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Back To Chiropractic CE Seminars
Neurology: The Dizzy Patient ~ Advanced ~ 6 Hours
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ADVANCED LECTURE ON THE
EVALUATION AND
MANAGEMENT OF THE DIZZY
PATIENTBy:Larry E. Masula, D.C., DACNB, FAVRB, FAFICCDipolmate American Chiropractic Neurology Board, Fellow American Vestibular Rehabilitation Board, Fellow Academy of Forensic and Industrial Chiropractic Consultants
mazu1021@gmail.com
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 3
Larry E. Masula, DC, DACNB, FABVR, FAFICC
Carrick Institute for Advanced Neurological Studies: Frederick C.Carrick, PhD, Cambridge University.
Diplomate American Chiropractic Neurology Board
Fellow American Board of Vestibular Rehabilitation
Fellow Academy of Forensic and Industrial Chiropractic Consultants
Evaluation and Management of Dizziness and Balance Disorders, NeilT. Shepard , PhD, director of the Dizziness and Balance DisordersProgram at the Mayo Clinic, Rochester, Minnesota, and professor ofaudiology in the Mayo Clinical School of Medicine. Joel A. Goebel,M.D., FACS. Director, Dizziness and Balance Center WashingtonUniversity School of Medicine, St. Louis, MO
American Institute of Continuing Medical Education, Certified in 101Vestibular Rehabilitation, 201 Ocular Motor Testing, 202 Gaze,Headshake and Positional Testing. Richard E. Gans, PhD., ExecutiveDirector American Institute of Balance
2/1/2020Larry E. Masula, D.C, DACNB.FABVR, FAFICC 4
Objectives
▪ General overview of the clinical anatomy and physiology
of the vestibular system and posterior fossa (cavity) will
be discussed with emphasis on diagnostics and
chiropractic management.
Larry E. Masula, D.C. DACNB, FABVR, FAFICC 2/1/2020 5
Recommended Reading▪ Clinical Neurophysiology of the Vestibular System, Edition 2,
Robert W. Baloh, Vicente Honrubia. Chapters 1-3
▪ Principles of Neural Science, 4th Edition, Eric R. Kandel, James H. Schwartz, Thomas M. Jessel, McGraw-Hill. Chapter 42: The Cerebellum
▪ Technique of the Neurological Examination, 4th Edition, DeMeyer, W. McGraw-Hill. Chapter 8: Examination of Cerebellar Dysfunction
▪ Neurological Differential Diagnosis, 2nd Edition, John Patten, Springer 1996. Chapter 12: The Extrapyramidal System and the Cerebellum
▪ The Neurology of Eye Movements, 3rd edition, Leigh & Zee
▪ The Brain That Changes Itself, Norman Doidge, M.D.
▪ Vestibular Rehabilitation, 4th Edition, Susan J. Herdman, Richard A. Clendaniel
Larry E. Masula, D.C. DACNB, FABVR, FAFICC 2/1/2020 6
IRISIS 1889
Larry E. Masula, D.C, DACNB, FABVR FAFICC 7
Almond Blossoms 1890
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At Eternity’s Gate 1890
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The Church at Auvers 1890
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Prisoners Exercising 1890
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Can You Find a Common Theme
Among These 5 Paintings
Can You Find a Common Theme
Among These 5 Paintings▪ 1. Yes, they have been painted by the same artist
▪ 2. Yes, they are all roughly painted within one year
▪ 3. Yes, the artist may well have had a disturbance of
spatial orientation (vertigo). Why? Much of the paintings
are leaning to the left.
▪ 4. If so, on which side is the artist’s problem?
▪ 5. What are the possible causes?
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2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 14
Answer: The left vestibular system was most
likely affected and may have failed.
Explanation: Due to the length of time, based on the painting
dates, (over a year) it was no longer an acute problem. We will
discuss the various problems which affect our sense of spatial
awareness. We will also discuss why in this case; the left
vestibular apparatus was no longer being inhibited by the right and
why the left vestibular system appeared overly active.
2/1/2020Larry E. Masula, D.C.DACNB, FABVR, FAFICC 15
Who is the
Artist?
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On the Verge of Insanity
Vincent cut off his left ear on December 23, 1888 after being
upset with a fellow painter. It was the first of several serious
breakdowns that plagued him until his tragic suicide a year
and a half later. We don’t know precisely what his illness
was, but it had a huge impact on his life.
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2/1/2020Larry E. Masula, D.C, DACNB, FABVR, FAFICC. 18
January 28, 1889
Van Gogh’s - Letter to his brother Theo from
Arles, France
“I well knew that one could break one’s arms and legs
before, and that then afterwards that could get better
but I didn’t know that one could break one’s brain and
that afterwards that got better too.”
Because▪ Patient Care and Safety are Preeminent
▪ Develop Improved Diagnostic Skills
▪ There is a Great Need for Skilled Practioners
▪ (9.47%) 31 million Americans experience Lower back
pain at any given time. www.acatoday.org/backpain
▪ (21.1%) 69 million US adults aged 40 years and older had
vestibular dysfunction. Disorders of Balance and
Vestibular Function in US Adults. Data From the National
Health and Nutrition Examination Survey, 2001-2004
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WHAT IS DIZZINESS AND
VERTIGO?
Historical Background
Prosper Meniere (1861) – first to recognize the association
of vertigo with hearing loss and to localize the symptoms to
the inner ear.
Robert Barany (1906)
▪ First clinical description of BPPV in 1921.
▪ Introduced Caloric testing – most widely used test of the
vestibulo-ocular reflex (VOR)
▪ Nobel Prize for mechanism of caloric stimulation
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Vertigo and Dizziness are considered:
▪ Either an unpleasant Disturbance of Spatial Orientation
▪ The Illusory perception of body movement (spinning,
wobbling, or tilting) and/or of the surroundings
Larry E. Masula, D.C, DACNB, FABVR, FAFICC2/1/2020 22
Dizziness / Vertigo
▪ Dizziness refers to various abnormal sensations relating
to perception of the body’s relationship to space.
▪ Dizziness – may represent a variety of symptoms which
may include spinning, or movement of the environment,
light-headedness, or presyncope, or imbalance while
walking
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Centers for Disease Control and Prevention
▪ Falls Are Serious and Costly
▪ One out of five falls causes a serious injury such as broken bones or a head injury.1,2
▪ Each year, 2.5 million older people are treated in emergencydepartments (visits) for fall injuries.3
▪ Over 700,000 patients a year (1/3) are hospitalized because of a fall injury, most often because of a head injury or hip fracture.3
▪ Each year at least 250,000 older people are hospitalized for hip fractures.5 More than 95% of hip fractures are caused by falling,6 usually by falling sideways.7
▪ Falls are the most common cause of traumatic brain injuries (TBI).8
▪ Adjusted for inflation, the direct medical costs for fall injuries are $34 billion annually.9Hospital costs account for two-thirds of the total.
Larry E. Masula, D.CDACNB, FABVR, FAFICC. 06/15/2019 24
The Burden Dizziness and Vertigo
Impose on the CommunityDizziness is the third most common major medical symptomreported in general medical clinics1 and accounts for about 3%–5% of visits across care settings.2 In the United States, thistranslates to 10 million ambulatory visits per year because ofdizziness,3 with roughly 25% of these visits to emergencydepartments.2 Many patients have transient or episodic symptomsthat last seconds, minutes or hours, but some have prolongeddizziness that persists continuously for days to weeks.4
▪ 1. Kroenke K, Mangelsdorff AD. Common symptoms in ambulatory care: incidence, evaluation, therapy, and outcome. Am J Med 1989;86:262–6 [PubMed] [Google Scholar]
▪ 2. Newman-Toker DE, Hsieh YH, Camargo CA, Jr, et al. Spectrum of dizziness visits to US emergency departments: cross-sectional analysis from a nationally representative sample. Mayo Clin Proc2008;83:765–75 [PMC free article] [PubMed] [Google Scholar]
▪ 3. Kruschinski C, Hummers-Pradier E, Newman-Toker D, et al. Diagnosing dizziness in the emergency and primary care settings [letter]. Mayo Clin Proc 2008;83:1297–8 [PubMed] [Google Scholar]
▪ 4. Neuhauser HK, von Brevern M, Radtke A, et al. Epidemiology of vestibular vertigo: a neurotologic survey of the general population. Neurology 2005;65:898–904 [PubMed] [Google Scholar]
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Ischemic Posterior Circulation Stroke:
Posterior circulation strokes (Posterior Fossa) patients
exhibit many neurological symptoms including vertigo. They
represent approximately 20% of all ischemic strokes.
In contrast to the anterior circulation, several differences in
presenting symptoms, clinical evaluation, diagnostic testing,
and management strategy exist presenting a challenge to
the treating physician.
▪ Ischemic Posterior Circulation Stroke: A Review of Anatomy,
Clinical Presentations, Diagnosis, and Current Management
Amre Nouh,1 Jessica Remke,2 and Sean Ruland1,*
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Normal Anatomy & Physiology
▪ The peripheral vestibular system consists of:
3 semicircular canals
Otolithic apparatus (utricle and saccule) and
The vestibular, 8th cranial, nerve
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Anatomy of Tympanic Cavity
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Important Structures include: Int. Auditory meatus, Cochlea, SCC’s, Cn7, Cn 8, Eustachiantube anteriorly, Mastoid air cells post.
Anatomy of Tympanic Cavity
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 29
The inner ear has two parts: the bony labyrinth and the membranous
labyrinth. The membranous labyrinth is contained within the bony
labyrinth, and within the membranous labyrinth is a K+ rich fluid called
endolymph. Between the outer wall of the membranous labyrinth and the
wall of the bony labyrinth is the location of perilymph.
Bony Labyrinth
The bony labyrinth (also
osseous labyrinth or otic
capsule) is the
rigid, bony outer wall of the
inner ear in the temporal
bone. It consists of three
parts: the vestibule,
semicircular canals, and
cochlea. These are cavities
hollowed out of the substance
of the bone and lined by
periosteum.
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Membranous Labyrinth
▪ The membranous labyrinth is a collection of fluid filled
tubes and chambers within the bony labyrinth which
contain the receptors for the senses of equilibrium and
hearing.
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Cochlea “unraveled”
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The middle ear functions as an amplifier. Sound enters the ear within the external auditory
meatus (EAC) - sound energy moves the tympanic membrane (ear drum) which transfers
this energy to the bony ossicles in the middle ear cavity. They in turn transfer compressed
sound energy to the Oval window of the cochlea via the stapes bone. Frequency from the
TM to the Oval window (force) increases. Mechanism one - TM is 17x larger than oval
window. Mechanism two - Ossicles transfer one unit of energy by factor of 1.3. Therefore,
17 x 1.3 = sound amplified ~ 22x Pathologically, Ossicular sclerosis = dampened sound.
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ANATOMY
Let’s Dive into the Anatomy
Middle Ear - Dimensions
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Dimensions of middle ear
a) 1/3 of the middle ear is above TM -“Epitympanic Recess”
b) Tympanic cavity proper (waist)
c) The Head of the Malleolus and Incus lie in the Epitympanic Recess
d) H = 15mm, AP = 15mm, Width-ETR = 6mmW, TC = 2mmW, Inf. Floor
= 4mmW
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The roof is small, and the floor is long.The tympanic Membrane is 9-10 mm thick and titled at 55° downward and forward
toward the floor, which together predispose foreign objects to lodge at bottom. Clinical
Note: Ear Lavage is best directed toward the roof for foreign body removal.
The Lateral Wall is made up o 2 parts. A membranous part and a bony part (Epitympanic
Recess). The TM consists of 3 layers. External-skin – derived from ectoderm. Internal –
mucosa of middle ear – derived from endoderm. Middle – fibrous layer is from
Mesoderm.
