Optokinetic Nystagmus: A Test for Parietal Lobe Lesions*

Optokinetic Nystagmus: A Test for Parietal Lobe Lesions*

LOW-VISION CLINICS group from each clinic represented a random sample from the files of that clinic, the only bias being that these patients had come...

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LOW-VISION CLINICS

group from each clinic represented a random sample from the files of that clinic, the only bias being that these patients had come to the particular clinic for attempted fitting of a visual aid in the case of low visual acuity. All information derived from the data has been obtained separately for near and distant vision with and without refractive correc­ tion ; also indicated is the aid which was pre­ scribed and the level of visual acuity so ob­ tained. These data were broken down into each individual disease group. It appears that

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the most valuable aid to vision is the proper correction of the refractive error. This ac­ counted for the largest improvement in visual acuity. Further improvement in reading and close work was obtained with the use of spe­ cial low-vision aids. In the case of the seven clinics analyzed the aid varied from clinic to clinic but in general the level of visual acuity was comparable from one clinic to the other. American Foundation for the Blind, Inc., 15 West 16th Street, New York 11.

O P T O K I N E T I C NYSTAGMUS: A T E S T FOR PARIETAL LOBE LESIONS* A STUDY OF 31 ANATOMICALLY VERIFIED CASES J. L A W T O N S M I T H ,

M.D.

Baltimore, Maryland AND D A V I D G. COGAN,

M.D.

Boston, Massachusetts

Optokinetic nystagmus is an induced jerky to-and-f ro involuntary oscillation of the eyes. It is symmetric or nearly so in the normal individual. A defective response to one side assumes significance if an intact response is elicited on rotating targets to the other side. Such a finding has been termed a "positive O.N. sign" (optokinetic nystagmus sign). 1 The normal or symmetric response is a "neg­ ative O.N. sign." Bârâny 2 was the first to note that some pa­ tients with homonymous hemianopia had a defective optokinetic nystagmus response when targets were rotated away from the de­ fective field, and yet intact to the opposite direction. He at first attributed this simply to inability to see the targets in the former instance, that is, an afferent visual lesion. However, Brunner, 3 Ohm,4 and Fox and * From the Howe Laboratory of Ophthalmology, Harvard University Medical School, and the Mas­ sachusetts Eye and Ear Infirmary. This work was supported by special traineeship BT-3S7, National Institute of Neurological Diseases and Blindness, Bethesda 14, Maryland.

Holmes 5 found that, whereas this was true in certain cases with homonymous field defects, in others with equally dense and absolute homonymous hemianopias the optokinetic re­ sponse was symmetric to both sides. This immediately revealed that the positive opto­ kinetic nystagmus sign was not due solely to an afferent lesion. Cords6 explanation for the asymmetric re­ sponse was that there must be an efferent optomotor lesion to account for the phenom­ enon, and that the most likely site was in the internal and external sagittal strata of the middle and posterior one third of the optic radiations, or deep in the parietal lobe. Kestenbaum 1 analyzed a series of 59 cases of homonymous hemianopia in which the lesions had been localized by autopsy, sur­ gery, or by roentgenogram. The number of cases in each of these three subdivisions was not stipulated. He considered a negative op­ tokinetic nystagmus sign as 100 percent re­ liable in excluding a parietal lobe origin for a homonymous hemianopia. Although opin-

TABLE 1 O P T O K I N E T I C NYSTAGMUS IN T H E AUTOPSY PROVED CASES

Case

Age

Sex

Vision

Fields*

O.N. Signt

Symptoms and Course

Anatomic Findings

Comment

32

Normal

Normal

Negative at first; later positive.

Uncinate fits and memory defect, 10 Glioblastoma multiforme, left parietomo. RHH developed after resection left temporal. Neoplasm involved lenticular posterior temporal lobe astrocytoma 47 nucleus, thalamus, internal capsule on mo. later, recurrence. Macular splitting left. No lesion in right hemisphere. Left RHH, with positive O.N. sign uncus herniated; midbrain shifted to right. Brain stem normal

At the time the glioma presumably in­ volved only the temporal lobe, the op­ tokinetic response was symmetrical. Later with involvement of parietal (and other) lobes, a positive O.N. sign was present

70

Good

RHH

Positive

Dysphasta and seizures 5 months. Gerstman's syndrome. Deceased after left parieto-temporo-occipital craniotomy, which revealed a necrotic gHoma

