Documenta Ophthalmologica 46,2: 339-344, 1979 NYSTAGMOGRAPHY AS A DIAGNOSTIC TOOL IN MULTIPLE SCLEROSIS A.G.M. VAN VLIET & G.H.M. VAN LITH

fRo tterdam] INTRODUCTION The diagnosis of multiple sclerosis is still a clinical one and depends on the demonstration of objective evidence of necessarily separate lesions in patients with a history suggestive of multiple sclerosis, in whom there is no satisfactory alternative explanation. Difficulty may arise in cases with symptoms referable to a single focal lesion of the spinal cord. In such cases it may be necessary to search for subtle defects, which give clinical evidence of a brain-stem lesion. We wonder whether a more systematically performed nystagmographicaI examination of patients with clinically definite multiple sclerosis would provide us with more objective evidence of clinically silent brain-stem lesions. The aim of the present investigation was to elucidate how frequently pathological changes in such patients with multiple sclerosis are demonstrated by nystagmographical examination and to obtain normative data especially in relation to the subtle defects, such as 'pathological slowness' of saccadic velocity, slowing of adduetion relative to abduction in conjugate gaze, impairment of smooth following movements of the eyes and 'pathological slowness' of the slow phase of optokinetic nystagmus. MATERIAL AND METHODS The material consists of two groups; one, the 'test' group, includes 18 patients with multiple sclerosis, referred for nystagmographical examination to the Department of Clinical Neurophysiology of the Erasmus University, Rotterdam, in the period from February 1977 to June 1977. Eight patients met the criteria of definite multiple sclerosis, and ten patients the criteria of probable multiple sclerosis, described by McAlpine (1972). It must be pointed out that the 'test'-group is not a sample of the entire population of multiple sclerosis patients. Those cases that simulated a spinal cord disorder but also had signs of a second lesion had a greater chance of entering the 'test' group. The other group, the 'control' group of 18 normal persons, matched with

339

Table 1. Sex and age distribution, duration and course of illness. Number of M.S. patients 18 (5 o', 13 ?) age groups 16 - 4 0 > 40

age d~strlbutlon

duration of il Iness

6 12

< 1 yr 1 - 5 yr > 5yr

number of patients 1 4 13

remitting course: 2 - 4 episodes > 4 episodes progressive after 3rd epTsede progressive course

6 2 6 4

severityof the illness: s[ight needs walking-aids wheelchair llfe

9 5 4

the test-group in sex and age, was kept as a standard for comparison in order to obtain normative data in relation to the subtle defects. Eye movements were recorded by direct current electronystagmography in a manner previously described for this laboratory (van Vliet, 1973). Asymmetry (e.g., of the angular velocity of the slow phase of optokinetic nystagmus) was calculated by means of the following formula: L-R D .... L+R

x 100%

We assumed a difference of 20% in angular velocity (~ or in total amplitude between the nystagmus to the right and that to the left, and an absolute diminution of 50% of the slow phase of optokinetic nystagmus in relation to the velocity of the optokinetic stimulus, to be the marginal values. RESULTS Sex and age distribution of the patient material, duration of the illness before nystagmographical examination, the course and the severity of the disease are presented in table 1. Table 2 shows the incidence of neurological deficiency symptoms in this material. It must be pointed out that in electronystagmographic examination only two of the 18 multiple sclerosis cases showed the normal pattern. In all the other cases (see table 3) one or more of the following abnormalities were found (in order of incidence): horizontal gaze induced nystagmus, weakness of adduction, vertical gaze induced nystagmus; spontaneous nystagmus with closed eyes, directional preponderance, obvious impairment of smooth

340

Table 2. Incidence of symptoms in 18 M.S. patients. spastic paraplegia

15

posterior column lesions

9

gaze nystagmus (dlssoclated)

8 (3)

optic atrophy

7

weakness of adduction

4

cerebel lar ataxia

3

hemiparesls

2

abducens paresis

1

dementia

1

symptomatic seizures

1

following movements of the eyes and diminution of the slow phase of optokinetic nystagmus elicited with stimuli of 30~ or slower. In the 'control' group four persons also had a spontaneous nystagmus with closed eyes of less than 5~ A slight gaze induced nystagmus and slight to moderate impairment of the following movements occurred in two cases. Finally, two persons of the 'control' group had a rather strong directional preponderance to the left, both with recruitment, possibly caused by an old, not yet completely compensated, peripheral vestibular disturbance. We also measured the peak velocity of the saccadic eye movements of each eye for 20 ~ and 40 ~ Table 4 shows the mean peak velocity with standard deviation of the saccadic eye movements for 20 ~ and 40 ~ in 18 normals and 18 multiple sclerosis patients. With the Student's t test it appeared that

Table 3. Incidence of ENG signs in

gaze nystagmus horizontal (dissociated) vertical

18M.S. pat.

10 (31 5

18normals

2 0

weakness oF adduction

6

spontaneous nystagmus with closed eyes

4

0 4

directional preponderance

3

2

impairment of following movements sllght - moderate considerable

6 3

2 0

dimlnubon of optokinetic nystagmus only when using stimulus of 60 o/s. when using stimulus of 30 o/s. or less

3 3

2 0

no abnorma l lties

2

12

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Table 4. Mean peak velocity with standard deviation of coniugate saccadic eye movements For 20 ~ and 40o ;n 18 M.S. patients compared with 18 normals (in degrees per sec.)

amplit.

