Pathophysiology of dizziness and Management

March 2008

Pathophysiology of Dizziness Signs and Symptoms

Common Disorders And Management Options

Symptoms of Dizziness
Dizziness

non-specific term; encompasses any and all 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 symptom descriptions that are specific in nature Detailed characterizations of the patients symptoms are of significant help in narrowing the etiologies

Pathophysiology of dizziness and Management

March 2008

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 or visual 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 < 24 hours Head movement provoked symptoms <2 minutes Vestibular crisis - - sudden onset vertigo slowly improving from continuous to head movement provoked symptoms in days More likely to have auditory involvement

Central

vestibular or nonvestibular Sx
Sudden onset of Vertigo, lightheadedness / Imbalance with one of the Ds Slow onset imbalance standing and walking Vague sx of any character Slow vertigo lasting 24 / 7

Pathophysiology of dizziness and Management

March 2008

Vertigo
Independent

of lesion site the underlying pathophysiology is that of asymmetrical neural activity The asymmetrical neural activity could occur anywhere from the labyrinth through lesions in the pons and even posterior cerebellum Highly unlikely to get true vertigo from lesion above the level of the pons --- more likely to get imbalance, lightheadedness Highly unlikely to get true vertigo from lesion in the area of the anterior circulation carotid arteries --- imbalance, lightheadedness Differentiation of labyrinthine versus posterior fossa by travelers --- especially the Ds

Asymmetrical Peripheral Activity

Sensation rotation rightward

Symptom head rotation rightward

Pathophysiology of dizziness and Management

March 2008

Labyrinthine Disorders without Vertigo-Is it Possible?

These

would fall in the realm of Chronic Dizziness Unilateral Labyrinthine/VIII n --- as long as the lesion develops slow and insidiously and central compensation is functioning. E.g. vestibular schwannoma, hereditary auditory/ vestibular degeneration Bilateral Labyrinthine lesions --- as long as the two labyrinths undergo symmetrical damage vertigo is not experienced. E.g. ototoxic drugs, idiopathic (thought to be hereditary), head trauma
VERSUS sequential unilateral sudden onset events result is bilateral hypofunction (chronic symptoms state) but vertigo is experienced at onset of each event

Differential Diagnosis
Temporal Characteristics
Episodic Seconds Episodic Sec Min < 60 Episodic Min Hours < 24 Episodic Min Hours < 24 Episodic Min Hours < 24

Dizziness Characteristics
HM- HP provoked Spontaneous HM HP provoked Spontaneous

Auditory Characteristics
Normal Normal or mild fluctuations Normal Fluctuant + Progressive Normal or mild Fluctuant

Differential Diagnosis
BPPV; Uncomp stable lab; VBI Migraine; TIA; Anxiety; Menieres Uncomp Stable lab; Migraine Lab Disorders eg Menieres & Autoimune Migraine; anxiety; cardiovascular

Spontaneous

Pathophysiology of dizziness and Management

March 2008

Differential Diagnosis
Temporal Characteristics
Days

Dizziness Characteristics

Auditory Characteristics
Normal

Differential Diagnosis
Vestibular neuritis; vascular event Labyrinthitis; PICA or AICA stroke Migraine; Vascular with other Neuro Symptoms Central vestibular disorders; anxiety; non-vestibular eg sensory motor neuropathy

Spontaneous HM HP provoked 1-3 days Days Spontaneous HM HP provoked 1-3 days Days typically < 7 Spontaneous or HM HP Relatively constant Continuous Possibly exacerbated by HM - HP

Sudden Onset at time of vertigo onset Normal

Normal

Signs: Generalizations
Labyrinthine / VIII n Direction fixed nystagmus horiz. Abnormal VOR via head thrust Nystagmus more likely to be seen with fixation removed Nystagmus more likely to be exacerbated when gazing in the direction of the fast component Alexanders Law Nystagmus more likely to be exacerbated post horizontal head shake horizontal nystagmus Pursuit tracking and saccade performance normal (or age dependent) If sudden onset can stand & walk with assistance Central

vestibular or nonvestibular Signs

Direction changing nystagmus Nystagmus more likely enhanced with fixation present Nystagmus more likely to be pure vertical or pure torsional Nystagmus post head shake vertical Likely to have abnormal performance on pursuit and/or saccades If sudden onset likely not to be able to stand & walk even with assistance

