Dizziness and Disturbance of Equilibrium and Coordination

Equilibrium
Ability to maintain orientation of the body and its parts in relation to external space. Depends upon continuous VISUAL, LABYRINTHE and PROPRIOCEPTIVE inputs Association occurs in the BRAINSTEM and CEREBELLUM

VISUAL

LABYRINTHE

PROPRIOCEPTION

BRAINSTEM and CEREBELLUM

ADAPTIVE MOVEMENTS

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

SPATIAL ORIENTATION SYSTEM DISORDERS

Important symptoms: 1. Vertigo 2. Ataxia/ Disequilibrium

Approach to a DIZZY patient

Medical history Physical examination Basic laboratory exam Physiologic diagnostic tools Radiologic diagnostic tools

MEDICAL HISTORY
Description of dizziness by the patient Secondary symptoms Previous history

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

DIZZINESS

disequi librium

vertigo

DIZZINE SS

Near syncop e

Illdefined lighthe adedne ss

VERTIGO

Physical sensation of MOTION of self and environment IMBALANCE of stance and gait Sensation of FAINTNESS Often accompanies anxiety and depression

DISEQUILIBRIUM/ ATAXIA NEAR SYNCOPE PRESYNCOPE/ SYNCOPE ILL DEFINED LIGHTHEADEDNESS (PSEUDOVERTIGO)

Dizziness
Rotating Spinning Whirling Oscillating Rocking Tilting Swaying

Dizziness VERTIGO
Rotating Spinning Whirling Oscillating Rocking Tilting Swaying

PATHOPHYSIOLOGY: Dysfunction of the VESTIBULAR SYSTEM

Dizziness DISEQUILIBRIUM / ATAXIA

Unsteadiness Imbalance Falling to one side Incoordination Wearing a new pair of eyeglasses feeling

Dizziness DISEQUILIBRIUM/ ATAXIA

PATHOPHYSIOLOGY: Unsteadiness Dysfunction of sensory Imbalance (proprioception), cereballer and vestibular Falling to one side pathways Incoordination Wearing a new pair of eyeglasses feeling

Dizziness NEAR SYNCOPE

Light-headedness Fainting Giddiness Passing out Candle being slowly exhausted If with loss of consiousness: SYNCOPE

NEAR SYNCOPE (PRESYNCOPE/SYNCOPE)

PATHOPHYSIOLOGY: Light-headedness Disturbed blood flow to the Fainting brain Giddiness (GLOBAL CEREBRAL ISCHEMIA) Passing out Candle being slowly exhausted If with loss of consiousness: SYNCOPE

Dizziness

Dizziness PSEUDOVERTIGO: PSYCHOLOGICAL

Feeling low Weakness Fatigue Feeling of unreality

III Defined Dizziness PSEUDOVERTIGO

Feeling low Weakness Fatigue Feeling of unreality

PATHOPHYSIOLOGY: Psychological Issues

NEUROLOGIC EVALUATION
Where is the lesion?
Peripheral vestibular
End Organ (Labyrinth) Vestibular Nerve

Central vestibular pathway

Brainstem Cerebellum

EAR

VESTIBULOCOCHLEAR

Vestibulocochlear Nerve CN VIII

Auditory Pathway
TRANSVERSE GYRUS OF HESCHL MEDIAL GENICULATE INFERIOR COLLICULUS LATERAL LEMNISCUS SUPERIOR OLIVARY NUCLEUS COCHLEAR NUCLEUS CRANIAL NERVE VIII

CONDUCTIVE HEARING LOSS

Patient speaks with normal or low volume voice Etiology: Clinical findings:
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 on the side of hearing loss (negative RT)

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) Unilateral hearing loss

Clinical findings

WEBER test: lateralized to the better hearing RINNE test: Air conduction > Bone conduction

Vestibular and Cochlear Sructures

SEMICIRCULAR CANALS

ANGULAR ACCELERATION

CRISTA

Rotational head movement causes displacement of the endolymph which pushes the cupula and deflection of the sensory hair cells This causes depolarization of the vestibular afferents

CRISTA: ANGULAR ACCELERATION

SEMICIRCULAR CANAL

END ORGANS UTRICLE AND SACCULE

Macula
Linear acceleration and gravitational pull OTOLITHIC MEMBRANE is pushed down with deflection of the sensory hair cells causing depolarization of the vestibular afferents

