SC3 Audiology Neil Shepard

7/27/2019 SC3 Audiology Neil Shepard

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Pathophysiology of dizziness and Management March 2008

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Pathophysiology of Dizziness

Signs and Symptoms

Common Disorders

And

Management Options

Symptoms of Dizziness

Dizziness non-specific term; encompasses any andall of the specific symptoms:

Vertigo

Imbalance general or actual ataxia and possible falls

Lightheadedness (near syncopal event), giddiness

Combinations of the above

In the history it is important to obtain symptomdescriptions that are specific in nature

Detailed characterizations of the patients symptomsare of significant help in narrowing the etiologies


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Characterizations of Dizziness Symptoms

Temporal course --- paroxysmal lasting sec, minutes, hours,days, weeks OR continuous with exacerbation lasting sec,minutes, hours, days, weeks

Type of dizziness --- vertigo, imbalance, lightheadedness,falls, disorientation; are there traveler symptoms:

nausea & vomiting, head aches, heart palpitations, feelings of panic,drop attacks, any of the Ds= diplopia, dysphasia, dysarthria,dysmetria, asymmetric muscle weakness

Onset of symptoms --- Spontaneous OR head motion orvisual motion provoked (most likely treated with VBRT)

Hearing --- involvement in the auditory system, e.g. tinnitus,aural fullness, progressive or fluctuant loss of hearing

Symptoms: Generalizations Labyrinthine / VIII n

Sudden memorable onset

Typically True vertigo at onset

Paroxysmal Spontaneous events 20 minutes 4 weeks apart

Prognosis excellent control with Gentamicin / surgeryotherwise time typically helps

Lesion site - Labyrinthine

Endolymphatic Hydrops & Menieres

New study S. Merchant et al Mass eye & ear,2005, Otology & Neurotology 26, 74-81

Human T-bone review + Experimental Hydrops inguinea pig reviewed in early post-surgical stage

7 T-bones with idiopathic hydrops no Menieres sx

1 patient with well defined Menieres and no hydrops

Guinea pigs all showed changes in the spiral ligament beforethe development of hydrops. Strongly suggests that hydropsresulted from disordered fluid regulation from spiral ligamentchanges.

Conclusion: EH is a good histological marker forMenieres but should not be considered directlyresponsible for the symptoms


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62 year old female

Spont. True vertigo - hours to 2-3 days 1/mo with mild head

movement provoked lightheadedness and imbalance between- no head ache with spells - > 3 years

Auditory Symptoms of tinnitus, aural fullness and fluctuanthearing on the right hearing tests all normal for the entire 3years even during a spell

Migraine head aches by IHS and ocular migraine-otherwisehx neg

Office exam NMLDx migraine related dizziness Treatment with life style change and Nortriptylene - 4

months symptom free at first follow up

Migraine Associated Dizziness Symptoms: History

Patient is determined as being a migraineur by IHS criteria

Dizziness can be of a variety of characterizations from true vertigo to onlychronic sensitivity to motion spontaneous or motion provoked sx only

May occur temporally related to headache or independent

If spontaneous the vertigo may last seconds to days

Signs: Direct exam & Typical Lab findings (including hearing test) No specific pattern may range from normal to indications for either

peripheral or central involvement can have hearing loss associated mildand NOT progressive

Classic treatments (including use of VBRT) Primary treatment is treatment for migraine risk factors / medications

The migraine treatment may be supplemented with use of VBRT

Prognosis good for reduction or elimination of the dizzinesssymptoms with control of migraine events

Lesion site Not known but speculated to involve the labyrinth andvestibular nuclei with other areas of the brainstem and midbrain


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Surgical Management of the Dizzy

patient

Reparative Middle ear procedures for

erosive process

Perilymphatic fistula both the

controversial form at OW or

RW & Superior SCC

dehiscence

Sac decompression or

endolymphatic shunt

Ablative procedures Labyrinthectomy

Vestibular nerve section

Canal plugging procedures

Chemical destruction - not

necessarily complete ablation

Rationale for Ablative Procedures

Compensation process difficult if not impossible with

fluctuating lesion

If lesion site is confined to the labyrinth then partial

or full destruction of this site produces:

A stable peripheral lesion

Thus changing the patient from group 1 to group 2where compensation is possible


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Medical & Dietary Control of the

