Topic presentation Vertigo Dr. Sadia Reza Baishakhi Indoor Medical Officer Dept. of Medicine EMCH CONTENTS • • • • Definition of vertigo Causes of vertigo How to know its central or peripheral Approach to a patient with vertigo Definition • Vertigo is defined as an abnormal perception of movement of the environment or self, and occurs because of conflicting visual, proprioceptive and vestibular information about a person’s position in space Causes of vertigo • Peripheral causes o Benign paroxysmal positional vertigo o Vestibular neuritis o Labyrinthitis o Meniere’s disease o Ethanol intoxication o Inner ear barotraumas o Semicircular canal dehiscence • Central causes o Seizure o Multiple sclerosis o Wernicke’s encephalopathy o Chiari malformations o Cerebellar ataxia syndromes • Mixed central and peripheral causes – Migraine – Stroke and vascular insufficiency • • • • Posterior inferior cerebellar artery Anterior inferior cerebellar artery Vertebral artery insufficiency Vasculitides – Cerebellopontine angle tumors • Vestibular schwannoma • Meningioma – Infections • Lyme disease • Syphilis – Vascular compression – Hyperviscosity syndromes Peripheral Vs Central Peripehral vertigo Central vertigo Onset Sudden Usually slow onset Severity of vertigo Intense Usually mild Pattern Paroxysmal Constant Exacerbate by movement Yes Variable Autonomic Frequent Variable Laterality Unilateral Uni or bilateral Nystagmus Horizontal Any Fatigable/fixation Yes No Auditory symptoms Yes No Tympanic membrane May be abnormal Normal CNS symptoms Absent Present Approach to a patient with vertigo • History: – Duration and frequency of episodes – Aggravating and provoking factors (position, head movement) – Associated ‘fullness in the ear’ during the episode (meniere’s disease) – Associated focal neurological sign (cerebrovascular event) – Fluctuating hearing loss or tinnitus – Associated headaches, nausea or aura (migrane) – Previous significant head injury; previous URTI Ask the Patient: • Do you feel that environment is moving or you moving around environment • Onset- is it sudden or gradual • Is it episodic or persistent • If recurrent what is the frequency and duration • Does it relate to head posture • How severe is it Cont… • Is it associated with tinnitus or hearing loss • Is it associated with double vision,focal weakness • Did you suffer any head trauma • Also take any drug • Physical examination: –Ear examination: • Otoscopic examination to visualize the tympanic membranes for any vesicles (herpes zoster infection) or retraction pockets as seen in cholesteatoma • vertigo triggered by pushing on the tragus or with the valsalva manoeuvre is seen in a perilymphatic fistula – Eye movements (the range of eye movements and whether they are equal in each eye should be observed) • peripheral eye movement disorders are usually disconjugate (different in the two eyes) • central pathology are usually associated with poor pursuit (the ability to follow a smoothly moving target) or inaccurate (dysmetric) saccades (the ability to look back and forth accurately between two targets) • alignment of the two eyes can be checked by a cover test – Cardiovascular examination: • pulse, blood pressure postural hypotension should be checked • carotid examination to identify bruits – Vestibular function test • • • • • • • Spontaneous nystagmus Head impulse test Fistula test Romberg test GAIT Hall –pike manoeuvre Test of cerebellar function Spontaneous nystagmus – Nystagmus of peripheral origin can be suppressed by optic fixation by looking at a fixed point and are typically causes unidirectional horizontal nystagmus – Nystagmus of central origin can not be suppressed by optic fixation, they include • Torsional nystagmus (lesions of branistem) • Vertical downbeat nystagmus (lesions of cranio cervical region) • Vertical upbeat nystagmus (lesions at the junctions of pons and medulla or pons and mid brain) • Pendular nystagmus (congenital or acquired) • Head impulse test – The vestibuloocular reflex (VOR) is assessed with small-amplitude rapid head rotations while the patient fixates on a target • Romberg test – The patient is asked to stand with feet together and arms by the side with eyes first open and then closed – In peripheral vestibular lesions, the patient sways to the side of the lesion – In central vestibular lesion disorder, patient shows instability • Gait – The patient is asked to walk along a straight line to a fixed point, first with eyes open and then closed – In peripheral vestibular lesions, the patient deviated to the affected side with eyes closed • Hallpike manoeuvre – Patients are asked to sit upright close to the edge of the couch. Turn their head 45 degree to one side and then rapidly lower them so that their head is now 30 degree below the horizontal. Ask them to