Neuro ophthalmological symptoms in vertigo and dizziness by jennyyingdi


									B-ENT, 2008, 4, Suppl. 8, 15-22

Neuro-ophthalmological symptoms in vertigo and dizziness
C. Van Nechel
Neuro-ophthalmological Unit, Erasmus University Hospital, Brussels
Neurological Department, Brugmann University Hospital, Brussels.
I.R.O.N., Paris

Key-words. Dizziness; vertigo; vestibular function tests; nystagmus; diplopia

Abstract. Neuro-ophthalmological symptoms in vertigo and dizziness. The vestibular and visual systems are closely
linked in the genesis of vertigo and dizziness. An examination of these two systems is helpful in the search for an
aetiological diagnosis. In ENT, this double approach can also help to avoid certain ophthalmological pitfalls such as the
mistaken idea that a squint cannot be of vestibular origin, that the absence of diplopia symptoms is enough to exclude
any recent oculomotor paresis, or even that eyelid asymmetry is not relevant to diagnosing dizziness.
This paper is intended to help in understanding the neuro-ophthalmological aspects of the guidelines. It is sometimes
limited to defining certain terms. However, on the whole, it covers diagnostic procedures.

1. Skew deviation and vertical           labyrinth to the eye muscles,               Let us remember that an ocular
diplopia of vestibular origin            through the vestibular nuclei and        misalignment does not necessarily
                                         the mesencephalic nuclei of Cajal,       imply diplopia. Monocular ambly-
A vertical diplopia (one image           can provoke a vertical misalign-         opia, alternating fixation or, para-
above the other) may be the con-         ment with torsion of the eyes and        doxically, a significant angle
sequence of a lesion in the              vertical diplopia if the patient has     between the ocular axes can
vestibular system, including a           binocular vision. This vertical          eliminate the diplopia. A contro-
lesion restricted to the labyrinth.      misalignment with torsion of the         lateral head tilt with a normal
The otolithic system contributes to      eyes consecutive to a lesion of the      counter-rolling reflex can also
the control of vertical eye move-        vestibular system is called “skew        sometimes counteract vertical
ments and alignment. In mammals          deviation”. The lower eye is             diplopia.
with lateral vision, a head tilt         ipsilateral to a labyrinthic or             There are two simple ways of
induces an upper movement of the         vestibular nucleus lesion, and           detecting ocular misalignment.
ipsilateral eye and a lowering of        contralateral to a lesion located        The first one consists of observing
the contralateral eye. The modifi-       higher on the otolithic pathways.        the reflection of a lamp in both
cation of eye-muscle implantation        The impairment of the otolithic          pupils. The position of this reflec-
associated with the shift to frontal     system means that this skew devi-        tion should remain relatively sta-
vision added a torsional (ocular         ation is often combined with a           ble during gaze deviations. The
rotation around the visual axis)         spontaneous head tilt, body latero-      second consists of placing a
action to the vertical muscles. So a     deviation and an error in the esti-      coloured filter in front of one of
head tilt in humans induces a tor-       mation of the visual vertical. This      the patient’s eyes. To exclude an
sional movement of both eyes             complete otolithic syndrome is           eye misalignment, we check that
with an amplitude of a few               called “Ocular Tilt Reaction”            the patient does not see two
degrees, the “counter-rolling            (OTR).1                                  different points in binocular vision,
reflex”. Normally, this reflex does         Horizontal diplopia is never a        while one point is indeed seen when
not result in any vertical misalign-     consequence of a direct lesion of        we hide each eye. This last method
ment between the eyes because of         the vestibular system. However, it       can lead to some false positive
accurate balance in the antagonist       can result from impaired struc-          results when there is phoria or a
vertical eye muscles. A dysfunc-         tures very close to the vestibular       lack of binocular fusion. These two
tion in any structure associated         pathways and so contribute to the        techniques will allow for the easy
with this otolithic reflex, from the     localisation diagnosis.                  detection of a vertical diplopia.
16                                                                                                     Van Nechel

