Chronic VertigoChronic Vertigo

A young lady complains of 3 months of dizziness. She had a road traffic accident then and sustained a mild head injury. She has otherwise recovered fully.

Causes of VertigoCauses of VertigoCentral Vertebrobasilar

Insufficiency

Multiple Sclerosis

Acoustic NeuromaPeripheral

Acute Vestibular Neuronitis

BPPV

Meniere’s Disease

InfectionsCommon

RH Syndrome

Labyrinthitis

Structural

Cholesteatoma

Perilymphatic fistula

Temporal Bone Fracture

Serous OM

Labyrinthine Concussion

HistoryHistoryWhen it beganConfirm vertigoTime courseAggravating factors- Head movement- Coughing, sneezing, exertion,

loud noises

HistoryHistoryAssociated symptoms- Nausea and vomitting- Postural instability- Deafness, tinnitus- Headache, photophobia- Neurological dysfunction- Drop attacks- Loss in spatial orientation

Past medical history and Past medical history and drug historydrug historyTrauma: site, nature Viral illnessesPast history of vertigoFamily historyDrug history

Physical ExaminationPhysical Examination Vital signs - presence of fever - rapid/irregular pulse - supine and standing BP:

any drop in BP on standing up? (orthostatic hypotension)

standing provokes symptoms?

If standing does provoke symptoms, postural symptoms should be distinguished from those triggered by head movement by returning the patient supine until symptoms dissipate and then rotating the head.

Physical ExaminationPhysical Examination Checking for Nystagmus

- With the patient supine, the eyes are checked for presence, direction, and duration of spontaneous nystagmus

- Direction and duration of nystagmus and development of vertigo are noted.

What is Nystagmus?What is Nystagmus? - Rhythmic movement of the eyes

- Vestibular disorders can cause nystagmus because the vestibular system and the oculomotor nuclei are interconnected.

- Presence of vestibular nystagmus helps identify vestibular disorders and sometimes distinguishes central from peripheral vertigo.

- The direction of the nystagmus is defined by the direction of the quick component

- Nystagmus may be rotary, vertical, or horizontal and may occur spontaneously, with gaze, or with head motion.

How to check for Nystagmus?How to check for Nystagmus? - Initial inspection for nystagmus is done with the patient lying

supine with unfocused gaze

- Patient is slowly rotated to a left and then to a right lateral position.

- Direction and duration of nystagmus are noted.

- If nystagmus is not detected, then the Dix-Hallpike maneuver is performed.

   Peripheral CentralNystagmusDirection Unidirectional, fast

phase toward the normal ear; never reverses direction

Sometimes reverses direction when patient looks in the direction of slow phase

Type Horizontal with a torsional component, never purely torsional or vertical

Can be any direction

Effect of visual fixation Suppressed Not suppressed

Other neurologic signs

Absent Often present

Postural instability Unidirectional instability, walking preserved

Severe instability, patient often falls when walking

Deafness or tinnitus May be present Absent

Difference between nystagmus Difference between nystagmus secondary to peripheral nervous secondary to peripheral nervous system and CNS causesystem and CNS cause - Nystagmus secondary to peripheral nervous system disorders

has a latency period of 3 to 10 sec and fatigues rapidly

- Nystagmus secondary to CNS causes has no latency period and does not fatigue.

- During induced nystagmus, the patient is instructed to focus on an object. Nystagmus from peripheral disorders is inhibited by visual fixation.

Inducing NystagmusInducing Nystagmus - Caloric stimulation of the ear canal induces nystagmus in a person with an intact

vestibular system.

- Failure to induce nystagmus or > 20% difference in duration between sides suggests a lesion on the side of the decreased response

- Quantification of caloric response is best done with formal (computerized) electronystagmography.

- Care should be taken not to irrigate an ear with a known tympanic membrane perforation or chronic infection.

- With the patient supine and the head elevated 30°, each ear is irrigated sequentially with 3 mL of ice water. Alternatively, 240 mL of warm water (40 to 44°C) may be used

- Cold water produces nystagmus to the opposite side; warm water produces nystagmus to the same side. A mnemonic device is COWS (Cold to the Opposite and Warm to the Same).

