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Vertical Ocular Dysmetria
VERTICAL OCULAR DYSMETRIA ROBERT L.
LESSER,
M.D.
New Haven, Connecticut AND J. L A W T O N S M I T H , M.D.,
D A V I D S. L E V E N S O N , M.D.,
A N D J O H N O. S U S A C ,
M.D.
Miami, Florida
The eye signs characteristically seen in cerebellar system disease are: (1) nystag mus, (2) skew deviation, (3) ocular dysmetria, and (4) ocular flutter.1 Ocular dysmetria consists of an overshooting of the eyes on rapid refixation movements.2 Customarily, horizontal eye movements are assessed in test ing for ocular dysmetria, and the fact that ocular dysmetria also occurs in the vertical plane is not well recognized. In this report, vertical ocular dysmetria is described. It was the only abnormal eye finding in a patient with cerebellar disease. To our knowledge, this is the first report of ocular dysmetria re stricted to the vertical plane as a neuro-ophthalmic sign. CASE REPORTS
Case 1—This 65-year-old white man was in good health until 1961 when he developed a slowly pro gressive ataxia. By 1964 his speech was slurred and he was unable to stand without support. On neuro logic examination he was oriented, but mildly de mented, and he had a short attention span. He was dysarthric and exhibited marked ataxia of all ex tremities. Eye examination revealed his visual acuity was 20/30 in the right eye and 20/25 in the left. Visual fields, pupillary light reflexes, and ophthalmoscopic findings were all normal. Motility examination showed that the extraocular movements were full and without nystagmus. When his eye movements were checked for dysmetria in the horizontal plane, no overshoot was observed. However, when he refixated rapidly from upgaze to the primary position, striking dysmetric overshoots of up to 30 degrees were noted. From the Department of Ophthalmology, Uni versity of Miami School of Medicine, Miami, Flor ida (Drs. Smith, Levenson, and Susac), and the Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, Connecticut (Dr. Lesser). Reprint requests to J. Lawton Smith, M.D., De partment of Ophthalmology, Bascom Palmer Eye Institute, 1638 N.W. 10th Avenue, Miami, Florida 33136.
Chest and skull x-ray findings were normal and a brain scan was negative. Pneumoencephalography showed dilated lateral ventricles as well as a dilated fourth ventricle without evidence of obstruction. A diagnosis of cerebral and cerebellar atrophy was made, and the patient was discharged to a nursing home. In summary, in the absence of horizontal dys metria and nystagmus, striking vertical ocular dys metria was the only neuro-ophthalmic sign in this 65-year-old man with florid cerebellar system dis ease and cerebral atrophy, probably degenerative. Case 2—A 25-year-old white man was admitted to Jackson Memorial Hospital in 1971 because of episodic irrational behavior and personality change. At another hospital in 1965, he had had a subtotal resection of an astrocytoma involving the floor of the fourth ventricle and thereafter he was confined to a wheelchair because of ataxia. On neurologic examination, the patient was alert and oriented and his mental status was normal. He had a left peripheral facial palsy, scanning speech, and was ataxic in all four extremities. Eye exami nation revealed his visual acuity was 20/30 in the right eye, but in the left he had only light percep tion because of a dense cataract. The pupils were equal in size and reacted briskly to light. The right disk was normal. The left fundus could not be visu alized. The ocular motility was of great interest. He had bilateral sixth-nerve palsies as well as a partial left third-nerve paresis. The vertical ver sions were full and there was no nystagmus. How ever, when the patient moved his eyes from upward gaze to the primary position, vertical ocular dys metria was noted. A brain scan showed no abnormality, and right brachial and vertebral angiography showed no evi dence of recurrent tumor. The patient declined pneumoencephalography and was discharged to a nursing home. In summary, this 25-year-old man with a fourth ventricle astrocytoma, scanning speech, ataxia, in volvement of the third, sixth, and seventh cranial nerves, showed striking vertical ocular dysmetria on looking from upgaze to the primary position. Case 3—This 37-year-old black man was in good health until 1962 when he suddenly developed diplopia, oscillopsia, malaise, and severe headaches. Ex amination at another hospital revealed blepharoptosis, a bilateral internuclear ophthalmoplegia, slurred speech, left-sided tremor, and incoordination. Lum bar puncture revealed a xanthochromic fluid with a nonreactive VDRL test. The results of a right ca-
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VERTICAL OCULAR DYSMETRIA
