Ataxia&vertigo

Ataxia and Vertigo

Prepared by Jason Pillet
Presented by Dr. Donze

Introduction
 Ataxia is the failure to produce smooth
intentional movements.
 Gait disorders include ataxic gait as
well as a variety of other conditions.
 The presenting complaint may be
weakness, dizziness, stroke, falling, or
another nonspecific complaint.

Pathophysiology
 Ataxia may categorized into motor and sensory
ataxias.
 Motor ataxias (cerebellar ataxias) are usually
caused by disorders of the cerebellum. The
sensory receptors and afferent pathways are
intact, but integration of the proprioceptive
information is faulty.
 Involvement of the lateral cerebellum may lead
to a motor ataxia of the ipsilateral limb.
 Lesions affecting the midline portion of the cerebellum
cause problems with axial muscle coordination
reflected in difficulty maintaining a steady upright
standing or sitting posture.

Pathophysiology
 Sensory ataxias occur with failure in transmission of
proprioception or position sense information to the
CNS.
 This may arise from disorders affecting the
peripheral nerves, spinal cord, or cerebellar input
tracts.
 Sensory ataxias may be compensated to a degree
with visual sensory information. Loss of visual
information leads to the observation that sensory
ataxia often worsen in poor lighting conditions and
may by brought out during examination.

Clinical Features
 Obtain orthostatic vital signs
 Gait testing - Observe the patient sit upright in the
stretcher, rise, stand, walk, and turn around. The patient
should be asked to walk at a normal speed, then walk on
the heels, and then toes. Tandem gait is toe-to-toe
walking and tests many elements of the nervous system.
 Cerebellar functions are tested by asking the patient to
perform smooth voluntary movements and rapidly
alternating movements:
 dyssynergia (breakdown of movements into parts),
 dysmetria (inaccurate fine movements), or
 dysdiadochokinesia (clumsy rapid movements) may be
indicative of a problem in the lateral cerebellum.

Clinical Features
 A test for cerebellar function that emphasizes the
lower extremities is the heel-to-shin test.
 Romberg test is primarily a test of sensation and, if
positive, may distinguish sensory from motor ataxia.
 The inability to maintain a steady standing posture confirms
that an ataxia is present but does not give information
about the type of ataxia.
 If the ataxia worsens with eyes closed, then the
Romberg sign is present, suggesting sensory ataxia with a
problem of proprioceptive input (posterior column,
vestibular dysfunction), or a peripheral neuropathy.
 In patients who show no change in their unsteadiness with
eye closure (Romberg negative), a motor ataxia is
suggested with possible localization of that problem to the
cerebellum

Tabes Dorsalis
(Neurosyphilis)
 Sensory ataxia.
 loss of proprioceptive information from the lower
extremities renders the patient dependent on
visual cues for correct gait.
 The classic description is of a patient who walks
slowly with wide gait while staring at the
ground.
 In darkness or with interruption of vision, the patient is
unable to walk. The gait is peculiar with the foot first
raised and then slapped to the ground with each step.
These abnormalities reflect the loss of proprioceptive
information from the posterior roots and posterior
columns.


Clinical Features
 A cerebellar or motor ataxic gait is wide
based with unsteady and irregular steps,
and compensation to barriers in the
environment may be lacking.
 The gait of sensory ataxia resulting from
loss of proprioception is notable for abrupt
movement of the legs and slapping impact
of the feet with each step.

Classification of Gait Disorders
Low-level gait disturbance refers to disorders of
proprioception or dysfunction of the
musculoskeletal system.

Middle-level gait disturbance causes distortion of
appropriate interaction of postural and motor
processes or synergies. This might include stroke
with paralysis, cerebellar dysfunction, or diseases
of the basal ganglia such as Parkinson's disease.
On examination, patients might have findings of
spasticity, muscular tone, paralysis, or abnormal
movements.

High-level gait disturbances involve structures or
processes that choose the appropriate responses
for the support surface, ie: Cautious gait, apraxic
gait, and the frontal gait disorder conceptually
fall into this group with pathology that correlates
with lesions in the frontal cortex or thalamus.

Children and gait disturbances

Vertigo and dizziness
 Dizziness may mean vertigo, syncope,
presyncope, weakness, giddiness, anxiety, or a
disturbance in mentation to various patients.

 Vertigo is the perception of movement
where no movement exists.

 Disequilibrium refers to a feeling of
unsteadiness, imbalance, or a sensation of
"floating" while walking.

Pathophysiology
 The central nervous system (CNS) coordinates
and integrates sensory input from the visual,
vestibular, and proprioceptive systems.
 The three streams of information help form an
impression of the orientation of the head and
body as well as the perception of motion.
 Vertigo arises from a mismatch of information
from two or more of the involved senses, which,
in turn, can be caused by dysfunction in the
sensory organ or its corresponding pathway.

