Vertigo –The Dizzy Patient:-An Evidence-Based Diagnosis and Treatment strategy

Dr. Sachin Verma MD, FICM, FCCS, ICFCFellowship in Intensive Care Medicine

Infection Control Fellows Course Consultant Internal Medicine and Critical Care

Ivy Hospital Sector 71 MohaliWeb:- http://www.medicinedoctorinchandigarh.com

Mob:- +91-7508677495

Table of Contents:

1. What is vertigo?2. Anatomical aspects.3. Pathophysiology.4. Causes of vertigo.5. General Examination 6. Neurological examination7. Lab investigations.8. Management.

1.What is vertigo?

Vertigo is a symptom of illusory movement and Vertigo is a symptom of illusory movement and not a not a diagnosis .It is due to asymmetry of vestibular system due diagnosis .It is due to asymmetry of vestibular system due to damage or dysfunction of the to damage or dysfunction of the

Labyrinth and vestibular nerve, or Labyrinth and vestibular nerve, or Central vestibular structures in the brainstem. Central vestibular structures in the brainstem.

It is subjective and objective illusion of movement

Differential Diagnosis Differential Diagnosis Is it vertigo ?

1. Lightheadedness: - which includes nonspecific

symptoms related to multiple sensory disturbances, side effect of medications that alter the sensorium or certain psychiatric disturbances.

2. Disequilibrium: - caused by motor dysfunction that impairs balance and gait. ( “Dizziness of feet”)

3. Presyncope: - a sense of impending loss of consciousness due to hypoperfusion of brain or metabolic causes such as hypoglycaemia.

4. Vertigo: - a sensation of movement due to disorder of labyrinth or its central connection.

Usually benign Rule out PSEUDOVERTIGO

Vertigo can be easily differentiated from other causes of dizziness by a “sensation of motion”. The sensation can be

1. subjective (patient is moving) 2. or objective (environment is moving).

2. Anatomical aspects

Ear has auditory system and vestibular system

Auditory system –CochleaVestibular system – It has a set of -Three-dimensional angular

velocity transducers, the semicircular canals,

First, each canal within each labyrinth is perpendicular to the other canals, which is analogous to the spatial relationship between two walls and the floor of a rectangular room.

Second, the planes of the semicircular canals, between the labyrinths, are close to each other.

-A set of three-dimensional linear acceleration transducers, the otoliths (saccule and utricle ).

SCC - mainly for Angular motion- do not have otoliths Otoliths (saccule and utricle ).In an upright person, the saccule is

vertical (parasagittal), whereas the utricle is horizontally oriented (near the plane of the lateral semicircular canals ( SCC )

The otoliths are also arranged in such a way that they can respond to motion in all three linear dimensions.

The otolithic membranes contain calcium carbonate crystals called otoconia

2. Anatomical aspects -cont

3.Pathophysiology. WHY DOES VERTIGO DEVOLOP?HY DOES VERTIGO DEVOLOP?

The three stabilizing systems

(mentioned earlier) overlap

sufficiently to compensate

(partially or completely) for

each other's deficiencies.

Vertigo may represent either

physiologic stimulation or

pathological dysfunction in

any of the three sensory

systems.

When Otoconia come in SCC ,

then cause BPPV.

4.Common causes of vertigo:-

A.Peripheral etiology

a. Acute labyrinthitis and Vestibular neuronitisb. Meniere’s diseasec. Benign Peroxysmal positional vertigo (BPPV)d. Toxins - alcohol. Aminoglycosides, Quinine (Tinnitus ,Hearing loss vomiting and vertigo)

Peripheral and Central causes

B.Central etiology

a. Vertebrobasilar insufficiency (TIA )b. Brainstem Stroke - Ischemia or Haemorrhage c. Demyelinating disorder eg Multiple

Sclerosis(MS). d. Space occupying lesion in brain stem (rare)-

CP angle SOL – -CP angle Tumor of the Schwann cells around the 8th cranial

nerve. -Vertigo with hearing loss and tinnitus -With tumor enlargement, it encroaches on the cerebellopontine angle causing neurological signs. -Mostly in women during 3rd and 6th decades

A.Peripheral etiology(i) Labrynthitis and Vestibular Neuronitis(i) Labrynthitis and Vestibular Neuronitis

Common term for an acute unilateral loss of peripheral vestibular function associated with nausea, vomiting,

vertigo

spontaneous nystagmus, and disequilibrium.

It is generally peaking during the first day, then gradually improving over the next few days

Generally due to a viral infections.

Vestibular Neuronitis

• It is also termed as acute vestibular failure. • Sudden onset acute severe vertigo but there is no auditory

symptom.• The single episode of severe vertigo -for one or two days but

patients may remain symptomatic for months. • Etiology -viral infection in young patients causing injury to

the vestibular apparatus, but in older patients, vascular causes are more likely.

