dizziness and disturbance of equilibrium and coordination.pdf

7/27/2019 Dizziness and Disturbance of Equilibrium and Coordination.pdf

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Dizziness and Disturbance of

E uilibrium and Coordination


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Equilibrium

Ability to maintain orientation of the body and its

parts in relation to external space.

Depen s upon cont nuous VISUAL, LABYRINTHE

and PROPRIOCEPTIVE inputs

Association occurs in the BRAINSTEM and

CEREBELLUM


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VISUAL LABYRINTHE PROPRIOCEPTION

BRAINSTEM and

CEREBELLUM

ADAPTIVE

MOVEMENTS


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EQUILIBIURM

In response to these inputs, ADAPTIVE

MOVEMENTS necessary to maintain equilibrium

are carried out

Normally we are unaware of these adjustments

because they operate largely at a REFLEX level


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SPATIAL ORIENTATION SYSTEM

DISORDERSImportant symptoms:

1. Vertigo2. Ataxia/ Disequilibrium


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Approach to a DIZZY patient

Medical history

Physical examination

Basic laboratory exam Physiologic diagnostic tools

Radiologic diagnostic tools


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MEDICAL HISTORY

Description of dizziness by the patient

Secondary symptoms

Previous history


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DIZZINESSapplied to a number of different sensory experiences which falls under 4 categories

disequilibriumdisequilibrium

DIZZINESS

DIZZINESS

Nearsyncop

e

Nearsyncop

e

Ill-definedlightheadedne

ss

Ill-definedlightheadedne

ss

vertigovertigo


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Physical sensation of MOTION of selfand environment

VERTIGOVERTIGO

IMBALANCE of stance and gaitDISEQUILIBRIUM/DISEQUILIBRIUM/

Sensation of FAINTNESSNEAR SYNCOPE

PRESYNCOPE/ SYNCOPE

NEAR SYNCOPE

PRESYNCOPE/ SYNCOPE

Often accompanies anxiety anddepression

ILL DEFINED

LIGHTHEADEDNESS

(PSEUDOVERTIGO)

ILL DEFINED

LIGHTHEADEDNESS

(PSEUDOVERTIGO)


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Dizziness

Rotating

Spinning

Whirling Oscillating

Rocking

Tilting Swaying


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Dizziness

VERTIGO Rotating

Spinning

Whirling PATHOPHYSIOLOGY:

Oscillating

Rocking

Tilting Swaying

Dysfunction of the

VESTIBULAR SYSTEM


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Dizziness

DISEQUILIBRIUM / ATAXIA Unsteadiness

Imbalance

Falling to one side

Incoordination

Wearing a new pair of eyeglasses feeling


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Dizziness

DISEQUILIBRIUM/ ATAXIA

Unsteadiness

Imbalance

PATHOPHYSIOLOGY:

Dysfunction of sensory

(proprioception),

Falling to one side

Incoordination

Wearing a new pair of eyeglasses feeling

cereballer and vestibular

pathways


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Dizziness

NEAR SYNCOPE Light-headedness

Fainting

Giddiness Passing out

Candle being slowly exhausted

If with loss of consiousness: SYNCOPE


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Dizziness

NEAR SYNCOPE (PRESYNCOPE/SYNCOPE)

Light-headedness

Fainting

PATHOPHYSIOLOGY:

Disturbed blood flow to the

brain

Passing out

Candle being slowly exhausted

If with loss of consiousness: SYNCOPE

(GLOBAL CEREBRAL ISCHEMIA)


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Dizziness

PSEUDOVERTIGO: PSYCHOLOGICAL Feeling low

Weakness

Fatigue Feeling of unreality


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III Defined Dizziness

PSEUDOVERTIGO

Feeling low

Weakness

PATHOPHYSIOLOGY:Ps cholo ical Issues

Fatigue

Feeling of unreality


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NEUROLOGIC EVALUATION

Where is the lesion?