Pathophysiology of dizziness and Management

March 2008

Male 36 Years
Reports

sudden onset of vertigo with his first movement in the morning 3 weeks ago Indicates that the vertigo has been with him every day since onset when asked he says it has not stopped When pushed the history reveals that the vertigo is only present when he make a movement, primarily in the pitch plane or rolls in bed. If he holds still the symptoms are absent. The longest the vertigo has lasted is seconds Also reports general imbalance when standing and walking Has been place on Meclizine not sure how much it works but symptoms have lessened and he is now avoiding all the movements that cause the symptoms

Benign Paroxysmal Positional Vertigo

Symptoms: History
Sudden onset (usually with first movement in the morning) Vertigo of short duration (seconds) provoke by rolling from a supine position or sagittal plane head movements Most describe general imbalance with standing and walking May last for only a day or multiple days or weeks natural history is to resolve spontaneously

Signs: Direct exam & Typical Lab findings (including hearing test)
For pure BPPV all normal excepting Dix-Hallpike testing for BPPV Can be associated with other disorders of the labyrinth

Classic treatments (including use of VBRT)

Primary treatment is that of canalith repositioning maneuvers Surgical procedures have been developed but used very rarely

Prognosis excellent for dizziness may have residual imbalance or sensations for weeks after successful resolution of vertigo treatments are a management technique not a cure recurrence is common Lesion site labyrinthine vast majority posterior SCC

Pathophysiology of dizziness and Management

March 2008

In

the normal system since the specific gravity of the cupula = that of endolymph, static position of the head in a gravitational field has no effect on the cupula.

Pathophysiology of dizziness and Management

March 2008

77 yr old Female
CC

Sudden onset 8 months prior of severe spontaneous vertigo lasting continuously for 2 days slowly resolved into pitch plane provoked spells of vertigo lasting seconds in duration these stopped 8 weeks prior to the balance function testing. Now left with head and movement provoked imbalance and lightheadedness and brief vertigo with very rapid head movements PMH Negative for any past problems with balance and dizziness
Denies any significant changes in her hearing No neurological focal complaints before or since the event of vertigo except some progressive loss of sensation in her feet. Severe life long migraines now continuing with ocular events and ice pick pain multiple times per month

77 yr old Female

Pathophysiology of dizziness and Management

March 2008

Vestibular Neuritis
Symptoms:

History

Vestibular crisis improving over 1-4 days Left with head movement sensitivity No hrg loss
Signs:

Direct examination & Typical Lab findings (including hearing test)

Nothing specific peripheral no central

Classic

treatments (including use of VBRT)

Meds to control sx VBRT to push compensation

Prognosis

excellent with compensation common to have Posterior canal BPPV as a sequela Lesion site neural vascular causing selected labyrinthine damage

Pathophysiology of dizziness and Management

March 2008

Division of Labor
Likely

consequences of this division of arterial and neural supply:

When one structure of the group is damaged others are likely also In combination with the specific eye movements for each of the 6 canals and 4 otolith organs it becomes highly unlikely that peripheral damage can produce certain nystagmus types therefore these are central until proven otherwise:
Pure vertical (exception bilateral superior canal dehiscence) Pure torsional

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Pathophysiology of dizziness and Management

March 2008

G. Gianoli et al, Otology & Neurotology, 26, 2005: 489-494

55 yr old Male
Mild

URI - sudden onset of true vertigo with n/v slowly improving over 3 days Reports sudden hearing loss on the left. Resolved in mild hd movement provoked vertigo lasting seconds that have now continued for 6 months - comes with nml head MRI Signs seen on exam left side VOR abnormality and ongoing right beating nystagmus with fixation removed.