Post-traumatic Vestibular syndromesPost-traumatic Vestibular syndromesA rare cause of peripheral vertigo is perilymphatic fistula .Post-traumatic lesion involves an abnormal connection between the middle and inner ear. It can be caused by i. a direct blow to the ear, ii. a forceful Valsalva maneuver, iii. acute external pressure changes ( as in scuba diving or descent in an airplane)

(ii) (ii) Ménièr’s Disease Disease

Triad of –a) Tinnitus , b) Vertigo andc) Fluctuating Sensory neural deafness.

May occur in clusters and have long episode-free remissions

Usually low pitched tinnitus Symptoms subside quickly after attack No CNS symptoms No positional vertigo is present Often patients have eaten a salty meal prior to attacks

(iii)BPPV- (iii)BPPV- Benign Peroxysmal positional vertigo

Extremely common – 40 % of all vertigo patients BPPV Otoconia displacement.and drag endolymph. No hearing loss or tinnitus Short-lived episodes brought up by rapid changes in

head position Usually there may be a single position that elicits vertigo Top shelf vertigo Horizontal rotatory nystagmus after a short latency

period Less pronounced with repeated stimuli Typically can be reproduced at bedside with positioning

maneuvers

(iv) Toxins

(i)Streptomycin and gentamycin – These cause injury to peripheral end organ, since they are

concentrated in the endolymph and perilymph. Patients usually report progressive unsteadiness, particularly

when visual input is diminished, as happens at night or in a darkened room.

Extreme caution should be used in patients with even mild renal disease because most of these agents are primarily removed by the kidney.

(ii) Anticonvulsant toxicity, phenytoin or carbamazepine, may cause CNS depression, nystagmus, and ataxia

(iii) Benzodiazepines, barbiturates, (iv) Alcohol, and other CNS depressants may present as

nonspecific dizziness

What differentiates labyrinthitis or vestibular neuritis (VN)? from BPPVWhat differentiates labyrinthitis or vestibular neuritis (VN)? from BPPV

Labyrinthitis/VN

a) No head movement needed

b) Duration of hours/days

c) Any age

d) Viral syndrome usually

precedes

a) Epley maneuver is ineffective

BPPV

a. Requires head movement

b. Duration of seconds

c. Usually in elderly

d. No relation to viral syndrome

e. Responds to Epley maneuver

Central vertigo –features Central vertigo –features

Symptoms associated with brainstem ischemia include

a. Diplopia, b. Dysarthriac. Ataxia d. facial weakness or sensory symptomsUnlike their peripheral counterparts, they have little nausea

or any auditory symptoms.

Causes include disorders with significant potential morbidity .

a) Vertebrobasilar Insufficiencyb) Stroke - Cerebellar Hemorrhagec) Multiple Sclerosisd) Tumors

Vertigo :Peripheral v/s CentralVertigo :Peripheral v/s Central

i. Onset Sudden Slow, gradual

i. Intensity Severe ILL defined

i. Duration Paroxysmal Constant

i. Nausea Frequent Infrequent

i. CNS signs Absent Usually present

i. Tinnitus/hearing loss

Can be present Absent

i. Nystagmus Torsional /horizontal

Fatigable

Vertical

Non-fatigable

i. Course Limited usually Non specific

PERIPHERAL CENTRAL

Step 5.General Examination of a patient.Step 5.General Examination of a patient.

1. General examination Orthostatic vital signs

BP and pulse in both arm2.Eye and Cranial nerves examination3.Ear examination4.Neurological examination

Gait and Cerebellar function

2.Eye examinaton –Eye movements and Nystagmus 2.Eye examinaton –Eye movements and Nystagmus

In peripheral vertigo – Spontaneous nystagmus

continues in only one direction even when the direction of gaze changes.

Nystagmus is typically

horizontal-rotary with a slow and fast component

In central disorders, Spontaneous nystagmus may

change its direction whenever there is a change in the direction of gaze (gaze-evoked nystagmus)

Vertical nystagmus is due to a central neurological cause until proved otherwise.

Patient is seated in front of the examiner or lies supine in the bed. The examiner keeps his finger about 30 cm from the patient’s eye in the central position and moves it to the right or left, up or down, but not moving at any time, more than 30° from the central position to avoid gaze nystagmus. Presence of spontaneous nystagmus always indicates an organic lesion.

Vestibular nystagmus has a slow and a fast component and, by convention, the direction of nystagmus is indicated by the direction of the fast component. Intensity of nystagmus is indicated by its degree.

i. 1st degree It is weak nystagmus and is present when patient looks in the direction of fast component.i. 2° degree It is stronger than degree nystagmus and is

present when patient looks straight ahead.

i. 3rd degree It is stronger than 2nd degree nystagmus and is present even when partial looks in the direction of slow component.

