вход по аккаунту


Assessment of vestibulo-ocular reflexes in congenital nystagmus.

код для вставкиСкачать
Assessment of Vestibulo-Ocular Reflexes
in Congenital Nystagmus
Michael A. Gresty, PhD,’ Hilary J. Barratt, MSc,’ Nicholas G. R. Page, MRCP,’ and Jonathan J. Ell, FRACPt
The vestibulo-ocular reflex and its suppression by fixation of a target rotating with the subject were tested in 18
subjects with congenital nystagmus using steps of constant velocity rotation and sinusoidal stimuli swept in frequency
between 0.01 and 1.0 Hz. Responses to stopping stimuli were abnormal in waveform and of short duration in most
subjects tested. This pattern was attributed to masking of the response by spontaneous eye movements and to adaptation. In contrast, during both oscillation in the dark and attempted suppression of the vestibulo-ocular reflex, all
subjects had nystagmus that was modulated with the stimulus during all frequencies of stimulation. The phase
relationship of the nystagmus to the motion stimulus was the same as in normal subjects. Estimates of the gain of the
vestibuloscular reflex respoqe were not meaningful because of contamination of the vestibular response by the
congenital nystagmus wavefosms. Modulation of amplitude and reversal of nystagmus in phase with the vestibular
stimulus at all frequencies of oscillation were shown most clearly during attempted suppression of the vestibulo-ocular
reflex. This finding is clinically useful because it establishes suppression as a test of the presence of vestibular function
in congenital nystagmus.
Gresty MA, Barratt HJ, Page NGR, Ell JJ: Assessment of vestibulo-ocular reflexes in congenital nystagmus.
Ann Neurol 17:129-136, 1985
Individuals with congenital nystagmus appear to have
intact vestibular function; in general, they are neurootologically asymptomatic and possess normal righting
reactions 171. The interpretation of vestibulo-ocular
reflex (VOR) responses in congenital nystagmus is
difficult, however, because the spontaneous nystagmus
may interact with and mask the VOR, thereby producing complex eye movements in which the vestibular
contribution is unclear {lOl. It is perhaps for this reason that investigations of vestibular function in congenital nystagmus have produced widely differing interpretations, as exemplified by two recent studies that
used objective recordings. Forssman [Gf concluded
that vestibulo-ocular reactivity was absent in 44% of
his patients because of “central influence,” whereas
Yee and colleagues {I 11 also found abnormal patterns
of response in 45% of their cases but concluded that
the underlying VOR was probably normal.
In view of this apparent contradiction, we investigated VOR responses to rotatory stimuli in subjects
with congenital nystagmus. In particular, oscillatory
stimuli over a wide range of frequencies, for assessment of both VOR and vestibulo-ocular reflex suppression (VORS), were used.
Subjects were 18 individuals with congenital nystagmus
whose names were retrieved from the diagnostic index of the
From the *Medical Research Council, Neuro-Otology Unit, National Hospital, Queen Square, London WClN 3BG, England, and
Wdcombe Hospital, NSW Australia
National Hospitals; all had been investigated and found to
have no evidence of other neurological disease. All subjects
gave informed consent to the investigations. Ages ranged
from 10 to 53 years. Subjects with latent nystagmus were
excluded from the study.
The high-frequency performance of the VOR was assessed
by comparing visual acuity with the head stationary with
acuity during passive oscillation of the head at frequencies
above 1 Hz. Acuity was measured using a Snellen chart, and
passive oscillation was applied with the turntable for frequencies up to 2 Hz and by manual shaking of the subjects’
shoulders to induce higher frequencies. Acuity during highfrequency oscillation depends on normal vestibular function,
because visual stabilization in this frequency range of head
movement cannot be achieved by other eye movement systems {S}. Impairment of vestibular function results in oscillopsia and reduction of acuity at these frequencies.