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 36
Examination: of the tympanic membrane with an otoscope reveals various structures which
include: Pars flaccida which is quite perforable due to infection, Handle of malleus and Umbro,
Pars tensa – stiffer because it sits in a bony sulcus. Cone of Light which transmits downward
and forward because of the 55° angle to the floor
Lateral Wall – (Tympanic Wall)
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 37
Nerve Supply to Tympanic Membrane
The Auriculotemporal nerve (branch of mandibular div. of Cn5) exits the Foramen Ovale and suppliesthe pars tensa and the EAC . It also innervates the teeth which is the reason why teeth pain maycause referred otalgia. CN. VII, X innervate the pars flaccida. Clinical Note: when stimulated or waxirritates the TM, the patient can develop reflex bradycardia, cardiac arrest or a cough. CN. IXinnervates (medial) inner TM surface, parts of the external ear and the posterior 2/3 of the tongue
supplying touch, pain, and temperature.
Nerve Supply to Tympanic Membrane
▪ Clinical Gem: The glossopharyngeal nervesupplies the posterior 2/3 of the tongue andtonsillar region. I recently had a patient, Jim,who presented with vertigo, minimal ear andpharyngeal pain. He had developed tonsillarcancer. Cancer of either structure can refersymptoms via the glossopharyngeal nerve tothe middle ear.
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These few nerve fibers within the middle ear are
important in the differential of Stroke vs. Vestibular
Pathology. Why is this important? Because later on
we will learn that the Facial nerves Geniculate
Ganglion can contain a latent Herpes Zoster virus.
Sometimes this virus can be activated. It enters the
7th fiber that travels through the middle ear to the
skin of the tympanic membrane. In this case the
patient will develop severe ear pain and/or hemi-
facial paralysis like Bells Palsy or Stroke. During
otoscopy there may be hemorrhagic blisters on the
anterior 2/3 of the tongue, the TM or within the
middle ear. “Ramsey Hunt Syndrome”
Note: Varicella Zoster (Herpes)– can affect CN.7 and create Hemi-facial
paralysis often seen with stroke facies, Tympanic hemorrhagic blisters and
may cause hearing loss and vertigo
(Ramsey Hunt Syndrome)
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Medial Wall aka (Labyrinthine Wall)
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Medial Wall (labyrinthine wall)▪ Most prominent feature is a circular
inward bulge = Promontory, (Base of
Cochlea), Tympanic Plexus of nerves.
▪ Foot Plate of Stapes attaches to Oval
Window. Movement of Stapes: Annular
lig. holds stapes to Oval window.
Posterior part of annular lig, is shorter
and thicker causing the stapes to tap
the oval window like a door hinge and
not a piston. Stepes is innervated by Cn.
7.
▪ Hook in the superior anterior wall – NOT
SHOWN (processes cochleiformis) for
the tendon of tensor tympani which
bends the tendon to move it laterally to
attach to the handle of malleus. During
contraction the tensor tympani pulls the
malleolus and the TM medially creating
tension to dampen sound. It is
innervated by a branch of the
mandibular division of the trigeminal
nerve.
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Medial Wall (Labyrinthine Wall)
▪ One of the most important structuresis a longitudinal bulge (bony “Facial”canal) along the superior aspect ofthe Medial wall.
▪ It originates from the Facial Nucleusin the Pons and moves anteriorly andmedially to enter the internal acousticmeatus. It exits and travels across thetop of the Vestibule terminating in theGeniculate Ganglion which sits behindthe superior anterior surface of themedial wall. Its first branch is theGreater Petrosal nerve before itenters through the boney (facial)canal in the petrous part of thetemporal bone where it extendsbackwards to the posterior wall andwithin the posterior wall the facialcanal and nerve turn downward.
▪ It is not exposed within the middle earcavity.
▪ The superior bulge (upper left) iscreated by the Horizontal Semicircularcanal.
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 43
Posterior Wall (Mastoid Wall) Special window in superior medial aspect
of posterior wall- “Aditus to antrum” -
opening into the mastoid antrum.
Facial Canal descends within the
posterior wall.
The bony “Pyramidal Eminence” - is
hollow and contains the stapedius muscle
with an exiting tendon which attaches to
the neck of the stapes. Importance:
dampen stapes movement and sound.
Innervated by a branch of the Facial
nerve.
The Chorda Tympani nerve (CN.7) and
the Posterior tympanic artery (not shown)
also enter the posterior wall. The chorda
tympani traverses through the middle ear
to exit through the anterior wall.
Not Shown- the short process of the
Incus attaches to the posterior wall at the
Fossa Incudis.
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 44
Posterior Wall (Mastoid Wall)
The Facial nerve descends andwill eventually emerge throughthe styloid mastoid foramengiving off the posterior auricularbranch which supplies thestylohyoid and posterior belly ofthe digastric muscles, theoccipital region and auricularmuscles. Its terminal branchesmove forward in the face to thetemporal, zygomatic, buccal,marginal mandibular andcervical muscles.
2/1/2020, Larry E. Masula, D.C, DACNB, FABVR, FAFICC. 45
Anterior Wall (Carotid Wall)2 Special Structures
1. Upper canal is a bony canal. Houses
the Tensor Tympani muscle which takes
3 origins from the bony canal, w/ the
superior cartilage of the eustachian tube,
and from the undersurface of the greater
wing of sphenoid (skull). It then enters
the canal and then converts to a tendon
which turns and moves laterally and
attaches to the handle of malleus. Upon
contraction it pulls the handle of the
malleus inward to pull the TM and the
ossicular chain tense. Purpose: contracts
to dampen loud sounds. Innervation:
mandibular division (motor) of CN5.
2. Eustachian Tube (petrotympanic tube)
connects the tympanic cavity w/ lateral
wall of pharynx.
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 46
Anterior Wall (Carotid Wall)
▪ Which artery sits
anteriorly?
▪ Int. Carotid. Covered by a
sympathetic plexus from
the superior cervical
ganglion. Sympathetic
fibers enter the middle ear
as Superior and Inferior
fibers.
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 47
Anterior Wall (Carotid Wall) Summary
▪ How many features in the
Anterior Wall?
1. Canal for Tensor Tympani
2. Opening of Eustachian
Tube
3. Lesser Petrosal Nerve
4. Sympathetic Fibers
5. Chorda Tympani Nerve
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 48
Anterior Wall (Carotid Wall)
Jugular Fossa sits directly beneath the floorof middle ear. Contains the internal jugularvein, CN’s 9, 10, & 11.
CN.9 gives off a branch which enters thefloor (not shown) bringing parasympatheticand sensory fibers to the tympanic plexuscollectively supplying all walls of the middleear including the eustachian tube andmastoid.
A branch from the tympanic plexus (lesserpetrosal nerve) exits the anterior wall andascends through the foramen Ovale anddescends back downward carryingparasympathetic pre-ganglionic fibers fromthe tympanic plexus to the parotid gland.
Chorda Tympani nerve CN.7, traverses themiddle ear and exits the anterior wall viaPetrotympanic fissure and through which theanterior tympanic artery enters to supply themiddle ear.
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 49
Chorda Tympani - Middle Ear
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Chorda Tympani – Branch of Facial N.
What is the relationship of theChorda Tympani (facial n.)contents of the middle ear?
It passes completely throughthe middle ear between theneck of the Malleus and theIncus and is covered withmucosa. It supplies theanterior 2/3 of the tongue withtaste receptors. Infections,strokes, and middle-earoperations may be damagingcausing dysgeusia (distortedtaste).cial
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 51
Eustachian tube ▪ Clinically Important:
The initial 1/3 is bony and the last 2/3 is
fibrocartilage. Angles 30º downward and 35º
anteromedially to open in the nasopharynx.
Attached to the end of the tube are the
Salpingopharyngeus, Tensor Veli Palitini
muscles, and the Levator Palatini muscles
(CN.10) Function: to elevate the soft palate
and open the end of the tube to equalize
pressure within the middle ear.
Reason why PICA strokes, can generate
unilateral swallowing impairment or having
food get stuck in the throat.
Test: have the patient say AAH repeatedly
and observe for a soft or complete impairment
of palatal elevation. The unaffected side will
elevate, and the palate may deviate in thatdirection
2/1/2020Larry E. Masula , D.C., DACNB, FABVR, FAFICC 52
Inferior Wall (Jugular Wall)
▪ The floor is made by the
petrous part of the temporal
bone with one important
cuniculus.
▪ Sympathetic fibers which
start from the Inferior
Salivatory nucleus travel
with other fibers of the 9th
nerve to enter the floor of
the middle ear cavity and
extend to the Promontory
2/1/2020Larry E. Masula, D.C., DACNB, FABVR, FAFICC 53
Roof
▪ The roof is called the Tegmentum Tympani. The roof is very thin. Clinically it is important because middle ear infections may extend upward especially in children due to an overlying Petrous -Squamous suture which may not be ossified producing a subdural abscess, meningitis and a temporal lobe abscess or infection. Fractures likely resulting in CSF leak.
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Clinical Review
▪ If the horizontal SCC is affected from a middle earinfection, it will result in Vertigo.
▪ If the facial canal is damaged it will result in facial palsy.If it is damaged proximal to the nerve to the stapedius,it results in paralysis of the stapedius giving rise tohyperacusis.
▪ Middle ear infections may extend posteriorly creatinglife-threatening mastoiditis. If the infection exits theroof (Tegmentum Tympani) it can produce anextradural abscess, meningitis, or a Temporal lobeabscess.
▪ If it extends backward through the Mastoid, it candamage the Sigmoid Sinus resulting inthrombophlebitis, and further backward enter thecerebellum or brainstem.
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CSF Leak from Middle Ear
Fracture of the middle cranial fossa, typically damages the
roof of the middle ear (Tegmentum Tympani which is a thin
bone). This may also disrupt the ossicular chain, rupture the
tympanic membrane and may damage the roof of the
external acoustic meatus. Blood and CSF leak into the
middle ear cavity and through the ruptured TM.
▪ This is called “Otorrhea”
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Contents of Middle Ear summary
▪ Air
▪ Ossicles (Malleus, Incus,
Stapes) all attached via
synovial joints
▪ Muscles (Stapedius, Tensor
Tympani Tendon)
▪ Nerves
▪ Vessels (Anterior tympanic
artery, Posterior tympanic
artery)
▪ All structures lined by
mucosa
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Understanding Vestibular
Neurophysiology
Understanding Neurons – the Big
Picture
▪ Stimulation of receptors results in activation of the 1st
order afferent (sensory) neuron
▪ Activation of the 2nd order afferent neurons is
dependent on the FOF of its pre-synaptic neuronal
pool (1st order neurons).
▪ Activation of the thalamus and all cortical structures
is dependent upon the FOF of ALL pre-synaptic
neuronal pools of the somatosensory system).
▪ As a result, receptor injury will result in impaired
cortical representation. (Head Maps)
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 59
Central Integrative State (Health) of a Neuron and
Cellular Immediate Early Gene Response –
There is a constant influx of neuronal membrane potential differences due to:
1. Spatial Summation (multimodal) on the receptor
2. Temporal Summation (high frequency unimodal) on the receptor
3. pH
4. Glucose
5. Oxygen tissue saturation
6. Temperature changes
7. Summation of all presynaptic (+) and (-) input which includes all cortical and segmental integration
8. In summary: stability or fragility of a neuron is based on the FOF of its presynaptic pools or receptor potentials
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What Do We Do?
