VERTIGO

Group 5

VERTIGOGROUP 42016

VertigoWhat is vertigo? A sensation of rotation or

movement of one’s self or of one’s surrounding

The Environment is ‘Spinning’

ex: rotational, linear, or tilting movement

Vertigo vs DizzinessDizziness: Imprecise term : To describe a variety of symptomsIt could mean -Vertigo-Dysequilibrium-Lightheadedness/Presyncope-Rocking or swaying as if on a ship-Motion sickness-Nausea & Vomiting-Oscillopsia(visual disturbance in which objects in the visual field

appear to oscillate) https://www.youtube.com/watch?v=5Jj1NjFspaM

-Floating,swimming,spinning inside of head

Types of Dizziness PatientsExperience

Mechanism

Vertigo Illusion of movement of patients or Surroundings

Disturbance of peripheral or CNS pathways of vestibular system

Dysequilibrium Imbalance or unsteadiness while standing or walking

Vestibulospinal, propioceptive, visual or motor dysfunction, joint pain or instability , psychological factors

Syncope or Presyncope Impending loss of consciousness

Momentary reduce in blood flow to brain eg.) cardiac obstructive problem

Mal de débarquement Sense of rocking or swaying as if on a ship

Vestibular adaptive process to the continuous, passive motion,and must re-adapt once environment is stable

Motion sickness Episodic dizziness,tiredness,pallor, diaphoresis, salivation, nausea & vomiting

Visual-vestibular mismatchEg.) riding in a car or viewing action sequence in large screen theater

Nausea & Vomiting Stimulation of vagus centers in medulla

Types of Dizziness Patients Experience Mechanism

Oscillopsia Subjective illusion of visual motion

Spontaneous : acquired nystagmusHead induced : severe,bilateral loss of the VOR

Floating,swimming,spinning inside of head

Frequently psychological symptoms of anxiety,somatoform disorders, and depression

Vestibular System

Vestibular System

Contributor to our balance system Maintain spatial orientation & stabilize vision Provides information related to movement and

head position

Vestibular System

Detects angular and linear acceleration via these end organs : 1. Saccule 2. Utricle 3. Semicircular canals : Angular acceleration

Otolith : Linear accelerations

Semicircular Canal They respond to angular acceleration and

deceleration. Contain sensory hair cells that are activated by

movement of inner ear fluid (endolymph). As the head moves, hair cells in the semicircular canals send nerve impulses to the brain by way of the acoustic nerve.

Vestibular System

Utricle & Saccule Utricle and saccule is stimulated by linear

acceleration and deceleration or gravitational pull during the head tilts.

The utricle is sensitive to change in horizontal movement. The saccule is sensitive to the change in vertical acceleration (such as going up in an elevator). 

Vestibular System

Overview of vestibular system

Vertigo and Dizziness

Normally there is balanced input from both vestibular systems

Vertigo develops from asymmetrical vestibular activity

Abnormal bilateral vestibular activation results in truncal ataxia

Vertigo and Dizziness Nystagmus

Rhythmic slow and fast eye movement Direction named by fast component Slow component due to vestibular or brainstem

activity Slow component usually ipsilateral to diseased

structure Fast component due to cortical correction

Physiologic Vertigo “motion sickness” A mismatch between visual, proprioceptive and

vestibular inputs Not a diseased cochleovestibular system or

CNS

Vertigo-Differential Diagnoses Etiologies of Vertigo

BPPV Labyrintitis

Acute suppurative Serous Toxic Chronic

Vestibular neuronitis Vestibular ganglionitis Ménière’s Acoustic neuroma Perilymphatic fistula Cerumen impaction

CNS infection (TB, Syphillis) Tumor (Benign or Neoplastic) Cerebellar infarct Cerebellar hemorrhage Vertebrobasilar insufficiency AICA syndrome PICA syndrome Multiple Sclerosis Basilar artery migraine Hypothyroidism Hypoglycemia Traumatic Hematologic (Waldenstroms)

Vertigo-History Is it true vertigo? Autonomic symptoms? Pattern of onset and duration Auditory disturbances? Neurologic disturbances? Was there syncope?

Unusual eye movements? Any past head or neck

trauma? Past medical history? Previous symptoms? Prescribed and OTC

medications? Drug and alcohol intake?

