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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4440_Библиотеки_им_академика_М_И_Перельмана.pdf
148
Dissociated pendular nystagmus—This is dened as two eyes
having different nystagmus.
See-saw nystagmus—It is a pendular oscillation that consists of elevation and intorsion of one eye and
depression and extortion of the fellow eye that alternates every half
cycle. It may be due to loss of the
crossed visual inputs from the
decussating bres of the optic nerve
at the level of the chiasm or lesions
in the rostral midbrain. Most patients
with acquired see-saw nystagmus
have bitemporal haemianopias consequent to large parasellar tumours
expanding to third ventricle.
Classication according to severity of nystagmus (Table3.54)
Classication according to site of
lesion—The site of lesion may
present either in peripheral vestibular system or in central vestibular
system (Table3.55).
Table 3.54 Degree (severity) of nystagmus (Alexander’s
law)
First degree
(mild)
Second degree
(moderate)
Third degree
(severe)
Table 3.55 Difference between peripheral and central
nystagmus
Characteristics Peripheral Central
Latent period 2–20s None
Duration Less than 1min More than 1min
Fatigability Yes No
Direction Fixed
Intensity of
vertigo
It is weak nystagmus, present when
looked in the direction of fast
component, but absent on looking
straight and towards slow
component
It is stronger nystagmus than
rst-degree nystagmus and present
when patient looks straight and
towards fast component but absent
towards slow component
It is strongest nystagmus present in
all directions
Directional
(unidirectional)
Severe Mild
changing
3 History andExamination ofEar
Fig. 3.75 Vertical nystagmus
Classication according to direction of nystagmus—The direction
of nystagmus decided by the fast
component of nystagmus.
Vertical nystagmus (Fig. 3.75)
Downbeat nystagmus—It is
dened as nystagmus with fast
phase in downward direction present in disorder of craniocervical
junction (Arnold-Chiari malformation) and other central lesions.
Upbeat nystagmus—It is dened
as nystagmus with fast phase in
upward direction. It is of two
types: large amplitude nystagmus
(increase in intensity on upward
gaze) suggestive of lesion in
cerebellum and small amplitude
nystagmus (decrease in intensity
on upward gaze and increase on
downward gaze) suggestive of
lesion in medulla.
Rotary/torsional nystagmus—It
is dened as rotatory movement of
globe about its antero-posterior
(AP) axis which accentuates on
lateral gaze. It appears in lesion of
anterior (superior) and posterior
semicircular canal on the same side
(lateral medullary syndrome).
Horizontal nystagmus—The sideby- side abnormal movement of eye
is known as horizontal nystagmus.
This can be right or left beating nystagmus depending on fast phase of
nystagmus. The direction is nystagmus towards fast phase or hypofunctional labyrinth (Fig.3.76).
3.2 Examination ofEar
149
Rotatory nystagmus—Torsional
(rotary) nystagmus refers to a rotary
movement of the globe about its
visual axis. A pure torsional or
rotary nystagmus is rare and indicative of a disorder of the central vestibular system.
Torsional nystagmus is typically
accentuated on lateral gaze
(Fig.3.77).
Classication of nystagmus based
on conjugacy
Conjugate—if both eyes move in
the same direction.
Disconjugate—if eyes move in different direction. This type of nystagmus is caused by disorders of
cerebellum, midbrain and brainstem.
Classication according to
physiology
Physiological nystagmus
Physiologic end point nystagmus—
when examiner tests the lateral
movement more than 30° for testing
oculomotor nerve, a horizontal jerk
nystagmus appears.
Per-rotational nystagmus—It is
horizontal jerk nystagmus resulting
from sustained head rotation with
fast phase ipsilateral to rotation.
Postrotational nystagmus—It is
reexive horizontal nystagmus that
Fig. 3.76 Horizontal nystagmus
occurs when head is suddenly
stopped during unidirectional head
movement.
Pathological nystagmus—These
are results from diseases affecting
the cortex, anterior visual tract,
brainstem, cerebellum and peripheral vestibular apparatus.
Direction of nystagmus—The
direction of nystagmus is decided
by the fast phase of nystagmus.
Right beating nystagmus
Left beating nystagmus
Upbeating nystagmus
Downbeating nystagmus
• Nystagmus in infancy—There are several
types of benign nystagmus seen in infancy.