Eye movements were recorded using bitemporal DCcoupled electro-oculographywith a flat response to 100 Hz.
Spontaneous nystagmus in the light was examined over a
complete range of gaze eccentricity by asking subjects to
look at individual targets in an array of light-emittingdiodes.
Gaze holding in the dark was examined by asking subjects to
hold their eyes in the same direction as the target lights.
Rotational testing stimuli were applied using a turntable
driven by a 150 Nm torque motor that provided rotation in
the horizontal plane about a vertical axis (yaw). The stimuli
used were as follows: rotational starting and stopping stimuli
in both rightward and leftward directions with velocity steps
of 0 to 40 and 0 to 80 degreedsec (acceleration of 80 de-
Received Dec 2, 1983, and in revised form Apr 5 and May 29,
1984. Accepted for publication June 2, 1984.
Address reprint requests to Dr. Gresty.
greedsec'); sinusoidal oscillation swept in frequency between
0.01 and 1.2 Hz,with peak velocities of both 40 and 80
degreedsec. The latter stimulus provided just more than one
stimulus cycle at the lowest frequency and approximately six
cycles at the htghest frequency. The stimuli were given first
while the subject was in total darkness (VOR), and then
while the subject fixated a point source light-emitting diode
target attached to the chair at a distance of 0.5 m in front of
and rotating with the subject (VORS) and while the subject
fixated on an earth-stationary target at a distance of 2 m
(visually assisted VOR-for stimuli oscillating at more than
0.2 Hz).During stimulation in the dark, subjects were encouraged to remain alert and, if necessary, were given mental
arithmetic tasks. Pursuit of horizontal target motion was assessed using a red laser beam deflected by a scanning motor
and projected on a tangent screen at a distance of 1.5 m. The
target motion consisted of a sinusoid swept in frequency
between 0.05 and 0.4 Hz with a peak amplitude of 20 degrees.
Congenital Waveformr
The waveforms of spontaneous nystagmus in each direction of gaze were classified using a system based on
one proposed by Dell'Osso and Daroff 141. The
waveforms were not mutually exclusive, and in some
patients different waveforms were seen at different
times during examination. The subjects (numbered
consistently through this report from 1 through 18)
can be grouped according to waveform as follows:
Linear slow-phase jerk nystagmus
Exponentially decreasing slow-phase
jerk nystagmus
Exponentially increasing slow-phase
jerk nystagmus
Bidirectional jerk nystagmus
Mixed pendular and jerk nystagmus
Pure pendular
11, 13-15
8, 13
1, 3, 4, 6-18
3, 4 , 6 7, 9,
10, 16, 17
2, 5, 18
130 Annals of Neurology Vol 17 No 2 February 1985
Fig 1. Spontaneous nystagmus and responses to rightward velocity step (upper traces) and sinusoidal oscillation (lower traces) in
the durk (Subject 12).The nystagmus on primury, left, and right
gaze has an exponentially increasing slow-phase velocity. The
lower eye movement trace of the velocity step response is a continuation oftbe upper. Responses to oscillation (dark): eye movement
responses (upper trace) to high, medium and IOU, fflquencies of oscillation at a peak velocity of 40 degreeslsec (lower traces). The response patterns are similar to nortnul ones except that the induced
nystagmus has exponentially increasing slow-phase velocities.
Responses to Steps in Rotational Velocity
The duration of the responses to velocity steps was
measured from the time of onset of the stimulus. In
our laboratory the normal response duration to a 0- to
80-degredsec velocity step is between 30 and 60 seconds, with a peak slow-phase velocity of approximately
60 degreedsec in an alert subject. The 0- to 80-degree/
sec stimulus produced clearer responses than the
lower-velocity step stimulus, but in more than half of
our subjects, the responses to velocity steps were
highly abnormal. Four characteristic response patterns
were identified and are illustrated by recordings from
individual subjects. These patterns are not intended to
represent a rigid classification or to be mutually exclusive, and subjects varied in the degree to which they
displayed the various features. When responses to rotational stepping stimuli were apparently of unusually
short duration, it was not clear whether this was a
result of a short time constant or whether the response
duration was masked by spontaneous eye movements.