Glioblastoma multiforme. On section, tumor involved left thalamus, basai ganglia, and roof of lat. ventricle. Neo­ plasm extended posterior to occipital lobe. No gross neoplasm in temporal lobe except in roof of temporal horn of lateral ventricle. Herniation of left cingulate gyrus beneath falx, bilateral cerebellar pressure cones, midbrain and pons compressed on left. Medulla and cere­ bellum unremarkable

Right homonymous hemianopia, right hemianesthesia, and positive O.N. sign were seen with involvement of thala­ mus and optic radiations deep in left parietal lobe

Somnolence, headaches, fatigability, 14 mo. Craniotomy disclosed meningioma in right sylvian fissure. Expired one day later

Surgical specimen, a meningioma, had been removed intact. Necropsy dis­ closed marked cerebral edema, with right temporal pressure cone. A fresh hemorrhage was noted in right parietooccipital region. Cerebellum and brain stem were normal

This case demonstrated a focal tem­ poral lobe lesion producing a Meyer's loop field defect yet with a negative O.N. sign. Death was from uncontroll­ able cerebral edema and a postopera­ tive hemorrhage

Visual disturbance, 9 mo. Right III nerve palsy 1 mo. prior to death

Adenocarcinoma of lung, with métas­ Metastatic disease to left occipital tases to occipital lobes, bilateral; right lobe produced a right homonymous III nerve, and cauda equina. Metas­ paracentral scotoma and a negative tasis adherent to left occipital lobe, and O.N. sign. There was no evidence of involving almost entire lobe. Tumor parietal lobe involvement in this case also in méninges medial to right occipi­ tal lobe, but not involving underlying brain. Cerebral atherosclerosis, with several tiny foci of softening in cortex, most prominent in right frontal lobe. Tumor also in cerebellum, on falx, ve­ nous sinuses, and tentorium. Metastasis to right superior orbital fissure noted, with III nerve spared intracranially

20/40 OU

59

M

59

M

R 20/70 L 20/30

Normal

Left upper homonymous quadrantanopia

Right homon. para-central scotomas-macular splitting

Normal, pseudo­ hemianopia to left

* RHH = Right homonymous hemianopia. LHH =Left homonymous hemianopia. t O.N. Sign =Optokinetic nystagmus sign.

Negative

Negative

Negative

Forgetfulness, 8 mo. Ignored left side of Astrocytoma, grade 3-4, right frontal environment, 1 wk. Headache. Cranio­ lobe, infiltrating; left frontal lobe, well tomy revealed subcortical right frontal circumscribed nodule. Right temporal lobe tumor just rostral to premotor pressure cone; herniation falx. Few strip. Expired next day areas of necrotic tumor remained in right frontoparietal region. Small hem­ orrhage in right basal ganglia. Brainstem and cerebellum had no lesions

> H O

This patient had a pseudohemianopia. The only other abnormality on eye exam was a positive O.N. sign. Clini­ cal evidence pointed to a right frontal lobe lesion. This case of a frontal lobe tumor with a positive O.N. sign was shown at autopsy to extend into right parietal lobe

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TABLE 1 (Continued) Case

Age

Sex M

Vision Normal

45

M

M

R 20,40 L 20/50



20/20 O.U.

Fields*

O.N. Signt

Symptoms and Course

Anatomic Findings

Comment This mixed glioma of left frontal lobe produced symptoms for 3 yr. There was no field defect, but a pseudohem ianopia to the right. At autopsy basal ganglia and anterior internal capsule were involved on left, but ex­ tension into parietal lobes was lacking. This was a frontal lobe tumor without parietal extension, in which the O.N. sign was negative

Normal

Negative

Seizures, dizziness, lethargy, rigidity Mixed glioma, left frontal lobe. En­ right upper extremity, 3 yr. Left frontal larged left hemisphere; herniation left lobectomy for glioma; patient expired cingulate gyms beneath fabx; right cere­ bellar pressure cone. Softening left oc­ on 3rd day cipital lobe, peduncle, midbrain. Large operative defect, left frontal. In remain­ ing white matter of frontal cortex, left basal ganglia, and corpus callosum, brain tissue yellowish and soft

LHH incongruous

Positive·

Seizures, 10 yr. personality change 2 yr. Headaches and incontinence, 1 mo. Bi­ lateral papilledema. At right frontotemporal craniotomy, a glioma was seen astride sylvian fissure. Expired on 18th day