“Alterations in the neuron occur at the synapse,strengthening and increasing, or weakening anddecreasing, the number of connections between theneurons.” (Michael Merzenich, considered the world’s leadingresearcher on brain plasticity)
Our rehabilitative purpose is therefore to:
1. Strengthen and enhance synaptic activity
2. Improve motor function
3. Improve brain activity via cortical
re-organization
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Cellular Survival is dependent upon
FuelGlucose
O2
Activation
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Summary: Cellular Survival is Altered by
▪ FOF of all presynaptic input (Activation)
▪ Identify and manage Dysglycemia, Hypoglycemia,
Metabolic Syndrome, Insulin resistance. (Fuel - glucose)
▪ Identify and manage anemia (Fuel – O2)
▪ Adequate protein and fat intake
▪ Inflammatory conditions
▪ Infections
▪ Autoimmunity
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Anatomy and Physiology of the
Vestibular System
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Vestibular Function:
an Overview
▪ Expressed simply, the role of the vestibular sensory
organs is to transduce the forces associated with head
acceleration and gravity into a biologic signal.
▪ The control centers in the brain use this signal to develop
a subjective awareness of head position in relation to the
environment and to produce motor reflexes for
equilibrium.
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Vestibular Function: Overview
continued
▪ The force associated with head acceleration generates a
signal in the labyrinth that is proportional to head
acceleration, 1:1 ratio.
▪ The overall objective of the CNS is to compute head
position by performing the equivalent of a mathematical
integration of the labyrinthine and otolithic input signals.
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Vestibular Nerve Physiology
▪ The vestibular system monitors the forces associated with
Angular and Linear accelerations of the head by means of
5 organs located within the labyrinthine cavity of the
temporal bones on each side of the skull.
▪ The Cristae Ampularis sensory organ of the 3
semicircular canals senses angular acceleration of the
head
▪ The Otolithic Organs (saccule and utricle) sensory organ
the Maculae senses linear acceleration.
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The Semi-Circular Canals
The semicircular canals provide sensory input about head
velocity, which enables the VOR to generate an eye
movement that matches the velocity of the head movement.
The desired result is that the eye remains still in space
during head motion, enabling clear vision. Neural firing in the
vestibular nerve is proportional to head velocity over the
range of frequencies in which the head commonly moves
(0.5 to 7 Hz).
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the Semi-circular canals
The fluid filled SCC is filled
with K+ rich Endolymph which
has a viscosity slightly
greater than H2O.
The sensory epithelium of the
cristae is covered by the
gelatinous cupula.
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Cristae Ampularis - enlarged
Lateral Line System
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A similar system is found in fish in which water passing over the tiny pores
within the lateral line of the fish move the cupula resulting in depolarization of
the nerve inducing a motor output and digestion
Semicircular Canals
▪ The cupula has the same density as the endolymph
▪ Semicircular canals do not respond to gravity in
static head positions however, there is tonic firing of
approximately 100 spikes/sec.
▪ The canals lie roughly in the same planes as the
extraocular muscles
▪ Each canal excites a pair of muscles and inhibits a
pair of muscles in its same plane. Its partner excites
the muscles it inhibits, and vice-versa
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Eye Muscles
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The plane in which the eyes
deviate are the result of
vestibular activation by the
canals stimulated
▪ Once vestibular signals leave the vestibular nuclei - they
divide into vertical, horizontal, and torsional components
of a motor command.
▪ Lesion of the central vestibular pathways can cause a
pure vertical, pure torsional, or pure horizontal nystagmus
of the eyes
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Canal Related Eye Movements
E.g. If I rotate my head horizontally to the right activating theright horizontal canal, I activate the right medial vestibularnucleus, which activates the right oculomotor nucleus andthe left abducens nucleus activating the right medial rectusand the left lateral rectus. Right horizontal canal activationbiases conjugate eye movements to the contralateral side, inthis case to the left.
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Activation of the Sensory Hair Cells
▪ Angular movement of the head causes endolymph flow in
one of the semicircular canals to deflect the cupula
▪ Deflection of the stereocilia toward the kinocilium results
in depolarization, or increased firing rate
▪ Deflection of the stereocilia away from the kinocilium
results in hyperpolarization, or a decreased firing rate
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Semi-Circular Canals
The semicircular canals provide sensory input about
head velocity, which enables the (VOR) vestibular
ocular reflex to generate an eye movement that
matches the velocity of the head movement. The
desired result is that the eye remains still in space
during head motion, enabling clear vision. Normal
neural firing of the vestibular nerve is proportional tohead velocity over the range of frequencies in which the
head commonly moves (0.5 to 7 Hz).
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Semi-Circular Canals
The coplanar pairing of the canals is associated with
a push-pull change in the quantity of semicircular canals
output. When angular head motion occurs, the endolymph of
the coplanar pair of canals is displaced in opposite
directions. This results in a neural firing increase in one
vestibular nerve and a hyperpolarization (decrease) on the
opposite side.
For the lateral canals, displacement of the cupula towards
the ampulla (ampullopetal flow) becomes excitatory,
whereas vertical canal displacement of the cupula away
from the ampulla (ampullofugal flow) is excitatory.
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Semi-Circular Canals
Clinically, this push-pull mechanism is an important point
which explains why patients with Unilateral Peripheral
Vestibular loss avoid head motion towards the side of their
lesion.
More will be said about this when we discuss how the
central nervous system compensates for overload.
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OTOLITHIC ORGANS: Utricle and Saccule
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Otolithic SystemEven with the head at rest, the calcareous material, becauseof its mass, exerts a force upon the otolithic receptor equalto the product of its mass and acceleration due to thegravitational pull of the earth, which at sea level is 9.80m/sec².
The Fg (force) acting upon the underlying sensory cellschanges with different degrees of head tilt.
The otolithic system is sensitive to gravity and linearacceleration. Because of their orientation in the head, theutricle is sensitive to a change in horizontal movement, andthe saccule gives information about vertical acceleration(such as when in an elevator). Remember Utricle is lateralforward and backward – the Saccule is Sit and Stand.Exception: both are subject to A/P acceleration
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Otolith Function
The brain therefore has difficulty determining tilt vs translation without
accessory input from the canals
Otolithic System
▪ Remnant of the lateral eyed animals
▪ Turned on by near vision
▪ Primes the legs
▪ Turned off by long axis distraction of the cervical spine
▪ Fires into midline Cb specifically the Nodulus
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The Otolithic SystemAn otolith also called statoconium or
otoconium, is a structure in the
saccule or utricle of the inner ear,
specifically in the vestibular labyrinth
of vertebrates
Each macula consists of a sensory
membrane containing the receptor
cells that supports a “heavy load,”
the otoliths.
The otolith is composed of
calcareous (calcium carbonate)
material embedded in a gelatinous
matrix. This is important because
osteoporosis patients frequently are
subject to otolithic degeneration
resulting in BPPV.
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Vestibular Nerve Physiology
Each vestibular neuron fires
tonically at a resting rate of
approximately 90-100 spikes
per second.
Upon activation these
peripheral vestibular afferents
have two main targets: the
vestibular nuclear complex
and the cerebellum
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Vestibular Nuclei Complex
4 Major Nuclei1. Superior Vestibular Nucleus
VOR relay center
2. Medial Vestibular Nucleus VOR relay center
VSR relay center
3. Lateral Vestibular Nucleus VSR relay center (major-
ipsilateral LVST). Mainly LE extensor muscles for stability. Input is mostly from the Otoliths
4. Inferior Vestibular Nucleus Connected to all other nuclei
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Vestibular Nuclear Complex
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The 4 vestibular nuclei are: Super Vestibular Nucleus, Medial Vestibular Nucleus,
Lateral (Dieter’s) Vestibular Nucleus, and the Inferior (caudal) Vestibular Nucleus.
Vestibular Nucleus Function
The vestibular nucleus is a multi functional nucleus with two
very important functions.
1. it tells you where your head is relative to gravity and
where gravity is relative to your head.
2. it establishes appropriate postural reflexes i.e., the
vestibular ocular reflex (VOR) and the vestibular spinal
reflexes (VSR).
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Vestibular Nuclei Projections
The vestibular nuclei receiveprojections from the cortex,the cerebellum, subcorticalvisual centers, and the spinalcord. Vestibular circuitry istherefore embedded withinlarger networks involved in theintegration of vestibular,visual, and proprioceptiveinformation. This provides anongoing global control of eyeand body orientation in thedynamic context of voluntarymovement and externalperturbations.
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Vestibular Nuclei Commissure
▪ Commissures link thevestibular nuclei from eitherside of the brainstemthrough mutually inhibitoryconnections
▪ This allows for informationto be shared across thebrainstem (push-pull)
▪ Which means that duringactive head rotation to theright, the right vestibularapparatus is excited andvia the commissure and theleft side becomes inhibited
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VOR (vestibular ocular reflex)
VOR gives us the ability tomove our head and maintainvisual (foveal) fixation on atarget without developing anyretinal slip or blurring of vision.
The VOR has a directpathway and an indirectpathway which we will talkabout that at another time.The main ascending tracksare from the superior andmedial vestibular nuclei to theextraocular muscles travelingthrough the mediallongitudinal fasciculus to driveoculomotor activity
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VSR
The VSR has to do withmaintaining balance and thisis just one part of our balancesystems. The distributivespinal reflexes are importantwhen you becomedestabilized while walking ona sandy beach, wet slipperypavement, on ice or standingon a foam surface.
Vestibular spinal reflexes arehard wired reflexes that keepus upright against gravity byallowing us to create anappropriate motor commandto avoid a fall .
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The medial vestibular spinal nucleus
and tract The media vestibulospinal trackinterfaces with the ventral horn ofthe spinal cord to create motoractivation for cervical spinestabilization. it is therefore usefulin the rehabilitation of patientswith ligament laxity secondary toa traumatic cervical sprain andstrain.
I personally have had numerouspatients over the years who havecome into the office followingphysical therapy or chiropracticwhich the patient terminatedbecause they couldn't handle thecervical exercises or mobilization.
These same patients have doneexceptionally well by putting themin a rotational chair and rotatingthem while the head is stabilized,performing ocular motor therapy,implementing the SenMoCorhead laser target maze, utilizingtrigeminal stimulation, EMS andTENS stimulation
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The medial vestibular spinal
nucleus and tract As a chiropractor we often here of patients who repeatedly
bang their head against the roof of the car when getting in
and out of the vehicle. This is often secondary to poor head
and neck maps in the brain. Improved head/neck maps may
be obtained through vestibular rehabilitation. This can all be
done without further traumatizing an unstable region.
Stimulation in this manner is aligned at creating better
cortical representation of their head and neck by generating
better “Head/Neck Maps”
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Lateral Vestibulospinal Nucleus
and TractThe LVST also innervates the anterior horn to create motor
activation. It extends further down the spine than the medial
vestibular spinal tract to innervate the extensors of the trunk
and legs.
It is pretty much ipsilateral but there is some bilaterality to it
but, for the most part it is strictly ipsilateral and important for
postural responses and standing upright.
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The Caudal Vestibular Nucleus and
TractThese guys innervate the dorsal columns (sensory) region of
the spinal cord for the purpose of receiving an effort copy of
the motor commands thus gating all incoming information
that says the same thing and only allowing that information
which is leftover (the errors) to ascend
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CLASSIFICATION of
VESTIBULAR REFLEXES▪ Old thinking. Cristae is a kinetic receptor and maculae
are static receptors
▪ Both receptor organs produce motor reflexes that cannot
be totally differentiated
▪ It is therefore appropriate to differentiate the reflexes by
categories based on their functional role
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CLASSIFICATION of
VESTIBULAR REFLEXES▪ Vestibulo-Ocular Reflex, The VOR acts to maintain stable vision
during head motion. This means that the eyes precisely counter-rotate to compensate for the head and keep the eye stable in space.
▪ Angular VOR, The angular VOR is primarily responsible for gazestabilization
▪ Linear VOR, The linear VOR, is mediated by the otoliths,compensates for translation and acceleration in a linear direction(which is basically the same thing). The linear VOR is most importantin situations where near targets are being viewed and the head isbeing moved at relatively high frequencies.
▪ Vestibulospinal Reflex, The purpose of the VSR is to stabilize the body.