Six subjects (33%; Subjects 1, 2, 11-14) had a response that showed a clear pattern of jerk nystagmus
with a predominantly linear waveform and a welldefined end point (Fig 1).All but one of these subjects
had symmetrical response durations in excess of 25
In the second type of response, the waveform of the
congenital nystagmus was strongly preserved throughout the vestibular stimulus. The VOR seemed to be
superimposed on the congenital nystagmus, causing
either an increase or a decrease in slow-phase velocity
1 minute later
1 sec
Fig 2. Responses to 4O-dgreehec steps i n rotationalvelocity in
darkness (Subject 2). The efhct of the velocity steps is to reverse
the direction ofthe nystagmus.
(and thereby altering frequency of fast phases), or reversal of nystagmus (Fig 2). The vestibular response
was short and heavily disguised (see Fig 4, rightward
velocity step), particularly during the later stages of its
decline, because the overlying spontaneous nystagmus
had such high slow-phase velocities.
In some subjects vestibular stimulation induced extreme tonic gaze deviations (EGDs), which were in the
direction of the slow phase of vestibular nystagmus.
The gaze deviation was interrupted by intermittent
saccades; these took the eyes to a more central position, which then revealed nystagmus consistent with a
vestibular response. The intermittent nature of this
nystagmus hindered measurement of response duration. This type of response is illustrated in Subject 13
(Fig 3), in whom the apparent duration of response was
between 15 and 20 seconds.
In certain subjects responses were difficult to assess
because they were masked by wandering eye movements (WEMs), which could be of higher velocity than
vestibular responses (Fig 4).
All of the shortest-duration responses (less than 10
seconds) were obtained in subjects who also had
bidirectional jerk nystagmus and WEMs; these did not
occur in association with responses of 30 seconds’ duration or longer. In addition, there was a strong inverse
relationship between nystagmus amplitude, as measured in primary gaze, and duration of vestibular response. Thus, short-duration vestibular responses are
associated with bidirectional jerk nystagmus of large
amplitude, WEMs, and EGDs. These relationships are
illustrated in the histograms in Figure 5.
1 s
Fig 3. Eye movements in primavy, right, and left gaze in the
light and during velocity steps and sinusoidal rotational stimuli
in the dark {Subject 13). The spontaneous nystagmus at various
gaze displacements shows linear and exponentialh increasing and
decreasing slow-phase velocities. Leftward velocity step of 80 degreeslsec provokes rightward deviations of the pyes, during which
there is no nystagmus. C indicates central eye position. The lower
eye movement trace is a continuation of the upper. Responses t o oscillation: eye movement responses (upper trace) t o oscillation at low
frequency in the dark (lower trace). Note the change of time base.
Velocity in the rightward or leftward direction induces extreme
gaze deviations in the opposite direction. Approximte phase of
the response is shown by changes in the direction of the slow
phase of the nystagmus (arrows).
t o Oscilkatory Stimuli
All subjects exhibited clearly modulated nystagmus in
response to oscillatory stimuli in darkness at all fre-
Gresty et d.VOR in Congenital Nystagmus
80°/a R
1 s
80015 L
quencies of stimulation. The nystagmus beat in the
same direction as normal vestibular nystagmus but
could be asymmetrical in beat frequency and slowphase waveform andor have exponentially increasing
and decreasing slow-phase velocities. This pattern is
exemplified in Figures 1, 3, and 4 in subjects who had
different nystagmus waveforms and patterns of response to velocity steps. Evoked nystagmus was intermittent during EGD (see Fig 3 ) and during WEMs (see
Fig 4). The abnormalities of slow-phase waveform precluded meaningful estimates of the gain of the VOR in
darkness. Although the eyes tended to wander in darkness, in most instances the phase reversal of the response could be identified. Typically the phase of the
responses, as judged by the reversals of nystagmus,
was 0 degrees with respect to zero stimulus velocity at
the high frequencies, with slight phase advance of 20
to 40 degrees at 0.01 Hz. These phase characteristics
are in accord with normal vestibular responses { 3 ] .