Pathophysiology
 Visual inputs provide spatial orientation.
 Proprioceptors help relate body movements and
indicate the position of the head relative to that
of the body.
 The vestibular system establishes the body's
orientation with respect to gravity.
 There are three semicircular canals which sense
orientation to movement and head tilt and are filled
with a fluid called endolymph.
 The movement of fluid causes specialized hair cells
inside the canals to move, causing afferent vestibular
impulses to fire which travels to the nucleus of the
eighth cranial nerve.

Clinical Features
 Vertigo is usually categorized as
"peripheral" or "central."
 Peripheral vertigo is caused by
disorders affecting the vestibular
apparatus and the eighth cranial nerve,
whereas
 Central vertigo is caused by disorders
affecting central structures, such as the
brainstem and the cerebellum.

Peripheral vs Central

Peripheral vertigo tends to cause distressing symptoms, but is seldom life-threatening. Disorders causing central vertigo may produce less
distressing symptoms and have a slower onset than those due to peripheral vertigo, but they are generally of a more serious nature

Diagnosis
 Peripheral vertigo is more likely than central
vertigo to be intense and to be associated with
nausea, vomiting, diaphoresis, tinnitus, hearing
loss, and photophobia.
 Central vertigo is more likely to be associated
with neurologic symptoms and signs such as
diplopia, dysarthria, and bilateral visual
abnormalities.
 An associated headache or history of headache
suggests migraine, stroke, TIA or a space-
occupying lesion.

Physical Exam
 Patients with vertigo should have ear, neurologic,
and vestibular examinations.
 Insufflation of air by use of a pneumatic otoscope
that precipitates a burst of vertigo with
nystagmus is diagnostic of an inner ear fistula
 If central vertigo is considered, check for an
absent corneal reflex, facial paresis, difficulty
swallowing, dysphonia, and depressed gag
reflex. Test for limb and truncal ataxia, and test
the vestibulospinal system and cerebellum
through tandem gait and Romberg testing.

Physical Exam
 Nystagmus is the principal objective sign of
vertigo.
 The eyes should be examined for spontaneous
nystagmus, and the direction of the fast
component of nystagmus should be noted. The
diagnosis of BPPV involving the posterior canal is
aided by the Dix-Hallpike position test.
 http://www.accessmedicine.com.proxy.library.oh
(how to perform the Dix-Hallpike)

Dix Hallpike
 Should not be performed on patients with carotid bruits, cerebrovascular
disease, risk factors or concern for vertebrobasilar insufficiency, spinal injury,
or cervical spondylosis.
 May provoke vertigo and pretreatment with 50 mg benadryl makes the test
more tolerable but will not obliterate nystagmus.
 To test the right posterior semicircular canal, the head is initially rotated 30 to
45 degrees to the right. Keeping the head in this position, the patient is rapidly
brought to the recumbent position until the head is 20 degrees below the level of
the stretcher or examining table. A positive test is indicated by rotatory
nystagmus following a latency of no more than 30 seconds; the nystagmus
exhibits rapid eye torsions toward the affected ear and lasts for 10 to 40
seconds.
 The side exhibiting the positive test is the side of the lesion. The test is
about 50% to 80% sensitive for BPPV

Disorders causing Peripheral
Vertigo
 Peripheral vertigo is noted for its abrupt
(often explosive) onset. It is an intense
sensation of spinning or hurtling toward the
ground or surrounding walls. It is typically
worsened by rapid movement and by
changes in head position. It is frequently
associated with nausea, often severe
vomiting, diaphoresis, and bradycardia and
hypotension.

BPPV
 Disorder of the inner ear causing transient vertigo and associated
nystagmus that is precipitated by certain head movements
 According to the canalolithiasis hypothesis, BPPV is caused by
inappropriate activation of a semicircular canal, typically the
posterior semicircular canal and typically unilateral, by the
presence of free-floating particles or otoconia.
 Average age of onset: mid-50s. Women are twice as likely to be
affected. The onset is sudden, and an attack typically is
precipitated by rolling over in bed, assuming a supine position,
leaning forward, looking up at the sky or ceiling, or turning the
head. Nausea is often present.

BPPV
 Because the symptoms fatigue, they tend to be worse in the
morning and become less pronounced as the day progresses.
Patients may eliminate the offending activities. There is no
associated hearing loss or tinnitus, and no physical findings
on examination of the external auditory canal.

BPPV treatment
 Medications such as transdermal scopolamine
and antihistamines.
 Epley maneuver (particle-repositioning
maneuver)
 principle behind the particle-repositioning maneuver is
to use gravity to induce the particles to move along the
semicircular canals until they end up inside the utricle,
where they are unlikely to cause vertigo
 (http://www.accessmedicine.com.proxy.library.ohiou.edu/video
Player.aspx?file=vid_epleymaneuver)

Epley Maneuver

The patient is
seated as in the
Dix-Hallpike
position test, and
the head is
turned 45
degrees toward
the affected ear.