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rotid arteriogram were normal. Subsequently, this position (Fig. 1). When he looked from downgaze patient improved slightly. to the primary position, vertical ocular dysmetria In 1965, he was admitted to the VA Hospital. was also seen, but to a lesser degree. Very little On admission, he was alert and oriented, except for horizontal ocular dysmetria was noted, probably be occasional auditory hallucinations. Neurologic ex cause of the disturbed horizontal gaze. The optoki amination revealed oculopalatal myoclonus, dysarth- netic responses were dampened in all directions. ria, and a gross tremor of the left arm and leg. Pneumoencephalography showed no evidence of There was marked bilateral dysmetria on finger-to- tumor. The presumed diagnosis was basilar artery nose and heel-to-shin testing. thrombosis, and the patient was discharged to a Eye examination revealed his visual acuity was nursing home. 20/50 in the right eye and 20/20 in the left. There In summary, this 43-year-old white man with was slight blepharoptosis on the right. His right pu presumed basilar artery thrombosis showed striking pil measured 3 mm and the left measured 5 mm in vertical ocular dysmetria in association with oculo diameter. They reacted sluggishly to light but palatal myoclonus, spastic quadriparesis, bilateral crisply to accommodation. There was a constant, cerebellar ataxia, bilateral horizontal gaze paresis, pendular, rhythmic, to-and-fro movement of both and internuclear ophthalmoplegia, and a right Horeyes at a rate of about 160/minute. Bilateral inter- ner's syndrome. nuclear ophthalmoplegia was more marked on the right. Convergence was intact. No response to cold DISCUSSION caloric stimulation or to optokinetic stimulation could be elicited. A striking finding was vertical Ocular dysmetria was first noted by Orzeocular dysmetria, present more on moving from up3 gaze to the primary position than from downgaze to chowski in 1927 in two patients. The clini the primary position. Often, there were three gross cal diagnoses were multiple sclerosis and dysmetric vertical movements before his eyes set syphilitic endarteritis of branches of the basi tled down to their base-line myoclonic oscillations. lar artery in these patients. In 1954, Cogan8 The fundi were normal. The results of lumbar puncture, skull x-ray ex reported six patients with ocular dysmetria. amination, and electroencephalography were nor Three had cerebellar tumors, one had a tu mal, but the serum FTA-ABS test was reactive. mor of the fourth ventricle, one cerebellar In summary, this 37-year-old black man had an atrophy, and one had neurosyphilis. Cogan apoplectic onset of a bilateral internuclear ophthal moplegia, oculopalatal myoclonus, and striking ver concluded that dysmetria is a valuable sign tical ocular dysmetria. This was thought to be due of cerebellar system disease. Goldstein and to neurosyphilis. 4 Case 4—This 43-year-old Cuban man with hy Cogan pointed out that in unilateral cerebel pertension suddenly developed spasms of the right lar lesions the dysmetria is usually greater arm and leg, dysarthria, and dysphagia eight on looking toward the side of the lesion. months prior to admission. He was hospitalized 5 elsewhere where an air study reportedly showed a Smith and David noted ocular dysmetria as brain-stem tumor. a subtle indicator of internuclear ophthalmo On neurologic examination, he was alert and ori plegia. ented, but his speech was dysarthric and he had Ocular dysmetria consists of an overshoot myoclonus of the palate, mentalis muscles, and left sternocleidomastoid muscle. The gag reflex was of the eyes following rapid refixation from markedly depressed. In addition to a mild spastic quadriparesis, the patient showed a coarse tremor one position to another. This overshoot is followed by oscillations of decreasing ampli of the upper extremities when the arms were out stretched. This tremor increased with intention and tude around the fixation point until the eye was more marked on the right. comes to rest. Testing for ocular dysmetria Ophthalmic examination revealed 20/20 acuity in each eye, normal confrontation fields and fundi. is usually performed by asking the patient to Blepharoptosis and miosis were present on the look at the examiner's finger, which is right, and both pupils reacted well to light. The moved sufficiently far to the right or to the ocular motility findings were of special interest. He had spontaneous, small-amplitude nystagmoid eye left as to move the eyes moderately far into movements ; his eyes moved synchronously with the lateral gaze, and then requesting the patient palate. On testing the versions, there was a mild bilateral horizontal gaze paresis superimposed on a to look again at the examiner's nose. It is im bilateral internuclear ophthalmoplegia. Vertical portant that the eyes are not moved into ex gaze, however, was intact and mild vertical nystag treme lateral gaze, but that the eyes be di mus occurred on both up- and downgaze. Marked vertical ocular dysmetria could be elicited by having rected to perhaps two thirds of a full lateral the patient look from upgaze back to the primary version. This will allow visualization of any
210
tmkmmmj V
AMERICAN JOURNAL OF OPHTHALMOLOGY
,| jn> if
-
— T - --
AUGUST, 1973
— i jr"^*,V-*4
Q> » I Μ ^ — Μ » » * *W > ^ » » V I W I « I »
/ ^ ^ * y ^ # »
Fig. 1 (Lesser and associates). In the upper half of the tracing (A) is an electronystagmographic re cording of a normal person's eye movements. Recording of the right eye is shown above and that of the left eye, below. This person made a rapid refixation from primary position to upgaze (upgoing arrow) and back to the primary position (downgoing arrow). In the lower half of the tracing (B), a patient with vertical ocular dysmetria (Case 4) was asked to refixate from upgaze to the primary position (downgoing arrow) and the recording shows the typical overshoot oscillations. Again, the recording of the right eye is above and that of the left eye, below. In this case, however, the deflections show phase reversal because of a difference in electrode placement.