Attempted Suppression of the VOR
In all subjects the patterns of nystagmus produced by
attempted VORs in response to swept sinusoidal
stimuli were the most orderly and reproducible responses observed (Fig 6A; see Fig 7). All stimulus
frequencies produced nystagmus that was modulated
with the stimulus and beat in the direction appropriate
to a vestibular response. Reversal of the direction of
nystagmus was clearly delineated, indicating the phase
relationship between stimulus and response. The nystagmus produced during VORS could be asymmetrical
in beat frequency and slow-phase waveform and/or
have exponentially increasing and decreasing slowphase velocities. As with the VOR, these characteristics precluded meaningful estimates of gain of the slow
phase of the nystagmus with respect to the motion
In contrast, attempted VORS responses to rotational stepping stimuli, as with the VOR step responses, were difficult to assess. At the onset of the
132 Annals of Neurology
Vol 17 No 2 February 1985
Fig 4. Eye movements in primary, right, and Iej9 gaze in the
light and dark and during velocity steps and sinusoihl rotational stimuli in the akrk (Subject 6). In the light there is a
bidirectional jerk nystagmus in primary gaze. In the dark there
are wandering eye movements in all positions of gaze. Rightward
80-degreelsec velocity step provokes a right-beating nystagmus
with an exponentially increasing wavefrm. This rapidly decays
and is f i l l w d b~ a bidirec8ioopaaljerk nystagmus that changes to
a left-beating nystagmus. Velocity step to the leji pmokes two
large beats of nystagmusfol(owedby wandering eye movements
that take the eyes t o extreme positions. Eye movement responses
(upper trace) to high, medium, and low frequencies of oscillation
(lower trace) show modulation of the direction ofthe nystagmus
at all frequencies. The approximate change in direction of the
slow-phase component of the nystagmus shows the phase reiationship with the stimulus (arrows).Note the change of time base
for the low-frequencystimulus. C indicates central eye position.
stimulus, a clear nystagmus response was evident. This
could take the form of a reversal of direction or increase in velocity of the spontaneous nystagmus. The
apparent durations of the VORS responses to velocity
steps were highly variable, however, both between and
within subjects, with some appearing to endure for
only a few seconds. It is not clear whether the brevity
of response was attributable to a short time constant or
resulted from spontaneous eye movements masking
the true response duration. Frequently the rate of decay and the end point of the nystagmus induced by the
vestibular stimulus were difficult to assess because the
slow phase of the response was distorted or the response was masked by spontaneous nystagmus (Fig
When the VORS tasks were provoking nystagmus,
subjects reported that they saw the fixation target oscillate. When the tasks provoked a cessation of nystagmus (possibly a “null”), the target appeared stationary.
A comparison was made between pursuit performance and VORS responses to ramped sinusoidal
stimuli. The waveform of pursuit was highly variable
and frequently asymmetrical in rightward, as opposed
20 25
30 35 40 45
2 0 25
30 35 40 45
20 25
30 35 40 45
20 25
3 0 35
4 0 45
Duration of (visible) vestlbular response to 80°/s veloctty step
Fig 5 . Histograms showing thefrequency distribution of bidirectional jerk nystagmus (BDJs), nystagmus amplitude, extreme
gaze deviation (EGD),and wandering eye movements (WEMs),
as functions of the duration of response t o 80-degreelsecsteps in
rotational velocity. Each patient is indicated by number. For
BDJs, WEMs, and EGD, blank syuares indicate absence ofthe
characteristic. Durations for rightward and lejtward stimuli are
presented separately, and each is the average of the responses t o
two stimuli.