Epley Maneuver continued
 The patient is
gently brought to
the recumbent
position with the
head hanging
roughly 20 degrees
below the
examining table.
The head is gently
rotated 45 degrees
to the midline.

 The head is
then rotated a
further 45
degrees to the
unaffected
side.

 The patient rolls
onto the shoulder
of the unaffected
side, at the same
time rotating the
head a further 45
degrees.

Epley Maneuver finished
 The patient is returned to
the sitting position, and
the head is returned to the
midline.
 Each portion of the
maneuver should be done
slowly (about 5 minutes)
and evenly to permit the
particles to traverse their
intended course.
 If the maneuver is done
correctly, nystagmus in
the same direction as that
observed during Dix-
Hallpike position testing
may be observed.

Meniere Disease
 Associated with an increased endolymph within the
cochlea and labyrinth
 Equally seen in men and women aged 65 and older
and usually unilateral
 Onset of vertigo is usually sudden, with associated
nausea, vomiting, and diaphoresis. The duration of
vertigo ranges from 20 minutes to 12 hours
 Roaring tinnitus, diminished hearing, and fullness in
one ear.
 Between attacks, the patient is usually well,
although decreased hearing may persist

Meniere disease continued
 Diagnosis confirmed by gylyeral testing and
by vestibular-evoked myogenic potentials.
 managed symptomatically with antihistamines,
betahistine (H1 receptor agonist), and CCBs
 A salt-restricted diet <1 gram/d of added salt is
recommended for patients with a confirmed
diagnosis.
 Intratympanic gentamycin administration has
been shown to provide significant immediate
and long-term relief

Perilymph Fistula
 opening in the round or oval window that permits
pneumatic changes in the middle ear to be
transmitted to the vestibular apparatus
 Trauma, infection, or a sudden change in the
pressure inside the ventricular system
 Diagnosis suggested by sudden onset of vertigo
associated with flying, scuba diving, severe
straining, heavy lifting, coughing, or sneezing
 Confirmed by nystagmus elicited by pneumatic
otoscopy (Hennebert sign)
 Managed with symptomatic treatment and bed rest,
with referral to an ENT

Vestibular Neuronitis
 Suspected viral etiology.
 Lasts several days and does not recur.
 Sudden onset
 The vertigo is often so intense that the
patient requires several days of bed rest;
 Elderly patients may have persistent
unsteadiness of gait.
 Unilateral loss of hearing and tinnitus
may occur.
 Treated symptomatically.

Vestibular Ganglionitis
 Caused by varicella zoster that can be reactivated
 Multiple ganglia may be involved.
 Herpes zoster oticus, also known as the Ramsay
Hunt syndrome, is a neuropathic disorder thought to
be associated with vestibular ganglionitis.
 Characterized by deafness, vertigo, and facial nerve
palsy.
 diagnosis is confirmed by the presence of grouped
vesicles on an erythematous base inside the
external auditory canal.
 Managed with a combination of symptomatic
treatment and antiviral therapy started within 72
hours of the appearance of vesicles

Labyrinthitis
 Infection of the labyrinth producing peripheral vertigo and hearing loss.
 viral (measles and mumps), in which case the clinical course is similar to
that of vestibular neuronitis. Bacteria (otitis media) in which bacteria and
toxins diffuse across the membrane of the round window.
 A cholesteatoma can erode into the inner ear, creating a portal of entry
for bacteria.
 The hallmarks of this disease include sudden onset of vertigo with
associated hearing loss and middle ear findings.
 Patients with bacterial labyrinthitis are at risk for meningitis and require
antibiotics and referral to an otologist or ENT specialist for admission
and drainage.

Ototoxicity
 Ototoxicity has been associated with aminoglycoside and macrolide
antibiotics, loop diuretics, platinum-based chemotherapeutic agents,
some NSAIDs, and antimalarial preparations
 Aminoglycoside antibiotics produce hearing loss and peripheral
vestibular dysfunction by accumulating inside the endolymph, where
they cause the death of
cochlear and vestibular
hair cells. However,
because both inner ears
are affected, vertigo is
uncommon

Eighth Nerve lesion
 may produce mild vertigo.
 Meningiomas and acoustic schwannomas are
typical causes.
 The onset of vertigo is usually gradual,
remaining constant until central
compensation can take place.
 The vertigo is usually preceded by hearing
loss. Such patients require urgent diagnostic
imaging as well as referral to a neurosurgeon