2. Nystagmus                               essence, organised at the level        commanding ocular muscles.
                                           of the pons. It is at this level       When a nystagmus of this kind
This paper will not provide details        that we find the abducens              is binocular and conjugate, it is
about the most likely localisations        nucleus (VI), the starting point       generally caused by a failure of
depending on the manifestations            for the stimulation of the             the integrator of the horizontal
of all the different types of nystag-      lateral rectus muscle and the          and vertical eye movements
mus. Several syntheses of the              ascending pathway (medial              and always corresponds to a
contribution of nystagmus to               longitudinal fasciculus) which         central lesion. However, it
this localisation diagnosis are            stimulates the motoneurons of          should be kept in mind that the
available.2,3 From the physiopatho-        the medial rectus muscle at the        first cause of this failure is
logical point of view, it should be        level of the common oculomo-           associated with medication
remembered that, although there            tor nucleus. Oculomotor nuclei         (psychotropic, anti-epileptic).
are three mechanisms responsible           responsible for vertical and tor-
for nystagmus, only the first is of        sional eye movements are            c) Nystagmus caused by visuo-
vestibular origin.                         located higher in the brain-           motor-loop impairment
                                           stem, at the level of the mid-         Eye fixation and pursuit result
a) Nystagmus associated with               brain. As a result, nystagmus of       from the permanent correction
   impaired        vestibulo-ocular        central origin associated with a       of the position of the eyes to
   reflex                                  lesion situated at the brainstem       compensate for retinal slip. A
   These deficits are characterised        input level in the vestibular          change in the associated feed-
   by both eyes being “pulled in           pathways        (ponto-medular         back loops can induce ocular
   one direction”, with this move-         level) will be horizontal or –         oscillation or drift. The impair-
   ment corresponding to the slow          less frequently – vertical,            ment of these loops can affect
   phase of the nystagmus. This            whereas a lesion at the mesen-         both perception and motor ele-
   direction depends directly on           cephalic level will usually            ments. This group includes
   the site of the lesion. The plane       result in vertical, torsional and      congenital            nystagmus,
   orientations of the semicircular        – rarely – horizontal binocular        acquired pendular nystagmus
   canals are close to those of the        nystagmus.                             and non-nystagmic eye fixa-
   oculomotor muscles. Each                                                       tion instabilities (square waves
   canal has a privileged relation      b) Nystagmus resulting from               and ocular flutter, opsoclonus).
   with the muscle that moves the          inability to maintain one or
   eye in a direction opposite to          both eyes in an eccentric posi-     3. Vestibulo-ocular inhibition
   the head movement stimulating           tion
   that canal. Ocular muscle               Here, elastic elements try to       This is usually evaluated with
   implantation precludes a pure-          return the eye to the primary       electro-nystagmography or video
   ly vertical eye movement                position, resulting in the slow     nystagmography but it can be also
   through the stimulation of a            phase of the nystagmus, which       clinically tested by asking patients
   single vertical muscle. The             will therefore change direction     to stretch out their arms in front of
   movement will always be                 according to the position of        them and to look at their thumbs
   around a vertical axis associated       eyes. Accordingly, there will       while rotating the head and the
   with a torsional movement of            be right horizontal nystagmus       arms “together”. Any inability to
   the eyeball. It is reasonable           when looking to the right, left     maintain the gaze on the thumbs is
   to assume that this association         nystagmus in left gaze, up-beat     easily detected by the appearance
   excludes the possibility of nys-        nystagmus when looking up,          of a nystagmus during the rota-
   tagmus with a purely vertical           and down-beat nystagmus in          tion. The diagnosis of a deficit in
   or rotatory slow phase caused           the reverse gaze direction.         the inhibition of the vestibulo-
   by a unilateral peripheral              The inability to maintain one       ocular reflex is not always correct.
   lesion. At the central level it is      or both eyes in an eccentric        It should be remembered that this
   necessary to keep clearly in            position can result from a mus-     immediate inhibition results from
   mind that the conjugate hori-           cular paresis or a weakness         the genesis of another eye move-
   zontal eye movements are, in            of the neurological structures      ment in the opposing direction but
Neuro-ophthalmological symptoms in vertigo and dizziness                                                           17

