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OBJECTIVES At the end of the session the student should be able to: 1. Define Vertigo and different from dizziness. 2. Identify the cause of Vertigo and different diagnosis of Vertigo. 3. Describe the investigation and treatment of Vertigo.

Vertigo - negative impact on quality of life:

Vertigo - negative impact on quality of life General health perception Women with vertigo Weighted population mean Men with vertigo QoL parameter (SF-36) Limitations due to emotions Physical functioning Limitations due to physical problems Social functioning Mental health Bodily pain Vitality p<0.05 Mean score (scale of 0-100) Mean score (scale of 0-100) Do we take vertigo seriously enough? p<0.05 p<0.05 p<0.05

Epidemiology prevalence of vertigo:

E pidemiology prevalence of vertigo 5 % of patients - GP , 10 % - Otorhinolaryngologists 3rd most common symptom L ifetime prevalence in adults : 7.4% • Female preponderance is observed 1 : 2.7 3 times more in the elderly Vertigo patients are nobody’s baby Shunting between GPs, Physician, Neurologist, ENT specialist and psychiatrists. With or without investigations-it is vestibular Suppressant . PROBLEM

What do you prefer to do ? :

What do you prefer to do ? ? Do CT - ? Refer to ENT - ? Do Audiogram - ? Refer to Epileptologist - ? Do MRI - ? Refer to Cardiologist - ? Do Angiogram - ? Refer to Psychiatrist - ? Refer to Physician - Could be stroke Could be BPPV Could be Meiniere Could be Epilepsy Could be Schwannoma Could be Arrhythmia Vertebral Artery dissection Could be a Panic Disorder For Anything and everyother

Define Vertigo:

Define Vertigo Unsteadiness or imbalance F eel normal when stationary , but difficulty while walk Often ,they have no symptoms of dizziness. Disequilibrium suggests a central lesion , but it may be peripheral. Patients with bilateral peripheral vestibular loss may note unsteady gait Both vertigo and dysequilibrium imply a loss of balance, but vertigo involves a sense of motion. “ILLUSION” AND “HALLUCINATION” of movement. “As the world Turns”

Dizziness :

Dizziness Circulation Metabolic Endocrine Degeneration Psychologic Light headedness Sense of strangeness Faintness Giddy Imbalanced Syncope Presyncope Weak Giddiness Anxiety Anemia Depression Unsteady “ abnormal sensations relating to a person’s perception of their body in the environment “

Dizziness :

Dizziness True Vertigo (50%) Presyncope Disequilibrium Other subtypes An illusion of movement, usually rotation A feeling of faintness or loss of consciousness A sense of unsteadiness in the lower body No effect on feelings in head Relieved when sitting down Swimming or floating sensations Feelings of dissociation Difficult to describe


Patient complains of dizziness Does the patient have true vertigo? Ask: Possible cause Comment Q. Does the room spin around? A . Yes Vertigo An illusion of movement, often horizontal and rotatory . Associated nausea and vomiting indicate a peripheral rather than central cause. Q. Do you feel unsteady? A . Yes Dys -equilibrium May result from peripheral neuropathy , eye disease, musculoskeletal weakness or peripheral vestibular disorders. Q. Do you feel like fainting? A . Yes Pre-syncope Caused by cardiovascular disorders reducing cerebral perfusion Q. Do you feel lightheaded? A . Yes non-specific & hard to Diagnose It may result from panic attacks with Hyperventilation - Psychogenic

How do we maintain equilibrium?:

How do we maintain equilibrium ? Visual input EQULIBRIUM PROPRIOCEPTIUAL INPUT(body) VESTIBULAR INPUT LABYRINTHS .( cerebellum,brain sten ) Pathophysiology Complex interaction of visual, vestibular and proprioceptive inputs that the CNS integrates as motion and spatial orientation

Balance requires information of similar intensity from both vestibular systems:

Balance requires information of similar intensity from both vestibular systems 10 10 Head movement Activation of cells in right vestibular system Activation of cells in left vestibular system Central nuclei Normally, the input from left and right vestibular system is of similar intensity (e.g. of size ‘10’)

Neurophysiology Vertigo: Role of Neurotransmitters :

Neurophysiology Vertigo: Role of Neurotransmitters Acetylcholine : (m2)- Functions as an excitatory neurotransmitter in central and peripheral pathways Glutamate:2 Maintains the resting discharge of the central vestibular neurons; may modulate synaptic transmission in the VOR arc GABA: 2 Thought to be inhibitory for commissures of the medial vestibular nucleus Histamine- 3 diffusely in vestibular structures. H1& H2 receptors- Pre & >post synaptically on vestibular cells Dopamine (5) D1 to D5 Serotonin 5 HT (7) Nitric oxide

Pathophysiological Pathways:

Pathophysiological Pathways Endolymph movement, depending on the direction of flow and deflection of otoliths by gravity, either stimulates or inhibits neuronal output from the attached hair cells Nerve impulses from the vestibular system are transmitted to the vestibular nuclei in the brain stem and cerebellum through the eighth cranial nerve From there, connections are made to the oculomotor system, spinal cord, and cerebral cortex, which integrate the information to produce the perception of motion Vertigo results from lesions or disturbances along this pathway

1.Objective vertigo: the patient perceives that the environment is moving around him/her 2.Subjective vertigo: the patient feels himself/herself moving in a static environment 3. Pseudo-vertigo; something spinning inside :

1. Objective vertigo: the patient perceives that the environment is moving around him/her 2. Subjective vertigo: the patient feels himself/herself moving in a static environment 3. Pseudo-vertigo; something spinning inside 3.Peripheral Involving structures not part of the central nervous system, most frequently the inner ear 4.Central Involving structures in the central nervous system (e.g., cerebrum, cerebellum, brainstem)

Central vertigo results from a dysfunction in central processing:

Central vertigo results from a dysfunction in central processing 10 10 Central nuclei Input from left and right vestibular system remains of similar intensity Impaired information transfer between vestibular nuclei causes central vertigo (e.g. of size ‘10’) Central vertigo requires central treatment

Peripheral vertigo results from a dysfunction in vestibular system functioning:

Peripheral vertigo results from a dysfunction in vestibular system functioning 5 10 Central nuclei


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 PHYSIOLOGIC VERTIGO


CHARACTERISTICS PERIPHERAL CENTRAL SEVERITY Severe Mild ONSET Sudden Gradual DURATION( Pattern) < Minutes Paroxysmal Weeks to Months Absent POSITIONAL Yes No FATIGUABLE Yes No POSTURAL INSTABILITY Able to walk; unidirectional instability Falls while walking; severe HEARING LOSS OR TINNITUS Can be present Usually absent OTHER NEUROLOGIC SYMPTOMS(vomiting) Absent Present ASSOCIATED NYSTAGMUS Horizontal Vertical PERIPHERAL VS CENTRAL VERTIGO 19

Etiology :

Etiology INNER EAR Benign paroxysmal positional vertigo (BPPV) Meniere’s disease Labyrinthitis Trauma (labyrinthine concussion) Aminoglycoside toxicity VESTIBULAR NERVE Vestibular neuritis Nerve compression due to meningioma or schwannoma BRAIN STEM Physiological (visual-vestibular mismatch) Demyelination (multiple sclerosis) Migraine Vertebrobasilar insufficiency (as in stroke or TIA) Drug toxicities (with anticonvulsants, aspirin, alcohol)


Neurosurgical emergency Central Vertigo 1.Vertebrobasilar Insufficiency 1.Atheromatous plaque 2.Subclavian Steal Syndrome 3.Drop Attack 4.Wallenberg Syndrome 2.Cerebellar Hemorrhage 3. Multiple Sclerosis( 7-10%) 4. Vertebral Basilar Migrai ne EXTRA 1.Head Trauma 2.Neck Inju 3.Temporal 4.Metabolic abnormalities 1.Hypoglycemia 2.Hypothyroidism 5 . Acute anxiety 6.Acute panic 7.Hyperventilation


CLINICAL IMPORTANCE CENTRAL CAUSES VBI Post Circulation stroke Cerebellar lesion CVJn anomaly PERIPHERAL CAUSE Benign paroxysmal positional vertigo (BPPV) Labyrinthitis Ménière disease Vestibular neuronitis Acoustic Neuroma Trauma, Drug : alcohol, aminoglycoside Life threatening Alarmingly panic Investign , Mx are different OTHER CAUSES Migraine Epilepsy Cardiac Ortho Hypoten Psychogenic Ototoxic drugs

Benign Paroxysmal Positional Vertigo:

Benign Paroxysmal Positional Vertigo Extremely common Otoconia displacement No hearing loss or tinnitus Short-lived episodes brought on by rapid changes in head position Self limited within a few minutes Usually a single position that elicits vertigo Horizontorotary nystagmus with crescendo-decrescendo pattern after slight latency period Less pronounced with repeated stimuli Typically can be reproduced at bedside with positioning maneuvers


Labyrinthitis S/S hearing loss and tinnitus,Abrupt onset,Usually continuous, 4 types Serous , Acute suppurative,Toxic,Chronic Vestibular Neuronitis S/S viral , Sudden onset ,increases in intensity in hours and gradually subsides over days, may have auditory symptoms Vestibular Ganglionitis S/S virally (VZV), may affect multiple ganglions, Ramsay Hunt Syndrome -Deafness -Vertigo - Facial Nerve Palsy -EAC Vesicles

Ménière Disease:

Ménière Disease S/S (1861) Triad of vertigo, tinnitus and hearing loss, Due to cochlea- hydrops (Unknown etiology) autoimmune Abrupt, episodic, recurrent episodes with severe rotational vertigo Usually last for several hours Acoustic Neuroma S/S Earliest sign is decreased corneal reflex Later truncal ataxia Most occur in women Tumor of the Schwann cells around the 8 th CN