Fig 6. Attempted suppression of the vestibulo-ocular refex during ramped sinusoidal rotation and a rightward velocity step
(Subject 2). (A) Clear modulation of the nystagmus during all
frequencies of sinusoidal stimulation. (Bi Responses to a 40degreelsec velocity step. The lower eye movement trace is an expansion of the early portion of the upper trace. Stimulus onset for the
upper trace is indicated with an arrow. The stimulus reverses
the direction of the spontaneous nystagmus for 3 seconds. The
spontaneous nystagmus then reappears and resembles prestimulus
nystagmus 8 seconds after the stimulus. A simplistic estimate of
time constant for this process would be 2 t o 3 seconds. Note
changes of time base for stimulus and expanded eye mwement
trace. (VORS = vestibulo-ocular refex suppression; S PK =
second peak.)
Gresty et al: VOR in Congenital Nystagmus
to leftward, directions. This pattern is exemplified in
Figure 7 (upper traces), in which pursuit has the appearance of reversal of slow phase only in the rightward direction. Pursuit frequently induced a shift in
the null point of the congenital nystagmus in the direction opposite to the stimulus. During the null, the eyes
appear to pursue more normally (see Fig 7). It was not
clear how the nystagmus during VORS related to the
waveform during pursuit; however, there was a correspondence between the presence of a null during
pursuit and the presence of a null during VORS. In
subjects who had a clear null in pursuit, there was a
cessation of nystagmus at the point of phase reversal in
the VORS. In contrast, there was a reversal in the
direction of nystagmus during VORS without a quiescent period in subjects who showed no clear null during pursuit (see Fig 7; comparison of upper and lower
VisuaI Acuity
Corrected binocular visual acuity in our subjects
ranged from 20/18 to 20/60 in the preferred directions
of gaze. Acuity did not decrease significantly during
high-frequency oscillation of the head in the light, indicating that the waveform of nystagmus produced during such oscillation provided adequate foveation periods. Typical loss on the Snellen chart was only a
single line, which is comparable to normal performance. Subjects did not report oscillopsia during shaking. Eye movement responses during sinusoidal oscillation above 1 Hz while an earth-fixed target was being
viewed were similar to those seen in normal subjects
but with occasional superimposed nystagmus beats.
Because the VOR is the only mechanism capable of
providing visual stabilization at high frequencies, one
must presume that it is functioning adequately in the
frequency range above 1 Hz.
134 Annals of Neurology Vol 17 No 2 February 1985
Fig 7. Pursuit and vestibulo-ocular re$ex suppression (VORS)
responses (Subjects 12 {A} and 6 {B}).In A the VORS andpursuit movements show clear nullperiods; in B the pursuit has a
superimposed congenital nystagmus waveform and the VORS nystagmus reverses without a clear null point. (pk = peak.)
The findings of this study are in agreement with earlier
reports {b, 7, 101: the eye movement responses of
subjects with congenital nystagmus to rotational velocity steps are frequently abnormal in waveform and appear to be of short duration. In contrast, the responses
to sinusoidal stimuli had appropriate phase reversals at
all frequencies, indicating the presence of vestibular
sensitivity at low frequencies of stimulation. Furthermore, because the phase relationship of the sinusoidal
response in congenital nystagmus is the same as in
normal subjects, the gain at low frequencies may also
be normal. Thus, there appears to be a discrepancy
between the transient and the sinusoidal response in
subjects with congenital nystagmus. This relationship
is unlike that in the vestibular responses of most normal subjects, in whom the sinusoidal response can be
predicted from the transient response. There are two
possible explanations for short responses to stepping
stimuli. One is that the responses are masked by spontaneous eye movements. The alternative, but not
necessarily exclusive, explanation is that the time constant of the vestibular response is shortened, possibly
as a result of adaptation, which occurs preferentially
during transient responses because of the unidirectional, highly predictable nature of the stimulus.