BPPVBPPV Provoking a BPPV attack – Dix-Hallpike manoeuvre

With the patient sitting, the neck is extended and turned to one side. The patient is then placed supine rapidly, so that the head hangs over the edge of the bed. The patient is kept in this position and observed for nystagmus. Nystagmus usually appears with a latency of a few seconds and lasts less than 30 seconds. It has a typical trajectory, beating upward and torsionally, with the upper poles of the eyes beating toward the ground. After it stops and the patient sits up, the nystagmus will recur but in the opposite direction.

If nystagmus is not provoked, the maneuver is repeated with the head turned to the other side. If nystagmus is provoked, the patient should have the maneuver repeated to the same (provoked) side; with each repetition, the intensity and duration of nystagmus will diminish.

Other examinationOther examination - Complete head and neck examination

- Ear Canal and hearing:

Weber test and Rinne test are used to document sensorineural or conductive hearing losses

Ear canal is inspected for discharge and foreign body, and the tympanic membrane is checked for signs of infection or perforation using a otoscope.

- Neurological examination:

Cerebellar function is tested by assessing gait and doing a finger-nose test and Romberg's test.

Test the rest of the cranial nerves

- Nasopharyngoscopy and indirect laryngoscopy

- Fistula test

Fistula TestFistula Test• Entails making a sensitive recording of eye movements while pressurizing each ear canal with a pneumatic otoscope

• A positive test is good grounds for surgical exploration.

InvestigationsInvestigationsImaging- Xray, CT, MRI, MRAElectronystagmography (ENG) and

video-nystagmography (VNG)Vestibular evoked myogenic

potentials (VEMP)- tests otoliths of vestibular system

Audiometry – low frequency hearing loss can confirm Meniere’s disease, or reflect traumatic sensorineural loss

ENGENGOculomotor evaluationPositioning/positional testingCaloric stimulation of the

vestibular system (COWS). If poor reflex, means vestibular weakness of horizontal semicircular canal of the side being stimulated.

Can help to discriminate between central and peripheral etiologies

Labyrinthine concussionLabyrinthine concussionCan occur in the absence of

fracturePressure waves in skull base may

damage the membranous labyrinth, VIII nerve or even the brainstem due to shearing forces

a/w high-frequency hearing loss+/- tinnitusMay recover or not

““Whiplash”- Cervical Whiplash”- Cervical vertigovertigovertigo or dizziness that is provoked by

a particular neck posture no matter what the orientation of the head is to gravity

estimated that 20-58% of patients who sustain closed-head injuries or whiplash experience late onset symptoms of dizziness, vertigo and dysequilibrium

no hearing symptoms (other than tinnitus) or hearing loss but there may be ear pain (otalgia)

Cervical vertigo - Cont. Cervical vertigo - Cont. Possible causes:

◦Vascular compression (central vertigo)

◦Abnormal sensory input from neck propioceptors

◦Cervical cord compression (most common)

◦Etc.

Temporal Bone FractureTemporal Bone FractureBones in the

temporal region are usually the thinnest and therefore at the greatest risk of fracture

Types◦ Longitudinal (most

common)◦ Transverse◦ Oblique

Associated with basilar fracture◦ Battle’s sign◦ Racoon eyes◦ CSF rhinorrhoea◦ Cranial nerve palsy◦ Bleeding from eyes

and nose◦ Hemotympanum◦ Ocular nerve

entrapment

Longitudinal fracture

Oblique fracture

Perilymphatic FistulaPerilymphatic Fistula Infrequent complication of head injury Fistula develops at otic capsule (most

commonly at round or oval window) Allow communication of fluid-filled inner and

air-filled middle ear Permits transfer of pressure changes to

macular and cupular receptors Patients c/o episodic vertigo, tinnitus and/or

hearing loss provoked by sneezing, lifting, straining, coughing and loud sounds

Investigations for perilymph Investigations for perilymph fistulafistulaHistory is more sensitive than imagingMRI with intrathecal gadolinium

enhancement can detect inner and middle ear communication

Hennebert sign- apply positive and negative pressure to the intact eardrum using a pneumatic otoscope. Positive results include the elicitation of nystagmus or onset of dysequilibrium with the sensation of motion or nausea. May be used with ENG