Dizzy PatientMedical

Control of an underlining

Metabolic or hormonal

disorder

Steroid sensitive disorder

Migraines

Destructive or degenerative

disorders

Symptom control

Dietary Low sodium diet -- 1.5 to 2

grams daily

migraine control

Difficulty with use of Rx Medications

As a group they produce a sedentary effect with CNS

depression that can possibly prevent or slow down

the compensation process

There are patients that will need the medications to

cut the edge off the symptoms in order to get activeenough to drive compensation judicious use is the

order of the day


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55 FemaleMarch 1998 Vestibular Crisis slow improvement

over 7 days

Resolved in hd movement provoked vertigo allsx resolved completely in 3-4 months

Dx with Non-Hodgkin's lymphoma started chemo

Early spring part of the chemo was Cisplatin

March 1999 Second Vestibular Crisis characteristics same as 1st

Left with episodic BPPV / Persistent imbalanceand mild oscillopsia

Male mid 70s

Severe imbalance using walker at home and wheel

chair away from home following Gentamicin

treatment for endocarditis now 3 months s/p

Denies any vertigo symptoms reports blurring of

visual world with head movements

No CNS indicationsBilateral hip replacements within last 1.5 years

No nystagmus with or without fixation VOR

abnormalities bilaterally


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Bilateral Peripheral Vestibulopathy

Symptoms: History

Depending on etiology usually onset of imbalance &oscillopsia progressive or stationary

Signs: Direct exam & Typical Lab findings(including hearing test)

Bilateral peripheral hypofunction extent of lesion byrotational chair

Classic treatments (including use of VBRT)

VBRT only treatment typically VOR/balance

Prognosis improvement but continued sxLesion site bilateral labyrinthine/VIIIth n (NF2)

46 year old Male Right Tullio

46 year old male

Reports a 1 year history of sound induced vibration,

oscillopsia, mild imbalance and head ache began

after a violent carnival ride

Denies vertigo or past history of dizziness

Denies hearing loss

Listen to description of sx on video


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Perilymphatic Fistula / SSC Dehiscence

Symptoms: History

RW / OW fistula very controversial Sudden onset head mov sx w/ or w/o fluctuant hrg or prog

After CHI or severe whiplash event

Spont w/ T-bone congenital deformities

SSC Dehiscence Tullio complaints / HL/ autophony / may have antecedent event

Signs: Direct exam & Typical Lab findings (including hearing test) RW / OW non-specific peripheral possible pressure induced horizontal

nystagmus

SSCD ENG typically normal Tullio test and / or pressure+ for SSC eyemovements/ LF conductive HL with nml AR bone better than nml /Abnormally low VEMP threshold / positive on special HR CT of T-bone

Classic treatments (including use of VBRT) Bed rest / Surgery / loud sound management

Prognosis If true OW / RW good / SSCD good

Lesion site - labyrinthine


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46 year old Male Right Tullio

Right Temporal Bone Left Temporal Bone

46 yr female

Slow onset over the last 3-5 years of imbalancestanding and walking exacerbated with reciprocalhead movements now some symptoms of imbalancewhen seated on a stool

Denies any vertigo or hearing impairment

PMH negative

Social hx positive for significant alcohol abuse overa 15 year interval has been dry for 6 years

Direct examination showed no VOR abnormalitiesbut ocular motor control were abnormal


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Ocular Flutter & Opsoclonus

71 yrs - Female

Sudden onset vertigo

progressively worse

Outside ENG reported

unable to performed too

noisy

Breast CA

Cerebellar paraneoplastic

Syndrome

Cerebellar / Brainstem Degenerative Disorders & Spino-Cerebellar

Atrophy Symptoms: History

Slowly progressive motor complaints with gait and imbalance and finemotor coordination of upper and lower limb control

In some of the spino-cerebellar atrophies a family history may beprominent

Signs: Direct exam and Lab findings Postural control abn on routine and Postural Evoked Responses +

pursuit and saccade abn + abn tilt suppression testing from rotary chairand abn visual suppression of VOR (these will vary depending on theexact lesion sites) + saccade intrusions

Treatment mostly palliative with falls prevention andmaintenance of ambulation --- in some patients head movementsexacerbate the symptoms (possible VIIIth n) VBRT withhabituation may be useful

Prognosis poor and progressive disorders

Lesion site cerebellum and brainstem


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22 year old male

Playing soccer performs a routine header no pain noproblems --- 20 minutes later sudden onset vertigo, nausea,

vomiting loss of hearing right ear

Unable to stand and walk even with assistance 20 minutes

Reports severe cervical region pain more to right dorsal

surface of neck

Seen in ER now able to walk with assistance CT of head

and neck nml --- significant left beating nystagmus with

fixation present follows Alexanders law and enhance

slightly with fixation removed mild limb dysmetria right

Is this Labyrinthitis?