Peripheral vestibular

End Organ (Labyrinth)

Vestibular Nerve

Central vestibular pathway

Brainstem

Cerebellum


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EAR


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VESTIBULOCOCHLEAR


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Vestibulocochlear Nerve CN VIII


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Auditory PathwayTRANSVERSE GYRUS OF HESCHL

MEDIAL GENICULATE

INFERIOR COLLICULUS

LATERAL LEMNISCUS

SUPERIOR OLIVARY NUCLEUS

COCHLEAR NUCLEUS

CRANIAL NERVE VIII


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CONDUCTIVE HEARING LOSS

Patient speaks with normal or low volume voice

Etiology: Anything that interferes with ossicular movement

(otitis nedia with middle ear effusion), otosclerosis

Unilateral hearing loss

WEBER TEST: lateralizes to side of hearing loss

RINNE TEST: Bone conduction > Air conduction onthe side of hearing loss (negative RT)


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SENSORINEURAL HEARING LOSS

Patient tends to speak with loud voice

Etiology

Cochlear damage from noise exposure & ototoxic

drugs (aminoglycosides) Compression of the CN VIII by tumors (schwanomma)

Clinical findings

Unilateral hearing loss

WEBER test: lateralized to the better hearing

RINNE test: Air conduction > Bone conduction


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Vestibular and Cochlear Sructures


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SEMICIRCULAR CANALS


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CRISTAANGULAR ACCELERATION

Rotational head movement causes displacementof the endolymph which pushes the cupula anddeflection of the sensory hair cells

This causes depolarization of the vestibular

afferents


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SEMICIRCULAR CANAL

CRISTA: ANGULAR ACCELERATION


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END ORGANS

UTRICLE AND SACCULE Macula

Linear acceleration andgravitational pull

Linear Acceleration OTOLITHIC MEMBRANE

is pushed down withdeflection of thesensory hair cellscausing depolarizationof the vestibularafferents


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Vestibular Pathways


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VESTIBULAR LESIONS

PERIPHERAL

Affects the labyrinth of the inner ear or the

vestibular division of the cranial nerve VIII

CENTRAL

Affects the brainstem nuclei or theirconnections


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Vestibular Pathways

The vestibular nerve impulse enters thebrainstem and synapses with thevestibular nuclei resulting in 2 reflex

responses: Vestibulo-ocular reflex

Vestibulo spinal reflex

Some vestibular impulses enter theflocculonodular lobe and vermis


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CONTROL OF EYE MOVEMENT

E TIBUL R NU LEU transm ts mpu ses to t e

Medial Longitudinal Fasciculus (MLF). MLF sends

impulses to CN nuclei 3, 4 and 6 for CONJUGATE EYE

MOVEMENTS


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VESTIBULOSPINAL TRACTS

MEDIAL vestibulospinal tract inhibitory

LATERAL vestibulospinal tract excitatory

From the brain, descending tracts carry

comman s to t e motor neurons or ax a an

proximal muscles (via median descending

pathways)


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PERIPHERAL VS CENTRAL VERTIGO

PERIPHERAL OR

VESTIBULAR LESION

CENTRAL LESION

VERTIGO OFTEN INTERMITTENT

SEVERE

OFTEN CONTANT

LESS SEVERE

ASSOCIATED FINDINGS:

Hearing loss/ tinnitus Often present Rarely present

Focal neurologic deficits:

- brainstem Absent Typical

- cerebellar signs Absent Typical


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PERIPHERAL VS CENTRAL VERTIGO

Direction of nystagmus Maybe pure horizontal Pure horizontal

Pure vertical

Pure torsional

Influence of gaze Does NOT change

direction with gaze

Does change direction

with gaze

Visual fixation Inhibits nystagmus Does NOT affect

Nystagmus

Latency following

repositioning

movements

Up to 20 seconds None

Direction changing with

reversal of head

direction

Present and

characteristic

Absent


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ATAXIA/ DISEQUILIBRIUM

INCOORDINATION OR CLUMSINESS of

movement which are NOT the result of

muscular weakness

, ,

cerebellar or vestibular disorders

Can affect eye movement, speech (dysarthria),

individual limbs, trunk, stance and gait


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VESTIBULAR ATAXIA

produced by the same central and peripheral

lesions that cause vertigo

NYSTAGMUS is frequently present: TYPICAL,

AWAY FROM THE SIDE of vestibular

involvement

NO DYSARTHRIA


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VESTIBULAR ATAXIA

GRAVITY DEPENDENT: incoordination of limb

movements cannot be demonstrated when

patient is examined lying down, becomes

walk

STANCE: may be able to stand with feet

together, typically worse with eyes closed


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Vestibular Ataxia (cont.)