Astrocytoma. Bilateral cerebellar and On gross examination this might have temporal pressure cones. On section, been considered a frontal lobe tumor right superior and middle frontal con­ with a positive O.N. sign. However, on volutions were soft and necrotic. Fur­ section there was tumor in right ther posteriorly, right thalamus internal parietal lobe and microscopic exam re­ capsule, basal ganglia, and part of white vealed a diffusely infiltrative glioma matter of parietal and temporal lobes were smooth and firm to palpation. Small cavity in right thalamus. Brain stem and cerebellum were normal

Headaches, dizziness, hallucinations, 3 mo. Encephalography was consistent with deep large right temporal tumor. Subtotal removal of glioma at craniot­ omy. Expired on 3rd day

Glioblastoma multiforme, right tem­ poral lobe; ant. horns, both lateral ven­ tricles. Tumor presented on inferior surface right temporal lobe. Tumor not distinctly separated from brain tissue. It obliterated right inferior horn of lat. ventricle, and a part of R. globus pallidus. Subependyma of anterior horns involved

Although further anatomic study would have been helpful, as midportion of ant. horn of lateral ventricles courses through deep parietal lobe, parietal involvement probably oc­ curred in this temporal lobe glioma with positive O.N. sign

LHH, splitting fixation

Positive

o O

2 2 H

H

>

RHH, complete

Positive

Headaches and speech difficulty, 3 wk. Aphasia, R. central facial weakness, and diminished pinprick over entire R. body. Craniotomy revealed left temporoparietal glioma, extending deeply into thalamus. Expired 5 mo. later

Glioblastoma multiforme, extensive, involving almost entire left hemisphere, Cystic area 2.5 cm. in diameter filled with greenish coagulum in parietal cor­ tex. Tumor extended to frontal lobe, most extensive in temporal and parietal lobes, and extended posteriorly to with­ in 2 cm. of occip. lobe. Thalamus in­ volved on left. Brainstem normal

This extensive glioma involved almost entire left hemisphere, and was most extensive in the thalamus, temporal and parietal lobes. An asymmetric optokinetic response was present.

RHH, incongruous

Positive

Abrupt onset, global aphasia. Auricular Two external lesions: (1) neoplasm in fibrillation. 14 mo. later, right VII and right cerebellar hemisphere, involving VIII nerve weakness, nystagmus, posi­ V, VII, VIII. (2) Extensive infarct, left tive O.N. sign. Posterior fossa explora­ parietal, with atrophy of entire superior temporal gyms. Extended from ante­ tion. Death on 60th day rior sylvian fissure to occipital lobe. In temporal lobe extended to within 3 mm. of posterior horn, and radiations were involved. No other lesions seen in brain

Difficult interpretation in this case be­ cause of two lesions: (1 ) old left parie­ tal infarct, embolie. (2) more recent medulloblastoma of cerebellum. At any rate, a defective O.N. response was noted as well as a left parietal lobe infarct.

d

TABLE 1 Case

Age

11

60

Sex

Vision

O.N. Signt

Symptoms and Course

Vision and fields could not be done because of aphasia

Positive

Aphasia and R. hemiparesis, 2 mo. Papilledema. Death 3 wk. later

Glioblastoma multiforme, discrete, left Definite parietal lobe extension of this frontal and parietal lobes. Extended frontal lobe glioma, with a positive from 3.4 cm. behind frontal pole to plane O.N. sign of midthalamus. It lay above plane of sylvian fissure, and extended mesially to insula. Foremost part, sharply differ­ entiated from edematous centrum semiovale. Compression of right crus; small hemorrhage in basis pontis

Norma

Negative

Malignant melanoma on back, recurred after excision. Headaches, vomiting, dragging left foot, seizures 4 days. Died on 6th hospital day

Three large metastatic lesions in brain— largest in left parietal region. It was firm, brown, and surrounding white matter edematous; cortex did not ap­ pear to be involved. Similar métastases in right frontal and right posterior tem­ poral lobes. No other brain lesions

Although no defect was present in either visual fields or optokinetic nystagmus in this case, a definite left parietal metastasis was present. Death may have occurred too rapidly for clinical manifestation of these lesions

Numbness, right extremities; poor vi­ Advanced atherosclerosis of basilarsion to right, 3 mo. Diminished pin­ vertebral system; with complete basilar prick over right body and face. 2 yr. thrombosis. Both posterior cerebral later, basilar ischemia progressed. Cor­ arteries totally occluded. Softening both peduncles, midbrain, upper pons, & tical blindness, dysphagia, dysarthria both cerebellar hemispheres. Extensive softening left occipital lobe; similar, but more recent softening, right occipital lobe. Right ant. cerebral and a minor branch left middle cerebral both virtu­ ally occluded