▪ Vestibulocollic Reflex, this is not an ocular reflex but a neck reflex. The vestibulocollic reflex (VCR) acts on the neck musculature to stabilize the head. The reflex head movement produced counters the movement sensed by the otolithic or semicircular canal organs.
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Vestibular Reflexes summary
1. Maintain posture.
2. Evokes extensor musculature activity (tone) above T6
and below T6 to compensate for gravitational forces.
3. Produce “kinetic” contractions of muscles for
maintenance of equilibrium and ocular stability during
movement. Includes reflexes arising from BOTH the
canals during angular acceleration and the otoliths
during linear acceleration.
4. Help maintain muscular tone: a role of both maculae
and cristae
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Reflexes: continued
Labyrinthine contribution to skeletal-muscular tone is
demonstrated following unilateral labyrinthectomy studies in
cats which results in:
Tone is decreased in the ipsilateral extensors
Tone is increased in the extensor muscles of the
contralateral extremities due to loss of inhibition
Meaning that, a unilateral vestibular deficit (UVD) patient
will present with ipsilateral extensor muscle hypotonia
and contralateral hypertonia of the extensors.
WOULD THIS AFFECT HOW YOU MANAGE YOUR
CERVICAL SPINE PATIENTS?
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Does my dizzy patient have a
stroke?Craniocervical pain
Narrative reviews have suggested that craniocervical pain mayaccompany dizziness in patients with stroke in the posterior fossabecause of the stroke itself (mass effect or direct involvement of pain-sensitive structures) or its underlying cause (e.g., dissection or aneurysmof the vertebral artery).22
Two studies addressed this issue. Headache or neck pain was present in a minority of patients presenting with acute vestibular syndrome (38%, n = 9/24;9 and 29%, n = 29/1016). A statistically significant association with central causes (38% v. 12%, p < 0.05) was found in the larger study.
6. Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke 2009;40:3504–10 [PMC free article] [PubMed] [Google Scholar]
9. Norrving B, Magnusson M, Holtas S. Isolated acute vertigo in the elderly: Vestibular or vascular disease? Acta Neurol Scand 1995;91:43–8 [PubMed] [Google Scholar]
22. Edlow JA, Newman-Toker DE, Savitz SI. Diagnosis and initial management of cerebellar infarction. Lancet Neurol 2008;7:951–64 [PubMed] [Google Scholar]
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DIFFERENTIAL DIAGNOSIS
Differential Diagnosis Should Include:
▪ A good diagnosis is not like a batting average where
you play the percentages. You might strike out! A
thorough examination is essential. You need to know
whether you are looking at:
A One level lesion
Multifocal / multiple lesions
A Central Lesion
A Peripheral Lesion
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Peripheral causes of vertigo
▪ 1. Benign paroxysmal positional vertigo▪ 2. Vestibular neuronitis▪ 3. Recurrent vestibulopathy▪ 4. Meniere’s disease▪ 5. Head trauma (labyrinthine concussion)▪ 6. Otosclerosis▪ 7. Herpes zoster oticus▪ 8. Cholesteatoma▪ 9. Perilymph fistula▪ 10. Aminoglycoside (antibiotics) ototoxicity
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Central causes of vertigo
▪ Vascular: vertebrobasilar ,TIA, cerebellar or brain stem stroke
▪ Cerebellopontine angle tumors: acoustic neuroma, meningioma, cholesteatoma, metastatic tumor
▪ Demyelinating disease: MS, postinfectious demyelination
▪ Cranial neuropathy: focal involvement of VIII nerve or in association with systemic disorders
▪ Intrinsic brainstem lesions: tumor, arteriovenous malformations
▪ Seizure disorders (rare)
▪ Spinocerebellar degeneration
▪ Hypertensive medications
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Most Frequent Vertigo Syndromes Diagnosed in a
Dedicated Neurological Dizziness Unit(N=4790) Vertigo and Dizziness by Brandt, Dietrich, and Strupp-2005
▪ BPPV 18.3%
▪ Phobic Postural Vertigo 15.9%
▪ Central Vestibular Vertigo 13.5%
▪ Vestibular Migraine 9.6%
▪ Vestibular Neuritis 7.9%
▪ Meniere’s Disease 7.8%
▪ Vestibular Paroxysmia 2.9%
▪ Perilymph Fistula 0.4%
▪ Unknown 4.2%
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You must be a lot like Sherlock Holmes
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Nothing Replaces a Good Bedside Neurological Examination
▪ History and physical examination provide the most important information
▪ Often, patients have difficulty describing the exact symptom experienced
▪ The first step is to define the symptom
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A case history specific to balance
may include the following:▪ Collection of results from other health professionals
▪ Fall risk data
▪ Medical history including blood pressure and other vitals history of dizziness ,balance problems or falls Medication use alternative medicines presence of other comorbidities
▪ Nature of dizziness and or imbalance symptoms including the following : Aggravating factors Alleviating factors Accompanying symptoms (e.g., Hearing loss, tinnitus aural fullness Duration (seconds , minutes , hours , days ) Frequency initial onset (How did it begin (gradual / sudden)
▪ Pattern (time of day , , activity symptomatic )
▪ Quality and character ( spinning , imbalance , disorientation )
▪ Patient questionnaire on dizziness
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Physical Examination▪ A general medical examination is important. Physical
examination is very important in patients complaining of
Vertigo because it can be the earliest symptoms of a
neurodegenerative disorder
▪ Postural hypotension measurement
▪ Orthostatic hypotension – probably the most common
▪ Identifying an irregular cardiac rhythm may help
▪ Other measures to consider include a visual assessment
and a musculoskeletal inspection (significant for arthritis
and peripheral neuropathy)
▪ Vertigo can also be an important symptoms of stroke,
tumor, demyelination, or other pathologies of the nervous
system
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Frenzel Goggles are a diagnostic tool used
in ophthalmology, otolaryngology and audiovestibular medicine for the
medical evaluation of involuntary eye movement (nystagmus). They are
named after Frenzel, a German physician. The purpose of
the goggles is to disable the patient's ability to visually fixate on an
object while at the same time allowing the examiner to adequately
visualize the eye. This is done by using high-powered
(+20 diopters) magnifying glasses with an illumination system. With
such a high-powered lens, it is unlikely that the patient can adequately
focus and visually fixate on an object to suppress nystagmus.
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Videonystagmography (VNG) is a technology for testing inner
ear and central motor functions. It involves the use of infrared
goggles to trace eye movements during visual stimulation and
positional changes.
Computerized Dynamic Posturography
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Computerized Dynamic Posturography
(CDP) is well documented in the clinical and
scientific literature as an objective method of
differentiating sensory, motor, and central
adaptive functional impairments of balance.
AireX Pad®
The Airex® Balance Pad is a
reasonably priced product
which has a smooth surface,
making it ideal for barefoot
balance testing and training.
Due to the yielding foam, the
body is constantly challenged
to maintain balance. This pad
is also great for balance,
mobility, standing stability and
motor-skill training.
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BESS Test with Airex Balance Pad
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While this test is
frequently used for
mTBI evaluation it is a
very useful tool for
vestibular evaluation
by means of a
Romberg test, Tandem
Romberg and Unipedal
stance. These tests
are performed with
eyes open and closed
both on a compliant
and then again on a
non-compliant surface.
This form is
downloadable from the
Internet and serves as
a great patient handout.
Bedside Diagnostic Gems
mnemonic
▪ V – Vascular
▪ I _ Infectious
▪ N – Neoplastic, Neurological
▪ D – Degenerative
▪ I – Inflammatory
▪ C – Connective tissue/muscle
▪ A – Autoimmune
▪ T – Trauma
▪ E – Endocrine/environmental
▪ S - Soft tissue
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VASCULAR
VINDICATES
VASCULAR: Cardiovascular Disease and
Cerebrovascular Disease
▪ Many vascular disorders may generate dizziness or lightheadedness. Therefore, Everything should be Considered Vascular Until Proven Otherwise Arrhythmias
Tachycardia
Bradycardia
Ischemic cardiomyopathy
Vasovagal syncope
Carotid sinus hypersensitivity
Conduction blocks w/ elongation of the PR interval
Brain ischemia
Etc.
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Clinical Aspects of Brainstem
DisordersCommon symptoms found in the majority of brainstem
lesions include diplopia, dysarthria, VERTIGO nausea and
vomiting.
These lesions are typically vascular in nature but can be as
result of other disorders such as MS and pontine gliomas
etc.
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Clinical Case. Your patient presents with the
following: What is the diagnosis?
▪ Vertigo, nausea and vomiting
▪ Ipsilateral facial pain and temperature loss
▪ Ipsilateral Horner’s
▪ Ipsilateral Ataxia and dysmetria
▪ Weakness of palate, pharynx and larynx
▪ Dysphagia, hoarseness, diminished gag reflex
▪ Contralateral pain and temperature loss
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2 Types Medullary Vascular Lesions
There are typically only 2 kinds ofmedullary ischemic attacks,
▪ Dorsal lateral
▪ The paramedian and basil arelumped together.
▪ Dorsal lateral infarction causesdamage typically referred to as aWallenberg syndrome. Typically,you will have:
▪ Ipsilateral Horner’s syndrome,loss of pain and temperature overthe face on the same side of thelesion. There can be cerebellarfindings on the ipsilateral sidecausing ataxia.
▪ Contralateral loss of pain andtemperature with..
▪ You can get severe nausea,vomiting, vertigo, and nystagmusdue to vestibular influence.Hiccups may be common do tolesion in the 9th and 10th nerveswith difficulty swallowing.
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Wallenberg Syndrome
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Lateral Medullary Syndromeaka: Wallenberg Syndrome (posterior inferior Cb artery)
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Regional territories
Lateral Medullary Syndrome
“Wallenberg Syndrome”
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Note the cranial nerve locations and their trajectories which become affected
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Labyrinthine Artery - Vascular Supply
It is important at this point to also review the clinically important Labyrinthine artery.
45% from AICA
▪ 24% superior cerebellar artery
▪ 16% basilar
▪ Two divisions: anterior vestibular artery
common cochlear artery
▪ Vascular pathologies can give pulsatile tinnitus or deafness
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Vestibular Migraine
I include vestibular migraines because of its seeminglyneurovascular nature even though it is not necessarily anischemic lesion. It is important to know due to the clinicalpresentation of headaches and dizziness.
Vestibular Migraine is associated with dizziness and vertigoas a common aura in migraineurs. It is estimated that about30% of migraineurs will be affected with this form of aura.
You could get dizzy and have balance problems without havinga migraine at all. Other times, the vertigo symptoms happenbefore, during, or after the headache. Sometimes, you mighthave migraines for years before the vertigo symptoms begin.
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Acute Vasculature
Vestibular Syndrome
Ocular Motor Assessment
1st step is to observe normal ocular movements and search
for any Nystagmus of the eyes, with a fast movement in one
direction and a slow movement in the other.”
Nystagmus can be classified as spontaneous, gaze-evoked,
or positional. The direction of nystagmus – conventionally
described by the direction of the fast phase, which is the
direction it appears to be “beating” toward. Fast phase
component may be horizontal, vertical, rotatory, or any
combination of these.
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Acute Vestibular Syndrome
H.I.N.T.S. to I.N.F.A.R.C.T.
“H.I.N.T.S.” Battery
1. Head Impulse Test
2. Nystagmus
3. Test of Skew
▪ STROKE FINDINGS:
“I.N.F.A.R.C.T.”
▪ Head Impulse test -Normal
▪ Fast-phase Alternating
nystagmus
▪ Re-fixation on Alternating
Cover Uncover Test
▪ Any ONE of these points to
a Stroke
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Nystagmus Testing
▪ Performed in
Primary Gaze
Lateral Gaze
Vertical Gaze
▪ In a normal volunteer: there is No nystagmus inprimary gaze. During lateral gaze some nystagmusmay be normal. Learn to suppress this with fixationby placing a piece of paper between their head andthe wall and ask them to look at the wall as if thepaper was not present. Otherwise, you might seenystagmus which would not be there without the
sheet of paper.