Vertigo-Physical Exam Cerumen/FB in EAC Otitis media Pneumatic otoscopy Tympanosclerosis or TM

perforation Nystagmus Fundoscopic exam Pupillary abnormalities Extraocular muscles Cranial nerves Internuclear

ophthalmoplegia

Auscultate for carotid bruits Orthostatic vital signs BP and pulse in both arms Dix-Hallpike maneuver Gross hearing Weber-Rinne test External auditory canal

vesicles Muscle strength Gait and Cerebellar function

Classification of VertigoDisorder of vestibular system PeripheralWhich involve vestibular end organs and their first order neurons (i.e. the vestibular nerve). The cause lies in the internal ear or the Vlllth nerve. They are responsible for 85% of all cases of vertigo. CentralWhich involve central nervous system after the entrance of vestibular nerve in the brainstem and involve vestibulo-ocular, vestibulo-spinal and other central nervous system pathways.

Acoustic Neuroma

CENTRAL

Vertebrobasila Insufficiency

Multiple sclerosis

Trauma/Head Injury

Benign paroxysmal postural vertigo(BPPV)

PERIPHERAL

Meniere’s Disease

Labyrinthitis Vestibular

Insufficiency,ex: Vestibular Neuronitis

Peripheral Vestibular Disorder Benign paroxysmal positional vertigo (BPPV). Labyrinthitis. Meniere's disease (endolymphatic hydrops). Acoustic neuroma.

Benign paroxysmal

positional vertigo

(BPPV).

Benign Paroxysmal Positional Vertigo (BPPV)

Acute attacks of transient vertigo lasting seconds to minutes initiated by certain head position accompanied by torsional (rotatory) nystagmus.

Most common cause of vertigo Not associated with auditory or

neurological symptoms Epidermiology: women (64%), 40 – 50

y/o Aetiology: head trauma, viral infection,

degenerative disease, idiopathic.

How it occurs?• As a result of otoliths, tiny crystal of

calcium carbonate (normal part of inner ear) detach from otolithic membrane in the utricle and collected in one of the semicircular canals.

• Head still -> gravity cause otoliths clump and settle

• Head moves -> otoliths shift -> stimulates cupula to send false signal to brain -> vertigo and nystagmus occur

Clinical presentation Symptoms: VERTIGO onset: 5-10s

after changing head position (getting out of bed, looking upward, rolling position last for seconds to min.

Often rotatory vertigo,Dizziness (lightheadedness), imbalance, difficulty concentrating, N+V, visual disturbance (nystagmus)

Signs: Hallpike maneuver: rotatory nystagmus. The top pole of the eyes rotates toward the undermost (affected) ear.

Dix-Hallpike maneuver

Rapidly moving the patient from a sitting position to the supine position with the head hanging over the end of the table, turned 45° to one side.

Hold for 15-20s to elicit nystagmus.Onset of vertigo and rotary nystagmus indicate positive test for the

dependent side

Dix-Hallpike Maneuver

Figure 1. Dix-Hallpike maneuver (used to diagnose benign paroxysmal positional vertigo). This test consists of a series of two maneuvers: With the patient sitting on the examination table, facing forward, eyes open, the physician turns the patient's head 45 degrees to the right (A). The physician supports the patient's head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table. The patient remains in this position for 30 seconds (B). Then the patient returns to the upright position and is observed for 30 seconds. Next, the maneuver is repeated with the patient's head turned to the left. A positive test is indicated if any of these maneuvers provide vertigo with or without nystagmus.

Diagnosis History Positive Dix-Hallpike maneuver

Treatment Reassure patient that process resolves

spontaneously Particle repositioning maneuvers Main Aim: Reposition the otoliths back to

utricle- Epley maneuver (performed by MD)- Brandt-Daroff exercise (performed by patient) Surgery for refractory cases Anti-emetics for nausea and vomiting

Epley maneuver

Brandt Daroff exercise

Labyrinthitis

Labyrinthitis

Labyrinth is the structure of the inner ear :

Consist of :

1. Semicircular canals

2. Vestibule

2. Cochlea

Balance & equilibriumHearing

Labyrinthitis - (inflammation of the labyrinth) occurs when an infection affects the whole structure of inner ear (labyrinth). Affect both the vestibular apparatus and cochlea

Resulting in hearing changes as well as dizziness or vertigo.

Different from..

Vestibular neuritis- ‘Neuritis’ (inflammation of the nerve) affects the branch associated with balance, resulting in dizziness or vertigo but no change in hearing.