The congenital nystagmus is the most
common infantile nystagmus followed by
latent/manifest latent nystagmus and pendular nystagmus of spasmus nutans. The
characteristics of congenital nystagmus
are as follows: it is binocular, has similar
amplitude in both eyes, is unipolar (horizontal), is diminished by convergence, is
increased by xation attempt, has superimposition of latent component, has inversion of the optokinetic reex, has
associated head oscillation and is abolished in sleep.
• Procedure to assess nystagmus—The
examiner keeps a nger at the distance of
30 cm from eyes in midline. The nger
should be moved right and left, up and
down but not more than 30° from centre.
The presence of nystagmus, type of nystagmus, direction of nystagmus, severity
of nystagmus, duration of nystagmus,
plane of nystagmus and degree of nystagmus are noted (Fig.3.78).
Fig. 3.77 Rotatory
nystagmus
150
Fig. 3.78 Procedure to elicit spontaneous nystagmus
• Type of nystagmus—peripheral or
central.
• Direction of nystagmus—It is towards the
fast component of nystagmus. In peripheral nystagmus, the fast component is
always towards hyperactive labyrinth.
• Fatigability—It is dened to be reduced
in severity with repeated positioning.
• Duration of nystagmus—It should be
noted to diagnose it is either peripheral or
central in origin.
• Plane of nystagmus
Horizontal—This is dened as involuntary rhythmic side-to-side movement of eye.
Vertical—This is dened as upward or
downward beating nystagmus.
Rotatory—This is dened as circular
beating nystagmus.
• Severity of nystagmus
First degree—If nystagmus is present
on gaze towards the fast phase only.
Second degree—Nystagmus is present
on gaze towards fast phase and
central.
Third degree—Nystagmus is present
on gaze towards all sides.
Advantage
Best results obtained soon after VS
damage.
Limitations
Cannot diagnose end organ disorder.
Spontaneous nystagmus cannot be
observed after a few days.
Cannot be used as bedside evaluation
to diagnose unilateral vestibular dysfunction without quantitative testing.
3 History andExamination ofEar
Degree and site of impairment from
the direction of spontaneous nystagmus cannot be determined due to intersubject variability and quality of
central compensation.
Only the presence or absence of spontaneous nystagmus to diagnose unilateral peripheral VS hypofunction is
unacceptable with this test; only the
presence and absence of nystagmus
can be noted.
The sensitivity for unilateral vestibular
hypofunction is less than 50%.
• Tests to induce nystagmus
Fistula test—It is a bedside vestibular
method of examination that detects
the existence of an abnormal communication between the middle and inner
ear. As described by Lucae in 1881,
when applying pressure in the external
ear, vertigo and nystagmus are elicited
and remain for a period of time. This
test is done with the help of Siegel’s
speculum (Fig.3.79). In this test, pressure in EAC increases to stimulate the
labyrinth to induce nystagmus.
Results
Negative—normal
Positive—erosion in HSCC, fenestration
operation, poststapedectomy stula,
ruptured round window membrane
False positive (Hennebert’s sign)—
Congenital syphilis, Meniere’s disease,
hypermobile stapes footplate syndrome
False negative—CSOM (cholesteatoma
seal of the stula)
Positioning test (Dix-Hallpike test)—
This is a classic manoeuvre described
to detect a posterior canal BPPV. It
causes nystagmus with the head hanging down or when switching to upright
position from lying down. This test is
3.2 Examination ofEar
151
specic for posterior canal BPPV
which precipitates the nystagmus and
dizziness.
Procedure—The examiner holds the
head of the patient and turns it 45°
towards one side, and then, patient will
be moved from sitting to supine position; afterwards, head is lowered 30°
by the side of couch. Nystagmus
should be checked. Repeat the test on
contralateral side (Fig. 3.80, Tables
3.56 and 3.57).
Pursuit movement of eyes—These are
tracking or slow eye movements used
to stabilize the image of a moving
object of interest on the fovea. Smooth
pursuit movement stabilizes the projection of the moving target onto the
fovea and corrects for any velocity
error between eye and target, i.e. for
any retinal slip. Pursuit is initially
driven by visual feedback when
responding to unexpected object
motion. However, internal (extraretinal) mechanisms rapidly take over and
sustain pursuit if object velocity is
constant.
Saccade movement of eyes—
Saccades are fast eye movements that
bring the image of an object of interest
onto the fovea. Saccadic movements
serve to realign the image if it falls outside the fovea, the area of highest acuity. They consist of a hierarchy of rapid
eye movements, from quick phases of
vestibular and optokinetic nystagmus,
to reexive saccades, to higher level
volitional saccades.