This patient had progressive atheromatous disease of basilar system. Findings support early involvement of left posterior cerebral artery. The O.N. sign was positive early. Later ex­ tensive basilar thrombosis compro­ mised efferent optomotors in brain stem so that no conclusions could be drawn about cortical localization. The left parietal lobe was involved in this case

m

>

26

18

M M

Normal

RHH, complete, splitting fixation

M

M

Fields*

(Continued)

Cortical blindness; transient RHH, then clearing

Positive

Anatomic Findings

Comment

No O.K. Headaches, 3 wk. Hypertension. Sudresponse to den cortical blindness, cleared to RHH either side in 12 hr. Patient named direction of drum correctly but had no response to either side. 24 hr. later, full fields but still O.N. response totally absent. Con­ vulsions, aphasia, coma, and later death

Diffuse encephalopathy, probably vas­ cular, with small scattered lesions throughout brain. Slightly larger lesions in deep right parieto-occipital cortex, which were relatively recent infarcts. Arteries showed markedly proliferated endothelium. Similar changes in cerebel­ lum

This patient died of a diffuse vascular disease of unknown cause within 8 wk. Transient cortical blindness, with RHH, and clearing, occurred later. Despite cooperation and ability to tell side of rotation, no O.K. response at all. Lesions seen in R. parietal lobe; left parietal not studied histologically, but similar process there appeared likely

20/20 OU

IHH. macular splitting

Positive

Seizures, 2 wk. Left hemianesthesia. Craniotomy disclosed right parietal tu­ mor

Glioblastoma multiforme

Parietal lobe lesion; positive O.N. sign

20/20 OU

Normal early; 3 mo. later, LHH

Negative; later, equivocal.

Headaches and seizures, 1 mo. Craniotomy disclosed right occipital tumor

Glioblastoma multiforme

Occipital lobe lesion; negative O.N. sign

R 20/30 L 20/20

Left upper quadrant-anopia

Negative

Seizures. Right temporal lobectomy had been done previously for tumor; fields unchanged in 21 month follow-up

Astrocytoma

Temporal lobe lesion; negative O.N. sign

LHH, complete, incongruous

Positive

Seizures, 10 mo. Craniotomy disclosed right parieto-occipital tumor

Glioblastoma multiforme

Parietal lobe lesion; positive O.N. sign

15/100 OU

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g H >

d O

3 n o o > 3

TABLE 1 (.Continued) Case

Age

Sex

Vision

19

60

F

20/20 OU

20

23

F M

22

19

F

23

56

M

Personality change, 12 yr. Craniotomy: large right occipital parasagittal tumor

R 16/30 L 16/20

LHH, complete, macular sparing

Negative

Occipital headaches,3 mo. Craniotomy: Glioblastoma multiforme right occipital tumor

Occipital lobe lesion; negative O.N. sign

OU: counts fingers

RHH, complete

Positive

Confusion, headache, disturbed vision, 3 wk. Glaucoma. Craniotomy: left parieto-occipital tumor

Parietal lobe lesion; positive O.N.sign

RHH macular splitting

Negative

Dysphasia, alexia, R. hemiparesis. Arteriovenous malformation, ■* (gr< Bloody spinal fluid Craniotomy: vas­ exam; biopsy not done) cular lesion on surface of left parietal region

Parietal lobe lesion; negative O.N. sign

LHH. denser below

Positive

Headaches, 5-6 wk. Nephrectomy 8 yr. before for hypernephroma. Craniotomy disclosed solitary metastasis to right parietal lobe

Parietal lobe lesion; positive O.N. sign

LHH, macular splitting, denser below

Positive

Headaches 12 hr., left hypalgesia. Right Arteriovenous malformation thalamic lesion suspected. Craniotomy: arteriovenous malformation, R tem­ poral lobe, with intracerebral hematoma

Temporal lobe lesion; positive O.N. sign, but extent of intracerebral hema­ toma could not be exactly defined

RHH, macular splitting, incongruous

Positive

Headaches, intermittent episodes con­ Meningioma fusion 1 i yr. Craniotomy revealed large left temporal lobe tumor

Temporal lobe lesion; positive O.N. sign. Large tumor present, as 85 grams of tissue resected at surgery