Abnormal vestibular responses occurred in subjects
who had congenital nystagmus of large amplitude with
bidirectional jerk waveforms and whose eyes wandered
and drifted to EGDs in the dark. These features indicate an insensitivity to eye position and velocity that
may account for the absence of vestibular nystagmus.
In a normal subject, an induced slow-phase eye movement in the dark elicits a corrective saccade, which is
triggered by a velocity or position threshold C11. These
saccades interrupt the slow-phase eye movement, thus
producing the pattern of nystagmus. With low sensitivity to position and velocity, the triggering of fast phases
will be impaired. In subjects with EGDs, vestibular
stimuli produced uncorrected tonic deviations of the
eyes without corrective fast phases. This response is
similar to the vestibular responses in patients with saccadic palsy, in whom vestibular stimulation also produces tonic gaze deviation without nystagmus. Vestibular responses could also be disguised by wandering
movements, which often had higher velocities than vestibular responses.
All our subjects had stimulus-modulated nystagmus
during sinusoidal VORS, with reversals in the direction
of nystagmus that had the same phase relationship to
the stimulus as normal vestibular responses. Because
the stimuli consisted of swept sinusoids, which are relatively unpredictable, the response would be determined largely by the stimulus and not by anticipatory
eye movements. The presence of modulation at all frequencies indicates that some vestibular function is present. Furthermore, assuming that gain is closely related
to phase, as in normal subjects, the finding of a normal
phase relationship with the stimulus suggests that the
underlying vestibular function is normal.
The nystagmus observed during VORS may have
several components. First, the slow phases may have a
component of unsuppressed vestibular response. During attempted suppression the eye returns to the target
with fast phases, which, overall, maintain a steady line
of sight. During the task, however, all subjects saw the
target oscillate with their nystagmus, indicating some
failure of visual stabilization. Second, the nystagmus
during attempted VORS may be congenital nystagmus,
as is suggested by the exponentially increasing velocity
of the slow phases. If this is so, then the stimulus influences the direction of the congenital nystagmus so
that it is in the same direction as a vestibular response.
Thus, the null of the nystagmus has been shifted (e.g.,
acceleration rightward brings the nystagmus seen on
right gaze into the primary position of gaze; therefore,
the null shifts in the direction opposite to the stimulus).
Finally, the nystagmus during attempted VORS may
result from the subjects’ abnormal pursuit responses.
There is a close relationship between pursuit and
VORS in normal subjects C2, 5,73, and impairment of
pursuit commonly accompanies failure of VORS. It has
been proposed that suppression of a vestibular response by fixation is mediated by pursuit, which cancels
the eye movements caused by the VOR. If this is the
mechanism of VORS in subjects with congenital nys-
tagmus, then the nystagmus seen during attempted
suppression could be the abnormal waveform of their
pursuit. In the case of an apparently reversed pursuit
waveform (see Fig 7, upper traces, rightward pursuit),
the nystagmus during suppression could theoretically
be enhanced such that the VOR gain appeared greater
than normal.
It is highly likely that the nystagmus seen during
attempted suppression derives in part from the congenital nystagmus. This possibly is consistent with both
the waveform of the VORS nystagmus and the theory
that the vestibular stimulus andor the pursuit movement used to suppress the vestibular response shifts
the null point of the spontaneous nystagmus. It is not
possible to estimate how much unsuppressed vestibular
response contributes to the VORS nystagmus; it is
clear, however, that even at the lowest frequencies
tested, there is a significant VOR to be suppressed.
VORS responses to velocity step stimuli were not
clearly related to the sinusoidal responses. The apparent brevity of the transient response may be attributable to masking by spontaneous eye movements
or to rapid adaptation to the predictable unidirectional
stimulus. A possible explanation for the distinctiveness
of the low-frequency response is that the less predictable, direction-changing nature of the stimulus impairs
and invalidates adaptation.