Linear Acceleration

Vestibular Pathways

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 their connections

Vestibular Pathways
The vestibular nerve impulse enters the brainstem and synapses with the vestibular nuclei resulting in 2 reflex responses:
Vestibulo-ocular reflex Vestibulo spinal reflex

Some vestibular impulses enter the flocculonodular lobe and vermis

CONTROL OF EYE MOVEMENT

VESTIBULAR NUCLEUS transmits impulses to the Medial Longitudinal Fasciculus (MLF). MLF sends impulses to CN nuclei 3, 4 and 6 for CONJUGATE EYE MOVEMENTS

VESTIBULOSPINAL TRACTS
MEDIAL vestibulospinal tract inhibitory LATERAL vestibulospinal tract excitatory From the brain, descending tracts carry commands to the motor neurons for axial and proximal muscles (via median descending pathways)

PERIPHERAL VS CENTRAL VERTIGO

PERIPHERAL OR VESTIBULAR LESION OFTEN INTERMITTENT SEVERE Often present Absent Absent CENTRAL LESION OFTEN CONTANT LESS SEVERE Rarely present Typical Typical

VERTIGO

ASSOCIATED FINDINGS: Hearing loss/ tinnitus Focal neurologic deficits: - brainstem - cerebellar signs

PERIPHERAL VS CENTRAL VERTIGO

Direction of nystagmus Influence of gaze Visual fixation Maybe pure horizontal Does NOT change direction with gaze (UNIDIRECTIONAL) Inhibits nystagmus Up to 20 seconds Present and characteristic Pure horizontal Pure vertical Pure torsional Does change direction with gaze (BIDIRECTIONAL) Does NOT affect Nystagmus None Absent

Latency following repositioning movements Direction changing with reversal of head direction

ATAXIA/ DISEQUILIBRIUM
INCOORDINATION OR CLUMSINESS of movement which are NOT the result of muscular weakness Caused by sensory (proprioception, visual), cerebellar or vestibular disorders Can affect eye movement, speech (dysarthria), individual limbs, trunk, stance and gait

VESTIBULAR ATAXIA
produced by the same central and peripheral lesions that cause vertigo NYSTAGMUS is frequently present: TYPICAL UNIDIRECTIONAL, Most pronounced on gaze AWAY FROM THE SIDE of vestibular involvement NO DYSARTHRIA

VESTIBULAR ATAXIA
GRAVITY DEPENDENT: incoordination of limb movements cannot be demonstrated when patient is examined lying down, becomes apparent when patient attempts to stand or walk STANCE: may be able to stand with feet together, typically worse with eyes closed

 Vestibular Ataxia (cont.) Gravity dependent Incoordination of limb movements cannot be demonstrated when the patient is lying down but becomes apparent when the patient attempts to stand or walk Stance May be able to stand with feet together. Typically worse with the eyes closed

Posterior Column

 Sensory Ataxia Results from disorders that affect proprioceptive pathways in the peripheral sensory nerves, sensory roots, posterior columns of the 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 but cannot with eyes closed (Rombergs sign) 3. Absent ankle jerks 4. VERTIGO, NYSTAGMUS and DYSARTHRIA are characteristically absent

 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 of WILLED MOVEMENTS that are generated in the CEREBRAL HEMISPHERE None of these activities of the cerebellum reach CONSCIOUS KINETIC PERCEPTION

 Anatomical Division Anterior lobe, posterior lobe, flocculonodular lobe Superior surface- Primary fissure Inferior surface- Posterolateral fissure

CEREBELLAR NUCLEI

Cerebellar Cortex (GRAY MATTER) White matter (Arbor vitae) Site of cerebellar nuclei

Spinocerebellar Tracts

CEREBELLAR OUTPUTS

CEREBELLAR OUTPUT
FROM THE FASTIGIAL NUCLEUS

CEREBELLAR OUTPUT
(Flocculonodular Lobe) Flocculonodular Lobe Purkinje Cells

Lateral Vestibular Nuclei (brainstem)

Vestibulospinal tract (spinal cord)