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Pathophysiology of dizziness and Management

March 2008

Labyrinthitis
Symptoms:

History

Vestibular Crisis event improving 1-4 days Left w/ head movement sensitivity Change in hearing with crisis event
Signs:

Direct exam & Typical Lab findings (including hearing test)

Non-specific peripheral no CNS SN hearing loss

Classic

treatments (including use of VBRT)

Steroids early for hearing loss Suppressive meds for sx control at first VBRT to push compensation
Prognosis

excellent for dizziness hearing loss recovery depends on degree of initial loss (viral vs Bac) Lesion site - labyrinthine

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Pathophysiology of dizziness and Management

March 2008

In the Chronic Dizzy Patient Why are symptoms continuing? Why has the Natural Compensation process not worked?
Group

Group

The patient has an UNSTABLE lesion, ie, the locus of the lesion is changing over time. The historical hallmark is spontaneous events More likely to be assisted with medicine or surgery

The patient has a STABLE lesion yet uncompensated by the central process The historical hallmark is symptoms are provoked by something More likely to be served with VBRT

Handling BPPV
Treat

first Then treat the residual symptoms left after the BPPV resolved. In many cases with the BPPV resolved the residual symptoms may be reduced dramatically.

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Pathophysiology of dizziness and Management

March 2008

Who is appropriate for VBRT

This

is a symptom driven indication system Test from laboratory studies play only a minor roll in assisting to determine who is appropriate
SOT to help design and monitor DVA to help design and monitor Caloric asymmetries and Chair time constant abnormalities indicate abnormal VOR This can be an indication for a type of therapy (Adaptation) if sx are appropriate for VBRT
Work

to date would indicate that the indications for a VBRT program are the same for adults and children

Vestibular Rehabilitation
z

Appropriate

Inappropriate

Head, visual motion Only spontaneous events provoked or too freq. (unstable / progressive periph.) Continuous with motion exacerbation No provocative activity or balance dysfunction Functional balance or gait dysfunction Progressive Central lesion (balance/gait) Stable peripheral or central lesion Any age

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Pathophysiology of dizziness and Management

March 2008

Techniques for assessment and exercises

The

assessment tools for determining specific system and functional deficits are generally applicable to:
Peripheral vestibular lesions Central vestibular lesions Children as well as adults

There

are reasonable normative data for children 3-4 and above on most of the major tools used for therapy assessment and for all of the laboratory studies (ENG, rotary chair, Dynamic posturography, postural evoked EMG responses, dynamic visual acuity and otolith function testing Multiple work by Rose Rine et al

System Integration
By Direct exam or via lab testing Organization & use of Sensory inputs (SOT of Dynamic Posturography or office technique of Clinical Test of Sensory Interaction on Balance Reaction to unexpected perturbations (clinical or machine) Functional use of Vestibulo-Ocular Reflex (DVA / GST) Gait & Balance (clinical tests) Movement sensitivity via MSQ (16 fast movements coding intensity duration)

Vestibular and Balance Rehabilitation Technique

Individual

Systems Review

By Direct exam or via lab testing Vision / Ocular motor control Vestibular Status and Vestibulo-Ocular Reflex Musculoskeletal Neurological Cognitive status

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Pathophysiology of dizziness and Management

March 2008

Vestibular and Balance Rehabilitation

Adaptation

Exercises

Goal - to improve Vestibulo-Ocular Reflex functional performance (indications are that gain in hypofunction patients does not actually change) X1 & X2 gaze exercises with horizontal or vertical head rotation
Habituation

Exercises

Goal - to reduce or eliminate response to a specific stimulus with repeated exposure repeated head movements with or without total body movement
Dose

related activities Do not appear to generalize

Vestibular and Balance Rehabilitation

Balance

Exercises Exercises

Static and Dynamic Postural Control

Substitution Gait

Use of one sensory input when another system is out

Exercises

Ambulation over short and long courses Should be combined with horizontal head rotations
General

Conditioning

Life style change Maintenance program

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Pathophysiology of dizziness and Management

March 2008

Case Female 58
1

year prior began with spontaneous spells of vertigo with n & v lasting 1-6 hours. These were as frequent as 1 time per week but no spells from 6 weeks prior to visit Tinnitus, aural fullness and fluctuant hearing reported with the onset of the spells in the left Denies neurological focal complaints Strong history of Migraines, with the head aches improving with menopause. Family hx of migraines with vertigo in her son and mother born deaf