How to elicit nystagmus

Nyst video

Eye examination

3.Ear examination3.Ear examination

a. Examine the tympanic membranes and

external auditory canals (EAC) for the presence of infection, tympanic membrane rupture, or foreign body

b. Ipsilateral facial nerve palsy with presence of vesicles within the EAC suggest herpes zoster infection (Ramsay hunt’s syndrome)

c. The presence of recent unilateral hearing loss in the setting of vestibular symptoms suggests Meniere’s disease

d. Acoustic neuromas, due to their slow growth, typically present with gradual decline in hearing and are rarely accompanied by symptoms of vestibulopathy.

Dix-Hallpike Test method-

1.Patient sits on a couch. Examiners holds the patient’s head ,turns it 45° to the right

2.Then places the patient in a supine position so that his head hangs 30* below the horizontal.

3.Patient is asked to look to opposite side and eyes are observed for nystagmus.

4.If patient is made to sit with head rotated , there is change in the direction of nyatagmus .

The test is repeated with head turned to left and then again in straight head-hanging position.

Four parameters of nystagmus are observed :

i. latency, ii. duration,iii. direction and iv. fatigability

Dix video

Finding Peripheral Central ( ?King )

Latency Yes 3-10 sec. No

Fatigability Yes No

Nystagmus direction Fixed, typically mixed rotational

Changing, variable and pure vertical or pure horizontal

Suppression by visual fixation

Yes No

Severity Marked severe Mild to moderateBut patient can not walk easily

Consistency Less consistent More consistent

Past pointing In direction of slow phase

In direction of fast phase

Interpretations of Nystagmus in Hallpike

6.Neurological examination6.Neurological examination

One should begin with a thorough cranial nerve exam, including evaluation of cranial nerves and cerebellar function using finger to nose and rapid alternating movement tests

Involvement of other cranial nerves in addition to the vestibulocochlear nerve strongly suggests central disease

Patient with peripheral vertigo are typically able to walk without assistance, although they tend to veer to one side.

Video – Cerebellar and Rhomerg;s

7.Lab investigations.7.Lab investigations.

1. Routine lab test include complete blood count, electrolytes, glucose and creatinine levels

2. Cardiac – Holtor monitoring and EKG- When evaluating the dizzy patient who complains of

near syncope, the EKG is very important. Look for Rapid or slow rates Prolongation of QT interval. A wide QRS complex with slurred upstroke- in association

with a short PR interval may indicate Wolff-Parkinson-White (WPW) syndrome.

3. Caloric test 4. Electronystagmography (ENG )5. Optokinetic test 6. Imaging (CT and MRI)

NeuroimagingNeuroimaging

1. Patients with severe headache and with hard neurological findings - ( include motor deficits, particularly crossed hemiplegia; dysarthria or dysphagia; inability to walk; bidirectional or vertical nystagmus; and sings of cerebellar dysfunction )

2. Patient with prolonged vertigo symptoms with no other neurological deficits They may have evidence of vertebrobasilar insufficiency by MR angiography, with the greatest incidence in elderly patient

CT is more sensitive for hemorrhage, but MRI is more likely to detect subtle brainstem or cerebellar infarction

CT / MRI findings

8.Treatment

1. General treatment symptomatic treatment -is useful to lessen the abnormal

sensations and to alleviate vegetative symptoms . It includes - antibiotics for infections , bed rest, low salt diet, adaptation exercises , diuretics for meniere’s and surgical repair for fistulas. Symptomatic treatment of nausea, vomiting and dizziness is done.2. Specific drug treatment

3. Exercise

4. Surgery

Treatment of specific conditions -

(i)Labyrinthitis – Bed rest and hydration . Severe nausea and vomiting-benefit from IV fluid Cinnarizine -25-75 mg TDS Short course of steroid i.e.methylprednisolone may help. Antivirals like acyclovir, famciclovir may help in hastening

the recovery in viral causes.(ii)Vestibular neuronitis – (a) Vestibular suppressants – Meclizine, promethazine or prochlorperazine - may be given for short period to tackle severe vertigo and vomiting if present. Cinnarizine -25-75 mg TDS (b) methyl prednisolone 3 week course tapered from 100 mg down to 10 mg daily may reduce long term loss of vestibular function.

Tr Treatment of specific conditions -cont

(iii)Meniers disease - Needs Low salt diet

Vestibular suppressant Vasodilators and Diuretics .

(iv)BPPV –

The treatment of choice for BPPV is -CRP (Canalith repositioning procedure). It is also known as the Epley maneuver.

