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Paralysis of Conjugate Gaze
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Horizontal Gaze Palsy Cerebral Origin An acute lesion of one frontal lobe, such as an infarct, usually causes impersistence or paresis of contralateral gaze, and the eyes may for a limited time turn involuntarily toward the side of the cerebral lesion In most cases of frontal lobe infarction, the gaze palsy is incomplete and temporary, lasting for a day or two or for as long as a week Almost invariably, it is accompanied by hemiparesis In this circumstance, forced closure of the eyelids may cause the eyes to move paradoxically to the side of the hemiparesis rather than their deviating upward (Bell phenomenon), as would be expected During sleep, the eyes may deviate conjugately from the side of the lesion to the side of the hemiplegia Also as indicated above, pursuit movements away from the side of the lesion tend to be fragmented or lost (Posterior parietal lesions reduce pursuit movements but do not cause a gaze palsy) With bilateral frontal lesions, the patient may be unable to turn his eyes voluntarily in any direction but retains xation and following movements, probably because pursuit movements are initiated in the parieto-occipital cortex Occasionally, a deep cerebral lesion, particularly a thalamic hemorrhage extending into the midbrain, will cause the eyes to deviate conjugately to the side opposite the lesion ( wrong-way gaze); the basis for this anamolous phenomenon is not established, but interference with descending oculomotor tracts in the midbrain has been postulated by Tijssen It should be emphasized that cerebral gaze paralysis is not attended by strabismus or diplopia, ie, the eyes move conjuugately The usual causes are vascular occlusion with infarction, hemorrhage, and abscess or tumor of the frontal lobe Brainstem Origin With regard to conjugate and horizontal gaze palsy, a unilateral lesion in the rostral midbrain tegmentum, by interrupting the cerebral pathways for horizontal conjugate gaze
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before their decussation, will cause a gaze palsy to the opposite side More common is a lesion in the pontine horizontal gaze complex (PPRF) also involving the abducens nucleus, which causes ipsilateral gaze palsy and deviation of the eyes to the opposite side As a rule, the horizontal gaze palsies of cerebral and pontine origin are readily distinguished Both may be accompanied by hemiparesis, particularly cerebral lesions, in which case gaze toward the side as the hemiparesis is impaired When there is a tonic deviation of the eyes from a cerebral lesion, this relationship is expressed as the eyes look toward the brain lesion and away from the hemiparesis The opposite pertains to brainstem gaze palsies, that is, gaze is impaired toward the side opposite the lesion, and if there is gaze deviation, the eyes are turned toward a hemiparesis Palsies of pontine origin need not have an accompanying hemiparesis but are associated with other signs of pontine disease, particularly peripheral facial and external rectus palsies and internuclear ophthalmoplegia on the same side as the paralysis of gaze Gaze palsies due to cerebral lesions tend not to be as long-lasting as those due to pontine lesions If there is a tonic gaze deviation away from the lesion, it too tends to be transient in the case of a cerebral paralysis of gaze and longer-lasting with a brainstem lesion Also, in the case of a cerebral lesion (but not a pontine lesion), the eyes can be turned to the paralyzed side if they are xated on the target and the head is rotated passively to the opposite side (ie, by utilizing the VOR) Vertical Gaze Palsy Midbrain lesions affecting the pretectum and the region of the posterior commissure interfere with conjugate movements in the vertical plane Paralysis of vertical gaze is a prominent feature of the Parinaud or dorsal midbrain syndrome Upward gaze in general is affected far more frequently than downward gaze because, as already explained, some of the bers subserving upgaze cross rostrally and posteriorly between the riMLF and INC and are subject to interruption before descending to the oculomotor nuclei, whereas the pathways for downgaze apparently project directly downward from the two controlling nuclei Optokinetic nystagmus in the vertical plane is usually lost in association with any interruption of vertical gaze The range of upward gaze is frequently restricted by a number of extraneous factors, such as drowsiness, increased intracranial pressure, and particularly aging In a patient who cannot elevate the eyes voluntarily, the presence of re ex upward deviation of the eyes in response to exion of the head ( doll s-head maneuver ) or to voluntary forceful closure of the eyelids (Bell