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Nystagmus
https://youtu.be/1q-VTKPweuk?t=105
Patient with vestibular neuritis. Note: here it is again, when
he looks to the left see that the nystagmus increases. It is
left beating and there is a rotatory component towards the
left and it increases when he looks to the left and you can
see the torsional component.
When he looks to the right it lessens but the fast component
is still towards the left.
Unidirectional nystagmus, does not change direction and
this exam is reassuring.
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Nystagmus
https://youtu.be/1q-VTKPweuk?t=157
Compare to this lady who when she looks to the right, she
has small horizontal nystagmus with the fast component to
the right. Then, when she moves more central and to the
left, you can see that the nystagmus beats towards the left.
So, she has direction beating nystagmus or bidirectional
nystagmus which is worrisome.
Note: nystagmus is named for the direction of the fast
phase
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Test of Skew
(Vertical)
Cover / Uncover test
https://youtu.be/1q-VTKPweuk?t=201
Examiner takes their hand and covers the eye and then
quickly covers the other eye to observe if there is any
vertical movement of the eye when it is uncovered.
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Test of Skew
https://youtu.be/1q-VTKPweuk?t=214
Observe that when the hand is taken away from the right
eye, the eye will go medially and upward and when the
examiners hand is taken away from the left eye it goes
medially and downward.
This abnormal skew deviation is worrisome
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Head Thrust Test
A unilateral or bilateral vestibulopathy can be identified using theHead-Thrust test. The head thrust test is a test of vestibularfunction that is performed as part of the bedside examination. Thismaneuver tests the vestibulo-ocular reflex (VOR).
The patient sits in front of the examiner and the examiner holds thepatient's head steady in the midline. The patient is instructed tomaintain gaze on the nose of the examiner. The examiner thenquickly turns the patient's head about 10–15 degrees to one sideand observes the ability of the patient to keep the eyes locked onthe examiner's nose. If the patient's eyes stay locked on theexaminer's nose (i.e., no corrective saccade) (A), then theperipheral vestibular system is assumed to be intact. Thus in apatient with acute dizziness, the absence of a corrective saccadesuggests a CNS localization. If, however, the patient's eyes movewith the head (B) and then the patient makes a voluntary eyemovement back to the examiner's nose (i.e., corrective saccade),then this suggests a lesion of the peripheral vestibular system andnot the CNS.
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Bedside Head Thrust Test
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Head Impulse Test
https://youtu.be/1q-VTKPweuk?t=295
Hold onto the patients skull while the patient fixates on
examiners nose (or camera). Move head (maybe 20
degrees), slowly to the right, then BRISKLY to midline. What
you are looking for are catch-up Saccades of the eyes
In this video her eyes remain fixed on the camera =
NORMAL or Abnormal?
2/1/2020, Larry E. Masula, D.C., DACNB, FABVR, FAFIICC 143
Head Impulse Test
▪ https://youtu.be/1q-VTKPweuk?t=324
Abnormal
Notice that this man presents with nystagmus when he looks
to the left and when his head is turned to the right. Do you
see that there is a larger movement of the eyes from the
right back to the midline? That is an abnormal HIT which is
reassuring which shows that he has a peripheral nerve
problem and probably does not have a brain problem.
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Head Impulse Test
https://youtu.be/1q-VTKPweuk?t=389
This lady has a rock-solid head impulse test. She is
WORRISOME because she has acute vertigo and
nystagmus and we cannot find a nerve problem. She
probably has a BRAIN problem.
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INFECTIOUS
VINDICATES
Infectious Disorders
Otitis ExternaPathophysiology
Typically begins with otitisexterna in elderly diabetics.
Infection spreads to surroundingtissues and adjacent temporo-occipital bones, almost alwayssecondary P. aerugiosa.
Commonly affects the facial nerve in the fallopian canal or at the stylomastoid foramen and can spread across the dura to produce purulent meningitis.
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 06/22/2019 150
INFECTIOUS DISORDERS:
Malignant Otitis ExternaDiagnosis – CT scan of the temporal bone may reveal:
1. External canal mass
2. Clouding of the mastoid air cells
3. Sequestra of the bony canal
4. Erosion at the base of the skull
5. Soft tissue masses within the parapharynx and
nasopharynx
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 151
INFECTIOUS DISORDERS:
Otitis MediaPathophysiology
The middle ear is involved with most viral URI’s. The nasal,paranasal, and pharyngeal mucositis spreads to involve theEustachian tube and middle ear mucosa, since the mucosa ofthe pharyngeal end of the Eustachian tube is continuous withmucociliary system of the middle ear. If the eustachian tubebecomes inflamed it swells and closes. If the tube is closed /blocked, then the middle ear and mastoid system becomedisconnected with the air in the nasopharynx and atmosphericsystem. This results in the air within the middle ear and mastoidbeing absorbed by the mucosa and a negative pressuredevelops. The negative pressure causes the TM to becomesucked inward and secondly the microcirculation within thetympanic cavity is encouraged to release fluid and mucusresulting in an inability for the TM to generate sound energycausing conductive deafness. Secondary bacterial infectionmay develop leading to otitis media.
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 152
INFECTIOUS DISORDERS:▪ Otitis Media (Inflammation of the middle ear)
Is a common cause of conductive hearing loss, particularly in
children. 2 Forms
A- Suppurative Otitis (infected)
B- Serous Otitis (non-infected)
Larry E. Masula, D.C.,DACNB, FABVR, FAFICC 2/1/2020 153
INFECTIOUS DISORDERS:
Otitis MediaDiagnosis
Most common organisms:
Streptococcus Pneumonia
Hemophilus Influenza
Translucency of TM is lost. The TM may be retracted and
the middle ear- atelectic. Impaired mobility may be observed
during pneumatic otoscopy.
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INFECTIOUS DISORDERS:
Chronic OtomastoiditisPathophysiology
From an untreated / unresponsive acute Otomastoiditis.
Characterized by thickened mucosa with obliteration of the
mastoid air cell lumen, perivascular fibrosis, and osteitis.
Polypoid granulomas may fill the mastoid antrum, the middle
ear, and extrude through a tympanic perforation.
Cholesteatoma (keratinized squamous epithelium) can
invade the middle ear destroying the ossicles and labyrinth
and pneumatized temporal bone cells. Producing conductive
hearing loss and vertigo.
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INFECTIOUS DISORDERS:
Cholesteatoma
Larry E. Masula, D.C.,DACNB, FABVR, FAFICC 2/1/2020 156
INFECTIOUS DISORDERS:
Mastoiditis
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 157
Intracranial Extension of Ear Infections
Background-from either acute otitis media or mastoiditis and
bone destruction. Febrile patient w/ continued ear pain,
mastoid pain, headache despite antibiotic treatment.
▪ Route of Spread may spread backward-
▪ 1. Direct extension
2. Hematogenous
3. Thrombophlebitis
Resulting in:
Meningitis
Epidural Abscess
Sigmoid Sinus Thrombophlebitis
Brain AbscessLarry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 158
INFECTIOUS DISORDERS:
Viral Vestibular NeuritisPathophysiology-part of a systemic viral illness, i.e. measles, mumps and mono, HERPES SIMPLEX II
A unilateral vestibular deficit (UVD), arising from a viral causein most patients, results in either sudden deafness or acuteprolonged vertigo with nystagmus rapidly beating (fastphase) toward the side of the lesion. This also results in aYaw rotation toward the side of the lesion and a Roll tilt in thesame direction. Acute symptoms usually abate within 3-5days, but the patient may be left with the equivalent of avestibular neuropathy.
▪ Diagnosis-
1. Caloric responses are decreased and/or absent on the side of the lesion. Ultra-high hearing loss. VNG abnormalities
2. Must be differentiated from other forms of labyrinthitis
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INFECTIOUS DISORDERS
Labyrinthitis
▪ A viral or bacterial infection of the fluid within the inner ear.
▪ Within one-week sufferers are usually able to situp and after two weeks will begin to compensatefor the dizziness/vertigo. Acute episodesusually end after one to two months. Althoughpermanent vestibular damage may remain insome cases, most people recover fully fromviral labyrinthitis.
▪ Labyrinthitis will classically affect hearing as wellas balance which are also symptoms of an AICAstroke
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Differential Diagnosis of Acute Peripheral Vestibulopathy
History Examination Laboratory
Viral Neurolabyrinthitis
Developing over hours, resolving over days, prior flu-like illness
Normal except for signs of acute unilateral vestibular loss
ENG: caloric hypo excitabilityAudio: may show ultrahigh frequency loss
Bacterial Labyrinthitis Abrupt onset, hearing loss, prior ear infections
Signs of otitis mediaor meningitis
ENG: absent caloric Audio: sensorineural loss. CSF: Pleocytosis
Labyrinthine Ischemia Abrupt onset w/ neurologic symptoms, prior vascular disease
Signs of brainstem or cerebellar infarction
ENG: absent caloric Audio: sensorineural lossImaging: Brain infarction
Perilymph Fistula Abrupt onset w/ head trauma, barotrauma, or sudden strain lifting, coughing, sneezing
Positive fistula test, may be chronic otitis w/ TM perforation
ENG: caloric hypo excitabilityAudio: usually sensorineural lossImaging: CT may show erosion from cholesteatoma
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Endolymphatic Hydrops(Meniere’s Syndrome)
Pathophysiology
1. An increase in the volume ofendolymph distending theendolymphatic system
2. The labyrinth dilates until thesaccular wall makes contactwith the stapes footplate andthe cochlear Scala
3. Hearing loss and vertigo arecaused by ruptures in themembranes separatingendolymph from perilymphcausing a sudden increase inpotassium which inhibitslabyrinth receptors
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 162
Meniere’s cont.
Bacterial and viral. Majority unknown
1. Family history 50% of cases
2. Considered to be rare based on AMA epidemiological
studies, perhaps as low as 1% of vertiginous patients
... Meniere's disease is an inner ear disease that typically
affects one ear. This disease can cause a fullness, pressure
or pain in the ear, severe cases of dizziness or vertigo,
hearing loss and a ringing or roaring noise, also known as
tinnitus.
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 163
Perilymph Fistula’s
A perilymph fistula (PLF) mayalso cause vertigo, It is anabnormal connection (a tearor defect) in one or both of thesmall, thin membranes (theoval window or the roundwindow) that separate the air-filled middle ear and the fluidfilled perilymphatic space ofthe inner ear. This smallopening allows perilymph(Na+ rich fluid) to leak into themiddle ear. - See more at:http://vestibular.org/perilymphfistula#sthash.bcdq3m49.dpuf
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Perilymph Fistula’s
Leaks through the round and oval windows can occurfollowing; severe nose blowing, strenuous exercise,barotrauma, and surgical trauma.
The symptoms of perilymph fistula may includedizziness, vertigo, imbalance, nausea, and vomiting.Usually however, patients report an unsteadiness whichincreases with activities that elevate CSF pressure andwhich is relieved by rest. Some people experienceringing or fullness in the ears, and many notice ahearing loss. Most people with fistula’s find that theyget worse with changes in altitude (fast elevators,airplanes, and travel over mountain passes.
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Perilymph Fistula Test
▪ The development of nystagmus in response to the
application of pressure on the external auditory canal
constitutes a positive result for the perilymph fistula test
and suggests the presence of a fistula between the air-
filled middle ear and the fluid-filled inner ear.