Vascular Events Symptoms: History

If in the vertebrobasilar supply system with AICA and PICA symptomscan involve episodic vertigo with imbalance and typically otherbrainstem signs and symptoms

Cerebellar and cerebral hemispheric ischemic events loss ofcoordination and imbalance

Signs: Direct exam & Lab findings AICA / PICA could be a mix of central ocular and peripheral

hypofunction with postural control abnormalities

Cerebellar / cerebral ocular abn with cerebellar and postural controland gait abn with both

Treatment neurology + balance and gait therapy and fallsprevention

Lesion site AICA / PICA central brainstem / cerebellar and may have a labyrinthine

component

Cerebellar and cerebral hemisphere


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Female 40s

Sudden onset true vertigo with nausea and vomiting

Severe imbalance with falls and right mild hemiparesis Right lateralpulsion

Very slow improvement in symptoms with continuing headmovement sensitivity months post onset

On direct exam --- negative head thrust; pure right torsionalnystagmus primary and left gaze changing to right torsional+ right beating horizontal on gaze right; ocular dysmetria,dysphasia, diplopia on lateral gaze, hoarseness, right ocularlateralpulsion

Treatment change of glasses to fix Rx lenses; VBRT forhead movement sensitivity and ataxic gait

Improvement overall no falls but ongoing symptoms

Wallenbergs Syndrome (dorsal lateral medullary infarct) Symptoms: History

Sudden onset vertigo, nausea & vomiting associated with severe imbalance and mostif not all of the Ds

May also have hoarseness and hiccups

Lateralpulsion (being pulled or pushed to one side)

Signs: Direct exam and lab findings Torsional / yaw plane nystagmus beating ipsilesional w/ fixation can be pure

torsional on straight gaze

Ocular lateralpulsion

Hypoesthesia for pain & temperature on trunk contralesional with loss of pain &temperature sensation on face ipsilesional

Horners syndrome (ptosis, anhidrosis of face, pupilar contraction & enophthalmos allipsilesional)

Treatment --- symptom control use of VBRT for chronic symptoms ofhead movement sensitivity and imbalance

Lesion site --- PICA distribution stroke with possible involvement of theVth, IXth, Xth, XIth CN brainstem and cerebellum


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Vestibular and Balance Rehabilitation General

summary of Results - Adults Controlled Studies

CRP for BPPV

Customized vs generic

Customized vs sham vs Medicine

Post -operative recovery Gait improvement with bilaterals

Balance improvementdemonstrated with CDP

Migraine & anxiety associateddizziness

Reduction in fall risk in young &elderly with unilateral vestibular

hypofunction General reduction in fall rate from

prevention programs in young andelderly

Observational Studies

Overall 85 - 90% improvement

with all patients

Central brainstem as well as

peripherals

Cerebellar and progressive CNS

show only minimal improvement

in ambulation

Elderly do as well as young -

longer course

Suppressive Meds slow course -

outcome same Reduction in the injury rate from

falls in elderly

Outcome Measures forVestibular Rehabilitation

z Want quantitative measures (pre / post)

z Measures different from tx activities

Questionnaires / Subjective reports

Global, eg, DHI

Disability scale

ABC / Tinnette falls risk scales / Berg Balance Scale

Visual Analog Scales ADL tasks

Clinical measures such as DGI (FGA)/TUG/Functional

reach/Gait speed/Single leg stance/DVA

Dynamic Posturography (SOT)


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Outcome Measures continued

z Measures not different from therapy activities

performed

Some of the clinical tests; Single leg stance /

some features of the DGI

Motion Sensitivity (eg MSQ)

Dynamic Posturography (SOT) in some cases

Male 54 yrs - Imbalance

Sudden onset of Imbalance on a continuous basis

without vertigo, with diplopia 1.5 years prior

Diplopia resolved in 1 month imbalance has persisted

with dysarthria and memory difficulty

Patient on medical leave as symptoms have progressed

motion provocation denied

Presents a normal MRI with contrast performed within

6 months of onset


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Multiple Sclerosis History

5-7% will have true vertigo as initial onset symptom

Others will have lightheadedness and imbalance but may come on suddenly withresolution and repeat

Classically the patient has history starting in 1st-2nddecades of life of unrelatedneurological events may involve change in unilateral vision female > male

presenting 2nd3rddecade

Lab findings Usually central may include INO, gaze-evoked nystagmus, saccadic dysmetria, pursuit

abnormalities, pendular nystag

May have peripheral hypofunction from VIIIth n involvement

Treatment Neurological care / vestibular rehab may be useful in exacerbations for imbalance and

in some head movement sensitivity

Prognosis --- guarded

Lesion site Central vestibular and possible VIIIth n unlikely labyrinthine

Down-Beat Lateral Gaze Nyst.

71 yrs - Female

History of repeated brief

spells of vertigo with

cervical hyperextension in

intervals of days to

several weeks worsening

Now with constantunsteadiness

Vertical Diplopia on

Lateral gaze


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Arnold-Chiari Cranial-Cervical Junction abn

Symptoms: History Episodic to continuous imbalance & lightheadedness exacerbated byhyperextension of neck

Diplopia on lateral gaze as it advances

Signs: Direct exam & Lab and direct examination findings

Hallmark is that of down-beat nystagmus in primary gaze usuallyexacerbated with lateral gaze seen with fixation present and absent may be elicited or exacerbated with hyperextension and / orintracranial pressure increase

Treatment neurology / neurosurgery

Prognosis guarded Lesion site cervical-cranial junction --- low midline

posterior fossa

54 Male

No balance or vertigo complaints unless pushed

with questioning.