Fig. 3.79 Siegelization to perform stula test
45˚
Fig. 3.80 Procedure of the Dix-Hallpike test
30˚
152
Table 3.56 Differential diagnosis of nystagmus
Type of nystagmus Denition Diagnosis
Congenital nystagmus
Latent nystagmus It is a congenital, jerk nystagmus
with either linear or decreasing
velocity
Pendular nystagmus in infant It is either bilateral or monocular
nystagmus present in infant. It
disappears by the age of 3years
Acquired pendular nystagmus This is multivectorial (i.e.
horizontal, vertical, diagonal, elliptic
or circular) nystagmus and usually is
associated with a head tremor.
Marked dissociation between the
two eyes often exists
Horizontal jerk nystagmus It is a horizontal- torsional or purely
horizontal primary- position jerk
nystagmus with a linear slow phase.
It has two phases, slow and fast
Downbeat jerk (beating) nystagmus It is dened as nystagmus gaze
position with the fast phase beating
in a downward direction
Downbeat nystagmus Spontaneous upward drift of the
eyes, slow phase waveform may
have constant decreasing or
increasing velocity
Upbeat nystagmus Spontaneous nystagmus with
downward slow phase
Upbeating torsional (rotatory) jerk
nystagmus
Gaze-evoked nystagmus It is elicited by the attempt to
Physiological nystagmus
Pendular nystagmus It has sinusoidal oscillation, and
See-saw nystagmus It is characterized by a conjugate,
Sea saw nystagmus (jerk) Disconjugate vertical torsional
Slow phase directed downwards
with torsional component in which
the upper pole of the eyes rotates
away from affected ear
maintain an eccentric eye position,
and it is the most common. It is
typically horizontal
may have complex waveform that
includes horizontal, vertical and
torsional component
pendular, torsional oscillation with a
superimposed disjunctive vertical
vector
nystagmus; during each cycle, one
eye moves upwards and intort, while
other moves downward and extort
3 History andExamination ofEar
Retrolental broplasia
Spasmus nutans
Brainstem or cerebellar lesion
Vestibular lesion
Cerebellar occulus lesion
Brainstem disease
Arnold-Chiari malformation
Drug intoxication
Spinocerebellar degeneration
Alcohol, B12 def
Mg def, Li toxicity
Lesion of vestibulocerebellum or its
pathway
Focal lesion of medulla or
cerebellum
Cerebellar degeneration
Wernicke’s encephalopathy
BPPV due to posterior SCC
MS, Whipple disease
Oculopalatal tremor syndrome
Severe visual loss
Large parasellar tumour extending
to third ventricle
Midbrain stroke
Parasellar mass
Congenital
M.S.
(continued)
3.3 Causes ofVertigo
Table 3.56 (continued)
Type of nystagmus Denition Diagnosis
Convergence retraction nystagmus Fast divergent movements followed
by a slow convergence
Periodic alternating nystagmus It is a horizontal jerk nystagmus that
periodically changes directions
every 2min
Rebound nystagmus It is either the diminution and
directional change of gaze-evoked
horizontal nystagmus during
sustained ocular deviation or a
horizontal gaze-evoked nystagmus
that, on rexation to primary
position, transiently beats in the
opposite direction
Muscle- paretic (myasthenic)
nystagmus
Bruns nystagmus Horizontal nystagmus beating
A paretic eye muscle, from whatever
cause, can fatigue quickly during
contraction, and muscle- paretic
nystagmus can be observed
contralateral to the lesion when
looking away from lesion, then a
beating ipsilateral, gaze-evoked
nystagmus (if tumour compresses
the brainstem)
Dorsal midbrain syndrome
Intraventricular haemorrhage
Lesion of vestibulocerebellum with
either occulus/paraocculus
Cerebellar disease
Myasthenia gravis
Acoustic neuroma
Extra-axial mass (cerebellar tumour)
153
Table 3.57 Examination ndings and diagnosis
Examination nding Diagnosis
The Dix-Hallpike test shows paroxysmal upbeat,
horizontal or downbeat torsional nystagmus
Spontaneous unidirectional, predominantly horizontal,
nystagmus
Gaze-evoked directional changing nystagmus Posterior fossa lesion
Skew deviation Posterior fossa lesion
Facial palsy and vesicle in EAC Ramsay Hunt syndrome
Asymmetric hearing loss Meniere’s disease, vestibular schwannoma
3.3 Causes ofVertigo
BPPV, involving posterior, horizontal or superior
semicircular canal, respectively
Acute peripheral vestibulopathy, vestibular neuronitis,
labyrinthitis
vestibulopathies (B/L vestibulopathies, uncompensated U/L vestibulopathy).