Cerebellopontine Angle
Tumors
 Associated with tumors of the
cerebellopontine angle.
 include acoustic neuromas, meningiomas,
and dermoids.
 They usually present with a cluster of
findings, including deafness and ataxia, as
well as ipsilateral facial weakness, loss of the
corneal reflex, and cerebellar signs.
 Require urgent diagnostic imaging as well as
referral to a neurosurgeon

Post-Traumatic Vertigo
 Acute post-traumatic vertigo is caused by a direct injury
to the labyrinthine membranes.
 Onset is immediate and accompanied by nausea and
vomiting.
 May have sustained a concomitant fracture of the
temporal bone. Vertigo associated with a closed head
injury warrants a CT scan or MRI to exclude an
extradural or intradural hematoma.
 Vertigo due to direct labyrinthine trauma tends to resolve
within several weeks.
 Postconcussive syndrome can be associated with
unsteadiness of gait and a vague sense of dizziness.

Central Vertigo
 Disorders affecting the cerebellum and
the brainstem.
 Gradual in onset and mild in intensity;
symptoms are not provoked by
changes in position.
 Unlikely to be associated with tinnitus
and hearing impairment.
 Nystagmus is more likely to be vertical

Cerebellar Hemorrhage &
infarction
 Causes acute vertigo and ataxia. Headache, nausea, and
vomiting may or may not be present.
 Sense of side-to-side or front-to-back motion.
 Truncal ataxia and may not be able to sit without support.
 Romberg testing and tandem gait will be abnormal.
Occasionally, there may be a sixth cranial nerve palsy or
conjugate eye deviation away from the side with the
hemorrhage.
 Cerebellar infarction has a similar clinical presentation.
Such patients require urgent diagnostic imaging, and
those with cerebellar hemorrhage require emergent
neurosurgical consultation.

Wallenberg Syndrome
 A lateral medullary infarction (Wallenberg
syndrome) of the brainstem can cause vertigo.
 Ipsilateral findings include facial numbness, loss of
corneal reflex, Horner syndrome, and paralysis or
paresis of the soft palate, pharynx, and larynx
(causing dysphagia and dysphonia).
 Contralateral findings include loss of pain and
temperature sensation in the trunk and limbs.
 Occasionally, lesions of the sixth, seventh, and
eighth cranial nerves can occur, causing vertigo,
nausea, vomiting, and nystagmus.
 usually require urgent diagnostic imaging and
referral to a neurologist

Vertebrobasilar insufficiency
 TIAs of the brainstem. Orthostasis can worsen symptoms.
 Vertigo may be of sudden onset and typically lasts from minutes to
hours.
 VBI-induced vertigo can present by itself or be accompanied by
diplopia, dysphagia, dysarthria, and bilateral loss of vision.
 Unlike other causes of central vertigo, VBI may be provoked by
position. Turning the head partially occludes the ipsilateral vertebral
artery. If the contralateral artery is stenotic, head turning could
cause transient ischemia to the brainstem, resulting in VBI.
 A sufficient loss of brainstem circulation caused by a head turn could
affect the reticular activating system, causing near-syncope or syncope.
 Patients with VBI should have imaging as well as referral to a
neurologist

Vertebral Artery dissection
 Lead to a stroke involving the posterior circulation.
 Symptoms and signs of vertebral artery
dissection include headache and vertigo, and a
unilateral Horner syndrome may be present.
 Sudden (and often violent) rotation or extension of
the neck may precipitate a dissection.
 Injuries may occur following high-velocity motor
vehicle crashes, diving injuries, coughing, sneezing,
and chiropractic neck adjustments.
 Emergency diagnostic imaging

Multiple Sclerosis
 Demyelinating disease can present with vertigo
that tends to last several hours to several days
or weeks and is usually nonrecurrent.
 Vertigo not usually intense, and nystagmus is
often more prominent than the vertigo
 Ataxia or optic neuritis may be present or may
have occurred previously.
 Diagnosis usually is confirmed using MRI.
 Patients with vertigo due to demyelination
require urgent referral to a neurologist.

Migraine related Vertigo

 Managed symptomatically with antivertigo therapy but require neurologic referral.
 Ergotamine or sumatriptin should not be used in basilar migraine.
 Migraine prophylactic agents, such as B-blockers and CCBs, may be instituted in consultation
with a neurologist

Disposition
 Patients with peripheral vertigo may be
discharged from the ED.
 All patients with a first episode of peripheral
vertigo should be referred to their PCP or an
otolaryngologist.
 Patients with BPPV who have had a particle-
repositioning maneuver should be referred to an
otologist or ENT
 Central causes of vertigo almost always require
urgent diagnostic imaging and neurologic or
neurosurgical consultation while in the ED and
admission.

Osteopathic Medicine
 Modified Muncie technique is type of
myofascial release administered inside the
patient's mouth
 Epley Maneuver
 Cervical Muscle energy or HVLA
 Cranial release

Ataxia&vertigo

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