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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.
Ataxia&vertigo
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.
Etiologies of Vertigo
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
Ancilliary tests
Treatment for Vertigo
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.
Epley Maneuver continued
                  The head is
                   then rotated a
                   further 45
                   degrees to the
                   unaffected
                   side.
Epley Maneuver continued
               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
Questions?

 ?

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Ataxia&vertigo

  • 1. Ataxia and Vertigo Prepared by Jason Pillet Presented by Dr. Donze
  • 2. 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.
  • 4. 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.
  • 5. 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.
  • 6. 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.
  • 7. 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
  • 8. 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. 
  • 9. 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.
  • 10. 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.
  • 11. Children and gait disturbances
  • 12. 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.
  • 13. 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.
  • 14. 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.
  • 16. 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.
  • 17. 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
  • 18. 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.
  • 19. 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.
  • 20. 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)
  • 21. 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
  • 24. 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.
  • 25. 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.
  • 26. 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.
  • 27. 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)
  • 28. Epley Maneuver The patient is seated as in the Dix-Hallpike position test, and the head is turned 45 degrees toward the affected ear.
  • 29. 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.
  • 30. Epley Maneuver continued  The head is then rotated a further 45 degrees to the unaffected side.
  • 31. Epley Maneuver continued  The patient rolls onto the shoulder of the unaffected side, at the same time rotating the head a further 45 degrees.
  • 32. 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.
  • 33. 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
  • 34. 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
  • 35. 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
  • 36. 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.
  • 37. 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
  • 38. 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.
  • 39. 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
  • 40. 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
  • 41. 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
  • 42. 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.
  • 43. 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
  • 44. 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.
  • 45. 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
  • 46. 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
  • 47. 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
  • 48. 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.
  • 49. 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
  • 50. 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.
  • 51. 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