Gravity dependent

Incoordination of limb movements cannot beemonstrate w en t e pat ent s y ng own ut

becomes apparent when the patient attempts tostand or walk

Stance

May be able to stand with feet together.Typically worse with the eyes closed


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Posterior Column


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Sensory Ataxia

Results from disorders that affect proprioceptive pathways inthe peripheral sensory nerves, sensory roots, posterior columns ofthe spinal columns and medial lemniscus

- From polyneuropathy or posterior column lesions

1. Impaired position and vibration sense

2. Stance- often able to stand with feet together and eyes open butcannot with eyes closed (Rombergs sign)

3. Absent ankle jerks 4. VERTIGO, NYSTAGMUS and DYSARTHRIA are characteristically

absent


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Cerebellum

Principally a motor organ

Responsible for COORDINATION of movements, esp. skilled

voluntary ones Control of POSTURE and GAIT

Regulation of MUSCLE TONE

Main role is to ASSIST in the initiation and modulation ofWILLED MOVEMENTS that are generated in the CEREBRAL

HEMISPHERE None of these activities of the cerebellum reach

CONSCIOUS KINETIC PERCEPTION


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Anatomical Division

Anterior lobe, posterior lobe, flocculonodular

lobe

Super or sur ace- Pr mary ssure

Inferior surface- Posterolateral fissure


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CEREBELLARNUCLEI

Cerebellar Cortex

(GRAY MATTER)

White matter

(Arbor vitae)

Site of

cerebellar nuclei


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Spinocerebellar Tracts


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CEREBELLAR

OUTPUTS


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CEREBELLAR OUTPUTFROM THE FASTIGIAL NUCLEUS


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CEREBELLAR OUTPUT(Flocculonodular Lobe)

Flocculonodular LobePurkinje Cells

Lateral Vestibular Nuclei

(brainstem)

Vestibulospinal tract

(spinal cord)

Axial and Proximal Muscles


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CEREBELLUMSOMATOTOPIC ORGANIZATION


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Vermian Lesion

Truncal Ataxia

Stands on wide

base

Rolling of trunk

from side to side


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Cerebellar Hemisphere Lesion

Ipsilateral Limb Ataxia

Uncoordinated,

clumsy

movements of

lower limbs


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Clinical Manifestations of Cerebellar

Disease

A. Hypotonia

B. Ataxia

Dysmetria

Decomposition of movement

Dysdiadokinesia

Rebound

Speech Disturbance scanning dysarthria

Nystagmus


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Cerebellar Ataxia

Produced by lesions of the cerebellum itself orof its afferent or efferent connections in thecerebellar peduncles

LIMB ATAXIA i silateral to the cerebellar

hemispherelesion

TRUNCAL ATAXIA vermis lesion

Stance unable to stand with feet togetherand eyes either open or closed


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what is the lesion?

Peripheral

A. Vertigo

Labyrinth

Benign Positional Vertigo (Cupulolithiasis) en ere s yn rome n o ymp a c y rops

Vestibulotoxic drug-induced vertigo

Posttraumatic vertigo

Vestibular nerve

Peripheral vestibulopathy (vestibular neuritis) B. Dysequilibrium

Vestibular Schwanomma


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NEUROLOGIC EVALUATIONWHAT IS THE LESION?

PERIPHERAL

A. VERTIGOLABYRINTH

Benign positional vertigo (Cupulolithiasis)

Menieres syndrome (Endolymphatic hydrops)-

Posttraumatic vertigoVESTIBULAR NERVE

Peripheral Vestibulopathy (Vestibular neuritis)

B. DISEQUILIBRIUM

Vestibular Schwanomma


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CAUSES OF VERTIGO AND

DISEQUILIBRIUM

Has it happened once?

Have there been multiple attacks?

