Vertigo 2016
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Transcript of Vertigo 2016
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