overshoot movements. When nystagmus is also present, as is frequently the case in these patients, it becomes difficult to differ entiate the eye movements noted on moder ate extremes of gaze. In these cases, the clin ical differentiation of ocular dysmetria from nystagmus is made as the patient refixates in the primary position, typically on the exam iner's nose. Usually, in central lesions, there is little if any nystagmus in the primary po sition, and here one can easily see the moder
ately large amplitude, overshoot oscillations of ocular dysmetria. It is also helpful for the examiner not to place his finger always in the same position when eliciting eccentric gaze so that the patient will not anticipate the position to which his eyes will be directed. This is because rapid reflex eye movements are much more likely to demonstrate dysmet ria than voluntary refixational movements. In vertical ocular dysmetria the same find ings are present but in the vertical plane.
VERTICAL OCULAR DYSMETRIA
VOL. 76, NO. 2
One should test for vertical ocular dysmetria both from moderately full upgaze to the pri mary position, and again from moderately full downgaze to the primary position. Con comitant vertical nystagmus is usually no problem when one evaluates the eye move ments on returning to the primary position. Electronystagmography may be helpful in visualizing the pattern. A normal refixation movement is shown in the upper portion of the figure and typical vertical ocular dys metria is shown in the lower portion. All of the patients included in this report had definite evidence of cerebellar dysfunc tion. In one, it was due to cerebellar degen eration, one to a fourth ventricle astrocytoma, one to neurosyphilis, and one to basilar artery disease. In one of these patients, ver tical ocular dysmetria was the only eye movement abnormality. This is, therefore, an important clinical test in suspected cere bellar disease. Testing for vertical and hori zontal ocular dysmetria should be routinely employed in the neuro-ophthalmic examina tion. SUMMARY
The four eye signs characteristic of cere
211
bellar system disease are nystagmus, skew deviation, ocular dysmetria, and ocular flut ter. Ocular dysmetria consists of an over shooting of the eyes on rapid refixation movements. The occurrence of ocular dys metria in the vertical plane has not been well recognized. This report documents four cases of vertical ocular dysmetria. Electronystagmographic demonstration of this motility pattern is provided in one case. On oc casion, vertical ocular dysmetria may be the only abnormal eye finding in cerebellar dis ease. To our knowledge, this is the first re port restricted to vertical ocular dysmetria as a neuro-ophthalmic sign. REFERENCES
1. Cogan, D. G. : Neurology of the Ocular Mus cles. Springfield, Charles C Thomas, 19S6, p. 154. 2. : Ocular dysmetria, flutter-like oscilla tions of the eyes, and opsoclonus. Arch. Ophth. 51 : 318, 1954. 3. Orzechowski, K: De l'ataxie dysmetrique des yeux. Remarques sur l'ataxie des yeux dite myoclonique (Opsoclonie, opsochorie). J. Psychol. Neurol. 35:1, 1927. 4. Goldstein, J. E., and Cogan, D. G. : Lateralizing value of ocular motor dysmetria and skew devi ation. Arch. Ophth. 66:517, 1961. 5. Smith, J. L., and David, N. J. : Internuclear ophthalmoplegia ; Two new clinical signs. Neurol. 14:307,1964.