Duration of the episode Any provoking factors

Associated manifestations


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ACUTE VERSIBULAR NEURITISSINGLE EPISODE

Vestibular Neuritis

Cerebellar / Brainstem Infarction of

Hemorrhage


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RECURRENT VERTIGO

Benign Positional Vertigo

Menieres disease

Transient Ischemic Attack (TIF) posterior

c rcu at on

Migraine

Anxiety


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INSIDIOUS SLOWLY PROGRESSIVE

COURSE

Disequilibrium associated with hearing loss

and later facial paralysis and numbness

VESTIBULAR SCHWANOMMA

increased intracranial pressure

CEREBELLAR MASS

(Neoplasms, abscess)


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INSIDIOUS SLOWLY PROGRESSIVE COURSE

Disequilibrium associated with hearing loss

and later facial paralysis and numbness

VESTIBULAR SCHWANOMMA

Associated with headache and signs of

increased intracranial pressure

CEREBELLAR MASS

(Neoplasms, Abscess)


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Duration of Common Causes of Vertigo

Benign positional vertigo

Vertebrobasilar

insufficiency, Migraine

Seconds

Minutes

Menieres Disease

Vestibular Neuritis

Hours

Days


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VERTIGO / DISEQUILIBRIUM OF

PERIPHERAL VESTIBULAR DISORDERS


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VESTIBULAR NEURITISACUTE UNILATERAL PERIPHERAL VESTIBULOPATHY

VESIBULAR NEUROPATHY Occurs mainly in young and middle aged adults

Most authorities attribute it to a VIRALINFECTION of the vestibular nerve

Usually sudden onset of severe vertigo withnausea and vomiting which subsides after severaldays

Lesser degrees of these symptoms made worseby rapid movements of the head

May persist for several weeks or months


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VESTIBULAR NEURITISACUTE UNILATERAL PERIPHERAL VESTIBULOPATHY

VESIBULAR NEUROPATHY

Tinnitus and deafness absent

Nystagmus to the OPPOSITE side Falling and fast pointing TOWARD side of lesion

Rapid Head Impulse Test and Caloric Test

Absent function of one lateral semicircular canal


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VESTIBULAR NEURITISTREATMENT

Acute Stage (to reduce symptoms)

Antihistaminics

Promethazine

Scopolamine

Methylprednisolone

100 mg orally tapered over 3 weeks

Vestibular Exercises


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BENIGN PAROXYSMAL POSITIONAL

VERTIGO (BPPV)

May be the most common cause of vertigo in thegeneral population

Patients typically experience brief episodes ofwith rapid changes in head position

May recur for several days or months

No abnormalities of hearing or other identifiablelesions in the ear or elsewhere


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BENIGN PAROXYSMAL POSITIONAL VERTIGO

Diagnosis

Dix Hallpike Maneuver


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Etiology

This condition is caused when calcium

carbonate debris, dislodged from the

otoconial membrane, enters a semicircular

CANALITHIASIS The debris can be free

floating within the affected canal or stuckagainst the cupula (CUPULOLITHIASIS)


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Treatment

EPLEY MANEUVER

Repositioning maneuver

Highly effective in removing the debris from the


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EPLEYS

MANEUVER

Canalith

Repositioning

Maneuver


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Treatment

Epley Maneuver

Repositioning Maneuver

Highly effective in removing debris from the canal


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Epleys Maneuver

Canalith

repositioningmaneuver


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Menieres Disease

Recurrent attacks of vertigo with FLUCTUATING

tinnitus and deafness; fullness in the ear may be

present

Attacks of VERTIGO Abrupt whirling or rotation for several minutes to an hour

or longer; severe with nausea and vomiting

NYSTAGMUS (+) during the acute attack with fast phase

OPPOSITE Past pointing and tendency to fall TOWARD the affected

side


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Menieres Disease

As the attack subsides, hearing improves

Attacks variable in duration; variable course with

further attacks, progressive increase in deafness

Attacks of verti o cease when the hearin loss is

complete


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Menieres Disease

Onset most frequently in the fifth decade

Female=Male

Etiology: endolymphatic hydrops


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Menieres Disease

Treatment

For protracted cases:

Transdermal scopolamine

For anxious patients in between attacks

M se at ves

Corticosteroid

Never proven effective

If the attacks are very frequent and severe

Permanent relief by surgery


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Menieres Disease

Prognosis

Majority of middle aged patients STABILIZE

spontaneously in a few years


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Menieres Disease

PROGNOSIS

Majority of middle aged patients STABILIZE

spontaneously in a few years


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TOXIC BILATERAL VESTIBULOPATHY

