Vertigo – from a neurologist’s point of view

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Transcript Vertigo – from a neurologist’s point of view

Vertigo – from a neurologist’s
point of view
Tung-Hua Chiang M.D.
Department of Neurology
Cheng-Ching General Hospital
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 Dizziness
and other sensations of imbalance are,
along with headache, back pain, the most frequent
complaints among medical outpatients (Kroenke
and Mangelsdorff).
 For the most part they are benign, but always there
is the possibility that they signal the presence of an
important neurologic disorder.
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 Diagnosis
of the underlying disease demands that
the complaint of dizziness be analyzed correctly the nature of the disturbance of function being
determined first, and then its anatomic localization
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“Vertigo” should be correctly defined
 “Dizziness”
: a feeling of rotation or whirling as
well as nonrotatory swaying, weakness, faintness,
light-headedness, or unsteadiness.
 “Vertigo” : subjective and objective illusions of
motion
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Mechanisms responsible for the
maintenance of a balanced posture
 Continuous
afferent impulses from the eyes,
labyrinths, muscles, and joints
 The adaptive movements necessary to maintain
equilibrium are carried out - at a reflex level.
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Afferent impulses (1)

Visual impulses from the retinas and possibly
proprioceptive impulses from the ocular muscles.
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Afferent impulses (2)