s phenomenon) usually indicates that the nuclear and infranuclear mechanisms for upward gaze are intact and that the defect is supranuclear However useful this rule may be, in some instances of disease of the peripheral neuromuscular apparatus such as Guillain-Barre syndrome and myasthenia gravis in which voluntary upgaze may be limited, the strong stimulus of eye closure causes upward deviation, whereas voluntary attempts at upgaze are unsuccessful, thereby spuriously suggesting a lesion of the upper brainstem However, about 15 percent of normal adults do not show a Bell s phenomenon; in others, deviation of the eyes is paradoxically downward In several patients who during life had shown an isolated palsy of downward gaze, autopsy has disclosed bilateral lesions of the rostral midbrain tegmentum ( just medial and dorsal to the red nuclei) In monkeys, a defect in downward gaze has been produced by bilateral circumscribed lesions centered in these regions (Kompf et al) An unusual case, described by Bogousslavsky and colleagues, suggests that a paralysis of vertical gaze may follow a
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strictly unilateral infarction in the posterior commissure, riMLF, and INC Hommel and Bogousslavsky have summarized the location of strokes that cause monocular and binocular vertical gaze palsies Several degenerative and related processes exhibit selective or prominent upgaze or vertical gaze palsies, as mentioned earlier (Table 14-1) In progressive supranuclear palsy, a highly characteristic feature is a selective paralysis of upward and then downward gaze, initially evident as dif culty with vertical saccades (page 926) Parkinson and Lewy body diseases (Chap 39), corticobasal ganglionic degeneration (Chap 39), and Whipple disease of the brain (Chap 40) may also produce vertical gaze palsies as these diseases progress Other Gaze Palsies Skew deviation is a poorly understood disorder in which there is vertical deviation of one eye above the other The deviation may be the same (comitant) in all elds of gaze, or it may vary with different directions of gaze The patient complains of vertical diplopia in all gaze positions (ie, it is comitant) A noncomitant vertical deviation of the eyes, most pronounced when the affected eye is turned down, is characteristic of fourth nerve palsy, described further on Skew deviation does not have precise localizing value but is associated with a variety of lesions of the cerebellum and the brainstem, particularly those involving the MLF With skew deviation due to cerebellar disease, the eye on the side of the lesion usually rests lower, but sometimes it is higher than the other eye (in a ratio of 2:1 in Keane s series), particularly in an internuclear ophthalmoplegia (The corresponding image, of course, rests higher in the rst instance and lower with INO) Skew deviation has been known to alternate from one side to the other ( alternating skew ) and has also been seen with the condition known as periodic alternating nystagmus Ford and coworkers described a rare form of skew deviation due to a monocular palsy of elevation stemming from a lesion immediately rostral to the ipsilateral oculomotor nucleus; a lesion of upgaze efferents from the ipsilateral riMLF was postulated, but an abnormality of the vertical gaze holding mechanism related to the function of the INC is an alternative explanation The ocular tilt reaction, in which skew deviation is combined with ocular torsion and head tilt, is attributed to an imbalance in otolith-ocular and otolith-collic re exes In unilateral lesions involving the vestibular nuclei, as in lateral medullary infarction, the eye is lower on the side of the lesion With lesions of the MLF or INC, which can also cause an ocular tilt reaction, the eye is higher on the side of the lesion Another unusual and now almost vanished disturbance of gaze is the oculogyric crisis, or spasm, which consists of a tonic spasm of conjugate deviation of the eyes, usually upward and less frequently laterally or downward Recurrent attacks, sometimes associated with spasms of the neck, mouth, and tongue muscles and lasting from a few seconds to an hour or two, were pathognomonic of postencephalitic parkinsonism Now this phenomenon is observed rarely as an acute reaction in patients being given phenothiazine drugs (page 1025) and in Niemann-Pick disease The pathogenesis of these ocular spasms is not known In the druginduced form, upward deviation of the eyes is associated with peculiar obsessional thoughts; it can be terminated by the administration of an atropinic medication Congenital oculomotor apraxia (Cogan syndrome) is a disorder characterized by abnormal eye and head movements during attempts to change the position of the eyes The patient is unable
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