Normal; but pseudohem ianopia

Negative

Headache, 2 wk. Dragging left leg, 1 wk. Craniotomy revealed right frontal lobe tumor

Glioblastoma multiforme

Frontal lobe lesion; negative O.N. sign

Negative

Auto accident, 8 days previously. Cra­ niotomy: left occipital subdural hematoma

Subdural hematoma

Occipital lobe lesion; negative O.N. sign

R 20/100 L 20/50 20/30 OU

57

20/70 OU

25 26

Symptoms and Course

Negative



Normal

44

Fields*

Cortical blindness; cleared to RHH

27

Anatomic Findings

Comment

O.N. Signf

LHH, macular sparing

Meningioma

Glioblastoma multiforme

Hypernephroma

Occipital lobe lesion; negative O.N. sign

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v> H

>

O

20/20 OU

LHH, denser below, incongruous

Negative

Headache, seizures 5 wk. Craniotomy: Adenocarcinoma of rectum metastasis to tip of right temporal lobe

51

20/20 OU

RHH, macular splitting

Negative

Visual difficulty, 2 mo. Craniotomy: small mass inferior portion of left posteterior temporo-occipital region

Carcinoma of ovary

Occipito-temporal lesion negative O.N. sign

30

14

20/20 OU

LHH, denser below

Positive

Weakness, right hand, 6 mo. Dragging R. foot, 2 wk. Craniotomy revealed a cyst, right parietal lobe

Cyst, right parietal lobe, probably gliomatous

Parietal lobe lesion; positive O.N. sign

31

54

20/20 OU

Normal

Positive

Carcinoma of breast, 2 yr., treated with X-ray. Seizures, dizziness, left hemi­ paresis 2 mo. Craniotomy revealed a solitary metastasis to right superior parietal lobule

Carcinoma of breast

Parietal lobe lesion; positive O.N. sign

M

28

o

Temporal lobe lesion; negativelO.N. sign

a

102

J. LAWTON SMITH AND DAVID G. COGAN

ions of the value of a positive optokinetic nystagmus sign have varied,2, ^ 8 most au­ thors have considered it as indicating disease of the posterior half of the cerebrum. The rare instances of alleged frontal lobe dis­ ease5' 7 causing an asymmetric optokinetic re­ sponse have not excluded parietal lobe in­ volvement. It is evident that more informa­ tion is needed on anatomically verified cases to resolve the significance of a positive opto­ kinetic nystagmus sign.. Our clinical experience has borne out the impression of Cords and Kestenbaum that this simple test is a reliable sign of parietal lobe localization in cerebral disease, and that one can with reasonable assurance differen­ tiate temporal and occipital lobe hemianopias from those of parietal origin by this method. The purpose of this report is to present briefly the clinical and pathologic findings in 31 patients in whom the optokinetic re­ sponse has been carefully studied, and which have been anatomically verified. In 14 of these, complete autopsy examinations are available. In 17 additional cases the findings were verified by craniotomy and biopsy. MATERIAL

Selected for review are 194 cases of cere­ bral disease seen by one of us (D.G.C.). Of this group, 29 have come to necropsy in the Massachusetts General Hospital. In 14 of the latter, and in 17 other cases confirmed by surgery, a specific statement regarding opto­ kinetic nystagmus is available. These 31 cases were further analyzed. The autopsy and sur­ gical cases are presented separately (table 1). DISCUSSION

Recent clinical experience with cases of cerebrovascular disease has strengthened our impression that a positive optokinetic nystag­ mus sign indicates parietal lobe disease. The anatomic evidence presented suggests that this is the case. A symmetric optokinetic re­ sponse was elicited to both sides in three of the autopsied cases (3, 4, and 6). These had lesions of temporal, occipital, and frontal

