and extent of brain damage from intracranial injury and to evaluate the response to therapy. Pupil size and prognosis in intracranial injury are shown in Table 16-3.


Table 16-3 Pupillary Reactions in Intracerebral Injury

























CONDITION PUPIL SIZE PROGNOSIS
Unilateral oculomotor nuclear or nerve contusion or compression* Anisocoria Guarded
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Compression of midbrain tectum Bilateral miosis Guarded
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Bilateral oculomotor nuclear or nerve contusion or compression Bilateral mydriasis Grave
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* Asymmetric interference with cerebral control of oculomotor neurons or the sympathetic upper motor neuron system, or both.


Bilateral sympathetic upper motor neuron deficiency or release of oculomotor parasympathetic neurons from cerebral inhibition.


Brainstem contusion with hemorrhage and laceration of the midbrain and pons is a common sequel of trauma. The parenchymal components of the oculomotor neurons are interrupted, causing both pupils to be widely dilated and unresponsive, a grave sign. Affected animals are also recumbent and semicomatose or comatose. Severe caudal brainstem lesions that are life threatening also result in partly dilated, fixed, unresponsive pupils.


Injuries that predominately involve the prosencephalon often result in very miotic pupils. Severe bilateral miosis is a sign of acute, extensive brain disturbance that by itself is not necessarily of any localizing value. The return of the pupils to normal size and response to light is a favorable prognostic sign and indicates recovery from the brain disturbance, especially following trauma. However, progression from bilateral miosis to bilateral mydriasis with fixed pupils that are unresponsive to light in trauma cases indicates that the brain disturbance (e.g., hemorrhage, edema) is advancing and the oculomotor neurons in the midbrain are nonfunctional (Figure 16-14). This progression often accompanies severe contusion of the midbrain with hemorrhage, usually along the midline, which may cause brain swelling and herniation of the occipital lobes ventral to the tentorium cerebelli, accompanied by compression and displacement of the midbrain or oculomotor nerve (or both).



The cause of unilateral or bilateral miotic pupils in acute brain disease is not known. It probably represents facilitation of the oculomotor parasympathetic neurons released from higher-center inhibition owing to its functional disturbance. Pupillary changes may take place hourly after head trauma. Unilateral mydriasis that in some cases may be accompanied by miosis of the other pupil is probably brought about by compression of the ipsilateral oculomotor nerve; the pupils, though anisocoric, may be slightly reactive. Experiments in dogs have shown that compression of the brainstem tectum at the level of the rostral colliculus causes miosis. Compression of CN III produces mydriasis.



Lesions Causing Pupillary Light Reflex Abnormalities in Visual Patients


Abnormalities in pupillary constriction that are not accompanied by visual deficits localize the lesion to the oculomotor nerve after it has exited the mesencephalon. As noted previously, the oculomotor nerve provides (1) somatic efferent inner-vation to the dorsal, medial, and ventral recti muscles, the ventral oblique muscle, and the levator palpebral muscles and (2) parasympathetic innervation to the iridal sphincter. Both functions may be affected by lesions to the nerve. There-fore such a patient will present with three clinical signs (see Figure 16-11):





Common sites for lesions of the oculomotor nerve are the cavernous sinus or orbital fissure. Therefore tumors or inflammations at these sites cause cavernous sinus syndrome and orbital fissure syndrome, respectively. Because CNs IV, V, and VI also pass through these sites, both syndromes are also characterized by deficits in the function of these nerves.


It is possible for patients with oculomotor nerve lesions to present with internal ophthalmoplegia, indicating loss of parasympathetic oculomotor function, without loss of innervation to the eyelid and extraocular muscles. In other words, these patients will present with fixed, dilated pupils but no strabismus or ptosis. This presentation is possible because of the topographical arrangement of the fibers in CN III: The parasympathetic fibers are superficial and medial to the motor fibers. Therefore compression during midbrain swelling or displacement may affect the former but not the latter.


Fixed, dilated pupils caused by parasympathetic denervation are also a characteristic sign of dysautonomia. Because patients also suffer from concomitant sympathetic denervaiton, the disease is discussed later in this chapter.


Additional Causes of Pupillary Light Reflex Abnormalities PLR abnormalities and anisocoria may also be caused by several processes that are unrelated to neurologic disease:








LESIONS CAUSING STRABISMUS



Function of the Extraocular Muscles


Innervation and action of the extraocular muscles are summarized inFigure 16-15 and Table 16-4. The globe has three axes of rotation, and the muscles are grouped into three opposing pairs. Each muscle in the pair acts in a reciprocal manner with its partner, similar to flexor and extensor muscles in the limbs. Such a pair of extraocular muscles is termed yoke muscles. When the two eyes move in the same direction the movement is called conjugate. Around a horizontal axis, passing transversely through the center of the globe, the medial rectus muscle adducts and the lateral rectus muscle abducts the globe. Around the anterior-posterior axis, through the center of the globe, the dorsal oblique intorts the globe (rotates the dorsal portion medially toward the midline), and the ventral oblique extorts the globe (moves the same point laterally away from the midline). The dorsal and ventral rectus muscles rotate the globe dorsally and ventrally, respectively.