keep their eyes open and to report any vertigo they experience.watch their eyes carfully for nystagmus. – Repeat the test,turning the pt’s head to the other side • Test of cerebellar dysfunction – Finger-nose test – Dysdiadochokinesis – Rebound phenomenon • Laboratory tests – Caloric test – Electronystagmography – Optokinetic test – Rotation test – Posturography – MRI of the brain – Carotid doppler Most commonly encountered vestibular disorders Benign paroxysmal positional vertigo • Pathophysiology: BPPV occurs due to the presence of otolithic debris from the saccule or utricle affecting the free flow of endolymph in the semicircular canals (cupulolithiasis). • It may follow minor head injury but typically spontaneous • Clinical feature: – Recurrent spells of vertigo – Episodes are brief (<1min and typically 15-20s) – Always provoked by changes in head position relative to gravity, such as lying down, rolling over in bed, rising from a supine position and extending the head to look upward • Diagnosis can be confirmed by Hallpike manoeuvre • Treatment: – Explanation and reassurance – reposition maneuvers (the Epley maneuver or Brandt-Daroff exercises) – Re-educate the brain to cope with the inappropriate signals (Cawthrone-cooksey exercises) Epley Maneuver Brandt- Daroff exercises – Start in an upright, seated position. – Move into the lying position on one side with your nose pointed up at about a 45-degree angle. – Remain in this position for about 30 seconds (or until the vertigo subsides, whichever is longer) – Repeat on the other side. Cawthrone-cooksey exercises Labyrinthitis • Clinical feature: – Acute onset of continuous, usually severe vertigo lasting several days to a week – Accompanied by hearing loss and tinnnitus • During recovery hearing may return to normal or remain permanently impaired in the involved ear • Treatment: – Antibiotics (if the patient is febrile or has symptoms of bacterial infection) – Vestibular suppressants (during acute phase of attack) (diazepam, meclizine) Vestibular Neuronitis • Clinical feature: – A paroxysmal, usually single attack of vertigo occurs without accompanying impairment of auditory function and will persist for several days to a week before gradually abating – On examination reveals nystagmus and absent responses to caloric stimulation on one or both sides • Treatment: – For acute stage: Diazepam (2-5mg every 6-12 hours) or Meclizine (25-100mg divided 2-3 times daily) – Vestibular therapy Vestibular migraine • Episodic vertigo lasting for minutes to hours or maybe for days to weeks • Associated with or without headache • Motion sensitivity and sensitivity to visual motion are common • Migraine features maybe present (such as photophobia, phonophobia, or a visual aura) • Treatment: treated with medications that are used for prophylaxis of migrane headaches (such as beta blocker, amitryptyline, flunarizine) Meniere’s disease • Clincial feature: – Episodic vertigo accompanied by tinnitus and fullness in the ear, each attack typically lasting a few hours. – Gradually patient may develop progressive deafness (typically low-tone on audiometry) • Management: – Low salt diet – Vestibular sedatives (cinnarizine or prochlorperazine) – Surgery to increase endolymphatic drainage from the vestibular system Superior Semicircular Canal Dehiscence • Clinical feature: – Deficiency in the bony covering of the superior semicircular canal maybe asscoaited with vertigo triggered by loud noise exposure, straining and an apparent conductive hearing loss – Autophony is also a common feature • Diagnosis is with coronal high resolution CT scan and vestibular evoked myogenic potential (VEMP) • Treatment: – Surgically resurfacing or plugging the dehiscent canal Psychosomatic and functional dizziness • Dizziness maybe somatic manifestation of some psychiatric condition • Major depression • Anxiety • Panic disorder • Or, patient may develop anxiety and autonomic symptoms as a consequence or co morbidity of an independent vestibular disorder. • This is now termed as persistent posturalperceptual dizziness (PPPD) Persistent postural-perceptual dizziness (PPPD) • Clinical feature: – Chronic feeling (3 months or longer) of fluctuating dizziness and disequilibrium that is present at rest and worst while standing – There is an increased sensitivity to self-motion and visual motion (e,g, watching movies) – Intensification of symptoms occurs when moving through complex visual environments such as super-markets – The neurootologic and vestibular function testing are normal • Treatment: – Selective serotonin reuptake inhibitors – Cognitive- behavioral psychotherapy – Vestibular rehabilitation Drugs causing vertigo • Antibioticsaminoglycisides,macrolides,nitrofurantoin • Anticonvulsantslevetiracetam,phenytoin,pregabalin • Antiinflammatory-