20 ~

20 ~

40 ~

40 ~

gaze to

right

left

right

left

18 normals

325

315

418

405

(305-345)

(297-333)

(383-453)

(375-435)

289

287

337

339

(226-312)

(260-314)

(297-377)

(304-374)

1 8 M . S . pat.

significant differences (P 0.05) existed between the slower peak velocity of the saccadic eye movements in multiple sclerosis patients and the saccadic eye movements in normal persons. Table 5 shows the mean peak velocity of saccadic eye movements for 20 ~ of 18 normal persons and 18 multiple sclerosis patients, subdivided into 6 patients with clinically proven weakness of adduction or dissociated gaze nystagmus and a second group of the 12 other multiple sclerosis patients. It appeared that significant differences (P 0.05 Student's t test) also existed between the slower adduction movements in multiple sclerosis patients and the adduction movements in normal persons. This applies mainly to the 6 patients with weakness of adduction or dissociated gaze nystagmus, and then only in relation to the saccadic eye movements for 20 ~ However, in measuring the peak velocities of the saccadic eye movements for 40 ~ , it appeared that no obvious differences existed between the slowing of adduction relative to abduction. Table 5. Mean peak velocity of monocu[ar saccadlc eye movements for 20 ~ Tn 18 M.S. patients compared w~th 18 norma[s (in degrees per sec.). L. to Centre

Centre to R.

R. to Centre

R.E.

L.E.

R.E.

L.E.

R.E~

L,E.

R.E.

L.E.

6 normaJs

376

336

394

307

390

391

263

314

6 MS + add. p~:resls or d~ssoc;at, nysf.

335

264

333

162

250

348

258

367

gaze from

Centre to k.

12 normals

404

401

390

357

339

407

302

390

12 MS without olin. add. paresis or dissociated gaze nyst.

371

337

382

298

358

356

289

350

significant differences existed between the M $. patients and the normals in the underlined values only.

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DISCUSSION In the 'control' group four persons had slight disturbances in the nystagmogram and in two cases borderline results were found. The other twelve normal nystagmograms included among others all the persons younger than 44 years. In the question whether nystagmography could detect subtle defects in the brain-stem it appeared that a spontaneous nystagmus (of less than 5~ with closed eyes, a directional preponderance or slight to moderate impairment of the following movements alone cannot be taken as a diagnostic criterion. Horizontal and especially vertical gaze nystagmus, considerable impairment of following movements and symmetrical diminution of the passive optokinetic nystagmus by use of stimuli of 30~ or less can be used as a fairly reliable diagnostic criterion for a second lesion. Although the mean peak velocity of conjugate saccadic eye movements for 20 ~ in the multiple sclerosis patients is higher than the lower limit of normal mean peak velocity of 188~ (Boghen and others, 1974) it appeared that a significant difference (P 0.05) existed between the peak velocity of the saccades in multiple sclerosis and that in normal persons. With nystagmography we could detect slowing of adduction relative to abduction in two additional cases to the four who showed this already without nystagmography. This applies only for relatively small saccades of 20 ~. This may be due to the pathological slowness of the gaze movements which will be more marked as the saccadic eye movement is larger. CONCLUSIONS Summarizing from this investigation we may conclude 1. It appeared that slight abnormalities in the nystagmograms can occur, but only in persons above 44 years of age. Because multiple sclerosis patients are usually younger than 50 years, disturbances in the nystagmogram are fairly often evidence of a brain-stem lesion. 2. In persons older than 44 years directional preponderance, spontaneous nystagmus with closed eyes and slight to moderate impairment of following movements alone cannot be taken as a diagnostic criterion for a brain-stem lesion. 3. Horizontal and especially vertical gaze nystagmus, considerable impairment of following movements and symmetrical diminution of the passive optokinetic nystagmus when using stimuli of 30~ or less can be used as a fairly reliable diagnostic criterion. 4. It appeared that the decrease in peak velocity of the saccadic eye

343

movements in our series of M.S. patients had pathological significance. 5. Slowing of the peak velocity of adduction relative to abduction is a reliable diagnostic criterion, provided that only relatively small saccadic movements (e.g. of 20 ~) are used. REFERENCES Boghen, D., Troost, B.T., Daroff, R.B. and others. Velocity characteristics of normal human saccades. Invest. Ophthalmol. 13:619 (1974). McAlpine, D., Lumsden, C.E. & Acheson, E.D. Multiple Sclerosis. Churchil Livingstone, Edinburgh and London, 1972. Pp. 224-226. Vliet. A.G.M. van. On the central mechanism of latent nystagmus. Acta Ophthalmol. 51:772-781 (1973). Author's address: A.G.M. van Vliet, M.D. Department of Neurology Academic Hospital 'Dijkzigt' Erasmus University Rotterdam The Netherlands

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Nystagmography as a diagnostic tool in multiple sclerosis.

Documenta Ophthalmologica 46,2: 339-344, 1979 NYSTAGMOGRAPHY AS A DIAGNOSTIC TOOL IN MULTIPLE SCLEROSIS A.G.M. VAN VLIET & G.H.M. VAN LITH fRo tterda...
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