LESSER,
M.D.
New Haven, Connecticut AND J. L A W T O N S M I T H , M.D.,
D A V I D S. L E V E N S O N , M.D.,
A N D J O H N O. S U S A C ,
M.D.
Miami, Florida
The eye signs characteristically seen in cerebellar system disease are: (1) nystag mus, (2) skew deviation, (3) ocular dysmetria, and (4) ocular flutter.1 Ocular dysmetria consists of an overshooting of the eyes on rapid refixation movements.2 Customarily, horizontal eye movements are assessed in test ing for ocular dysmetria, and the fact that ocular dysmetria also occurs in the vertical plane is not well recognized. In this report, vertical ocular dysmetria is described. It was the only abnormal eye finding in a patient with cerebellar disease. To our knowledge, this is the first report of ocular dysmetria re stricted to the vertical plane as a neuro-ophthalmic sign. CASE REPORTS
Case 1—This 65-year-old white man was in good health until 1961 when he developed a slowly pro gressive ataxia. By 1964 his speech was slurred and he was unable to stand without support. On neuro logic examination he was oriented, but mildly de mented, and he had a short attention span. He was dysarthric and exhibited marked ataxia of all ex tremities. Eye examination revealed his visual acuity was 20/30 in the right eye and 20/25 in the left. Visual fields, pupillary light reflexes, and ophthalmoscopic findings were all normal. Motility examination showed that the extraocular movements were full and without nystagmus. When his eye movements were checked for dysmetria in the horizontal plane, no overshoot was observed. However, when he refixated rapidly from upgaze to the primary position, striking dysmetric overshoots of up to 30 degrees were noted. From the Department of Ophthalmology, Uni versity of Miami School of Medicine, Miami, Flor ida (Drs. Smith, Levenson, and Susac), and the Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, Connecticut (Dr. Lesser). Reprint requests to J. Lawton Smith, M.D., De partment of Ophthalmology, Bascom Palmer Eye Institute, 1638 N.W. 10th Avenue, Miami, Florida 33136.
Chest and skull x-ray findings were normal and a brain scan was negative. Pneumoencephalography showed dilated lateral ventricles as well as a dilated fourth ventricle without evidence of obstruction. A diagnosis of cerebral and cerebellar atrophy was made, and the patient was discharged to a nursing home. In summary, in the absence of horizontal dys metria and nystagmus, striking vertical ocular dys metria was the only neuro-ophthalmic sign in this 65-year-old man with florid cerebellar system dis ease and cerebral atrophy, probably degenerative. Case 2—A 25-year-old white man was admitted to Jackson Memorial Hospital in 1971 because of episodic irrational behavior and personality change. At another hospital in 1965, he had had a subtotal resection of an astrocytoma involving the floor of the fourth ventricle and thereafter he was confined to a wheelchair because of ataxia. On neurologic examination, the patient was alert and oriented and his mental status was normal. He had a left peripheral facial palsy, scanning speech, and was ataxic in all four extremities. Eye exami nation revealed his visual acuity was 20/30 in the right eye, but in the left he had only light percep tion because of a dense cataract. The pupils were equal in size and reacted briskly to light. The right disk was normal. The left fundus could not be visu alized. The ocular motility was of great interest. He had bilateral sixth-nerve palsies as well as a partial left third-nerve paresis. The vertical ver sions were full and there was no nystagmus. How ever, when the patient moved his eyes from upward gaze to the primary position, vertical ocular dys metria was noted. A brain scan showed no abnormality, and right brachial and vertebral angiography showed no evi dence of recurrent tumor. The patient declined pneumoencephalography and was discharged to a nursing home. In summary, this 25-year-old man with a fourth ventricle astrocytoma, scanning speech, ataxia, in volvement of the third, sixth, and seventh cranial nerves, showed striking vertical ocular dysmetria on looking from upgaze to the primary position. Case 3—This 37-year-old black man was in good health until 1962 when he suddenly developed diplopia, oscillopsia, malaise, and severe headaches. Ex amination at another hospital revealed blepharoptosis, a bilateral internuclear ophthalmoplegia, slurred speech, left-sided tremor, and incoordination. Lum bar puncture revealed a xanthochromic fluid with a nonreactive VDRL test. The results of a right ca-
208
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VERTICAL OCULAR DYSMETRIA
209