at a speed identical to the slow        factors (obstacles, escalators).         tic correction in astigmatism,
phase of the vestibulo-ocular nys-      And secondly by allowing sub-            there may be interference with
tagmus.3 At the speeds usually          jects to estimate their own stabili-     space perception and particularly
tested, a pursuit movement can-         ty. This is done by analysing the        of the orientation of vertical or
cels the slow phase of the nystag-      movement of the projections on           horizontal lines.
mus. The inhibition will therefore      the retina of fixed visual targets,         If subjects can estimate their
be impaired if the pursuit system       or by measuring the eye move-            own stability by analysing the eye
is failing. A central lesion could      ments necessary to stabilise this        movements required to stabilise
very well spare this system of eye      projection on the retina. All the        the image on the retina, it is clear
pursuit. The correct interpretation     factors that may interfere with the      that any paresis of an ocular mus-
is therefore that a deficit in          movement of the projection of            cle or any modification in eye
vestibulo-ocular reflex inhibition      fixed visual targets on the retina       motility may induce vertigo symp-
signals a central lesion but the        may therefore affect the ability of      toms.
opposite is not necessarily true.       subjects to estimate their stability
The preservation of normal inhibi-      on the basis of visual information.      6. Ocular saccade impairments
tion does not indicate that the         The most common disruptive ele-
deficit is of labyrinthic origin.       ments include the prismatic effect       Two types of ocular saccade
                                        of lenses, any drastic modification      abnormalities are particularly sig-
4. Tilt of the visual fields (room      of refraction, for example after cata-   nificant for dizziness: saccade
tilt illusion)                          ract surgery, or ocular instabilities    hypermetria and the slowing of
                                        associated with abnormal eye             the vertical saccades.
Patients perceive a rotation, often     movements.
of 90 or 180 degrees, of the visual        Multifocal lenses merit particu-      a) Saccade hypermetria
fields with both eyes. This rotation    lar attention. The correction they          Saccades are fast and precise
can occur in the three spatial          bring about changes with the ver-           movements. These two charac-
planes. They are usually brief and      tical direction of the gaze. The            teristics make them particular-
found most commonly in brain-           prismatic effect, in other words the        ly sensitive to dysfunction in
stem4 or cerebellar infarcts, in cor-   deviation of light rays caused by           several structures of the brain-
tical lesions – more particularly       the curvature of the glasses, also          stem. In particular, lesions in
during vestibular epilepsies – but      varies according to the vertical            the cerebellar system will
also in peripheral lesions.5 They       position of the eyes. This modifies         impair the precision and some-
are a consequence of the faulty         the amplitude of the compen-                times also the speed of the sac-
integration of visual and otolithic     satory eye movement for a head              cades. This loss of saccade pre-
information. This visual tilt is        movement (vestibulo-ocular gain)            cision will appear as saccade
rarely present simultaneously with      as a function of the vertical posi-         amplitudes that are either too
abnormalities of the subjective         tion of the eyes. In other words,           weak (hypometric) or too
visual vertical line because the lat-   the same 10-degree movement of              strong (hypermetric). Although
ter is of otolithic origin and can be   a visual target will require the eye        dysfunctions in many struc-
corrected by adequate visual            to turn more than 10 degrees when           tures involved in saccade pro-
information.                            focusing for close vision, and less         gramming        can      produce
                                        than 10 degrees when focusing for           hypometria, saccade hyperme-
5. Visual symptoms associated           remote vision. The stabilisation of         tria is almost specific to lesions
with an improvement in visual           the visual environment and the              of the cerebellar vermis. Other
refraction                              estimation of subject stability             median cerebellar structures
                                        from fixed visual targets therefore         control vestibulo-ocular reflex
Vision contributes to balance           becomes much more complex                   gain and play an essential role
through two mechanisms. Firstly         because the analysis has to change          in balance. Hypermetric sac-
through the analysis of the content     for every vertical position of the          cades against a background of
of the visual fields, by extracting     eyes. Although a lot of subjects            vertigo or dizziness are there-
vertical or horizontal references       quickly adapt, others never do.             fore strongly suggestive of the
and anticipating destabilisation           Similarly, when there is a dras-         presence of a cerebellar
18                                                                                                       Van Nechel