▪ Hosuk Chu, M.D., and Won-Ho Chung, M.D. N Engl J Med 2012; 366:e8
January 26, 2012 DOI: 10.1056/NEJMicm1010568
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NEOPLASTIC -
NEUROLOGICAL
VINDICATE
Internal Acoustic Meatus for Facial Nerve
and Vestibular Nerves
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Acoustic neuromas are usually located in the angle between the cerebellum and the
pons, in the back of the skull (posterior fossa) applying pressure in and around the
internal acoustic meatus and may impair both Cn.7,8. Common symptoms are one-
sided hearing loss, tinnitus, vertigo/dizziness and facial paralysis
NEOPLASM: Cerebellopontine Angle
TumorsLesions in the area of
cerebellopontine angle cause
signs and symptoms secondary
to compression of nearby cranial
nerves, including CN V, VII, VIII.
I.E., involvement of CN V from a
cerebellopontine mass lesion
often results in loss of the
ipsilateral corneal reflex.
Patients with larger tumors can
develop Bruns nystagmus due to
compression of the cerebellar
flocculi.Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 169
NEOPLASM: CPA Tumors
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Br J Neurosurg. 2008 Jun;22(3):441-3. doi:
10.1080/02688690801911614.
Cerebellopontine angle epidermoid tumor
presenting with bilateral gaze nystagmus.
Han IB1, Huh R, Chung SS, Kim OJ.
Abstract
Vestibular symptoms have been rarely described in
cerebellopontine angle epidermoid tumors. We report a
case of CPA epidermoid tumor presenting with subacute
onset of vestibular symptoms such as vertigo, gait ataxia,
and nystagmus masquerading as acute vestibular neuritis
or central vertigo. The vestibular symptoms disappeared
after excision of the tumor.
PMID: 18568737 [PubMed - indexed for MEDLINE]
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Cerebellopontine angle epidermoid tumor
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Clin Exp Otorhinolaryngol. 2012 Dec; 5(4): 234–236.
Published online 2011 Sep 15. doi: 10.3342/ceo.2012.5.4.234
PMCID: PMC3506776
A Posterior Petrous Meningioma with Recurrent
VertigoSeong Jun Choi, MD,1 Jong Bin Lee, MD,1 Joon-Ho Bae, MD,1 Jung-Hee Yoon, MD,1 Ho-Jin
Lee, MD,1 Chan-Ho Kim, MD,1 Keehyun Park, MD,2 and Yun-Hoon Choung, MD2
Abstract
Meningioma's account for around 15% of all primary brain tumors
with some 10% of meningioma's arising in the posterior fossa. In
rare cases, a meningioma can form around the endolymphatic
sac. When formed in the posterior fossa, meningioma tumors can
produce vague, non-specific vertiginous symptoms. Research
has observed that a subset of these lesions could produce
symptoms indistinguishable from those of Meniere's disease.
Therefore, we described the clinical features of a case of
posterior petrous meningioma with recurrent vertigo as well as
the substantial resolution of symptoms after tumor removal via
transmastoid approach.
NEOPLASMA: Acoustic Neuroma (vestibular schwannoma)
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Cerebellum: the Brain Behind the
Brain
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Clinical Manifestations, (DDX)
▪ Tilting –
▪ Falling forward or backward –
▪ Exocentric Yaw axis (spinning) –
▪ Egocentric Yaw axis (spinning) -
▪ Most likely cortical
▪ Mesencephalic, medullary, Cb
▪ Peripheral Nerve i.e. BPPV or vestibular nerve loss
▪ Most likely cortical
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Case report Rotational vertigo caused by cerebral lesions: Vertigo and areas
3av, 2v, and 7
▪ Eiichirou Urasaki, Akira Yokota
▪ Source Journal of Clinical Neuroscience > 2006 > 13 > 1 > 114-116
Abstract - We describe two patients complaining of vertigo
associated with a small supra-tentorial convexity
meningioma. Symptoms disappeared after tumor removal,
providing evidence for an association between the vertigo
and the cerebral cortical lesions. Tumors were located in the
central and parietal areas, respectively, which are probably
analogous to the vestibular cortex in the areas designated
3av, 2v, and 7 in animal studies
*** Why you must check for non-vestibular cortical
findings
Larry E. Masula, D.C.,DACNB, FABVR, FAFICC 2/1/2020 177
Van GoghIn an acute right sided process
such as vestibular neuritis, the
nuclei are initially excited, and
the eyes exhibit a slow phase of
nystagmus pushing the eyes to
the left, the fast phase of
nystagmus to the right. But, as
time passes and the nerve dies
the right side, is no longer an
acute problem and the Left side
that is no longer being inhibited
through the commissure appears
overly active. The fast phase of
nystagmus then switches, and
the eyes beat Slow phase to the
right with a Fast phase back tothe left.
So, In Vincent's case on which
side is the probable lesion?
The Right side. The slow phase
gives an illusion that you are
moving to the right while the
world is moving left.
Assuming that in his case it was
no longer an acute problem, the
Left side was no longer being
inhibited by the right vestibular
nuclei and the left side appears
overly active.
The same is true in the acute
stage of a vascular insult
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Sir Gordon Morgan Holmes, (22 February 1876 – 29 December 1965) was a
British neurologist. He is best known for his pioneering research into
the cerebellum
Gordon Holmes, M.D.
1917, Dr. Holmes talked about the symptoms of acutecerebellar lesions due to WWI gun shot wounds andwhat he talked about is this,
“the brain (cortex) is fine but these people have thesepresentations that are very severe and involveaberrancies’ in the frontal cortex. It is also increasinglyclear that there are extensive connections between theCb and frontal associative areas of the cerebral cortexthat fall well outside the classical sensory-motor circuit.”
▪ The Cerebellum. 2007; 6: 268-279
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Functional ConceptsA “BAD” Cb is known to be involved with:
Cognitive functions (ataxia of thought and represents erratic attempts to correct errors of thought or behavior)
Psychiatric Disturbances
Autonomic concomitants
Sensory Disturbances
Maintenance of Equilibrium
Breakdown in Coordination/Sequenced motor activity – walking, intention and terminal tremors (not at rest), eye movements w/ diminished pursuits and overshooting saccades. Intention tremors and terminal tremors.
Motor learning – motor skills
Monitor & predict
Horizontal & Vertical nystagmus w/ & w/o fixation
Scoliosis – genetic calcium channel mutation affecting midline Cb
Head tilt
Ocular deviations
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Functional Concepts
▪ A “Bad” cerebellum may develop as a result of:
Alcohol degeneration
Thiamine deficiencies
Toxins
Concussion
Inflammation
Acute and hemorrhagic stroke
Inherited gene changes
Paraneoplastic disorders
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The cerebellum is organized anatomically
and physiologically
▪ “ArchiCerebellum”
Floculonodular Lobe
▪ “Paleocerebellum”
Anterior Lobe
▪ “Neocerebellum”
Posterior Lobe
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Floculonodular Lobe Aka (ancient)ArchiCerebellum
Aka Vestibulocerebellum▪ Receives Input from the
labyrinthine system with noinvolvement of the deep Cbnuclei
▪ This has influence over theaxial musculature, someinfluence over VestibularOcular Reflexes andVestibular Reflexes
▪ Flocculus/paraflocculusmodulates the smoothnessof pursuits and calibratesthe rotational VOR
▪ Nodulus – calibrates VOR(from otoliths)
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Anterior Lobe Paleocerebellum (old-not ancient)
Spinocerebellum
▪ Associated with upright
stance, posture and
bipedalism
▪ Limb coordination and
feedback from extremities
▪ Controls proprioception
related to postural muscle
tone
▪ Axons extend to the deep
Cb nuclei
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Medial Zone (Vermis)▪ Lesions in midline Cb (aka:
Spinocerebellum)
▪ Gait instability
▪ Ataxia of trunk
▪ Titubation
▪ Breakdown in movements
▪ Saccadic dysmetria
▪ Vertiginous activity
▪ Note: findings may improve when
lying down or with an increase in
integrity into the system
▪ Ex: distract the patient’s neck and
this fires midline Cb structures and
the symptoms of the lesion reduce
(ddx midline lesion versus lateral)
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Lateral Zone (aka
Neocerebellum)Input: from the parietal cortex via the ponto-cerebellar mossy fiber projections
▪ The information is specific to the location of the body in space
▪ Integration of body position information, strength and speed
Output: Dentate nucleus projects to the cortex for cognition of movement. Aids in timing and planning and higher cognitive functions
Note: no balance, equilibrium or gait disorders associated with the Neocerebellum
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Comparing and Contrasting
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Normal Cb Alcoholic Cb
Note the folia atrophy
Cerebellar Function
▪ Maintenance of Equilibrium
Balance, posture, eye movements
▪ Coordination/Sequenced motor activity
Walking gait
▪ Adjustment of Muscle Tone
▪ Motor Learning-Motor Skills
▪ Monitor & Prediction of Movement
▪ Cognitive Function-learning
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Cerebellar Stroke
▪ A cerebellar stroke is one of the least common types
of strokes. It occurs when a blood vessel is blocked or
bleeding, causing complete interruption to a portion of
the cerebellum. This type of stroke typically affects only
one side or section of the cerebellum. It's also referred to
as cerebellar stroke syndrome.
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Cerebellar Stroke
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Clinical Signs:
Ipsilateral Cerebellar Disease
(Flocculonodular Zone/Spinocerebellar lesions)
Abnormal Stance/Gait: a. Wide based, stumbling gait with truncal tremor, Falling/veering to side of the lesion, activities w/ increased speed/difficulty (tandem gait).
Titubation: rhythmic tremor of the body(trunk) and head. Note: must rule out BG lesion
Rotated/tilted head: not specific for side of lesion but related to eye movements
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Clinical Signs: Cerebellar
Disease
Dysdiadochokinesia: error in the rate of movements and
completion of movement (rapid alternating) vs loss of
smooth movement
Dysrhythmokinesis: errors in timing out a beat. Note:
Interactive metronome used for both testing and rehab.
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Clinical Signs: Cerebellar Disease
Dysarthria: tremulous voice with errors in prosody and
intonation (Vermal - medial zone lesions) Interference with
articulation, respiration and phonation; slowness, scanning
(stretch syllables)
Kinetic Tremor: (Cerebrocerebelar lateral zone lesions)
greatly increases as movement nears target, when accuracy
is most essential. Worse with fatigue
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Clinical Signs: Cerebellar Disease
Abnormal Tone: Hypotonia, joint laxity and pendular reflexes
Relates to the alpha-gamma co-activation
Abnormal check and rebound Check - arms outstretched and tap wrist. Should
return quickly to initial point
Rebound is excessive excursion during the attempted
return to initial point
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Clinical Signs: Cerebellar
DiseaseAbnormal Ocular Motor Function:
(Flocculonodular lobe lesions)Nystagmus: Gaze evoked
Skew Deviation: in primary position, oneeye is elevated () and other is depressed(hypotropia)
Saccadic dysmetria: usually hypermetriadue to failure to terminate the movementsecondary to lesions in the CerebellarFastigium
Impaired Smooth Pursuit
Glissades (post saccadic drift)
Alteration in VOR (due to improper termination/hypermetria)
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Cerebellar Tests
▪ Middle – Sharpened
Romberg’s, tandem gait,
finger-nose-finger, saccade
hypermetria, nystagmus,
post rotational nystagmus,
head thrust tests, smooth
pursuits
▪ Lateral – piano playing,
RAM w/ fingers, finer nose
finger
▪ Intermediate - rapid
alternating movements w/
arms front, bent utilizing
rapid pronation/supination,
then windshield wiper
motion, finger-nose-finger,
heel to shin
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Head tilts often have Cb lesions affecting
their otolithic pathways
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Normally, tilt in the (YAW) roll plane to the right normally produces a reflex
counter roll and Skew (hypertropic eye movement) towards the opposite
side. If I lose my Cb Pathways on the Rt. the right eye remains extorted
and what do I do to compensate for the extorsion? Tilt my head to the
(left) opposite side.
