Vertigo –The Dizzy Patient:-An Evidence-Based Diagnosis and Treatment strategy     Dr. Sachin Verma MD, FICM, FCCS, ICFC  ...
Table of Contents:1.   What is vertigo?2.   Anatomical aspects.3.   Pathophysiology.4.   Causes of vertigo.5.   General Ex...
1.What is vertigo?    Vertigo is a symptom of illusory movement and not a    diagnosis .It is due to asymmetry of vestibul...
Differential Diagnosis Is it vertigo ?Vertigo can be easily differentiated from other causes of dizziness by a    “sensati...
2. Anatomical aspectsEar has auditory system and vestibular   systemAuditory system –CochleaVestibular system – It has a s...
2. Anatomical aspects -cont                          SCC - mainly for Angular                          motion- do not have...
3.Pathophysiology. WHY DOES VERTIGO DEVOLOP?The three stabilizing systems   (mentioned earlier) overlap   sufficiently to ...
4.Common causes of vertigo:-            Peripheral   and Central causes A.Peripheral etiologya.    Acute labyrinthitis and...
B.Central etiologya.   Vertebrobasilar insufficiency (TIA )b.   Brainstem Stroke - Ischemia or Haemorrhagec.   Demyelinati...
A.Peripheral etiology(i) Labrynthitis and Vestibular Neuronitis   Common term for an acute unilateral loss of    peripher...
Vestibular Neuronitis     •   It is also termed as acute vestibular failure.     •   Sudden onset acute severe vertigo but...
(ii) Ménièr’s Disease      Triad of –a)     Tinnitus ,b)     Vertigo andc)     Fluctuating Sensory neural deafness.     ...
(iii)BPPV- Benign Peroxysmal positional vertigo   Extremely common – 40 % of all vertigo patients BPPV   Otoconia displa...
(iv) Toxins(i)Streptomycin and gentamycin –   These cause injury to peripheral end organ, since they are    concentrated ...
What differentiates labyrinthitis or vestibular neuritis (VN)? from BPPV    Labyrinthitis/VN                BPPV    a)   ...
Central vertigo –features Causes include disorders with significant potential morbidity .     a)   Vertebrobasilar Insuffi...
Vertigo :Peripheral v/s Central                      PERIPHERAL                   CENTRALi.   Onset            Sudden     ...
Step 5.General Examination of a patient.1.  General examination     Orthostatic vital signs     BP and pulse in both arm2....
2.Eye examinaton –Eye movements and Nystagmus   In peripheral vertigo –       In central disorders,Spontaneous nystagmus...
How to elicit nystagmus Patient is seated in front of the examiner or lies supine in the bed.       The examiner keeps his...
Eye examination
3.Ear examinationa.   Examine the tympanic membranes and     external auditory canals (EAC) for the     presence of infect...
Dix-Hallpike Test method-1.Patient sits on a couch. Examiners     holds the patient’s head ,turns it     45° to the right2...
Interpretations of Nystagmus in HallpikeFinding               Peripheral             Central      ( ?King )Latency        ...
6.Neurological examination    One should begin with a thorough cranial nerve exam,     including evaluation of cranial ne...
7.Lab investigations.1.   Routine lab test include complete blood count,     electrolytes, glucose and creatinine levels2....
Neuroimaging1.   Patients with severe headache and with hard     neurological findings - ( include motor deficits,     par...
CT / MRI findings
8.Treatment1.   General treatment             symptomatic treatment -is useful to lessen the abnormal      sensations and ...
Treatment of specific conditions   -(i)Labyrinthitis –    Bed rest and hydration .    Severe nausea and vomiting-benefit f...
Tr            Treatment of specific conditions -cont   (iii)Meniers disease -        Needs Low salt diet        Vestibular...
Drug treatment -Labyrinthine suppressants - mainly used in acute attack (i). Antihistamines Dimenhydrinate -50 mg thrice ...
Drug treatment -Labyrinthine suppressants - mainly used in acute attackiii) Anticholinergics• Meclizine 12 5mgTDS. SE- Dro...
3. Exercises (i)Epley’s maneuver (CRP)-                   first identify the side of lesionby neck extensionThe operator s...
ii)Brandt- Duroff exercises One sits in the positions as described .Patient needs to spend 30 seconds in each of the posit...
(iv) SurgeryThree surgical procedures have been used to control vertigo. (i)Singular neurectomy: The singular nerve suppl...
B For central vertigo -Vertebrobasilar insufficiency(TIA) BP control, lipid and blood sugars control,  smoking caesation....
Take home message         1.    First decide between true vertigo and pseudovertigo.         2.    Then differentiate betw...
Vertigo –the dizzy patient an evidence-based diagnosis and treatment strategy
Vertigo –the dizzy patient an evidence-based diagnosis and treatment strategy
Vertigo –the dizzy patient an evidence-based diagnosis and treatment strategy
Vertigo –the dizzy patient an evidence-based diagnosis and treatment strategy
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Vertigo –the dizzy patient an evidence-based diagnosis and treatment strategy

