Transcription
[Music] Diagnosis of paralytic strobismus of recent onset is not particularly difficult and is based on the presence of a motor deficiency in the field of action of the paralyzed muscle, as in right lateral rectus muscle paralysis or right medial rectus muscle paralysis. The terms periodic and paralytic often are used interchangeably in clinical ophthalmology, even though periodic denotes only a partial or incomplete paralysis. Another diagnostic symptom of recent paralytic strabismus is diplopia in the field of action of the paralyzed muscle, as in right lateral rectus muscle paralysis.
In paralytic strobismus, the secondary angle of deviation on fixating with the paralyzed eye is greater than the primary angle of deviation on fixating with the sound eye. Paralytic hyperdeviation is more difficult to diagnose because it is necessary to differentiate between a pair of elevators—the superior rectus and the inferior oblique muscles—and a pair of depressors—the inferior rectus and the superior oblique muscles—in each eye. In right elevators paralysis, when the patient is fixating with the right periodic eye, he exerts maximal innervational effort to move the right pair atikai into primary position. Consequently, according to Herring's law of equal innervation, excess innervations to the yoke elevator muscles of the other eye causing excessive elevation of the left eye. In a patient with a left superior oblique paralysis, who less than the normal amount of innervation will be required when he is looking up and to the right. Since the innervation flowing to the right normal eye is determined by the left inferior oblique muscle, the right superior rectus will seem peritic. This is termed as inhibitional palsy of the contralateral antagonist.
In right paralytic hyperdeviation, if the hyperdeviation is greatest on left gaze, then the paralyzed muscle is either the right superior oblique muscle or the left superior rectus muscle. If the hyperdeviation is greatest when the head is tilted to the right shoulder, then the paralyzed muscle is the right superior oblique muscle. If the deviation is greatest when the head is tilted to the left shoulder, then the paralyzed muscle is the left superior rectus muscle. In right paralytic hyperdeviation, if the hyperdeviation is greatest on right gaze, then the paralyzed muscle is either the right inferior rectus muscle or the left inferior oblique muscle. If the hyper deviation is greatest when the head is tilted to the right shoulder, then the paralyzed muscle is the left inferior oblique muscle. If the hyperdeviation is greatest when the head is tilted to the left shoulder, then the paralyzed muscle is the right inferior rectus muscle.
In left paralytic hyperdeviation, if the hyperdeviation is greatest on right gaze, then the paralyzed muscle is either the left superior oblique muscle or the right superior rectus muscle. If the hyper deviation is greatest when the head is tilted to the left shoulder, then the paralyzed muscle is the left superior oblique muscle. If the hyper deviation is greatest when the head is tilted to the right shoulder, then the paralyzed muscle is the right superior rectus muscle. If the hyper deviation is greatest on left gaze, then the paralyzed muscle is either the left inferior rectus muscle or the right inferior oblique muscle. If the hyper deviation is greatest when the head is tilted to the left shoulder, then the paralyzed muscle is the right inferior oblique muscle. If the hyper deviation is greatest when the head is tilted to the right shoulder, then the paralyzed muscle is the left inferior rectus muscle.
If the patient is asked to point to an object in the field of action of the paralyzed muscle while the sound eye is covered, his finger will point beyond the object toward the field of action of the paralyzed muscle, as in right lateral rectus muscle paralysis. This test is termed as past pointing. The forced duction test is a simple method to differentiate between muscle paralysis and the presence of mechanical restriction of ocular motility. If no resistance is encountered, the motility defect is clearly caused by paralysis. If resistance is encountered, mechanical restrictions do exist. To distinguish lateral rectus or medial rectus muscle paralysis from mechanical restriction, we apply the forceps at the 6 and 12 o'clock positions and move the eye into abduction and adduction. To distinguish superior rectus or inferior rectus muscle paralysis from mechanical restriction, we apply the forceps at the three and nine o'clock positions and move the eye into elevation and depression. The generated muscle force by a contracting muscle can be estimated by stabilizing the eye with forceps while the patient tries to move the eye against this obstacle. This test is used to distinguish muscle paralysis from mechanical restriction. The presence of a tug on the forceps indicates normal contraction of the muscle; then mechanical restriction is present. The absence of a tug on the forceps indicates muscle paralysis.
Estimation of saccadic velocity of the eye may be useful in distinguishing between a mechanical and a periodic limitation of ocular motility. If paralysis exists, the velocity of eye movement into the field of action of the paralyzed muscle will be markedly decreased. If the motility defect is caused by a mechanical obstacle, the saccadic velocity of an eye movement into the field of apparent basis will be normal. In isolated paralysis of the superior rectus muscle, the paralyzed eye is hypotropic in primary position; there is limitation of elevation in abduction; elevation is normal in adduction; there is overaction of the ipsilateral inferior rectus and the contralateral inferior oblique muscles; there is a small excyclotropia and absent Bell's phenomenon. Superior rectus muscle paralysis is frequently associated with weakness of the hemolateral levator palpebrae muscle. Since the upper lid elevates with elevation of the globe and drops when the eye moves downward, a true ptosis caused by levator weakness must be differentiated from pseudoptosis secondary to the hypotropic position of the globe. The differential diagnosis of a superior rectus muscle paralysis includes mechanical causes that limit elevation of the eye, such as contracture, fibrosis, high myopia, or heavy eye, myositis, endocrine orbitopathy, or a blowout fracture of the orbital floor. Whenever elevation is not restricted, the forced duction test will be negative; then paralysis of the superior rectus muscle is present. Whenever elevation is restricted mechanically, the forced duction test will be positive, and the restriction often involves the entire upper field of gaze.