     syndrome. For mechanical rea-         near the otolithic afferences of     to the position of the head with
     sons associated with the orbit,       oculomotor nuclei. When the          regard to the trunk, and the different
     the probability of detecting          vertical eye misalignment            segments of the body in space.
     hypermetric saccades is dou-          related to the otolithic deficit     Cervical somaesthetic informa-
     bled when we test the precision       is clear in the acute phase, the     tion, cutaneous, muscular and
     of centripetal saccades, in           slowing of the vertical saccades     articular data are therefore needed
     other words when the gaze             may be the only remaining            to estimate the orientation of the
     moves from an eccentric posi-         sign several months after            physical vertical axis correctly.
     tion, returning to the primary        the sub-thalamic lesion. This           The SVV relates only to the
     position. Clinical diagnosis          deficit is easily highlighted by     visual representation of the verti-
     involves asking patients to tar-      simply asking the patient to         cal axis and is measured in the
     get alternately one finger situ-      switch as quickly as possible        absence of any visual reference. It
     ated     between     20     and       between two targets (for exam-       seems particularly dependent on
     30 degrees laterally and the          ple the index fingers of the         the position of the head in space
     second situated in front of           examiner) located one above          and does not seem to be very sen-
     them. The clinician will look         the other.                           sitive to variations in the position
     for the eyes overshooting each                                             of the cervical column or the body
     target, followed by a corrective   7. The subjective visual vertical       [data submitted for publication].
     saccade. These hypermetric                                                 In binocular measurements, the
     movements are easily recog-        The subjective visual vertical          SVV is less sensitive to eye tor-
     nisable on saccade recordings      (SVV) of a subject is the angle         sions induced by oculomotor
     in so far as the saccades are      between the physical vertical line      paresis, even though a binocular
     unpredictable in terms of          (gravitational axis) and the posi-      approach can also reduce its sensi-
     amplitude and position, pre-       tion of a visual linear mark adjusted   tivity to some cases of otolithic
     venting      the    progressive    vertically by the subject. This         dysfunction. With methods of this
     improvement of precision by        SVV is probably built up on the         kind, the SVV can be considered
     anticipating saccades with the     basis of sensory vestibular, visual     to be an otolithic evaluation. The
     same amplitude.                    and proprioceptive information          SVV is frequently impaired after
                                        which include abdominal sensors.        labyrinthic lesions, lesions of the
b) Slowing of vertical saccades         Other perceptions such as the           vestibular nerve or vestibular
   A vestibular otolithic syn-          dynamic moments of inertia may          pathways in the brainstem and in
   drome is frequently the conse-       also contribute. The subjective         the cortical vestibular areas.
   quence of an ischaemic lesion        visual vertical is not an indicator        The distribution of the normal
   in the terminal territory of         of the postural vertical (the body      values obtained for binocular
   brainstem arteries. The lesion       axis when a subject thinks he/she       SVV measurements with the head
   is situated in the sub-thalamic      is vertical), because the impor-        straight using a glowing bar
   region, and extends up to the        tance of sensory information in         moving in rigorously controlled
   midbrain. This mesencephalic         the estimation of these two verti-      darkness (Vertical Test) in 81 sub-
   extension is responsible for the     cal references is different. This       jects shows a deviation greater
   otolithic syndrome, which is         explains the discrepancies found        than 2.8° in fewer than 5% of
   often associated with a slowing      between postural deviation and          normal subjects.6
   of the vertical saccades, with-      the SVV. The sensitivity of the
   out any abnormality in hori-         otolithic organs to gravity sug-        8. Visual dependence and visual
   zontal saccades. The pre-            gests that they play an essential       vertigo
   nuclear structures specifically      role in the estimation of the
   involved in the realisation of       physical vertical axis orientation.     Vision contributes to the preserva-
   vertical saccades (mesen-            Visual information may, however,        tion of balance, not only by allow-
   cephalic reticular formation         modify this perception. The effec-      ing us to detect and anticipate
   and, in particular, the rostral      tive use of these otolithic and visu-   obstacles or irregularities in the
   interstitial nucleus of the medi-    al data for postural control does       ground but, in particular, by sup-
   an longitudinal fasciculus) are      indeed imply a correction relative      plying vertical and horizontal
Neuro-ophthalmological symptoms in vertigo and dizziness                                                             19