NormalOcular tiltReflex
Head tilt
▪ You can no longer say that a left head tilt means a bad
left Cb. I know some people instruct that from classes
you may have taken but there are too many factors
involved and that assumption is incorrect
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Central Vestibular Disorders J Neurol (2007) 254:559-568
A tonic imbalance in YAW (rotation) is characterized by horizontal(torsional) nystagmus, lateralpulsion of the eyes, past-pointing,rotational and lateral body falls, and lateral deviation of theperceived straight-ahead. (Implicates a horizontal VOR type problem, i.e. vestibularnerve loss, Meniere’s, post vestibular neuronitis, or a Cb - fastigial n.). Turning ~ 35° in Fakuda test.DDX- CN8 entry into medulla, MVN, SVN, NPHypo., PPRF demyelination or ischemia)
A tonic imbalance in ROLL is defined by torsional nystagmus,skew deviation, ocular torsion, head tilt, body, and the perceivedvertical. (Central...remember Van Gogh?, midbrain, paramedian thalamus or PIVC –parieto-insular- vestibular cx lesions)
Finally, a tonic imbalance in PITCH can be characterized by someforms of upbeat or downbeat nystagmus, for-aft tilts and falls, andvertical deviation of the perceived straight-ahead. (Central problemsomething in the midline dying off i.e. central flocculus, PPRF or bilat. medullary)WARNING…NOT GOOD!!!
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EXAMINATION - VESTIBULAR
ASSESSMENT
Tests performed in lighted room
Various tests are performed to
evaluate the where and the
why the patient suffers
vertigo. The following tests
are performed in a lighted
room.
▪ Identify any Spontaneous nystagmus
▪ Identify any (Gaze holding) nystagmus
▪ Skew deviation
▪ Vergence
▪ Decreased VOR
i. Head thrust test
ii. Dynamic visual acuity
Visual tracking
i. Smooth pursuit
ii. Saccadic eye movement
iii. VOR cancellation
Gait and balance
i. Feet together
ii. Tandem
iii. Single leg stance
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Tests performed in dark
Tests performed using Frenzel lenses or infrared goggles
(Real Eyes®)
Spontaneous nystagmus
Gaze holding nystagmus
Decreased vestibular ocular reflex
Head thrust (head shaking nystagmus)
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VOR▪ The VOR maintains foveal fixation on a target during head movement.
▪ Head movement will not normally result in excessive eye movementand the eyes will remain focused on a target. This reflex functionsto stabilize images on the retinas (when gaze is held steady on atarget) during head movement by producing eye movements in thedirection opposite to head movement, thus preserving the image onthe center of the visual field(s). For example, when the head moves tothe right, the eyes move to the left, and vice versa.
▪ Since slight head movement is present all the time, the VOR isnecessary for stabilizing vision: patients whose VOR is impaired find itdifficult to read print, because they cannot stabilize the eyes duringsmall head movements, and also because damage to the VOR cancause vestibular nystagmus
▪ Patient symptoms of a bad VOR are therefore typically triggered bychanges in head and or body position/movement in specific directions atspecific speeds (frequencies)
▪ When Head and Eye coordination are out of sync during movement it islikely a sign of vestibulopathy.
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VOR (vestibulo-ocular reflex)
▪ A good Cb (flocculonodular lobe) is necessary for both
suppression of the VOR during head movement and for
slip-induced gain change i.e. OPK stimulation and head-
thrust testing.
▪ VOR suppression. It can be suppressed by focusing on
an object e.g., motion sickness, sea-sickness or ice
skating. It is effective for peripheral lesions and has no
effect on central pathologies
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2 Forms of Nystagmus. Peripheral
and Central
Peripheral Induced Nystagmus - Vertigo of peripheral origin
generally manifests by horizontal nystagmus, rotatory
nystagmus, or absent nystagmus, but
horizontal nystagmus is not a specific sign
of peripheral vertigo.
Direction changing nystagmus (Central Induced Nystagmus)
is the most common type of nystagmus observed in
patients with cerebellar infarction. Vertical nystagmus is
always considered specific for central pathology.
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Peripheral Causes of Nystagmus and
VertigoBPPV-otoconia most often in the PC w/ down beating nystagmus
Acute Viral Labyrinthitis
Alcohol- lighter than blood so the haircells float in the endolymph and thinsblood affecting the anterior
Meniere’s Disease
Toxins – especially antibiotics such as streptomycin and gentamycin
Sequeala of Peripheral Vestibular Dysfunction
Head tilt
Cb dysfunction
Vestibular system dysfunction
Ipsi Neocortex dysfunction
Torticollis
Difficulty compensating for perturbations of head position-functional imbalance
Worse with eyes closed because a normal Cb and Frontal lobes can use vision to suppress the nystagmus
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Here we seen in the far-left diagram, equal tonic input from both vestibular
nuclei, equal 100 spikes/second, thus no perceived movement. In the middle
diagram, during right head rotation, the right canal system and the right
vestibular nuclei become excited and motion is detected rightward. In the far-
right diagram there is a left sided vestibular deficit. The right side is no longer
being inhibited and again the perception is a rightward rotation.
Physiologic vs. Pathologic
Nystagmus
PhysiologicRotation-induced
Caloric-Induced (cows) remember fast phase names the nystagmus
Optokinetic stimulation induced
End Point- there is a point at which it usually slows and stops. The exception is a cupulolithiasis
Fixating on a target suppresses the nystagmus
PathologicSpontaneous-the nystagmus isspontaneous and is best seen indarkness w/ goggles, becausethe patient cannot fixate onobjects in the room. The slowphase points to or looks at thelesion
Central Nystagmus is not suppressed by fixating eyes on a target
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Central vs. Peripheral induced
Nystagmus and vertigo▪ Example – a patient presents with no nystagmus in light
during fixation, but you see nystagmus in darkness
without fixation
▪ Central or Peripheral lesion?
▪ Answer : fixation in light indicates central is ok therefore
problem is peripheral
▪ If they cannot suppress it in the light with fixation= a
central lesion
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Oculomotor ExaminationEye movement ROM (Cardinal Fields of Gaze)
Eye movement ROM Procedure (CFG): Hold patient’s head
with one hand. Ask the patient to follow your finger
(keeping it 18-24 inches away from the patient’s face) to test
for full vertical and horizontal eye movements. Look for: •
ROM • Conjugate eye movement
Note: •
Vertical movements decrease slightly in older people
A small amount of “end point” nystagmus may be
seen at the point of full ocular range in all directions,
minimal in young people and increases with age
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Tests performed in room light Spontaneous Nystagmus Procedure:
Hold patient’s head with one hand. Ask patient to look straight ahead at a point several feet away. Look for: Nystagmus and note direction.
Gaze Holding Nystagmus Procedure:
Hold patient’s head with one hand. Ask patient to follow your finger(keeping it 18-24 inches away from the patient’s face) while you moveyour finger 30 degrees to the left, right, up and down. Pause in eachposition to observe nystagmus, note direction.
Skew Deviation Procedure:
Hold patient’s head with one hand. Cover one eye. Switch the coverfrom one eye to the other eye. Look for: a vertical corrective movementof the eye as it is uncovered. Note: Effect of direction of gaze on the skewdeviation • Any spontaneous tilt of the head and the effect of tilt on theskew deviation
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Oculomotor ExaminationVergence
Hold the patient’s forefinger in your hand about 2 feet away from thepatient’s face. Ask the patient to focus on the finger while you move ittoward the patient’s nose. Look for : Convergence of the eyes •Conjugate eye movement • Pupillary constriction
Head thrust test
Used for evaluation of a decreased vestibular ocular reflex (VOR)
Seated slow and fast-abnormal start pt. supine, progress to seated,then standing. Inform the patient that you will be moving their headvery quickly, but only through a small range. Grasp patient’s headfirmly with both hands on the sides of the head. Tilt the head forward30 degrees so that the horizontal semicircular canal is level in thehorizontal plane. Instruct the patient to look at your nose. Move thepatient’s head side to side slowly. Then, suddenly move the patient’shead in one direction and stop. The head movement should be smallamplitude with the position held at the end.
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Vestibular Ocular Pathway
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As each FEF drive the eyes to the contralateral side, a lesion
on the right will result in the eyes being deviated toward the side
of the lesion
Dynamic Visual Acuity
While moving the patient’s head side to side at a frequency
of 2Hz (2 complete side to side cycles per second) through a
ROM of 1-2 inches in each direction, (so as to not restrict
the visual field which may occur in patients who wear
glasses) ask them to read the lowest line that they can until
they cannot correctly identify all the letters on a given line.
Note the line and where this occurs and or the number of
incorrect letters. A difference of less than or equal to 2
lines is normal. A difference of greater than or equal to 3
lines is abnormal. (likely vestibular deficit). If the patient has
restriction of the cervical movement which limits your ability
to perform the head movement the test cannot be properly
performed and should be ceased.
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Smooth Pursuit eye movements Smooth-pursuit movements allow
clear vision of a moving target by
holding the image steady on the
fovea.
Smooth pursuit may be “jerky,” (ie,
inability to maintain the target on the
fovea requiring a “catch-up”
saccade).
Patients with vestibular hypofunction
who also have a central lesion exhibit
impaired smooth pursuits.
Impaired smooth pursuit and
optokinetic nystagmus is mainly seen
ipsilateral to pontine damage which
is a crucial relay area between the
cerebral cortex and the cerebellum .
Ask the patient to follow your slowlymoving finger (< 20 degrees per second)horizontally, 30 degrees from the centerto the left and to the right
Ask the patient to follow your slowly moving finger (< 20 degrees per second) horizontally, 30 degrees from the center to the left and to the right
Repeat vertically, moving 30 degrees above and below the horizontal.
Abnormal is jerky (or saccadic) Note: Eye movements may be saccadic if you are moving your finger too fast. Slow the speed of your finger to see if the person can follow smoothly.
Smooth pursuit eye movements become more and more saccadic with age. Vertical eye movement is often interrupted by a saccades in younger individuals.
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Saccadic eye movements
Hold the patient’s head with one hand. Hold your finger
about 15 degrees to one side of your nose. Ask the
patient to look at your finger and then at your nose
several times. Perform this left, right, up and down.
Look for: The number of eye movements it takes for
the patient’s eyes to reach the target, normal is less
than 2. Abnormal is several small movements or a big
movement with an overshoot. (Hypermetria)
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VOR Cancellation
The test is used principally to assess whether patient
symptoms are attributable to a vestibulocerebellar lesion.
Remember visual fixation cancels the VOR if it is of
peripheral causation. The nystagmus can often times be
suppressed by visual fixation if the cause is peripheral
The VOR is essential for maintaining stable vision on a
target when the head is moving but the brain must also have
a mechanism for suppressing the VOR when it is necessary
to move the head and eyes in the same direction. This task
is managed by the vesstibulocerebellum (Flocculonodular
lobe). Failure to suppress the VOR indicates probable
vestibulocerebellar (central) contribution to the patient's
vertigo.
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VOR Cancellation
Grasp the sides of the patient’s head firmly with both hands.
Tilt the head forward 30 degrees so that the horizontal
semicircular canal is level in the horizontal plane. Instruct
the patient to look at your nose. Move the patient’s head
from side to side approximately 30 degrees while you move
in the same direction so that your face remains directly in
front of the patient’s face. Look for: Patient’s ability to
maintain visual fixation and/or if the patient makes saccadic
eye movements.
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BESS Test
The Balance Error ScoringSystem: provides a portable,cost‐effective, and objectivemethod of assessing staticpostural stability. In theabsence of expensive,sophisticated postural stabilityassessment tools, the BESScan be used to assess theeffects of mild head injury onstatic posturalstability. Information obtainedfrom this clinical balance toolcan be used to assistclinicians in making return toplay decisions following mildhead injury.
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While this is most often used for concussion assessment, it provides great patient
feedback as to the integrity of their balance system
Optokinetic Eye Movements
The optokinetic (OPK) tape is
an essential part of the
functional neurologist's toolkit.