EVALUATION History / Exam are key stone in arriving at diagnosis 1.Eyes / Ears / CVS / CNS / Vestibular System Exam in all CT is not very much useful MRI is most useful if the Dx is BS stroke The way of “Ruling-out” a central disorder is to “Rule-in” a specific vestibular disorder


VERTIGO PRESENTATION Acute severe Vertigo Recurr spont . Vertigo Recurr Positionl Vertigo EXAMINATION Evaluate Nystagmus Positional test Dix Hallpike test Supine positional test Head Thrust test 27


DIX – HALLPIKE TEST HALLPIKE TO THE LEFT or THE RIGHT The head is turned to the left or right by 45° in the upright position Pt is brought back to the left or right ear down head hanging position. The head should remain at least 15 sec in the head down position ( for latency) Help eyes to stay open manually Use your nose as a target to the patient First elicited during the straight back positional manoeuvre. The second clip shows the same nystagmus during the conventional right ear down Hallpike manoeuvre.

Vertigo-Ancillary Tests:

Vertigo-Ancillary Tests CT-if cerebellar mass, hemorrhage or infarction suspected Glucose and ECG in the “dizzy” patient Cold caloric testing Angiography for suspected VBI MRI Electronystagmography and audiology


Algorithm For various tests


Emergency Care Monitor / Maintain vitals Stabilize the Symptoms Identify the Causes – Central / Peripheral Prevent worsening Treat the Condition --Hierarchically Appropriately Antihistaminics ( Dimenhydrinate ) Dramamine H1 Antagonist / Antiemetic (Meclizine ( Diligan ) Antihistaminics (Promethazine) Avomine 7.Medical Tt for first few Days MANAGEMENT

Symptom Management:

Symptom Management Dizziness: Dimenhydrinate (Dramamine) 50 mg IV Nausea: Ondansetron ( Emeset ) Lorazepam / Steroids – Not found to be effective Vestibular Neuritis: Steroids + ? Vancyclovir  Superior effect, followed by Vestibular physical therapy

Management of Vertigo in Elderly:

Management of Vertigo in Elderly Identify etiology and treat BPPV accounts of 25% of vertigo in elderly Acute Vertigo -Vestibular sedatives Vestibular rehabilitation Exercises Labyrinthectomy may sometimes useful Labyrinthectomy : Symmetrically open all the semicircular canals and vestibules; the five individual groups of neurosensory epithelia are excised to eliminate abnormal vestibular input from the diseased ear


Treatment to reduce endolymphatic pressure Acetazolamide ( Diamox ) Low salt diet (1-2gm/d) Diuretics (HCT + Triampterine ) Decompression surgery Endolymphatic shunt Cochleo Sacculotomy Ablation of hair cells Intra tympatic gentamycin Meiniere’s Disease 34

Physiologic Vertigo:

Physiologic Vertigo Motion Sickness Bring Vestibular, Somato sensory and visual input back to congruence Looking into Horizon Scopolamine Patch 35


Vestibular rehabilitation exercises Head and neck Visual-vestibular interaction Postural stability Performed lying, sitting or standing Vertigo-provoking movements of head & neck in different planes (ex: flexion, extension, etc.) Uses cervical-ocular reflex Promotes visual-vestibular interaction Involves ocular and hand-eye co-ordination exercises Uses the vestibulo -ocular reflex Improves static and dynamic posture Manipulates visual, somatosensory and vestibular cues Involves trunk rotation, head rotations, and gait exercises Rehabilitation exercises differ in their target


: SURGERY ONLY A SMALL FRACTION PATIENTS Patient presents with Vertigo-inducing tumour (e.g., cerebellopontine tumour) Recurrent episodes of acute vertigo due to established unilateral vestibular damage unresponsive to medical therapy Clinical picture Surgery Tumour removal Ablative Non-Ablative Meniere’s disease or peripheral vestibulopathy : Labyrinthectomy Vestibular nerve section Meniere’s disease : Endolymphatic sac shunt or decompression BPPV : Posterior canal occlusion


SUMMARY ON TREATMENT Vertigo type Treatment Peripheral causes BPPV Canalith repositioning manoeuvre Labyrinthine concussion Vestibular rehabilitation Meniere’s disease Low-salt diet, diuretic, surgery, transtympanic gentamicin Labyrinthitis Antibiotics, removal of infected tissue, vestibular rehabilitation Perilymph fistula Bed rest, avoidance of straining Vestibular neuritis Brief course of high-dose steroids, vestibular rehabilitation Central causes Migraine Beta-blockers, calcium channel blockers, tricyclic amines Vascular disease Control of vascular risk factors, e.g., antiplatelet agents Cerebellopontine tumours Surgery

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