references which contribute to the       at least 2 Hz and greater than           consciousness level. However,
adjustment of our perception of          120°/second, which exceeds the           clinical practice suggests that the
the physical vertical. Finally,          limits at which it is possible to        link between vertigo and migraine
movements in the projections of          prevent compensation with antici-        is much more frequent, being
fixed visual targets on the retina,      patory slow eye movements and            found outside the group of
or the eye movements needed to           catch-up saccades.                       patients who fulfil these criteria,
stabilise this projection, allow us         The subjects are asked to iden-       and that vertiginous monosympto-
to estimate and therefore correct        tify symbols or letters on a visual      matic aura is common.
our own stability. Problems arise        acuity chart. This is continued on          Neuhauser et al.10 assess the
when this visual strategy is used in     successive lines until the subject       prevalence of migrainous vertigo
circumstances where the available        misses three of the five optotypes       in patients with migraine and in
visual information is not appropri-      on a line.                               patients with vertigo according to
ate.7 If most of the visual field is        This is done under two condi-         two different diagnoses.
occupied by mobile elements, or if       tions: head stationary (static              The diagnosis of definite
all fixed visual landmarks are           binocular visual acuity - SVA),          migrainous vertigo was based on
taken away, the subject must be          and with the head being passively        the following criteria:
able to disregard this visual infor-     rotated sinusoidally, 15° from cen-
                                                                                  1. Episodic vestibular symptoms
mation and use vestibular or             tre to the left and right, to the beat
                                                                                     of at least moderate severity
somaesthetic information more to         of a metronome at 2 Hz (dynamic
                                                                                     (rotational vertigo, other illu-
control balance. The use of visual       visual acuity - DVA).
                                                                                     sory self or object motion,
information in these conditions             A difference greater than two
                                                                                     positional vertigo, head motion
will not allow subjects to turn or       lines between SVA and DVA con-
                                                                                     intolerance, i.e., sensation of
stabilise themselves correctly in        stitutes a failure score.
                                                                                     imbalance or illusory self or
space, and often lead to a sensa-           This test has been shown to be
                                                                                     object motion that is provoked
tion of nausea as a result of the        sensitive for vestibular impair-
                                                                                     by head motion)
activation of the alarm system           ment in adults8 and children.9 The
                                                                                  2. Migraine according to the IHS
(parabrachialis nucleus - limbic         results of the study of Rine et al.9
cerebral cortex system). This per-       indicate that the clinical DVA test
                                                                                  3. At least one of the following
sistence in the use of inadequate        is a reliable and valid test of gaze
                                                                                     migrainous symptoms during
visual information can be the            stability in children, and can be
                                                                                     at least two vertiginous attacks:
result of a vestibular deficit or a      used to screen for vestibular hypo-
                                                                                     migrainous headache, photo-
loss of the ability to select an ade-    function in children as young as
                                                                                     phobia, phonophobia, visual or
quate source of sensory informa-         three years of age.
                                                                                     other auras
tion. This can persist in spite of the
                                                                                  4. Other causes ruled out by
recovery of normal vestibular func-      10. Migraine and vertigo
                                                                                     appropriate investigations
tion, when a subject has got used to
controlling balance with a visual        Vertigo has been found to occur          A separate diagnostic category of
strategy. Vestibular rehabilitation      significantly more frequently in         probable migrainous vertigo was
can be used in an attempt to help        patients with migraine than in           chosen for patients who did not
these patients regain the ability        control subjects. The international      entirely fulfil the above criteria for
to select adequate sensory infor-        classification of migraines (IHS)        migrainous vertigo but were still
mation.                                  includes the symptom “vertigo”           considered to have migrainous
                                         only as an aura of a basilar             vertigo as the most likely diagno-
9. Dynamic visual acuity                 migraine. This aura has to consist       sis.
                                         of at least two of a number of
                                                                                  The diagnosis of probable
The dynamic visual acuity (DVA)          symptoms, including: vertigo, tin-
                                                                                  migrainous vertigo was based on
test is a method for measuring the       nitus, dysarthria, binocular visual
                                                                                  the following criteria:
clinical functioning of the vestibu-     symptoms in the nasal and tempo-
lo-ocular reflex. This test mea-         ral fields, hearing loss, diplopia,      1. Episodic vestibular symptoms
sures visual acuity during hori-         ataxia, bilateral paraesthesia,             of at least moderate severity
zontal sinusoidal head rotations of      bilateral paresis or a decline of the       (rotational vertigo, other
20                                                                                                    Van Nechel