Axial and Proximal Muscles

CEREBELLUM
SOMATOTOPIC ORGANIZATION

Vermian Lesion Truncal Ataxia

Rolling of trunk from side to side

Stands on wide base

Cerebellar Hemisphere Lesion Ipsilateral Limb Ataxia

Uncoordinated, clumsy movements of lower limbs

Clinical Manifestations of Cerebellar Disease

A. Hypotonia B. Ataxia
Dysmetria Intention Tremor Decomposition of movement Dysdiadokinesia Rebound Speech Disturbance scanning dysarthria Nystagmus

Cerebellar Ataxia
Produced by lesions of the cerebellum itself or of its afferent or efferent connections in the cerebellar peduncles LIMB ATAXIA ipsilateral to the cerebellar hemisphere lesion TRUNCAL ATAXIA vermis lesion Stance unable to stand with feet together and eyes either open or closed

NEUROLOGIC EVALUATION what is the lesion?

Peripheral

A. Vertigo

Labyrinth
Benign Positional Vertigo (Cupulolithiasis) Menieres Syndrome (Endolymphatic hydrops) Vestibulotoxic drug-induced vertigo Posttraumatic vertigo

Vestibular nerve

Peripheral vestibulopathy (vestibular neuritis)

B. Dysequilibrium

Vestibular Schwanomma

NEUROLOGIC EVALUATION
WHAT IS THE LESION?
PERIPHERAL A. VERTIGO
LABYRINTH

VESTIBULAR NERVE

Benign positional vertigo (Cupulolithiasis) Menieres syndrome (Endolymphatic hydrops) Vestibulotoxic drug-induced vertigo Posttraumatic vertigo

Peripheral Vestibulopathy (Vestibular neuritis)

B. DISEQUILIBRIUM

Vestibular Schwanomma

CAUSES OF VERTIGO AND DISEQUILIBRIUM

Has it happened once? Have there been multiple attacks? Duration of the episode Any provoking factors Associated manifestations

ACUTE VERSIBULAR NEURITIS

SINGLE EPISODE

Vestibular Neuritis Cerebellar / Brainstem Infarction of Hemorrhage

RECURRENT VERTIGO
Benign Positional Vertigo Menieres disease Transient Ischemic Attack (TIF) posterior circulation Migraine Anxiety

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)

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)

Duration of Common Causes of Vertigo

Seconds Minutes Hours Days Benign positional vertigo Vertebrobasilar insufficiency, Migraine Menieres Disease Vestibular Neuritis

VERTIGO / DISEQUILIBRIUM OF PERIPHERAL VESTIBULAR DISORDERS

ACUTE UNILATERAL PERIPHERAL VESTIBULOPATHY VESIBULAR NEUROPATHY

VESTIBULAR NEURITIS

Occurs mainly in young and middle aged adults Most authorities attribute it to a VIRAL INFECTION of the vestibular nerve Usually sudden onset of severe vertigo with nausea and vomiting which subsides after several days Lesser degrees of these symptoms made worse by rapid movements of the head May persist for several weeks or months

ACUTE UNILATERAL PERIPHERAL VESTIBULOPATHY VESIBULAR NEUROPATHY

VESTIBULAR NEURITIS

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

VESTIBULAR NEURITIS
TREATMENT Acute Stage (to reduce symptoms)
Antihistaminics Promethazine Clonazepam Scopolamine

Methylprednisolone
100 mg orally tapered over 3 weeks

Vestibular Exercises

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV)

May be the most common cause of vertigo in the general population Patients typically experience brief episodes of vertigo (less than a minute) and nystagmus only with rapid changes in head position May recur for several days or months No abnormalities of hearing or other identifiable lesions in the ear or elsewhere

BENIGN PAROXYSMAL POSITIONAL VERTIGO Diagnosis Dix Hallpike Maneuver

BENIGN PAROXYSMAL POSITIONAL VERTIGO Etiology This condition is caused when calcium carbonate debris, dislodged from the otoconial membrane, enters a semicircular canal (posterior in 90%) CANALITHIASIS The debris can be free floating within the affected canal or stuck against the cupula (CUPULOLITHIASIS)

BENIGN PAROXYSMAL POSITIONAL VERTIGO Treatment EPLEY MANEUVER

Repositioning maneuver Highly effective in removing the debris from the canal

EPLEYS MANEUVER
Canalith Repositioning Maneuver

BENIGN PAROXYSMAL POSITIONAL VERTIGO Treatment Epley Maneuver

Repositioning Maneuver Highly effective in removing debris from the canal

Epleys Maneuver
Canalith repositioning maneuver

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

Menieres Disease
As the attack subsides, hearing improves Attacks variable in duration; variable course with further attacks, progressive increase in deafness Attacks of vertigo cease when the hearing loss is complete