Prolonged exoposure to gentamycin can cause

a vestibulopathy that is usually bilateral

Most prominent symptoms are OSCILLOPSIA

vertigo

Symptoms are especially troublesome when

the patient moves Some nonspecific dizziness occur


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VESTIBULAR SCHWANNOMA

Typically manifest with slowly progressiveunilateral hearing loss (affects high frequencyones) but VERTIGO can occur only rarely

Tumor rowth is slow so the vestibulo ath iscompensated by the CNS

Midle chronic imbalance with impaired caloricresponse

If untreated:

Involvement of CN VII and V, ipsilateral limb ataxia


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VERTIGO / ATAXIA OF

CENTRAL NERVOUS SYSTEM


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What is the lesion?

CENTRAL VERTIGO / ATAXIA

Brainstem / Cerebellar ischemia and infarction

Demyelinating disease ,

Intrinsic brainstem / cerebellar lesions Tumor, AVM

Degenerative diseases

Spinocerebellar ataxia Migraine

Seizure disorders (rare)


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TRANSIENT ISCHEMIC ATTACKS

Episodes of vertigo generally last minutes,

often accompanied by other posterior

circulation symptoms

BRAINSTEM OR CEREBELLAR


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BRAINSTEM OR CEREBELLAR

INFARCTION

Affecting vestibular pathways within brainstem orcerebellum

Wallenberg syndrome (PICA)

Vertigo

Crossed sensory syndrome

Impaired pain and temperature in ipsilateral face andcontralateral extremities

Horners syndrome

Dysphagia with uvula deviated to normal side

Ipsilateral limb ataxia


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MULTIPLE SCLEROSIS

Dizziness is a common symptom in patientswith MS; vertigo is the initial symptom in 5%of patients

T ical MS attack has a radual onsetreaching its peak within a few days

Key to diagnosis:

Lesions DISSEMINATED in time and SPACE within

the nervous system

Cranial MRI: multiple CNS white matter lesions


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MIGRAINE

Wide range of symptoms from brief attacks ofvertigo to prolonged disequilibrium

May be similar to Menieres disease but withouthearing loss

Vestibular symptoms often occur withoutheadache

There is a vestibular form of migraine in children(Benign Paroxysmal Vertigo of Childhood)


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NEURODEGENERATIVE DISORDERS

Not uncommon for a patient with the main

complaint of dizziness to have or later develop

Parkinsonian Syndrome

Usually however , dizziness in these patients is

better clarified as IMBALANCE


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NONVERTIGINOUS DIZZINESS:PRESYNCOPE/SYNCOPE

Sensation oflightheadedness, faintness, andgiddiness

Produced by conditions that IMPAIR BRAINSsupply of BLOOD, OXYGEN, AND GLUCOSE

Orthostatic hypotension Cardiac arrhythmia

Myocardial ischemia

Excessive vagal stimulation

Hypoxia

Hypoglycaemia

May culminate in loss of consciousness (syncope)


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SYSTEMIC CAUSES OF DIZZINESS

Drugs Anticonvulsants, hypnotics, antihypertensives,

alcohol, analgesics, tranquilizers

Hypotension, Presyncope

Primary cardiac causes, postural hypotension from

a wide variety of causes

Infection diseases

Syphilis, viral, bacterial meningitides, systemicinfection



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Endocrine diseases

Diabetes, hypothyroidism

Cellulitis

, ,induced vasculitis

Other systemic conditions

Hematologic disorders, polycythemia, anemia,

dysproteinemia, sarcoidosis, granulomatousdisease and systemic toxins.


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PSEUDOVERTIGO

Chronic hyperventilation syndrome

Anxiety and phobia

Depression


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FEATURES OR PSYCHOPHYSIOLOGIC DIZZINESS

Description

Floating, swimming, rocking, giddy, depersonalization,

spinning inside the head

Associated symptoms

Tension headache, palpitations, gastric distress,urinary frequency, backache, generalized weakness,

and fatigue

Common situations that provoke attacks

Walking on a brightly polished floor or down asupermarket aisle, driving on a freeway, shopping in a

crowded store, death of a loved one

dizziness and disturbance of equilibrium and coordination.pdf

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