Etiology Occurs as a complication of acute and

chronic otitis media, bacterial meningitis, cholesteatoma, and temporal bone fractures

Bacterial : S. pneumonia, H. Influenza, P. aeruginosa, P. mirabilis

Viral : rubella, CMV, measles, mumps, varicella zoster

Inner ear infections that cause vestibular neuritis or labyrinthitis are usually viral rather than bacterial

Clinical presentation Sudden onset of vertigo, nausea, vomiting,

tinnitus, and unilateral hearing loss, with no associated fever or pain

Age: Middle aged adults (30-40) peak around 41 years old

No male or female predominance Usually unilateral, sometimes can be

bilateral It usually preceded with URTI infection It can last for some days, or even weeks Meningitis is a serious complication

Investigation No specific test. The diagnosis can usually be made clinically. Lab test: FBC: To see elevated TWC (infection) Lumbar puncture, CSF culture & gram stain: if suspect

Meningitis

Other: MRI- MRI with gadolinium to exclude a retrocochlear

cause of hearing loss (such as acoustic neuroma) CT Head Pure Tone Audiogram- to document the extent of hearing

loss and to confirm the affected ear Electronystagmography (ENG)- Records eye movements

and responses to ocular and vestibular stimuli

Treatment

IV antibiotics Drainage of middle ear + mastoidectomy

Meniere’s Disease

(Endolymphatic hydrops)

Meniere’s Disease- an idiopathic peripheral vestibular disorder attributed to excess endolymphatic fluid pressure, causing episodic inner ear dysfunction.

Distension of endolymphatic system due to increased volume of endolymph

Risk factor High salt intake Caffeine Stress Nicotine Alcohol

S

Ductus reuniens

U

Cochlear duct

U = utricleS = saccule

Endolymphatic duct in vestibular aqueduct

Clinical presentation Early stage: Sudden, episodic vertigo (>20 min,<24hr) nausea and vomiting,

nystagmus and aural fullness. Intermediate stage: attacks of vertigo+tinnitus + fluctuating sensorineural

hearing loss. Late stage: hearing loss + balance difficulties + tinnitus.

Diagnosis criteria:by American Academy of otolaryngology, head & neck surgery

2 or > definitive spontaneous episodes of vertigo lasting 20 min/>

Audiometrically documented hearing loss >1 occasion Tinnitus /aural fullness in affected ear All other causes excluded.

Investigations No definitive test, depends on history Dix-Hallpike positional test: +ve indicates coexisting benign paroxysmal

positional vertigo (BPPV) Romberg test: instability while eye closed Tuning fork test: sensorineural hearing loss (Rinne: +ve, Weber lateralised to

unaffected ear) Caloric test MRI: vestibular schwannoma or superior canal dehiscence Audiometry, electrocochleography ( may indicate increased inner ear fluid

pressure in some cases of Ménières disease) & � electronystagmography( to evaluate balance function)

ManagementAcute Management Reassurance and psychological support Bed rest Vestibular sedatives to relieve vertigo – dimenhydrinate

(Dramamine), promethazine theoclate (Avomine)

Long term

Medical:

-Low salt diet, diuretics (e.g. hydrochlorothiazide, amiloride), intratympanic gentamicin therapy (control vetrtigo up to 80% of the patient)

Surgical:

- Decompression of endolymphatic sac

- Transtympanic labyrinthetomy

Acoustic Neuroma(vestibular scwannoma)

Acoustic neuroma(vestibular scwannoma)Definition Scwannoma of the vestibular portion of CN VIII Acoustic neuroma is the most common intracranial tumor causing

SNHL and the most common cerebellopontine angle tumour.

SNHL* Sensoryneural hearing loss

Pathogenesis Starts in the internal auditory canal and expends into cerebellopontine

angle (CPA), compressing cerebellum and brainstem When associated with type 2 neurofibromatosis (NF2) : bilateral

acoustic neuromas, café-au-lait lesions, and multiple intracranial lesions.

Clinical features Usually presents with unilateral SNHL or tinnitus Dizziness and unsteadiness may be present, but true vertigo is

rare as tumour growth occurs slowly and thus compensation occurs

Facial nerve palsy and trigeminal (V1) sensory deficit(corneal reflex) are late complications

Acoustic neuroma(vestibular scwannoma)

Diagnosis MRI with gadolinium(gold standard) Audiogram Poor speech discrimination relative to the hearing loss Stapedial reflex absent or significant reflex decay ABR- increase in latency of the 5th wave Vestibular test : normal or asymmetric caloric weakness(an early

sign)

Treatment Surgical excision Other: gamma knife, radiation

Acoustic neuroma(vestibular scwannoma)

Thank you