Table 16-4 Extraocular Muscles: Innervations and Actions



































MUSCLE INNERVATION ACTION
Superior (dorsal) rectus Oculomotor (CN III) Elevates globe (rotates upward)
Inferior (ventral) rectus Oculomotor (CN III) Depresses globe (rotates downward)
Medial rectus Oculomotor (CN III) Turns globe nasally (adduction)
Lateral rectus Abducens (CN VI) Turns globe temporally (abduction)
Superior (dorsal) oblique Trochlear (CN IV) Intorts globe (rotates 12 o’clock position nasally)
Inferior (ventral) oblique Oculomotor (CN III) Extorts globe (rotates 12 o’clock position temporally)
Retractor bulbi Abducens (CN VI) Retracts globe

CN, Cranial nerve.


The extraocular muscles of both eyes do not function independently. Rather, they act together in a synergistic or antagonistic manner to provide conjugate movements of the two eyes in the same direction at the same time. This is demonstrated, for example, by the action of the medial and lateral rectus muscles in horizontal conjugate movement. When the eyes move conjugately to the right, facilitation of abducent neurons to the lateral rectus of the right eye and inhibition to those of the left eye are required in conjunction with inhibition of the oculomotor neurons to the medial rectus of the right eye and facilitation to those of the left eye. The medial longitudinal fasciculus (MLF) functions in coordinating this activity.


Functions of the extraocular muscles in domestic animals do not compare exactly with those in humans because of anatomic differences in the position of the eye with respect to the muscle insertion. Another difference between humans and animals is the presence of a retractor bulbi muscle, which is present in many mammalian species (but absent in birds and reptiles). As the name implies, this muscle, innervated by CN VI, is responsible for retracting the globe in response to pain or threats.



Lesions Causing Strabismus


Strabismus, an abnormal position of the eye, results from lesions of the nuclei or cranial nerves that innervate the striated extraocular muscles (CNs III, IV, and VI). It may also occur in some head positions with lesions in the vestibular system. When a strabismus is suspected, the eye movements are tested to verify the paralysis of the extraocular muscles. The head of the patient is moved vertically or horizontally while symmetry of ocular movements is evaluated. Movements of the head require a simultaneous conjugate response by both eyes to maintain fixation on objects in the visual field. The vestibular and cervical proprioceptive systems exert considerable influence on the nuclei of the cranial nerves that innervate the extraocular muscles in order to move the eyes so that they remain fixated on the visual target. One of the major pathways involved in connecting the vestibular system to these nuclei is the MLF.


Lesions of the vestibular system or MLF may cause an abnormal ocular position when the head is in certain positions. This appears as strabismus but usually can be corrected by repositioning of the head (see following section). Strabismus resulting from faulty extraocular muscle innervation persists in all positions of the head.


It should be remembered that strabismus may be also be caused mechanical and muscular disorders within the orbit that restrict movement of the globe. Common causes include tearing of extraocular muscles following traumatic proptosis, and orbital fractures that cause incarceration of muscles.




Strabismus due to Lesions in Innervation of the Extraocular Muscles



OCULOMOTOR PARALYSIS.


Lesions of the oculomotor nucleus, or oculomotor nerve lesions, cause a lateral and slightly ventral strabismus— exotropia—primarily from loss of innervation of the medial rectus and secondarily from the denervation of the dorsal and ventral recti muscles and the ventral oblique muscle (see Figures 16-11 and 16-15, B). There is experimental evidence to support the direction of this strabismus, although it is difficult to explain the ventral deviation on the basis of the anatomy of the oblique muscle. Due to the lesion, eye adduction is deficient due to denervation of the medial rectus muscle. This can be observed on testing of normal vestibular nystagmus: As the head is moved in a dorsal plane, side to side, the eyes normally develop a jerk nystagmus with the quick phase in the direction of the head movement. The jerklike movement toward the nose is adduction resulting from contraction of the medial rectus innervated by the oculomotor nerve (CN III). This adduction, as well as lid opening and pupillary constriction, will be reduced by lesions to CN III.




Causes of oculomotor nerve dysfunction were discussed in previous sections (see Pupils in Patients with Intracranial Injury and Lesions Causing Pupillary Light Reflex Abnormalities in Visual Patients). Depending on the location of the lesion, patients may present with or without other CNS and visual deficits.


Exotropia may also be seen in hydrocephalic animals that have an enlarged cranial cavity. Both eyes often deviate ventrolaterally, and therefore the syndrome is called sunset eyes. This abnormality is thought to result from a malformation of the orbit that occurs when the cranial cavity is distorted by the early development of the brain abnormality. The eyes adduct and abduct normally on testing of normal vestibular nystagmus, and no ptosis or pupillary abnormality is present. Therefore this exotropia is not related to oculomotor dysfunction.





LESIONS CAUSING EYELID ABnoRMALITIES



Third Eyelid Abnormalities


Normally the mammalian third eyelid is kept in its position ventromedial to the eye by the tone in its smooth muscle, which keeps it retracted. This is a function of its sympathetic innervation. The normally protruded position of the eye in the orbit also contributes to the normal position of the third eyelid.


The third eyelid may protrude for a number of reasons. Except possibly in the cat, this protrusion is a passive event. The third eyelid protrudes passively when the globe is retracted actively by the retractor bulbi (CN VI). In the cat, slips of striated muscle from the lateral rectus and levator palpebrae superioris attach to the two extremities of the membrane and may contract and contribute actively to this protrusion.


Aug 11, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Neuroophthalmology
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