BPPVBPPV Benign paroxysmal positional vertigo Symptoms:

Patients c/o recurrent episodes of vertigo, lasting one minute or less

Lasts for weeks to months (median duration 2 weeks)

Vertigo provoked by specific head movements (e.g. Looking up while standing, getting up from bed, rolling over in bed)

Associated with nausea and vomiting

BPPVBPPV Mostly due to calcium debris (otoconia – loose

calcium carbonate crystals) Usually deposit in posterior semicircular canal –

canalithiasis less commonly, can also be anterior canal or

horizontal canal Semicircular canals normally detect head

accelerations Debris in the canal causes inappropriate

sensation of spinning when head moves with respect to gravity

BPPVBPPV In the setting of trauma:

Prior head trauma present in approximately 15% of BPPV

Head injury can cause displacement of otoconia, which can then settle into one of the semi-circular canals

May be a delay of weeks or even months between injury and onset of BPPV

BPPVBPPV Important to differentiate from central

positional nystagmus, as central lesions often require intervention Dix-Hallpike manoeuvre helps to confirm BPPV,

and establish it as peripheral Typical features suggest peripheral lesion:

Peripheral CentralLatent period before onset

2 to 20 seconds None

Duration of nystagmus < 1 min > 1 min

Fatiguability Fatiguing with repetition

Non-fatiguing

Direction Only one type; horizontal/rotatory

May change direction with given head position

Intensity of vertigo Severe Less severe

Benign paroxysmal Benign paroxysmal positional vertigopositional vertigo

1. Particle repositioning maneuver2. Vestibular rehabilitation3. Surgical options?

Particle repositioning Particle repositioning maneuvermaneuverEpley maneuverModified Epley maneuverModified Semont maneuver

In patients with benign paroxysmal positional vertigo due to canalithiasis, the particle repositioning maneuver encourages the calcium carbonate debris to migrate toward the common crus of the anterior and posterior canals and exit into the utricular cavity. Step 1 is the standard Dix-Hallpike positioning test.

This maneuver should be carried out three times a day. Repeat this daily until you are free from positional vertigo for 24 hours. Reproduced from Http://www.charite.de/ch/neuro/englishL.htm

Modified semont maneuver

http://www.youtube.com/watch?v=NQr7MKJBAJY&NR=1

VIDEO ON EPLEY’S MANEUVER

Brandt-Daroff exerciseBrandt-Daroff exercisehttp://www.tchain.com/otoneurology/disorders/bppv/brandt/first.html

Vestibular rehabilitationVestibular rehabilitationactivities should involve using the eyes while the head and body are in motion.

Surgical options?Surgical options?POSTERIOR CANAL PLUGGING

MENIERE’S DISEASEMENIERE’S DISEASENon-Interventional: • Lifestyle modifications• Medication• Rehabilitation

Interventional

Lifestyle adjustmentsLifestyle adjustmentsSalt restrictionLimiting caffeine

MedicationMedicationAcute episodes: vestibular

suppressants and antiemeticsDiuretics and betahistine

InterventionalInterventionalDestructive : intratympanic

gentamicin injection, surgical labyrinthectomy, and vestibular nerve section.

Non-destructive:◦Surgical: endolymphatic sac

procedures (enhancement or shunting or both) and sacculotomy.

◦Intratympanic glucocorticoids ◦Positive pressure pulse generator

(Meniett) 

Brainstem concussion - Vestibular rehabilitation

Labyrinthine concussion – Vestibular suppressants and vestibular rehabilitation, Labyrinthectomy or vestibular nerve section are options.

Perilymphatic fistula – Bed rest for at least 5 days and the avoidance of the Valsalva maneuver. Middle ear exploration and tympanotomy and placement of soft tissue graft over the fistula are options.

Cervical vertigo - Vestibular rehabilitation and anti-inflammatory medications

Meniere’s DiseaseMeniere’s Disease

Definition: Disorder of the inner ear characterized by episodic vertigo, fluctuating sensorineural hearing loss, tinnitus, and aural fullness with progressive sensorineural hearing loss.