rotid arteriogram were normal. Subsequently, this position (Fig. 1). When he looked from downgaze patient improved slightly. to the primary position, vertical ocular dysmetria In 1965, he was admitted to the VA Hospital. was also seen, but to a lesser degree. Very little On admission, he was alert and oriented, except for horizontal ocular dysmetria was noted, probably be occasional auditory hallucinations. Neurologic ex cause of the disturbed horizontal gaze. The optoki amination revealed oculopalatal myoclonus, dysarth- netic responses were dampened in all directions. ria, and a gross tremor of the left arm and leg. Pneumoencephalography showed no evidence of There was marked bilateral dysmetria on finger-to- tumor. The presumed diagnosis was basilar artery nose and heel-to-shin testing. thrombosis, and the patient was discharged to a Eye examination revealed his visual acuity was nursing home. 20/50 in the right eye and 20/20 in the left. There In summary, this 43-year-old white man with was slight blepharoptosis on the right. His right pu presumed basilar artery thrombosis showed striking pil measured 3 mm and the left measured 5 mm in vertical ocular dysmetria in association with oculo diameter. They reacted sluggishly to light but palatal myoclonus, spastic quadriparesis, bilateral crisply to accommodation. There was a constant, cerebellar ataxia, bilateral horizontal gaze paresis, pendular, rhythmic, to-and-fro movement of both and internuclear ophthalmoplegia, and a right Horeyes at a rate of about 160/minute. Bilateral inter- ner's syndrome. nuclear ophthalmoplegia was more marked on the right. Convergence was intact. No response to cold DISCUSSION caloric stimulation or to optokinetic stimulation could be elicited. A striking finding was vertical Ocular dysmetria was first noted by Orzeocular dysmetria, present more on moving from up3 gaze to the primary position than from downgaze to chowski in 1927 in two patients. The clini the primary position. Often, there were three gross cal diagnoses were multiple sclerosis and dysmetric vertical movements before his eyes set syphilitic endarteritis of branches of the basi tled down to their base-line myoclonic oscillations. lar artery in these patients. In 1954, Cogan8 The fundi were normal. The results of lumbar puncture, skull x-ray ex reported six patients with ocular dysmetria. amination, and electroencephalography were nor Three had cerebellar tumors, one had a tu mal, but the serum FTA-ABS test was reactive. mor of the fourth ventricle, one cerebellar In summary, this 37-year-old black man had an atrophy, and one had neurosyphilis. Cogan apoplectic onset of a bilateral internuclear ophthal moplegia, oculopalatal myoclonus, and striking ver concluded that dysmetria is a valuable sign tical ocular dysmetria. This was thought to be due of cerebellar system disease. Goldstein and to neurosyphilis. 4 Case 4—This 43-year-old Cuban man with hy Cogan pointed out that in unilateral cerebel pertension suddenly developed spasms of the right lar lesions the dysmetria is usually greater arm and leg, dysarthria, and dysphagia eight on looking toward the side of the lesion. months prior to admission. He was hospitalized 5 elsewhere where an air study reportedly showed a Smith and David noted ocular dysmetria as brain-stem tumor. a subtle indicator of internuclear ophthalmo On neurologic examination, he was alert and ori plegia. ented, but his speech was dysarthric and he had Ocular dysmetria consists of an overshoot myoclonus of the palate, mentalis muscles, and left sternocleidomastoid muscle. The gag reflex was of the eyes following rapid refixation from markedly depressed. In addition to a mild spastic quadriparesis, the patient showed a coarse tremor one position to another. This overshoot is followed by oscillations of decreasing ampli of the upper extremities when the arms were out stretched. This tremor increased with intention and tude around the fixation point until the eye was more marked on the right. comes to rest. Testing for ocular dysmetria Ophthalmic examination revealed 20/20 acuity in each eye, normal confrontation fields and fundi. is usually performed by asking the patient to Blepharoptosis and miosis were present on the look at the examiner's finger, which is right, and both pupils reacted well to light. The moved sufficiently far to the right or to the ocular motility findings were of special interest. He had spontaneous, small-amplitude nystagmoid eye left as to move the eyes moderately far into movements ; his eyes moved synchronously with the lateral gaze, and then requesting the patient palate. On testing the versions, there was a mild bilateral horizontal gaze paresis superimposed on a to look again at the examiner's nose. It is im bilateral internuclear ophthalmoplegia. Vertical portant that the eyes are not moved into ex gaze, however, was intact and mild vertical nystag treme lateral gaze, but that the eyes be di mus occurred on both up- and downgaze. Marked vertical ocular dysmetria could be elicited by having rected to perhaps two thirds of a full lateral the patient look from upgaze back to the primary version. This will allow visualization of any
210
tmkmmmj V
AMERICAN JOURNAL OF OPHTHALMOLOGY
,| jn> if
-
— T - --
AUGUST, 1973
— i jr"^*,V-*4
Q> » I Μ ^ — Μ » » * *W > ^ » » V I W I « I »
/ ^ ^ * y ^ # »
Fig. 1 (Lesser and associates). In the upper half of the tracing (A) is an electronystagmographic re cording of a normal person's eye movements. Recording of the right eye is shown above and that of the left eye, below. This person made a rapid refixation from primary position to upgaze (upgoing arrow) and back to the primary position (downgoing arrow). In the lower half of the tracing (B), a patient with vertical ocular dysmetria (Case 4) was asked to refixate from upgaze to the primary position (downgoing arrow) and the recording shows the typical overshoot oscillations. Again, the recording of the right eye is above and that of the left eye, below. In this case, however, the deflections show phase reversal because of a difference in electrode placement.