Progressive loss of hearing on the left with constant

tinnitus and aural fullness reason for seeking

medical opinion

Retrosigmoid approach


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54 male

54 male retro-

sigmoid approach


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Vestibular Schwannoma

Symptoms: History

Rare to have vestibular sx typically hearing loss Can appear as brief spell of imbalance or vertigo

Sx and lab findings depend on growth site Sup vs Inf

Signs: Direct exam & Typical Lab findings (includinghearing test) Typically Unilateral hypofunction ; HL; +/- CNS; VEMP neg in

superior div growth, + inferior div

Classic treatments (including use of VBRT) Surgical and VBRT pre & post-op

Prognosis-Good with VBRT

Lesion site-Vestibular portion of VIIIth cn / labyrinth /possible brain stem and cerebellum --- all contingent onsize

Male 45Aeronautical Engineer at U of MI life long history of

motion sickness in all vehicles

Typically could avoid sx by being the driver or the pilot of

small crafts

PMH completely negative Family history of motion

sickness in mother and all siblings

Seen for work up secondary to invitation by USSR to fly as a

passenger in a newly designed Mig fighterDirect exam + all lab findings completely normal

Used habituation techniques of brief repeated exposure to

reduce (not eliminate) sensitivity

He flew with only minimal nausea


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Classic Motion Sickness (not related to labyrinthine disorder) History

As a passenger in a moving vehicle (car, train, plane, boat) or whilevisualizing the simulated motion in order of development -gastrointestinal awareness, lightheadedness, yawning, increasedsalivation, nausea, facial pallor, cold sweats, vomiting --- recovery inhours to 1 day after motion stops

Lab tests --- typically all routine test are normal

Treatment

Be the driver

Prophylactic medication (Rx or homeopathic); desensitization therapy(limited but some help)

Prognosis prophylactic control is good

Lesion site susceptibility varies widely not a lesion likelygenetically predisposed common with migraine

Male 50sOnset of rocking sensation following a cruise 3 months prior

symptoms only present when sitting, lying or standing still absent when in motion

Denied any vertigo, hearing loss or imbalance currently or inpast

Direct examination and lab work up completely normal

Treated with reassurance and short trial of putting him inmotion that would cause symptoms (swinging) in ahabituation format

All symptoms resolved in about 5 months until he dutifullywent with his wife on another cruise sx returned hechecked in but all sx resolved in 4-7 months this cyclecontinued for at least another 4 years after which he stoppedcoming to the lab for work ups.


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Mal de Debarquement (MDD) (potentially an otolith or otolithpathway central receptor site involvement ? Anxiety or OCD)

History

Sensation of persistent rocking (no vertigo or true imbalance) followinga prolonged sea, train or sometime air travel that continues for days tomonths

Spontaneous resolution typically in months

Symptoms improve or are absent when in motion

Very common in most individuals, even seamen for up to 24 hours aftertravel typically resolves in hours

Lab testing all normal occasional swaying on postural controltesting

Treatment reassurance and possible mild anti-anxiety, time

Prognosis good to excellent

Lesion site & pathogenesis - unknown

38 year Female 2 years prior sudden onset of true vertigo with imbalance

when getting out of bed and with other pitch planemovements

Treated with unknown meds and movements by PT.

Sx resolved but returned in two weeks. PT treatment repeated helped but since then constant imbalance standing andwalking mild spinning in the head 24/7 cannot lie flat asshe does spinning feels like it is increasing and persists evaluated by PT with additional maneuvers no help

Sx worsened in mall, grocery store, at work lunch room better at home

Evaluated by psychiatrist has mild anxiety tendencies but noclinically significant generalized anxiety

PMH migraine, treated for anxiety and depression in thepast for brief interval otherwise non-contributory


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Psychological Issues (dominated by Anxiety disorders)

History May or may not have a past history of a classic vestibular event of central or

peripheral involvement

Present sx are 24 / 7 vertigo is usually subjective, slow moving. Sx are the samelying, sitting, standing may be increased with walking, especially sensitive tohigh visual complex environment

Testing ranges based on whether there was an antecedent vestibularevent normal if a primary psych problem anxiety disorders canproduce positional nystagmus vertigo complaint but no nystagmus

Treatment VBRT to full cognitive/behavioral therapy +/- use of meds

Prognosis Good if recognized early

Lesion site for anxiety disorder likely a neurotransmitter problem butthe specific transmitter and site of action still in question

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by Neil T Shepard

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