An isolated paralysis of the medial rectus muscle is very rare. With this type of paralysis, the greatest defect of ocular motility occurs when the affected eye moves into adduction, since the action of the antagonistic lateral rectus muscle is unopposed. Exotropia usually is present in primary position. The differential diagnosis of an isolated medial rectus paralysis includes internuclear ophthalmoplegia, synergistic divergence, and Duane's syndrome. In isolated paralysis of the inferior rectus muscle, the affected eye is hypertrophic in primary position with limited depression in abduction and normal depression in adduction. When the patient fixates with the peritic eye, there is hypotropia, and pseudoptosis may occur in the sound eye, creating diagnostic difficulties. An isolated inferior oblique muscle paralysis is the least likely muscle to become paralyzed. In primary position, the affected eye is hypotropic; the greatest deviation occurs when the patient attempts to elevate the abducted periodic eye; limited elevation in adduction and overaction of the unopposed ipsolateral superior oblique muscle. The differential diagnosis of inferior oblique muscle paralysis is Brown syndrome, since the defect of ocular motility in is clinically similar; both show limitation of elevation of the adducted eye. The forced duction test is necessary in differentiating between Brown syndrome from paralysis of the inferior oblique muscle; the forced duction test is positive in Brown syndrome and negative in inferior oblique muscle paralysis.
Vertical muscle paralysis following cataract surgery consists of limitation of elevation or depression with diplopia. This complication is caused by the myotoxic effect of the anesthetic agent or by accidental injection of the muscle belly or the nerve supplying the muscle. When the oculomotor nerve is completely paralyzed, the paralyzed eye will be in a position of abduction, slight depression, and intorsion. Concurrent paralysis of the levator palpebrae will cause ptosis of the upper lid. The motility of the affected eye will be limited to abduction to small degrees of depression in abduction. The intrinsic muscles of the eye also are involved, causing the pupil to be dilated and non-reactive. Aberrant regeneration of the oculomotor nerve fibers may result in failure of the upper lid to follow the eye as it moves downward, causing retraction of the upper lid in downward gaze. This is known as pseudo-Graefe sign.
In trochlear nerve paralysis, the affected eye is hypertrophic; the hypotropia is greatest in the nasal field of the involved eye; the Bielschowsky head tilt test is diagnostic, with increase of the hypotropia on tilting the head to the same side of the involved eye. In bilateral paralysis of the trochlear nerve, there is right hypotropia in left gaze and a left hypotropia in right gaze; positive Bielschowsky head tilt test with the head tilted to either side; bilateral excyclotropia and V pattern. The diagnosis of sixth cranial nerve paralysis should not present any difficulties; esotropia will be present with the fixating eye in primary position; the greatest esotropia occurs on attempts to abduct the peritic eye; most patients will complain about double vision in lateral gaze and assume a compensatory face turn in the direction of the paralyzed muscle. The differential diagnosis includes the Duane retraction syndrome and with congenital esotropia, abducens paralysis simulated by crossed fixation, and the nystagmus blocking syndrome. In bilateral paralysis of the sixth cranial nerve, both eyes may be in a position of adduction with bilateral limited abduction. A benign and often recurrent form of sixth cranial nerve palsy occurs in children, usually following upper respiratory infections or other forms of mild viral illness, immunizations, or impetigo. Möbius syndrome is congenital bilateral abducens paralysis associated with facial diplegia and microglossia; various degrees of esotropia may be present in primary position, and the abducens paralysis may be incomplete or asymmetrical.
Skewed deviation is a transient vertical divergence of the eyes whereby one eye is elevated and the other depressed. It may occur in association with brainstem, cerebellar, or vestibular disease. Upshoot of the abducted eye and downshoot of the abducted eye in skew deviation may easily be confused with overaction of the oblique muscles. Double elevator paralysis is paralysis of both elevator muscles—the superior rectus and the inferior oblique muscles. When the patient fixates with the nonparetic eye, the paretic eye will take a hypotropic position, and the upper lid may be slightly ptotic. Elevation of the paretic eye from any position of gaze is severely restricted; hence the term double elevator palsy. The ductions of the paretic eye are normal in all other positions of gaze. Fixation with the paretic eye will cause a hypotropia of the nonparetic eye, and the pseudoptosis will disappear. The differential diagnosis of double elevator paralysis is restricted elevation of the eye, which occurs in blowout fracture of the orbital floor, congenital or acquired fibrosis of the extraocular muscles, and endocrine myopathy. Negative forced duction test will confirm the diagnosis of double elevator paralysis.
Double depressor paralysis is paralysis of both depressor muscles of one eye—the inferior rectus and the superior oblique. When the nonparetic eye is fixating, the paretic eye is hypertrophic in primary position. Ductions are restricted in the entire lower field of gaze and normal in all other gaze positions. Lesions of the supranuclear ocular motor pathways or centers cause bilateral conjugate paralysis of associated muscle groups. Gaze palsies may occur in dextroversion, levoversion, elevation, or depression, depending on the site of the lesion. Internuclear ophthalmoplegia is caused by lesions in the medial longitudinal fasciculus; adduction is limited, and an asymmetrical nystagmus is present involving the abducting eye.