Transcript Vertigo - Southern Neurology

Vertigo
Southern Neurology
Dizziness – is it vertigo ?
Is the dizziness is vertiginous in nature, or more
suggestive of near-syncope or non-vestibular dizziness
Is the dizziness is affected by movements of the head,
if so it suggests a peripheral vertigo
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a patient with peripheral acute vertigo often
prefers to sit upright and not lie down, or prefers to lie
still with the unaffected ear undermost; and the patient
also prefers to avoid any sudden head movements
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a patient with central vertigo often has a lesser
degree of dizziness, which is less affected by head
movements and not specifically related to a particular
head position
Dizziness and head movement
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Vertigo lasting seconds, which is only precipitated
by sudden movements of the head (looking up,
suddenly twisting the head, suddenly getting up from a
supine position or when suddenly rolling over in bed)
suggests benign positional vertigo
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a patient with benign positional vertigo may be
able to identify a particular movement or position of
the head that precipitates vertigo, which usually occurs
after a latent period of 10 - 20 seconds
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patients with BPV may complain of non-specific
nausea, dysequilibrium and dizziness between attacks
Dizziness – duration assists
differential diagnosis
The duration of the vertigo provides useful information
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vertigo lasting seconds suggests benign
paroxysmal positional vertigo
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vertigo lasting minutes suggests transient
cerebrovascular ischaemia (posterior circulation TIA)
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vertigo lasting hours suggests Meniere's
syndrome
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vertigo lasting hours-days suggests vestibular
neuronitis or posterior circulation strokes
Dizziness and otological
symptoms
Deafness and/or tinnitus suggests peripheral vertigo
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Many patients with vestibular neuronitis have a
history of a recent viral illness in the past few weeks.
Otological symptoms in a patient with acute vestibular
neuronitis suggests acute (serous) labyrinthitis
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Recent severe earache +/- ear discharge +/- fever
suggests a middle ear infection and a possible acute
(purulent) labyrinthitis
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Recent head trauma, sudden coughing/sneezing +
sudden 'pop' in the ear, or recent scuba diving suggests
a possible peri-lymphatic fistula (vertiginous symptoms
may also be exacerbated by valsalva-type maneuvers or
a loud noise)
Benign positional vertigo theory 1
Cupulolithiasis theory
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In 1962, Dr Harold Schuknecht proposed the cupulolithiasis
(heavy cupula) theory. Via photomicrographs, he discovered
basophilic particles or densities that were adherent to the
cupula. He postulated that the PSC was rendered sensitive to
gravity by these abnormal dense particles attached to, or
impinging on, the cupula. This is analogous to the situation of
a heavy object attached to the top of a pole. The extra weight
makes the pole unstable and thus harder to keep in the neutral
position. This produces persistent nystagmus and also explains
the dizziness when a patient tilts the head backward.
Benign positional vertigo theory 2
Canalithiasis theory
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In 1980 Epley published his canalithiasis theory. He believed
that the symptoms of BPPV were more consistent with freemoving densities (canaliths) in the PSC rather than fixed
densities attached to the cupula. While the head is upright, the
particles sit in the PSC at the most gravity-dependent position.
When the head is tilted back supine, the particles are rotated
up to about 90 degrees along the arc of the PSC. After a
momentary (inertial) lag, gravity pulls the particles down the
arc. This causes the endolymph to flow away from the ampulla
and causes the cupula to be deflected. The cupular deflection
produces nystagmus.
Benign positional vertigo epidemiology
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In one U.S. study, the age- and sex-adjusted incidence was 64
per 100,000. Incidence in general population is higher in
persons older than 40 years. In a recent study of a group of
elderly patients, the incidence was found to be approximately
8%. BPPV may represent a health hazard to the elderly.
Estimates suggest that approximately 20% of all falls that
result in hospitalization for serious injuries in the elderly are
due to vertigo of end-organ origin (most often related to
BPPV).
Average age of onset 51 years. M=F, although some studies
show a slight predilection for women.
It is rarely seen in persons younger than 35 years without a
history of antecedent head trauma.
Causes of BPV –in a study of 240
patients
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Idiopathic – 118 cases
Posttraumatic – 43 cases
Viral neurolabyrinthitis – 37 cases
Other
–
VBI 11 cases
Meniere’s disease 5 cases
Post-surgical 10 cases (including
5 ear surgery)
Ototoxicity 4 cases
Nystagmus
Central
Peripheral
Appearance
Latency
Duration
Fatigability
Localisation
Pure vertical,
usually downbeat
Unusual
Persistent
Unusual
Brainstem or
cerebellum
Torsional upbeat or
horizontal
geotropic
Usual
Brief
Usual
Posterior or
horizontal semicircular canal
Epley manouevre
Exercise therapy at home
Horizontal and anterior canal BPV
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Vast majority are due to posterior semicircular involvement.
Anterior canal BPV – torsional downbeating not upbeating
nystagmus during Hallpike test induced when the abnormal
anterior canal (which lies at right angles to posterior) is
uppermost. Repositioning manouevre starts with abnormal ear
uppermost – moving across to opposite head hanging position.
Horizontal canal BPV – rare, paroxysmal horizontal direction
changing nystagmus –beats towards ground when head turned
to side while patient lies supine. Nystagmus lasts 1 minute,
minimal latency and no fatiguability. Occurs with head to
either side but stronger on one side. Treatment is a 360 degree
log roll in 90 degree steps to normal side prone, to abnormal
side and then supine.
Vestibular neuronitis
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Acute, prolonged vertigo of peripheral origin is
commonly called vestibular neuritis, although other
terms such as "vestibular neuronitis," "labyrinthitis,"
"neurolabyrinthitis," and "unilateral vestibulopathy of
unknown cause" have also been used.