Impulses from the labyrinths, the three
semicircular canals sense angular acceleration of
the head, and the saccular and utricular maculae
sense linear acceleration and gravity
Vestibulo-ocular reflex - stabilizes the eyes
Vestibulo-spinal reflex - stabilizes the position of
the head and body
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Afferent impulses (3)
 Impulses
from the proprioceptors of the joints and
muscles, which are essential to all reflex, postural,
and volitional movements.
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 All
connected with cerebellum and certain
ganglionic centers and pathways in the brainstem,
particularly the vestibular nuclei, and, via the
medial longitudinal fasciculi, with the red and
ocular motor nuclei.
 Any disease that disrupts these neural mechanisms
may give rise to vertigo
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Cerebral cortical lesion
 vertigo may constitute the aura of an epileptic
seizure
 electrical stimulation of the cerebral cortex
(posterolateral aspects of the temporal lobe,
inferior parietal lobule, adjacent to the sylvian
fissure) may evoke intense vertigo
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Vertiginous epilepsy vs Vestibulogenic seizures
 Vestibulogenic seizures : an excessive vestibular
discharge serves as the stimulus for a seizure - a
rare form of reflex epilepsy
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Ocular motor disorders
 abrupt onset of ophthalmoplegia with diplopia - a
source of spatial disorientation and brief sensations
of vertigo (maximal : when looks in the direction
of action of the paralyzed muscle; receipt of two
conflicting visual images)
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Cerebellum
 depend on which part of this structure is involved
 large, destructive processes in the cerebellar
hemispheres and vermis may cause no vertigo
 lesions involving the territory of the medial branch
of the PICA may cause intense vertigo,
indistinguishable from that due to labyrinthine
disorder.
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 Infarction
extended to the midline and involved the
flocculonodular lobe : falling toward the side of
the lesion; nystagmus was present on gaze to each
side but was more prominent on gaze to the side of
the infarct
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Labyrinthine disease
 unidirectional nystagmus to the side opposite the
impaired labyrinth and swaying or falling toward
the involved side, direction of the nystagmus is
opposite to that of the falling and past pointing
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Cervical vertigo
 Biemond and DeJong
 originating in the upper cervical roots and the muscles and
ligaments that they innervate
 Spasm of the cervical muscles, trauma to the neck, and
irritation of the upper cervical sensory roots are said to
produce asymmetrical spinovestibular stimulation and
thus to evoke nystagmus and prolonged vertigo, and
disequilibrium.
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 Downbeat
nystagmus, vertigo and postural
instability have been observed with paramedian
lesions at the craniocervical junction.
 Upbeat nystagmus with oscillopsia and vertigo has
been traced to two separate brainstem lesions : one
in the perihypoglossal nuclei and the other in the
pontomesencephalic tegmentum (Brandt)
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 Cervical
vertigo has also been attributed to VBI
 Occasionally, vertigo lasting a few minutes occurs
as a prelude to a basilar migraine headache (Grad
and Baloh).
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Meniere disease
 Recurrent
attacks of vertigo associated with
fluctuating tinnitus and deafness.
 Meniere disease affects the sexes about equally
and has its onset most frequently in the fifth
decade of life, although it may begin earlier or later.
 Usually sporadic, but rare hereditary forms, both
AD AR
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 The
main pathologic change : increase in the
volume of endolymph and distention of the
endolymphatic system (endolymphatic hydrops)
 Paroxysmal attacks of vertigo : ruptures of the
membranous labyrinth and a dumping of
potassium-containing endolymph into the
perilymph, which has a paralyzing effect on
vestibular nerve fibers and leads to degeneration of
the delicate cochlear hair cells
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 A small
proportion of patients with Meniere
disease experience sudden, violent falling attacks :
"otolithic catastrophe of Tumarkin," : deformation
of the otolithic membrane of the utricle and
saccule. Consciousness is not lost
 An initial attack must be distinguished from other
types of drop attacks, occurrence of more typical
vertiginous attacks with deafness and tinnitus,
clarify the diagnosis.
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 The
hearing loss in Meniere disease usually
precedes the first attack of vertigo
 There is frequently a decrement in hearing with
each attack; hearing may improve after a few hours,
but later the loss becomes irreversible
 Early : low tones; Later : high tones
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 The
attacks of vertigo usually cease when the
hearing loss is complete.
 Sensorineural type of deafness
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 During
an acute attack of Meniere disease, rest in
bed is the most effective treatment
 Destruction of the labyrinth should be considered
only in patients with strictly unilateral disease and
complete or nearly complete loss of hearing.
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 Bilateral
disease or significant retention of hearing,
the vestibular portion of the eighth nerve can be
sectioned or decompressed (by separating the
nerve from an aberrant vessel).
 Endolymphatic-subarachnoid shunt is the
operation favored by some surgeons
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Vestibular Neuronitis (Neuropathy)
 Originally
by Dix and Hallpike
 Disturbance of vestibular function, paroxysmal and
usually single attack of vertigo and absence of
tinnitus and deafness.
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 Mainly
in young to middle-aged adults, equal sex.
 Antecedent URI
 Examination discloses vestibular paresis on one
side
 Nystagmus (quick component) and sense of body
motion are to the opposite side, whereas falling
and past pointing are to the side of the lesion.
 Auditory function is normal.
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 A benign
disorder.
 The severe vertigo subside in several days, but
lesser degrees of these symptoms, made worse by
rapid movements of the head, may persist for
several weeks.
 In some patients there has been a recurrence
months or years later.
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 Primarily
affected the superior part of the
vestibular nerve trunk, which was observed to
show degenerative changes
 The cause is uncertain, may be a viral infection,
many neurologists prefer the term vestibular
neuropathy.
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Other Paroxysmal Vertigo
 A single
abrupt attack of severe vertigo, nausea,
and vomiting without tinnitus or hearing loss, with
permanent ablation of labyrinthine function on one
side -> suggested occlusion of the labyrinthine
division of the internal auditory artery;
Labyrinthine hemorrhage has been demonstrated
by MRI in some of these patients.
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In childhood : good health, sudden onset of brief vertigo,
pallor, sweating, and immobility, and occasionally
vomiting and nystagmus.
 Recurrent but tend to cease spontaneously after a period of
several months or years
 Impairment or loss of vestibular function, bilateral or
unilateral, frequently persisting after the attacks have
ceased. Cochlear function is unimpaired.
 Unknown pathologic basis

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Young adults in which a nonsyphilitic interstitial keratitis
is associated with vertigo, tinnitus, nystagmus, and rapidly
progressive deafness.
 The prognosis for vision is good, but the deafness and loss
of vestibular function are usually permanent.
 Unknown cause and pathogenesis
 Half of the patients later develop aortic insufficiency or a
systemic vasculitis that resembles polyarteritis nodosa.

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 There
are many other causes of aural vertigo, such
as purulent labyrinthitis complicating meningitis,
serous labyrinthitis due to infection of the middle
ear, "toxic labyrinthitis" due to intoxication with
alcohol, quinine, or salicylates, motion sickness,
and hemorrhage into the inner ear.
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 Head
trauma, cerebral concussion or whiplash
injury, vertigo due to loosening or dislodgement of
the otoconia in the otoliths.
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Thanks!
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