                                                      Figure 1

   illusory self or object motion,     The results of this study show           any headaches, and patients with
   positional vertigo, head motion     that the prevalence of migraine          recurring dizziness and without a
   intolerance)                        according to the IHS criteria was        history of the usual signs of
2. At least one of the following:      higher in the dizziness clinic group     migraine.
   migraine according to the cri-      (38%) compared with the age- and
                                                                                Benign paroxysmal vertigo in
   teria of the IHS; migrainous        sex-matched control group (24%,
                                                                                childhood is also included in the
   symptoms during vertigo;            p <0.01). The prevalence of
                                                                                IHS classification of migraine.
   migraine-specific precipitants      migrainous vertigo was 7% in the
                                                                                The criteria are:
   of vertigo, e.g., specific foods,   dizziness clinic group, and 9% in
   sleep irregularities, hormonal      the migraine clinic group. In 16 of      1. Episodes of vertigo or disequi-
   changes; response to anti-          33 patients, vertigo occurred both          librium without hearing loss
   migrainous drugs                    with and without headache, and in           or tinnitus
3. Other causes ruled out by           two patients headache and vertigo        2. Accompanied by visual flashing,
   appropriate investigations          never occurred together. The dura-          nausea/vomiting, pallor, agita-
                                       tion of attacks varied from minutes         tion and ataxia. Headache not a
Vestibular symptoms were defined       to days.                                    usual feature
as “mild” if they did not interfere       Moreover, Dieterich et al.11          3. First decade of life, commonly
with daily activities, “moderate”      have effectively treated migrainous         at ages of one to four years
if they interfered with but did        patients with vertiginous aura who       4. Duration: usually minutes,
not impede daily activities, and       do not fulfil the criteria for basilar      sometimes hours
“severe” if patients could not         migraine, as well as migrainous          5. Positive family history of
continue daily activities.             patients suffering vertigo without          migraine, and many develop
Neuro-ophthalmological symptoms in vertigo and dizziness                                                       21

                                                    Figure 2

   migraine with aura at older        half-light. The anhydrosis of the      pathetic fibres at the level of the
   ages                               ipsilateral hemi-face present in       cervical cord or in the pathway
6. Other causes ruled out.            CBH syndromes of central origin        along the carotid arteries. We
   Differential        diagnosis:     is not obvious. It is often transi-    should also bear in mind that a
   Ménière’s disease, vestibular      tional because it is compensated       CBH syndrome can result from a
   epilepsy, perilymphatic fistula,   by denervation hypersensitivity to     migraine crisis and this can also
   posterior fossa tumours and        circulating adrenergic substances.     lead to dizziness and vertigo.
   psychogenic disorders              The diagnosis can be confirmed
                                      by eye-drop tests from ophthal-        12. Facial sensitivity deficit
11. The    Claude        Bernard      mologists (cocaine test followed
Horner syndrome                       by the hydoxy-amphetamine test).       In the brainstem, post-synaptic
                                      At the ponto-medullar level, the       pain sensitivity fibres of the
The interruption of the orthosym-     orthosympathetic fibres pass just      trigeminal nerve extend down to
pathetic eye fibres is known as       inside the vestibular nuclei. There    the first cervical levels. They con-
Claude-Bernard-Horner syndrome        is therefore a high probability that   stitute the downward root of the
(CBH). It is characterised by ipsi-   a lesion of the vestibular nucleus     trigeminal nerve and reach the
lateral ptosis consecutive to the     is associated with CBH syndrome.       upper spinal cord. At the bulbar
denervation of the Müller superior    Only larger lesions will result        level, these fibres are situated just
eyelid muscle and also by a dis-      in the classic syndrome of             inside vestibular nuclei. They are
creet rise of the lower eyelid        Wallenberg. The presence of CBH        a part of the same vascular territo-
caused by denervation of its          signs can still indicate a central     ry as the vestibular nuclei, and are
retractor muscle. In addition this    origin months after a vestibular       irrigated by the terminal branches
syndrome includes anisocoria          deficit.                               of the antero-inferior cerebellar
with ipsilateral miosis. The aniso-      In a post-traumatic context,        artery. Other branches of the same
coria may be moderate and not         CBH syndrome can result from           artery irrigate the internal ear. A
exceed 1/2-1 mm. It is clearer in     the impairment of the orthosym-        sensory deficit of the face
22                                                                                                              Van Nechel

associated with acute dizziness       oscillations, superior   oblic                 8. Tian JR, Shubayev I, Demer JL.
indicates the presence of a lesion    myokimia and spasmus nutans.                      Dynamic visual acuity during passive
                                                                                        and self-generated transient head rota-
at the level of the floor of the
                                                                                        tion in normal and unilaterally
fourth ventricle, associated or not   An overview of abnormal eye                       vestibulopathic humans. Exp Brain
with a labyrinthic lesion. Since      movement in adults and in infants                 Res. 2002;142:486-495.
topography is inverted in this        is given in Figures 1,2.13                     9. Rine RM, Braswell J. A clinical test
downward root of the trigeminal                                                         of dynamic visual acuity for children.
nerve, it is mostly in the upper      References                                        Int J Pediatr Otorhinolaryngol. 2003;
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