Case Female 58

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Pathophysiology of dizziness and Management

March 2008

Menieres Disease
Symptoms:

History

Spont event >20 minutes <24 hours Fluctuant hrg with documented loss Tinnitus and aural fullness No CNS indicators

Signs:

Direct Exam & Typical Lab findings (including hearing test)

Nothing specific peripheral no CNS Progressive SN hearing loss

Classic

treatments (including use of VBRT)

Diet / suppressive meds / Surgery Gent / VBRT if sx between and spells >4 weeks apart
Prognosis

excellent control with Gentamicin / surgery otherwise 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 in guinea 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 before the development of hydrops. Strongly suggests that hydrops resulted from disordered fluid regulation from spiral ligament changes.

Conclusion:

EH is a good histological marker for Menieres but should not be considered directly responsible for the symptoms

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Pathophysiology of dizziness and Management

March 2008

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 fluctuant hearing on the right hearing tests all normal for the entire 3 years even during a spell Migraine head aches by IHS and ocular migraine-otherwise hx neg Office exam NML Dx 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 only chronic 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 mild and 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 dizziness symptoms with control of migraine events Lesion site Not known but speculated to involve the labyrinth and vestibular nuclei with other areas of the brainstem and midbrain

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Pathophysiology of dizziness and Management

March 2008

Surgical Management of the Dizzy patient

Reparative Ablative

procedures

Middle ear procedures for erosive process Perilymphatic fistula both the controversial form at OW or RW & Superior SCC dehiscence Sac decompression or endolymphatic shunt

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 2 where compensation is possible

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Pathophysiology of dizziness and Management

March 2008

Medical & Dietary Control of the Dizzy Patient

Medical Dietary

Control of an underlining Metabolic or hormonal disorder Steroid sensitive disorder Migraines Destructive or degenerative disorders Symptom control

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 are patients that will need the medications to cut the edge off the symptoms in order to get active enough to drive compensation judicious use is the order of the day

There

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Pathophysiology of dizziness and Management

March 2008

55 Female
March

1998 Vestibular Crisis slow improvement over 7 days Resolved in hd movement provoked vertigo all sx 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 imbalance and 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 indications Bilateral hip replacements within last 1.5 years No nystagmus with or without fixation VOR abnormalities bilaterally

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Pathophysiology of dizziness and Management

March 2008

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 by rotational chair

Classic

treatments (including use of VBRT)

VBRT only treatment typically VOR/balance

Prognosis

improvement but continued sx Lesion 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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Pathophysiology of dizziness and Management

March 2008

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 eye movements/ 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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Pathophysiology of dizziness and Management

March 2008

46 year old Male Right Tullio

Right Temporal Bone

Left Temporal Bone

46 yr female
Slow

onset over the last 3-5 years of imbalance standing and walking exacerbated with reciprocal head movements now some symptoms of imbalance when seated on a stool Denies any vertigo or hearing impairment PMH negative Social hx positive for significant alcohol abuse over a 15 year interval has been dry for 6 years Direct examination showed no VOR abnormalities but ocular motor control were abnormal

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Pathophysiology of dizziness and Management

March 2008

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 fine motor coordination of upper and lower limb control In some of the spino-cerebellar atrophies a family history may be prominent
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 chair and abn visual suppression of VOR (these will vary depending on the exact lesion sites) + saccade intrusions
Treatment

mostly palliative with falls prevention and maintenance of ambulation --- in some patients head movements exacerbate the symptoms (possible VIIIth n) VBRT with habituation may be useful Prognosis poor and progressive disorders Lesion site cerebellum and brainstem

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Pathophysiology of dizziness and Management

March 2008

22 year old male

Playing

soccer performs a routine header no pain no problems --- 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 symptoms can involve episodic vertigo with imbalance and typically other brainstem signs and symptoms Cerebellar and cerebral hemispheric ischemic events loss of coordination 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 control and gait abn with both
Treatment

neurology + balance and gait therapy and falls

prevention Lesion site

AICA / PICA central brainstem / cerebellar and may have a labyrinthine component Cerebellar and cerebral hemisphere