Menieres Disease
Onset most frequently in the fifth decade Female=Male Etiology: endolymphatic hydrops

Menieres Disease Treatment

For protracted cases:
Transdermal scopolamine

For anxious patients in between attacks

Mild sedatives

Corticosteroid
Never proven effective

If the attacks are very frequent and severe

Permanent relief by surgery

Menieres Disease Prognosis

Majority of middle aged patients STABILIZE spontaneously in a few years

Menieres Disease PROGNOSIS

Majority of middle aged patients STABILIZE spontaneously in a few years

TOXIC BILATERAL VESTIBULOPATHY

Prolonged exoposure to gentamycin can cause a vestibulopathy that is usually bilateral Most prominent symptoms are OSCILLOPSIA and DISEQUILIBRIUM (IMBALANCE) without vertigo Symptoms are especially troublesome when the patient moves Some nonspecific dizziness occur

VESTIBULAR SCHWANNOMA
Typically manifest with slowly progressive unilateral hearing loss (affects high frequency ones) but VERTIGO can occur only rarely Tumor growth is slow so the vestibulopathy is compensated by the CNS Midle chronic imbalance with impaired caloric response If untreated:

Involvement of CN VII and V, ipsilateral limb ataxia

VERTIGO / ATAXIA OF CENTRAL NERVOUS SYSTEM DISORDERS

NEUROLOGIC EVALUATION What is the lesion?

CENTRAL VERTIGO / ATAXIA Brainstem / Cerebellar ischemia and infarction Demyelinating disease Intrinsic brainstem / cerebellar lesions Degenerative diseases
Tumor, AVM Spinocerebellar ataxia Multiple sclerosis, postinfectious demyelination

Migraine Seizure disorders (rare)

TRANSIENT ISCHEMIC ATTACKS

Episodes of vertigo generally last minutes, often accompanied by other posterior circulation symptoms

BRAINSTEM OR CEREBELLAR INFARCTION

Affecting vestibular pathways within brainstem or cerebellum Wallenberg syndrome (PICA)
Vertigo Crossed sensory syndrome
Impaired pain and temperature in ipsilateral face and contralateral extremities

Horners syndrome Dysphagia with uvula deviated to normal side Ipsilateral limb ataxia

MULTIPLE SCLEROSIS
Dizziness is a common symptom in patients with MS; vertigo is the initial symptom in 5% of patients Typical MS attack has a gradual onset, reaching 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

MRI showing lesions of MS in brainstem, cerebellum, and spinal cord

 MIGRAINE Wide range of symptoms from brief attacks of vertigo to prolonged disequilibrium May be similar to Menieres disease but without hearing loss Vestibular symptoms often occur without headache There is a vestibular form of migraine in children (Benign Paroxysmal Vertigo of Childhood)

 NEURODEGENERATIVE DISORDERS Not uncommon for a patient with the main complaint of dizziness to have or later develop typical features of Parkinson Disease Parkinsonian Syndrome Usually however , dizziness in these patients is better clarified as IMBALANCE

 NONVERTIGINOUS DIZZINESS: PRESYNCOPE/SYNCOPE Sensation of lightheadedness, faintness, and giddiness Produced by conditions that IMPAIR BRAINS supply of BLOOD, OXYGEN, AND GLUCOSE
Orthostatic hypotension Cardiac arrhythmia Myocardial ischemia Excessive vagal stimulation Hypoxia Hypoglycaemia

May culminate in loss of consciousness (syncope)

 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, systemic infection

SYSTEMIC CAUSES OF DIZZINESS

Endocrine diseases Cellulitis
Diabetes, hypothyroidism Collagen vascular disease, giant cell arteritis, drug induced vasculitis Hematologic disorders, polycythemia, anemia, dysproteinemia, sarcoidosis, granulomatous disease and systemic toxins.

Other systemic conditions

PSEUDOVERTIGO Chronic hyperventilation syndrome Anxiety and phobia Depression

 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 a supermarket aisle, driving on a freeway, shopping in a crowded store, death of a loved one