Eye movement disorders
- Eye movement, oculomotor, trochlear and abducens nerve:
- Saccadic (rapid) eye movements
- Focused eye movements
- Convergent eye movement
- Retention of eye in a specific position
- Eye movements in acceleration and gravity changing
- Extraocular muscles and gaze palsy:
Oculomotor muscles provides eye movement. Oculomotor muscles receive innervation from III, IV, VI cranial nerves.
Oculomotor nerve's (III cranial nerve pair) motoneurons located on either side of the midline in the rostral part of the midbrain. These nuclei of the oculomotor nerve (III pair of cranial nerves) innervate five extraocular muscles of the eyeball, including the muscle that elevate upper eyelid. The nucleus of the oculomotor nerve also contain parasympathetic neurons (Edinger-Westphal nucleus) involved in the processes of pupil constriction and accommodation.
Displaying the normal position of the eyeballs and exotropia with the weakness of the medial (inner) eyes right rectus muscle (III pair of cranial nerves).
There is a division of supranuclear motor neuron groups for each individual eye muscles. Oculomotor nerve fibers that innervate the medial rectus, inferior oblique and inferior rectus muscles are located on the same side. Subnucleus of oculomotor nerve for upper rectus muscle is located on the contralateral side. Elevate upper eyelid muscle is innervated by the oculomotor nerve's central group of cells.
Trochlear nerve (IV cranial nerve pair) motoneurons closely adjacent to the main part of the complex nuclei of the oculomotor nerve. Left trochlear nerve nucleus innervate the upper right oblique muscle of the eye, right nucleus - innervate the eyeball's upper-left oblique muscle.
Motoneurons of the abducent nerve (VI cranial nerve) innervating the lateral (outer) rectus muscle of the eye on the same side and located in the nucleus abducens in the caudal part of the pons (part of the brainstem). All three oculomotor nerves, coming from the brain stem, pass through the cavernous sinus and enter the orbit through the upper orbital fissure.
Clear binocular vision provided by joint activity of individual eye muscles (oculomotor muscles). Friendly eye movements controlled by supranuclear sight centers and their connections. Functionally, there are five different supranuclear systems. These systems provide various kinds of movements of the eyeballs. Among them there are centers that control:
- saccadic (rapid) eye movements;
- focused eye movements;
- convergent eye movement;
- retention of eye in a certain position;
- vestibular centers.
Shown the weakness of the lateral (outer) rectus muscle of the right eye (VI pair of cranial nerves) before and after treatment.
Saccadic (fast) movements of the eyeball appear as a command in the opposite visual field of the cortex of the brains frontal region (field 8). Exceptions are the fast (saccadic) movement arising during stimulation fovea of the retina, which come from the occipital-parietal region of the brain. These frontal and occipital control centers in the brain have projections in the supranuclear stem centers on both sides. The activity of these stem supranuclear visual centers exposed by influences from the cerebellum and the vestibular nuclei complex. Paracentral sections of the reticular formation of the pons are the stem center that providing friendly fast (saccadic) eye movements. Simultaneous innervation of internal (medial) rectus and opposite the rectus (lateral) rectus muscle while moving eyeballs horizontally provided by medial longitudinal fasciculus. This medial longitudinal fasciculus connects the abducent nerve nucleus with subnucleus complex of oculomotor nuclei, which are responsible for the innervation of the opposite internal (medial) rectus muscle of the eye. For the beginning of vertical rapid (saccadic) eye movements requires bilateral stimulation paracentral departments of the reticular formation in the pons from the cortical brain structures. Paracentral sections of the pons reticular formation transmit signals from the brain stem to the supranuclear centers that controlling eye movement vertically. Such supranuclear eye movement center is relates an intermediate rostral nucleus of the medial longitudinal fasciculus, located in the midbrain.
Cortical center for smooth tracking or focused movements of the eyeballs is located in the occipital-parietal region of the brain. Control performed with same side, i.e., the right occipital-parietal area of the brain controls the smooth eye movement focused to the right.
Checking purposeful eye movements performed by tracking an object from the center to the periphery in fixed patient's head.
Control mechanisms of convergent movements are less well understood, however, as is known, the neurons responsible for converging eye movement are arranged in the reticular formation of the midbrain, surrounding the complex of the oculomotor nerve nuclei. They provide projections in the motor neurons of the internal (medial) rectus muscle of the eye.
Stem centers of eye movements called neural integrators. They are responsible for holding the gaze in a certain position. These centers are changing the signals of the eyeballs movement speed in information about their location. Neurons possess their property, located in the pons below (caudal) the abducens nucleus.
Coordination of the eyeballs movements in response to changes in gravity and acceleration carried out by vestibular system (vestibulo-ocular reflex). In case of lesion, coherence movements of both eyeballs will be developed double vision, because the images projected onto the disparate (inappropriate) portions of the retina. In congenital strabismus or squint, impaired muscles balance, leading to the wrong eyeballs location (non parethic strabismus), can help to ensure that the brain will suppress one of the images. Such decrease in visual acuity in non-locating eyeball called amblyopic without anopsia. In paralytic strabismus, double vision occurs in resulting of the eyeball muscles paralysis, usually due to lesions of the oculomotor (III), trochlear (IV) or abducens (VI) cranial nerves.
There are three types of the eyeball extraocular muscles paralysis:
Typical clinical manifestations occur with isolated lesions of the oculomotor (III), trochlear (IV) or abducens (VI) nerve.