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Pathophysiology of dizziness and Management

March 2008

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 head movement sensitivity months post onset On direct exam --- negative head thrust; pure right torsional nystagmus primary and left gaze changing to right torsional + right beating horizontal on gaze right; ocular dysmetria, dysphasia, diplopia on lateral gaze, hoarseness, right ocular lateralpulsion Treatment change of glasses to fix Rx lenses; VBRT for head 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 most if 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 all ipsilesional)

Treatment --- symptom control use of VBRT for chronic symptoms of head movement sensitivity and imbalance Lesion site --- PICA distribution stroke with possible involvement of the Vth, IXth, Xth, XIth CN brainstem and cerebellum

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Pathophysiology of dizziness and Management

March 2008

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 improvement demonstrated with CDP Migraine & anxiety associated dizziness Reduction in fall risk in young & elderly with unilateral vestibular hypofunction General reduction in fall rate from prevention programs in young and elderly

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 for Vestibular Rehabilitation

z z

Want quantitative measures (pre / post) 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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Pathophysiology of dizziness and Management

March 2008

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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Pathophysiology of dizziness and Management

March 2008

Multiple Sclerosis

History
5-7% will have true vertigo as initial onset symptom Others will have lightheadedness and imbalance but may come on suddenly with resolution and repeat Classically the patient has history starting in 1st-2nd decades of life of unrelated neurological events may involve change in unilateral vision female > male presenting 2nd 3rd decade

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 constant unsteadiness Vertical Diplopia on Lateral gaze

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Pathophysiology of dizziness and Management

March 2008

Arnold-Chiari Cranial-Cervical Junction abn

Symptoms:

History

Episodic to continuous imbalance & lightheadedness exacerbated by hyperextension 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 usually exacerbated with lateral gaze seen with fixation present and absent may be elicited or exacerbated with hyperextension and / or intracranial 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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Pathophysiology of dizziness and Management

March 2008

54 male

54 male retrosigmoid approach

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Pathophysiology of dizziness and Management

March 2008

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 (including hearing 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 on size

Male 45
Aeronautical

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 fighter Direct 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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Pathophysiology of dizziness and Management

March 2008

Classic Motion Sickness (not related to labyrinthine disorder)

History

As a passenger in a moving vehicle (car, train, plane, boat) or while visualizing the simulated motion in order of development gastrointestinal awareness, lightheadedness, yawning, increased salivation, nausea, facial pallor, cold sweats, vomiting --- recovery in hours 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 likely genetically predisposed common with migraine

Male 50s
Onset

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 in past Direct examination and lab work up completely normal Treated with reassurance and short trial of putting him in motion that would cause symptoms (swinging) in a habituation format All symptoms resolved in about 5 months until he dutifully went with his wife on another cruise sx returned he checked in but all sx resolved in 4-7 months this cycle continued for at least another 4 years after which he stopped coming to the lab for work ups.

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Pathophysiology of dizziness and Management

March 2008

Mal de Debarquement (MDD) (potentially an otolith or otolith

pathway central receptor site involvement ? Anxiety or OCD)

History

Sensation of persistent rocking (no vertigo or true imbalance) following a prolonged sea, train or sometime air travel that continues for days to months 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 after travel typically resolves in hours
Lab

testing all normal occasional swaying on postural control testing 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 plane movements 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 and walking mild spinning in the head 24/7 cannot lie flat as she 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 no clinically significant generalized anxiety PMH migraine, treated for anxiety and depression in the past for brief interval otherwise non-contributory

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Pathophysiology of dizziness and Management

March 2008

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 same lying, sitting, standing may be increased with walking, especially sensitive to high visual complex environment

Testing ranges based on whether there was an antecedent vestibular event normal if a primary psych problem anxiety disorders can produce 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 but the specific transmitter and site of action still in question

Digitally signed by Neil T Shepard Reason: I am the author of this lecture Date: 2008.02.02 18:47:49 -06'00'

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