The vertigo typically develops over a period of hours,
is severe for a few days, and then subsides over the
course of a few weeks.
Some patients can have residual nonspecific dizziness
and imbalance that lasts for months or longer. with
known viral disorders of the inner ear, such as
measles and mumps.
Vestibular neuronitis pathophysiology
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The condition is thought to result from a selective
inflammation of the vestibular nerve, presumably of viral
origin.
The facts that the disorder often has a viral prodrome, that it
occurs in epidemics, that it may affect several members of the
same family, and that it occurs more commonly in spring and
early summer all support a viral cause.
Postmortem studies have found atrophy of the vestibular nerve
and the vestibular sensory epithelium that is similar to the
pathological findings.
Clinical features of vestibular
neuronitis
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Mean age 41.5 years, 55% are males
Sudden vertigo, often overnight; 66% noted on
awakening. Severity peaks within first day.
Direction-fixed horizontal nystagmus with fast phase
towards healthy ear. Intensity of nystagmus increases
with gaze toward healthy ear and decreases with gaze
towards affected ear.
Frenzel glasses, which prevent visual fixation, may
be needed to observe spontaneous nystagmus.
Head-impulse test is positive
Frenzel glasses
Head impulse (or thrust) test
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A simple bedside test of the horizontal vestibulo-ocular reflex
performed by grasping the patient's head and applying a brief,
small-amplitude, high-acceleration head turn, first to one side
and then to the other.
To start, the eyes should be about 10 degrees away from the
primary position in the orbit so that after a 10-degree head
turn, the eyes will be near the primary position.
The patient fixates on the examiner's nose and the examiner
watches for corrective rapid eye movements (saccades), which
are a sign of decreased vestibular response (i.e., the eyes move
with the head rather than staying fixed on the nose).
In ‘peripheral’ lesions (labyrinth or the 8th nerve including the
root's entry zone in the brain stem) a"catch-up" saccades occur
after head thrusts in one direction but not the other.
Vestibular neuronitis – time
course
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Disabling severe vertigo lasts less than 1 week
in 70%; and less than 2 weeks in 96%.
However, caloric testing shows partial canal
paresis in 30% and absent responses in 10-20%
at 1 year.
In one long term clinical follow-up study, minor
symptoms (transient vertigo with rapid head
movements or slight unsteadiness) persisted for
3 months in 60%, 1 year in 50% and more than
5 years in 25%.
Meniere’s disease
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15-46/100,000 population per year affected in
USA.
By definition – idiopathic endolymphatic
hydrops.
2 phases – early (almost always unilateral and
symptoms episodic) and late (symptoms present
more or less all the time with episodes of
exacerbation consisting of an increased severity
of symptoms).
Clinical features of Meniere’s
disease
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Vertigo – well defined episodes, 20 min – 24 h
duration, frequent nausea/vomiting, vestibular
nystagmus may be present.
Deafness – sensorineural, fluctuating,
progressive. During attacks hearing loss may be
sudden, lasts minutes to hours to days to weeks.
May remain as permanent deficit.
Tinnitus – variable, episodic, begins slowly, may
reach crescendo over minutes to hours,
continues for hours to days to weeks.
Aural pressure – most variable of symptoms.
Treatment of Meniere’s disease
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Meniere’s crisis has been reported after high sodium meal.
This has led to treatments recommending moderate sodium
restriction (1-2 g sodium/day). Often strict sodium restriction
(<1g/day) required.
Diuretics – mixed results in double blind studies. A
retrospective study showed beneficial hearing effects of
diamox and chlorthalidone in short-term (2-6 weeks) but not
long term (5 years).
Histamine (vasodilates labyrinth vasculature)– short-term
benefits only; vestibular suppressants – no long term
advantage.
Surgery – destructive (need to warn patient of risks if
contralateral ear becomes affected) and non-destructive (eg
endolymphatic sac decompression) procedures
ENG and calorics
Caloric testing – cold and warm
water irrigation
Other causes of peripheral vertigo
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Migraine-associated vertigo
Post-traumatic – “whiplash” injury is frequently
associated with vertigo – often difficult to explain
particularly if neuro-imaging is negative for high
cervical nerve damage.
Perilymphatic fistula – penetrating ear trauma,
temporal bone or head trauma, prior stapedectomy
and barotrauma. Patients experience stepwise
progressive sensori-neural hearing loss with episodes
triggered by exertion or Valsalva and episodic and/or
positional vertigo triggered by exertion or Valsalva.
Causes of central vertigo
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Infarcts - the absence of associated neurological symptoms
does not exclude central vertigo because as many as ~ 25% of
middle-aged/elderly patients with risk factors for stroke, who
present to the ED with isolated severe vertigo + postural
instability may have an inferior cerebellar infarction
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Cerebellopontine angle tumors
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Multiple sclerosis
Vertebral artery or PICA infarct causing
lateral medullary syndrome
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Vertigo, nystagmus
Gait and limb ataxia
Dysphagia, decreased gag
Ipsilateral facial hemianaesthesia
Ipsilateral Horner’s syndrome
Contralateral arm/trunk/leg pain and
temperature (spinothalamic) loss
Lateral medullary infarction
Multiple sclerosis
Visual evoked potentials
Vertigo in multiple sclerosis
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At least 5% of patients with MS report vertigo as
an initial symptom.
Vertigo may be rotatory with a positional
component in some patients.
Diplopia, facial paraesthesia and weakness may
co-exist.
Eye signs in MS patients with vertigo can
include nystagmus, internuclear
ophthalmoplegia and abnormal saccades (eg
dysmetria, slow saccades), impaired pursuit and
impaired convergence.
Cerebello-pontine angle tumours
Other central causes