Epidemiology•Incidence: 0.5–7.5 per 1000 persons annually, often other causes of peripheral vertigo are misdiagnosed as this disorder.•Onset most frequently in the fifth decade of life, may also occur in young adults or the elderly•Sex : Affects males and females equally

Etiology•Etiology is unknown. •Pathophysiology: Accumulation of fluid within the endolymphatic system of the inner ear (endolymphatic hydrops) leading to degeneration of vestibular and cochlear hair cells•Most cases are idiopathic (the term Ménière’s disease should be applied strictly to these patients). Secondary causes of this pathology include: Infection, Trauma , Autoimmune disease, Inflammatory causes, Tumor.

Signs and symptoms:•Episodic vertigo

•Often occurs with nausea and vomiting •Usually not positional

•Aural fullness or pressure in the ear often accompanies these vertiginous episodes. •Fluctuating sensorineural hearing loss

•Any pattern of hearing loss can be observed. •Low-frequency, unilateral sensorineural hearing impairment is typical. •Gradual progression of hearing deficit is common.

•Tinnitus •Usually low pitch •May be absent during the initial attacks of vertigo •Invariably appears as the disease progresses •Increases in severity during an acute attack •Often associated with distortion of auditory perception

Ddx: Damage to hair cells/Damage to central auditory pathways

Diagnosis There is no definitive test for Ménière’s disease. Careful history and physical examination of the patient with episodic

vertigo ◦ Vertigo ◦ Hearing loss

Audiometry should be used to document sensorineural hearing loss in the affected ear at least once during the course of the disease and can be used to follow progression and response to treatment.

◦ Tinnitus ◦ Aural fullness

Appropriate testing to exclude other etiologies Electrocochleography can be useful.

Lab tests: to exclude other suspected diseases.Imaging: MRI Best imaging study for sensorineural hearing loss May obtain to exclude retrocochlear pathology

◦ Vestibular schwannoma ◦ Meningioma ◦ Other lesions/tumors of cerebellopontine angle ◦ Demyelinating lesions/disorders of the brainstem (which only

rarely mimic this condition) Superior to CT for imaging retrocochlear pathology

Diagnostic Procedures Audiometry Brainstem auditory evoked potentials Electronystagmography Otoscopy Caloric test/electronystagmography (ENG) Electrocochleography

◦ Measures the earliest evoked potentials generated in the cochlea and the auditory nerve

◦ An elevation of the ratio of summating potential to action potential is seen in Ménière’s disease.

Treatment Approach There is no cure for Ménière’s disease. Control of vertigo is the focus of treatment. There is no effective treatment for the other manifestations of

the disease. ◦ Hearing loss ◦ Tinnitus ◦ Aural fullness

Specific TreatmentsTherapy for vertigo Low-salt diet

◦ Mainstay of control of rotatory vertigo ◦ Many clinicians also recommend discontinuation of caffeine and tobacco products.

Vestibular therapy ◦ Can be provided by special vertigo clinics and rehabilitation centers ◦ Only a minority of patients experience significant improvement.

Medications ◦ Meclizine: 25–50 mg PO q6h prn ◦ Scopolamine: 1.5-mg transdermal patch behind the ear q3d prn ◦ Diazepam: 5–10 mg PO q 6 h prn ◦ Prochlorperazine: 5–10 mg PO q6h prn; 25 mg PR q12h prn ◦ Promethazine: 25–50 mg PO/PR q6h prn ◦ Diuretics ◦ Short course of glucocorticoids for acute attacks ◦ Intratympanic gentamicin ◦ Many patients will end up taking a combination of 2 or more of these medications.

Surgical therapy: reserved for unresponsive cases ◦ Endolymphatic sac decompression ◦ Labyrinthectomy (resolves rotatory vertigo in >90% of the cases) ◦ Vestibular nerve section (resolves rotatory vertigo in >90% of the cases)

Therapy for tinnitus Hearing aids Tinnitus maskers Antidepressants Monitoring Monitor response to treatment. Periodically monitor hearing status through audiometry.

Complications Hearing loss/deafness Injury due to falls Inability to work Anxiety regarding symptoms

Prognosis Course is variable.

◦ It is not fatal. ◦ There are usually alternating periods of attacks and remissions. ◦ Over time, tinnitus and hearing loss usually progress.