overshoot movements. When nystagmus is also present, as is frequently the case in these patients, it becomes difficult to differ entiate the eye movements noted on moder ate extremes of gaze. In these cases, the clin ical differentiation of ocular dysmetria from nystagmus is made as the patient refixates in the primary position, typically on the exam iner's nose. Usually, in central lesions, there is little if any nystagmus in the primary po sition, and here one can easily see the moder
ately large amplitude, overshoot oscillations of ocular dysmetria. It is also helpful for the examiner not to place his finger always in the same position when eliciting eccentric gaze so that the patient will not anticipate the position to which his eyes will be directed. This is because rapid reflex eye movements are much more likely to demonstrate dysmet ria than voluntary refixational movements. In vertical ocular dysmetria the same find ings are present but in the vertical plane.
VERTICAL OCULAR DYSMETRIA
VOL. 76, NO. 2
One should test for vertical ocular dysmetria both from moderately full upgaze to the pri mary position, and again from moderately full downgaze to the primary position. Con comitant vertical nystagmus is usually no problem when one evaluates the eye move ments on returning to the primary position. Electronystagmography may be helpful in visualizing the pattern. A normal refixation movement is shown in the upper portion of the figure and typical vertical ocular dys metria is shown in the lower portion. All of the patients included in this report had definite evidence of cerebellar dysfunc tion. In one, it was due to cerebellar degen eration, one to a fourth ventricle astrocytoma, one to neurosyphilis, and one to basilar artery disease. In one of these patients, ver tical ocular dysmetria was the only eye movement abnormality. This is, therefore, an important clinical test in suspected cere bellar disease. Testing for vertical and hori zontal ocular dysmetria should be routinely employed in the neuro-ophthalmic examina tion. SUMMARY
The four eye signs characteristic of cere
211
bellar system disease are nystagmus, skew deviation, ocular dysmetria, and ocular flut ter. Ocular dysmetria consists of an over shooting of the eyes on rapid refixation movements. The occurrence of ocular dys metria in the vertical plane has not been well recognized. This report documents four cases of vertical ocular dysmetria. Electronystagmographic demonstration of this motility pattern is provided in one case. On oc casion, vertical ocular dysmetria may be the only abnormal eye finding in cerebellar dis ease. To our knowledge, this is the first re port restricted to vertical ocular dysmetria as a neuro-ophthalmic sign. REFERENCES
1. Cogan, D. G. : Neurology of the Ocular Mus cles. Springfield, Charles C Thomas, 19S6, p. 154. 2. : Ocular dysmetria, flutter-like oscilla tions of the eyes, and opsoclonus. Arch. Ophth. 51 : 318, 1954. 3. Orzechowski, K: De l'ataxie dysmetrique des yeux. Remarques sur l'ataxie des yeux dite myoclonique (Opsoclonie, opsochorie). J. Psychol. Neurol. 35:1, 1927. 4. Goldstein, J. E., and Cogan, D. G. : Lateralizing value of ocular motor dysmetria and skew devi ation. Arch. Ophth. 66:517, 1961. 5. Smith, J. L., and David, N. J. : Internuclear ophthalmoplegia ; Two new clinical signs. Neurol. 14:307,1964.