Total damage to the oculomotor (III) nerve leads to the appearance of ptosis. Ptosis manifested in the form of weakening (paresis) muscles that lifting the upper eyelid and the impairment of any movements of the eyeball upward, downward and inward, and exotropia due to safety features lateral rectus muscle. In case of damage of the oculomotor (III) nerve there are as pupil dilation (mydriasis) and the absence of his reaction to light (iridoplegiya) and paralysis of accommodation (cycloplegia). Isolated paralysis of the muscles of the iris and ciliary body called internal ophthalmoplegia.
Shows the normal position of the eyeballs and esotropia with weakness of the lateral direct right eye muscles (VI cranial nerve).
Damage of trochlear (IV) nerve cause paralysis of the eyeballs superior oblique muscle. Similar damages of trochlear (IV) nerve lead to a deviation of the eyeball outwards and gaze downward movement difficulty (paresis). Gaze downward paresis mostly clearly manifested in turning the eye inward. Diplopia (double vision) disappears when the head is tilted to the opposite shoulder, at which the compensatory deviation of intact eyeball medially.
Damage of abducens (VI) nerve leads to paralysis of the muscles, which move the eyeball sideward. Damage of abducens (VI) nerve develops esotropia due to the predominance of eyeball's normally working medial rectus muscleís tone exposure. With a partial paralysis of the abducens (VI) nerve patient can turn his head to the side of affected eye abductor to eliminate double vision through a compensatory effect on the eyeball's weakened lateral rectus muscle.
Intensity of listed above symptoms with damage oculomotor (III), trochlear (IV) or abducens (VI) nerve will depend on the lesions severity and its localization in patient.
Friendly gaze called simultaneous movement of both eyes in the same direction. Acute lesions one of the frontal lobes, such as cerebral infarction (ischemic stroke), can lead to a transient paralysis random friendly movements of the eyeballs in a horizontal direction. At the same time, independent of eyeballs movements in all directions fully preserved. Paralysis friendly random movements of the eyeballs in the horizontal direction revealed in the dolls eye phenomenon during passive head rotation horizontally lying person or by caloric reflex test (vestibular caloric stimulation - infusion into the ear canal with cold water).
Unilateral damage of pons disposed downwardly of paracentral reticular formation at the abducens nerve nucleus level causes persistent gaze palsy toward destruction side and oculocephalic reflex loss. Oculocephalic reflex (or vestibulo-ocular reflex) - is a eyeballs motor reaction on vestibular apparatus mechanical or thermal irritation, as in the phenomenon of the dolls head and eyes or caloric stimulation of the external auditory canal walls with cold water. Optical image stabilization (OIS) systems in digital cameras work at the same principles.
The damage of the rostral interstitial nucleus of the medial longitudinal fasciculus in front of the midbrain and/or damage of posterior commissure cause gaze supranuclear upward palsy to this focal neurologic symptom added of pupilís dissociated reaction on light:
- pupils on light weak reaction;
- pupils fast reaction to the accommodation (eyeballs focal length changing) and view on close objects.
In some cases in a patient is also being developed paralysis of convergence (eyeballs toward each other movement, when gaze will focus on the nose). This symptom called Parinaud syndrome. Parinaud syndrome common in tumors of the pineal gland, in some cases with cerebral infarction (ischemic stroke), multiple sclerosis and hydrocephalus.
An isolated downward gaze palsy occurs rarely in patients. When this occurs, the most commonly cause is a blockage of the lumen (occlusion) of penetrating artery and bilateral midline infarction (ischemic stroke) of the midbrain. Some hereditary extrapyramidal disease (Huntington's chorea, progressive supranuclear palsy) can cause restriction of movements of the eyeballs in all directions, especially upwards.
Simultaneous combination of the patient gaze palsy and paralysis of certain oculomotor muscles, usually a sign of midbrain or pons lesions. Lower pons parts lesions with destruction of located there abducens nucleus can lead to paralysis of fast (saccadic) movements of the eyeballs and horizontal abducens (VI) nerve paralysis on affected side.
Lesions of medial longitudinal fasciculus lead to various eye disorders in the horizontal direction (internuclear ophthalmoplegia).
Unilateral damage of medial longitudinal fasciculus caused by infarction (ischemic stroke), or demyelination process, lead to the eyeball toward movement weakness (to the nose). This may manifest clinically as complete paralysis, eyeball inwards abduction inability from the midline, or form of moderate paresis, which will manifest itself in lower speed abduction fast (saccadic) eye movements to the nose (adduction delay). Lesions on the opposite side of the medial longitudinal fasciculus, usually observed abduction nystagmus: nystagmus arising in eyeballs abduction outwards with a slow phase directed to the midline, and fast horizontal saccadic movements. Asymmetrical arrangement of eyeballs to the vertical line often develops in unilateral internuclear ophthalmoplegia. The eye on the affected side will be located higher (gipertropiya).
Bilateral internuclear ophthalmoplegia occurs in demyelinating processes, tumors, infarcts, or arteriovenous malformations. Bilateral internuclear ophthalmoplegia leads to a more complete eyeballs movementís syndrome disorder that manifest bilateral paresis of the muscles, eyeballs toward movement, a impairment of the vertical movements, tracking purposeful movements and movements, caused by the vestibular system. Noted vertical line gaze disorders, upward nystagmus during looking up and downward nystagmus when looking down. Lesion of medial longitudinal fasciculus in the midbrain overlying (rostral) sections accompanied by convergence damage (convergent eye movements to each other in the direction of the nose).
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