lobes, respectively, with no parietal involve­ ment. Six of the autopsied cases had positive (asymmetric) optokinetic nystagmus signs, and parietal lobe involvement was present in each (1, 2, 5, 7, 9, and 11). However, five of the autopsied cases present difficulties in interpretation. Thus, Cases 10 and 13 both have dual lesions (basilar artery thrombosis and medulloblastoma of cerebellum). Case 12 presented a metastatic malignant mela­ noma to left parietal region, and yet normal visual fields and optokinetic nystagmus were found clinically. This patient died within 10 days of onset of symptoms from massive cerebral edema, and perhaps death occurred too rapidly for clinical manifestation of the lesions. The fact that no field defect was present in this case substantiates the fact that there was little parietal lobe dysfunction present at the time of admission. Case 8 is a temporal lobe neoplasm with an asymmetric optokinetic nystagmus sign. However, pari­ etal lobe extension probably occurred in this case, and further anatomic study would have been helpful. Finally, the same factor arises in Case 14, in which only one parietal lobe was studied histologically. Of the surgically corroborated cases, seven instances of a negative optokinetic nystag­ mus sign were seen with lesions of occipital, frontal, or temporal lobes, without evident parietal involvement. Further, in six in­ stances of positive optokinetic signs, there was proven parietal lobe disease. Cases 25 and 26 deserve scrutiny, however. In Case 25, an arteriovenous malformation of the temporal lobe presented a positive optokinetic nystagmus sign. However, an intracerebral hematoma was evident in this case, and the extent of the latter could not be definitely determined. Likewise, Case 26 was a left temporal lobe meningioma which presented a positive optokinetic nystagmus sign. Whether or not parietal lobe involvement occurred is not definitely known. The neoplasm was large, however, with 85 gm. of tissue being resected at time of craniotomy. The method of testing was by rotating a

OPTOKINETIC NYSTAGMUS

large optokinetic drum at a moderate rate, and held about 20 inches from the patient. This was done several times to both sides in order to compare the responses. It should be noted that slight asymmetry may be seen at times in normal persons. Only either an ab­ sence of response to one side, or a definitely defective and asymmetric response should be called a "positive O.N. sign." An absent re­ sponse to both sides is nearly always without significance. The most common causes for this finding are that the patient is obtunded, has very low vision, or is ignoring the test. It should be noted that optokinetic nystagmus has been found to be inaccurate in lateralization of brain stem disease in the experience of one of us (D.G.C.), so that the statements made previously apply to its use only in cere­ bral lesions. The vertical optokinetic re­ sponse was not interpreted in this study. SUMMARY

The optokinetic response was analyzed in 14 cases of cerebral disease which came to autopsy examination. Six of these had posi­ tive (asymmetric) optokinetic nystagmus signs and were found to have parietal lobe lesions. Three cases presented lesions of temporal, occipital, and frontal lobes respec­ tively, with no parietal involvement. The optokinetic nystagmus sign was negative in these cases. Complicating factors in inter­

193

pretation of the other five cases have been discussed. Seventeen cases were studied from the standpoint of optokinetic nystagmus, which were subsequently verified by craniotomy and biopsy. Six of these had parietal lobe lesions with asymmetric optokinetic re­ sponses. Four had occipital lobe lesions with a normal optokinetic response to both sides. Likewise, a negative optokinetic nystagmus sign was seen with three temporal lobe le­ sions and with one frontal lobe lesion. In the three other cases, two were temporal lobe lesions with positive optokinetic nystagmus signs in which rather extensive lesions were present (one intracerebral hematoma, and one neoplasm). One patient was seen to have an arteriovenous malformation of the sur­ face of the left parietal region, with a nega­ tive optokinetic nystagmus sign, however. A frequent occurrence noted in cases with a positive optokinetic nystagmus sign was concomitant involvement of the thalamus. This would not be unexpected with lesions involving the middle and posterior one-third of the optic radiations, deep in the parietal lobe. It is concluded that a positive opto­ kinetic nystagmus sign in cortical lesions is most suggestive of involvement of the parietal lobe. 900 Lenton Avenue (12). 243 Charles Street (14).

REFERENCES

1. Kestenbaum, A.: Clinical Methods of Neuro-ophthalmologic Examination. New York, Grune and Stratton, 1946. 2. Bârâny, R.: Z. Klinik u. Theorie d. Eisenbahnnystagmus. Acta oto-laryngol., 3:261, 1921. 3. Brunner, H.: Zur klinischen Bedeutung des optischen Drehnystagmus. Klin. Monatsbl. f. Augenh., 68:783, 1922. 4. Ohm, J. : Cited by Kestenbaum.1 5. Fox, J. G, and Holmes, G.: Optic nystagmus and its value in the localization of cerebral lesions. Brain, 49:333, 1926. 6. Cords, R.: Optisch-motorisches Feld und optische-motorische Bahn. Arch. f. Ophth., 117:58, 1926. 7. Cogan, D. G., and Loeb, D. R.: Optokinetic response and intracranial lesions. Arch. Neurol. & Psychiat., 61:183, 1949. 8. Enoksson, P.: Optokinetic nystagmus in brain lesions. Acta Ophth., 34:163, 1956.