Acute vestibular syndrome—Patients with AVS
present with more than 24h of continuous vertigo (lasting days to weeks and monophasic) with
nausea/vomiting, imbalance, head motion intolerance, spontaneous nystagmus. The causes are
acute labyrinthitis, stroke, Ramsay Hunt syndrome, demyelinating diseases, U/L vestibulopathy (Fig.3.81).
Chronic vestibular syndrome—Patients
with CVS have constant vestibular symptoms for
weeks to years (e.g. bilateral vestibular loss). The
causes are stroke, PPPD, central vestibular lesion,
Episodic vestibular syndrome—Patients
with EVS have similar symptoms and signs such
as AVS, lasting seconds to hours (e.g. Meniere’s
disease, VM).
Causes of episodic vestibular syndrome
(provoked) (Table 3.58)
Causes of episodic vestibular syndrome
(unprovoked) (Table 3.59 and Fig.3.82)
Approach to tinnitus (Fig. 3.83)
Approach to patient with tinnitus to differential diagnosis (Table 3.60, Figs. 3.84, 3.85,
and 3.86)
154
3 History andExamination ofEar
Fig. 3.81 Approach to a patient with acute vestibular syndrome
Table 3.58 Causes of episodic vestibular syndrome
(provoked)
Provoked nystagmus Causes
Head motion/visual Central vestibular lesion
Peripheral vestibular lesion
Position Central positional
Peripheral positional (BPPV)
Head turn Rotational vertebral syndrome
Vestibular paroxysmia
Hyperventilation Vestibular paroxysmia
Orthostatic Orthostatic hypotension
Valsalva Vasovagal
SCDS
Sound Perilymph stula
Evaluation of tinnitus
3.3 Causes ofVertigo
Table 3.59 Causes of episodic vestibular syndrome (unprovoked)
Isolated vertigo Non-isolated vertigo
Hypoglycaemia
Vasovagal
Arrhythmia
Epilepsy
TIA
Drop attack Auditory Vegetative Neurogenic Anxiety
Meniere’s
disease
Arrhythmia
Epilepsy
Vestibular
paroxysmia
Meniere’s
disease
Vestibular
Meniere’s
disease
Vestibular
migraine
TIA
migraine
TIA
Vestibular
migraine
TIA
155
Panic attack
Fig. 3.82 Algorithm of approach to cause differential diagnosis of vertigo
Tinnitus
Duration
Acute < 3 weeks
H/O Noise exposure, head neck
Otitis media, Ototoxic medication
Examine for wax, TMJ, Head
neck, Ear, Neurologic deficiet
trauma
Investigations
Treat the
cause
Suspect
Arterial
lesions
MRI, CT
angiogram
Vascular lesions
Arterial lesion or
Venous lesion
Suspected venous
lesions
Venogram
Ye s
Meniere
disease
Ye s
Non vascular lesions
Palatal myoclonus
Tensor tympani
Stapedial myoclonus
Intermittent hearing loss
myoclonus
Chronic > 3 weeks
No -
Pulsatile tinnitus
Cholesteatoma
Fig. 3.83 Evaluation of tinnitus
Abnormal ear
findings
Wax
CSOM
Abnormal hearing
Unilateral
Vestibular
schwannoma
No
Normal ear findings
Bilateral -
Presbyacusis
dysfuntion
Normal
hearing
TMJ
156
Table 3.60 Grades of dysplasia of pinna
Grade of dysplasia Subgroup
First-degree
malformation
Second-degree
malformation
Third-degree
malformation
Prominent ear, macrotia, cryptotia or pocket ear, coloboma, Satyr ear
Slight deformities (absent crus of helix, Darwin tuberculum, deformity of tragus)
Deformities of lobe (xed lobe, aplasia, hypoplasia, cleft)
Cup ear deformity type 1, type 2A and type 2B
Cup ear deformity type 3
Mini-ear (hypoplasia of upper pinna, hypoplasia of middle pinna and hypoplasia of lower
pinna)
Unilateral microtia Grade 3, B/L microtia Grade 3, anotia
3 History andExamination ofEar
Fig. 3.84 Approach to differential diagnosis in a patient of tinnitus
3.3 Causes ofVertigo
Fig. 3.85 Approach to a patient with pulsatile tinnitus
157
Fig. 3.86 Approach to causes of prelingual deafmute child