The behavior of the null is a further factor to be
considered when attempting to reconcile transient and
sinusoidal responses. During sinusoidal VOR and
VORS, the null is clearly related to the stimulus, occurring at the time of the zero eye velocity of a normal
vestibular response. It is not clear how the null behaves following a transient stimulus. One must presume that at the onset of the stimulus the null shifts
(e.g., acceleration rightward induces a null shift leftward, bringing out the nystagmus that is usually present on right gaze). Thereafter the null may drift, return
in a jump, or be subject to adaptive processes, as with
the VOR. Thus, the behavior of the null also contributes, in some unknown way, to the complex patterns
of response to step stimuli seen in subjects with congenital nystagmus.
We have determined that sinusoidal rotational
stimuli over a range of frequencies are superior to
velocity steps for demonstrating the presence of vestibular function in congenital nystagmus. The duration
of responses to velocity steps is difficult to assess because of masking of the responses by spontaneous eye
movements and possibly because of adaptation. In
contrast, the responses to sinusoidal stimuli showed a
clear modulation of nystagmus at all frequencies, with
changes in direction of nystagmus that have the same
phase relationship in the stimulus as normal vestibular
Gresty et al: VOR in Congenital Nystagrnus 135
responses. This modulation is seen most clearly during
VORS. This finding is of clinical significance, because
the modulation of nystagmus during VORS may be
used to demonstrate the presence of vestibular function. The patterns of abnormality that occur in subjects
with congenital nystagmus who have confirmed labyrinthine disorders remain to be demonstrated.
J. J. Ell held an Alexander Werner Piggott Commonwealth Training
Fellowship. N. G. R. Page is supported financially by the Smith's
1. Barnes GR: Vestibulo-ocular responses to head turning move-
ments and their functional significance during visual target acquisition. Unpublished PhD dissertation, University of Surrey,
Guilford, England, and Royal Air Force Institute of Aviation
Medicine, Farnborough, Hants, England, 1976.
2. Barnes GR, Benson AJ, Prior ARJ: Visual-vestibular interac-
136 Annals of Neurology Vol 17 No 2 February 1985
tion in the control of eye movement. Aviat Space Environ Med
49:557-564, 1978
3. Benson AJ: Interactions between semicircular canals and
gravireceptors. In Busby DE (ed): Recent Advances in Aerospace Medicine. Dordrecht, Holland, Reidel, 1970, pp 249261
4. Dell'Osso LF, Daroff RB:Congenital nystagmus waveforms and
foveation strategy. Doc Ophthalmol 29155-182, 1975
5. Dichgans J, Reutern GMV, Rommelt U: Impaired suppression
of vestibular nystagmus in cerebellar and non cerebellar patients. Arch Psychiatr Nervenkr 226:183-199, 1978
6. Forssman B: A study of congenital nystagmus. Acta Otolaryngol
571427-449, 1964
7. Forssman B: Vestibular reactivity in cases of congenital nystagmus and blindness. Acta Otolaryngol 57:539-555, 1964
8. Gresty MA, Hess K, Leech J: Disorders of the vestibulo-ocular
reflex producing oscillopsia and mechanisms compensating for
loss of labyrinthine function. Brain 100:693-716, 1977
9. Halmagyi GM, Gresty MA: Clinical signs of visual vestibular
interaction. J Neurol Neurosurg Psychiatry 42:931-939, 1979
10. Suzuki J-I: A study of pendular nystagmus. Acta Otolaryngol
53:381-390, 1961
11. Yee RD, Baloh RW, Honrubia V, Young S K A study of congenital nystagmus: vestibular nystagmus. J Otolaryngol 10:8998, 1981
Без категории
Размер файла
688 Кб
vestibular, reflexes, nystagmus, congenital, assessment, ocular
Пожаловаться на содержимое документа