-Brandt- Duroff exercises

(i). Antihistamines Dimenhydrinate -50 mg thrice daily.SE – Drowsiness .Useful in acute attacks Promethazine Hcl -10-20 mg TDS. SE- Sedation or extrapyramidal synd. Useful in acute attacks, Used with caution in prostatic hypertrophy, glaucoma and CVS pathology. Cinnarizine -25-75 mg TDS . SE -drowsiness. (ii) Phenothiazines • Prochorperazine Orally/I V/IM 5-25 mg SOS/TDS.

SE- Hypotension Useful in acute attacks; acts on vomiting centre.• Trifulpromazine 10mg SOS/TDS - SE-Hypotension .

Useful in acute attacks; acts on vomiting center.

Drug treatment -Labyrinthine suppressants - mainly used in acute attack

iii) Anticholinergics• Meclizine 12 5mgTDS. SE- Drowsiness . in acute attacks; acts on vomiting center • Scopolamines 0.6mg BD ,TDS Use with caution in glaucoma .

(iv) Newer vasodilator - Histamine Agonist/H2 antagonist• Betahistine dihydrochioride 8-16mgTDS SE-GI upset . • Betahistine Mesylate, Chemical name: 2-(2-methylamino ethyl) pyridine dimethane sulfonte , C/I in bronchial asthma and phaeochromocytoma . Maximum efficacy of betahistine is obtained with long periods of treatment of 3-8 weeks and with daily doses of 32 to 36 mg

Drug treatment -Labyrinthine suppressants - mainly used in acute attack

3. Exercises (i)Epley’s maneuver (CRP)- first identify the side of lesion by neck extension

The operator stands behind the patient with the assistant on the side One repositioning cycle has five positions.

PositionA:The patient sits on the table so that when lying, the head is positioned beyond the edge of table.

Position B: The head is placed over the edge of the table, 45 degrees to one side.

Position C While the head is tilted down it is rotated 45 degrees to the opposite side.

Position D: The head and body are rotated until they face downwards 135 degrees from the supine position. Face should face the ground –This step is ignored by clinicians.

Position E: With the head still tilted, the patient is made to sit. The head is turned forward and chin down by 20 degrees.

There should be pause at each position until there is no nystagmus or there is slowing of the nystagmus before changing to the next position. This ejects crystals from the Utricle .

The patient is instructed to wear a neck brace for 24 hours and to not bend down or lay flat for 24 hours after the procedure. One week after the CRP, the Dix-Hallpike test is repeated. If the patient does experience vertigo and nystagmus, then the CRP is repeated with a vibrator placed on the skull in order to better dislodge the otoconia.

One sits in the positions as described .Patient needs to spend 30 seconds in each of the positions .It is repeated 5-6 times twice a day.

ii)Brandt- Duroff exercises

(iv) Surgery

Three surgical procedures have been used to control vertigo. (i)Singular neurectomy: The singular nerve supplies the

ampulla and can be approached through the middle ear. The nerve lies close to the round window membrane at a depth of 1- 2 mm.

(ii)Posterior canal occlusion: The posterior canal is exposed through a transmastoid approach. Drilling is done to reach the perilymphatic space and then plugged with fascia and bone dust. Again, sensorineural hearing loss can occur in about 5 of cases. It is an effective procedure to control vertigo and has been recommended as the procedure of choice.

(iii)Vestibular nerve section: Vestibular nerve is sectioned through the middle cranial fossa. Although this procedure controls vertigo, it entails an intracranial operation with its attendant risks.

B For central vertigo -

Vertebrobasilar insufficiency(TIA) BP control, lipid and blood sugars control,

smoking caesation. Aspirin, anticoagulation as per requirement. Vestibular suppressant medications plus initiation

of rehabilitation procedures. Cerebral activators – (i)Piracetam –

2.4 to 3.6 gm daily in 3 divided doses .Side effects -Insomnia, Hyperkinesia, GI upset Contra indicated in recent MI, pregnancy, renal and hepatic diseases.

(ii)Priabedil - 50 mg once daily.

Take home message1. First decide between true vertigo and pseudovertigo.2. Then differentiate between peripheral and central vertigo.3. Peripheral causes are common .Cervical spondylitis is not

usually a cause of Vertigo.4. Vertical nystagmus is due to a central neurological cause until

proved otherwise. Central causes are not too many but need urgent recognition as they have different treatment and prognosis.

5. Cinnarizine can be prescribed in both central and peripheral causes of vertigo.

6. Betahistine is prescribed mainly in meniere’s disease and also in other peripheral vertigo cases. Both the vestibular suppressants should be prescribed for minimum possible interval of time and not for long .

7. BPPV occurs in 40 % cases of peripheral vertigo. It is treated by Epley’s method.

8. Adaptation exercise should be highlighted in clinical practice.

Reality is merely an illusion, albeit a very persistent one- Reality is merely an illusion, albeit a very persistent one- Albert EinsteinAlbert Einstein