It can be used to evaluate
optokinetic nystagmus, which
provides a window of
assessment into the
functionality of the frontal
lobe, parietal lobe, cerebellum
and other brain regions
involved in the generation and
control of optokinetic eye
movements.
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Tests best performed using Frenzel lenses or IR
goggles
Look for any horizontal nystagmus which is the most
common form of nystagmus observed with cerebellar
infarction.
Spontaneous nystagmus denotes movement of the eyes
without a cognitive, visual or vestibular stimulus.
Most commonly spontaneous nystagmus is caused by a
vestibular imbalance. Normally, both vestibular nerves fire
equally at a tonic rate.
Hold patient’s head with one hand. Ask patient to look
straight ahead. Look for: Nystagmus and note direction.
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Head Shaking Nystagmus Test
Used to determine the presence of a decreased VestibularOcular Reflex (VOR)
Procedure: Inform the patient you will be moving their headfrom side to side. Grasp patient’s head firmly with one handon either side of the head. Tilt the head forward 30 degreesso that the horizontal semicircular canal is level in thehorizontal plane. Have the patient close their eyes. Move thehead side to side 20 times, asking the patient to help withthe movement.
Ask patient to open their eyes quickly. Look for: Nystagmus,noting direction . 1 or 2 beats of nystagmus is notsignificant. If horizontal head shaking induces persistentnystagmus the procedure should be repeated vertically, butonly moving the patient’s head 10 times.
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Positional Testing
▪ Can help identify peripheral or central causes of vertigo.
▪ The most common positional vertigo is BPPV due to free-floating calcium carbonate debris from the otolithic organswhich enters one of the semicircular canals – usually inthe posterior semicircular canal – occasionally horizontalcanal and rarely the anterior canal
▪ The characteristic burst of upbeat torsional nystagmus istriggered in patients with BPPV by a rapid change fromthe sitting-up position to supine head-hanging left orhead-hanging right (Dix-Hallpike test for BPPV).
▪ A burst of nystagmus in the opposite direction (downbeattorsional) occurs when the patient sits up
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Dix Hallpike Test for Posterior Canal
BPPV
Patient seated on table and head is rotated 450 The head
and trunk are quickly taken straight back so the head is over
the edge of the table. Hold 30-45 seconds, observing for
nystagmus and question for vertigo. (latency of 5-10 sec.).
Patient is then brought up slowly to a sitting position with the
head maintained in 450 rotation. Again, observe for
nystagmus and question for vertigo. Test is repeated with
head rotated 450 in opposite direction. Look for: Up beating
or down beating Nystagmus, indicative of central lesion.
Note: Critical element is position of the head in space (not
relative to the body).
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Head roll test for Horizontal canal
BPPV
Procedure: patient is supine with the headflexed 20 degrees. Head is turned quickly toone side. Hold 30 seconds, observing fornystagmus and question for vertigo. Rollthe head slowly back to the supine position,hold for 30 seconds. Roll the head quicklyto the other side. Observe fornystagmus/vertigo. Observe nystagmus,noting direction, latency and duration. Askthe patient which side is worse.
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Imaging
▪ To rule out central causes of vertigo
▪ CT scan can rule out a large mass withexception of smaller lesions due to infarct andpoor resolution in the posterior fossa. (Chalela etal. 2007)
▪ MRI imaging is the modality of choice especiallyif the patient has focal neurological symptoms oris having unexplained neurological deficits,direction changing nystagmus, or an otherwiserapid, unexplained progression of symptoms.
▪ BPPV, vestibular neuritis, or Meniere’s diseasedo not require imaging
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Additional Testing
▪ Berg Balance Scale
▪ Dynamic Gait Index
▪ Modified Clinical Test of Sensory Interaction in Balance
(mCTSIB)
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VESTIBULAR ASSESSMENT
AND TREATMENT
VRT(vestibular rehabilitation therapy)
Therapeutic Goals▪ Enhance existing vestibular capabilities
▪ Strengthen compensatory mechanisms
By improving Proprioceptive input
By increasing Visual Input
Other sensory systems
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Vestibular Adaptation and
Compensation Thomas P. Wellings*, Alan M. Brichtaand Rebecca Lim
School of Biomedical Sciences and Pharmacy, The University of Newcastle, and Hunter Medical
Research Institute, NSW, Australia
The balance or vestibular system is often overlooked as a
major sensory system (Goldberg et al. 2012). Even less
appreciated is the vestibular system’s inherent plasticity
and capacity for self repair.
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Vestibular Adaptation
(compensation) Exercises▪ Vestibular adaptation describes the routine changes in
sensitivity (gain) of reflexive eye movements (VOR)
responsible for stabilizing images on the retina during
head movements.
▪ This may not be possible with an MS patient who
develops demyelination of the vestibular nerve and the
medial longitudinal fasciculus which yokes eye
movements and may result in (Yaw) rotation
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Vestibular Habituation ExercisesA large amount of end point
nystagmus may be seen with
increasing age.
The goal
of habituation exercise is to
reduce the dizziness through
repeated exposure to specific
movements or visual stimuli that
provokes the patients'
dizziness.
These exercises are designed
to mildly, or at the most
moderately, provoke the
patients' symptoms of dizziness.
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Benign Positional Vertigo (BPPV)There are Two Forms: Canalithiasis and Cupulolithiasis.
Canalithiasis (otoconia is free in the canal) and is the single
most common cause of vertigo lasting less than 30 seconds
with position change-typically when turning over in bed,
getting in and out of bed, bending over and straightening up,
and extending the neck to look up. Cupulolithiasis (otoconia
stuck to the cupula) causes immediate vertigo and
nystagmus and does not fatigue.
Barany- found lesions of the otolith organs. Dix-Hallpike-
found unilateral degeneration of the utricular macula at
necropsy. Schuknecht-found basophilic deposits on the
cupulae of the posterior canal proposing otoconia from
degenerating utricular macula settles on the cupula of the
posterior canalsLarry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 237
BPPV
▪ Most common cause of vertigo in the general population
▪ Patients typically experience brief episodes of vertigo
when getting in and out of bed, turning in bed, bending
down and straightening up, or extending the head back to
look up
▪ Repositioning maneuvers are highly effective
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It is important to realize that eye movement alone or head movements alone, will
have extremely limited benefit. Introduction of head movement together with
visual acuity, (within the frequency of the VOR) , is extremely beneficial at repairing a
damaged system.
Management
He following therapies are specific for lesions in
the affected canal system
1. Epley Maneuver - PC
2. Semont Maneuver – PC
3. Lempert Maneuver – HC
4. Gufoni Maneuver – HC
5. Reverse Dix Hallpike – AC
6. Reverse Epley - AC
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Posterior Canal BPPV
Two most convincing pieces of clinical evidence supporting a posterior canal are:
▪ 1. The positional nystagmus is in the plane of the posterior canal
▪ 2. Sectioning of the ampullary nerve from the posterior canal stops BPPV
▪ Schuknecht’s cupulolithasis theory is supported byany type of damage to the inner ear (trauma,infection, ischemia, age related degeneration) whichcan lead to dislodging of the calcium carbonatecrystals from the otolith and deposition on the cupulaof the posterior semicircular canal
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Posterior Canal BPPV
Diagnosis-
1. Rests on finding the characteristic fatigable paroxysmal positional nystagmus. The Nystagmus is torsional and in the plane of the affected canal.
2. Caloric hypo excitability is seen on the ipsilateral side presumably involving both the horizontal and posterior canals
3. Canals may also be tested w/o eye fixation in a Dis-Halpike position (Frenzel lenses) for better optimization
▪ Management- positional exercises. Epley or Semont. Resume upright position once the vertigo has ceased. Repeat x 3 - t.i.d.
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Dix-Hallpike Test for posterior canal
BPPVExplain procedure to patientbeforehand that it mightinduce vertigo. Ensure thatthere are no neck/backproblems that would beaggravated by sudden changein posture. Stand to the sideof the patient • Pt sitting withhead turned to examiner • Ptsat so that when supine, thehead will be beyond the endof the couch • Patient lain flatin one quick, smoothmovement • Eyes must stayopen • Repeat on other side.
Positive test: – Rotatory (torsional) nystagmus (& vertigo): • Diseased ear downmost
3 important features include:
▪ Latency – delay of up to 20 seconds before onset of nystagmus
▪ Fatigueability – nystagmus fades if head held in provoking position
▪ Habituation – Repeating DH test produces less vigorous response
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Interpretation of Dix Hallpike Test
Consider central problem if
any of the following occur:
▪ Non-rotatory nystagmus
▪ No latency
▪ No fatiguability
▪ No habituation
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Posterior Canal Rehab.
▪ Semont
▪ Epley
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Epley Maneuver-posterior canal
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Semont Maneuver - Right PC
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Roll Test for Horizontal Canal
BPPV(Herdman, 2007)
Patient lies supine with neck flexed 20º, head is quickly
rolled 90º to one side to orient the horizontal canal. Hold for
up to one minute and observe presence & direction of
nystagmus, and then return slowly to midline; maintaining
the neck flexion, the procedure is repeated to the other side.
Note patient report of vertigo.
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Roll Test, Interpretation
Horizontal canalithiasis –nystagmus is geotropic(toward the earth) when thehead is rolled to the right andleft, and lasts a short duration(approximately <60 seconds)
Horizontal cupulolithiasis –nystagmus is apogeotropic(away from the earth) whenthe head is rolled right andleft, and it is persistent (>60seconds)
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Horizontal Canal Rehab.
▪ Gufoni Maneuver
▪ Lempert Maneuver
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Gufoni Maneuver - Horizontal Canal rehab.
Larry E. Masula, D.C.,DACNB, FABVR, FAFICC 2/1/2020 251
Lempert Maneuver (BBQ Roll)
Horizontal Canal rehab.
Larry E. Masula, D.C., DACNB, FABVR, FAFICC 2/1/2020 252
Rehab. Gem
▪ Vestibular rehabilitation utilizing Otolith stimulation (A/P
and Up/down) also provides lot of frontal lobe stimulation.
This application may also useful for ADD kids with right
frontal lobe problems.
▪ Special Note: All the testing maneuvers previously
mentioned are aides to identify the canal most likely to be
generating the vertigo, but they are also extremely
beneficial and frequently used for canal rehabilitation as
well.
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VOR Gaze stabilization rehab.
X1 viewing exercise, may be
used for rehabilitating the
dizzy patient with gaze
holding failure. While seated
keep eyes fixed on single
stationary target held in hand
or placed on wall move head
side to side. Repeat while
moving head up and down.
This like all tests should be
performed both sitting and
standing.
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VOR rehab: X1 viewing
Head/eyes moving in same
direction Holding a single
target, keep eyes fixed on
target. Slowly move target,
head and eyes in same
direction up-down/ side to
side/diagonally
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VOR rehab: X2 viewing
Head/eyes moving in opposite
direction Holding a single
target, keep eyes fixed on
target. Slowly move target up-
down/side to side/diagonally
while moving head in opposite
direction of target
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Saccades Rehabilitation
Holding two stationary targets
placed inches apart side-to-
side/up-down/diagonally,
move eyes quickly from target
to target as head stays still.
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Cawthorne Cooksey Exercises
▪ Were devised in the 1940’s
▪ Mainly for vestibular lesions
▪ Initially, the exercises performed are slow gradually
increasing speed as patient tolerates the movement
▪ The patient should experience an increase in symptoms
with movement
▪ Exercises performed for at least 1 minute several times
each day for adaptation to occur
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Have a Vestibular Questionnaire
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Additional Rehab. Strategies
▪ OPK
▪ Cb Rehab Exercises
▪ Head Laser Maze
▪ NSI Unit
▪ Metronome
▪ Simon
▪ Gaze Stability - Dots on Wall
▪ Wii
▪ Fit Ball
▪ Wobble Board
▪ Mini Trampoline
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2/1/2020Larry E. Masula, D.C.DACNB, FABVR, FAFICC 261
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