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Vertigo is a symptom of illusory movement and not a diagnosis .It is due to asymmetry of vestibular system due to damage or dysfunction of the
Labyrinth and vestibular nerve, or
Central vestibular structures in the brainstem

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Vertigo –the dizzy patient an evidence-based diagnosis and treatment strategy

  1. 1. Vertigo –The Dizzy Patient:-An Evidence-Based Diagnosis and Treatment strategy Dr. Sachin Verma MD, FICM, FCCS, ICFC Fellowship in Intensive Care Medicine Infection Control Fellows Course Consultant Internal Medicine and Critical Care Ivy Hospital Sector 71 Mohali Web:- http://www.medicinedoctorinchandigarh.com Mob:- +91-7508677495
  2. 2. Table of Contents:1. What is vertigo?2. Anatomical aspects.3. Pathophysiology.4. Causes of vertigo.5. General Examination6. Neurological examination7. Lab investigations.8. Management.
  3. 3. 1.What is vertigo? Vertigo is a symptom of illusory movement and not a diagnosis .It is due to asymmetry of vestibular system due to damage or dysfunction of the Labyrinth and vestibular nerve, or Central vestibular structures in the brainstem.It is subjective and objective illusion of movement
  4. 4. Differential Diagnosis Is it vertigo ?Vertigo can be easily differentiated from other causes of dizziness by a “sensation of motion”. The sensation can be1. subjective (patient is moving)2. or objective (environment is moving).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
  5. 5. 2. Anatomical aspectsEar has auditory system and vestibular systemAuditory 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 ).
  6. 6. 2. Anatomical aspects -cont 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
  7. 7. 3.Pathophysiology. WHY DOES VERTIGO DEVOLOP?The three stabilizing systems (mentioned earlier) overlap sufficiently to compensate (partially or completely) for each others 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.
  8. 8. 4.Common causes of vertigo:- Peripheral and Central causes A.Peripheral etiologya. Acute labyrinthitis and Vestibular neuronitisb. Meniere’s diseasec. Benign Peroxysmal positional vertigo (BPPV)d. Toxins - alcohol. Aminoglycosides, Quinine (Tinnitus ,Hearing loss vomiting and vertigo)
  9. 9. B.Central etiologya. Vertebrobasilar insufficiency (TIA )b. Brainstem Stroke - Ischemia or Haemorrhagec. 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
  10. 10. A.Peripheral etiology(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.
  11. 11. 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 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 byi. 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)
  12. 12. (ii) Ménièr’s 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
  13. 13. (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
  14. 14. (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
  15. 15. What differentiates labyrinthitis or vestibular neuritis (VN)? from BPPV Labyrinthitis/VN BPPV a) No head movement a. Requires head movement needed b) Duration of hours/days b. Duration of seconds c) Any age c. Usually in elderly d) Viral syndrome usually d. No relation to viral syndrome precedes e. Responds to Epley a) Epley maneuver is maneuver ineffective
  16. 16. Central vertigo –features Causes include disorders with significant potential morbidity . a) Vertebrobasilar Insufficiency b) Stroke - Cerebellar Hemorrhage c) Multiple Sclerosis d) Tumors Symptoms associated with brainstem ischemia includea. Diplopia,b. Dysarthriac. Ataxiad. facial weakness or sensory symptomsUnlike their peripheral counterparts, they have little nausea or any auditory symptoms.
  17. 17. Vertigo :Peripheral v/s Central PERIPHERAL CENTRALi. Onset Sudden Slow, graduali. Intensity Severe ILL definedi. Duration Paroxysmal Constanti. Nausea Frequent Infrequenti. CNS signs Absent Usually presenti. Tinnitus/heari Can be present Absent ng lossi. Nystagmus Torsional /horizontal Vertical Fatigable Non-fatigablei. Course Limited usually Non specific
  18. 18. 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
  19. 19. 2.Eye examinaton –Eye movements and Nystagmus In peripheral vertigo –  In central disorders,Spontaneous nystagmus Spontaneous nystagmus may continues in only one change its direction whenever direction even when the there is a change in the direction of gaze changes. direction of gaze (gaze-evoked nystagmus)Nystagmus is typically Vertical nystagmus is due to a horizontal-rotary with a central neurological cause until slow and fast component proved otherwise.
  20. 20. How to elicit nystagmus 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. Nyst video
  21. 21. Eye examination
  22. 22. 3.Ear examinationa. Examine the tympanic membranes and external auditory canals (EAC) for the presence of infection, tympanic membrane rupture, or foreign bodyb. 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 diseased. Acoustic neuromas, due to their slow growth, typically present with gradual decline in hearing and are rarely accompanied by symptoms of vestibulopathy.
  23. 23. Dix-Hallpike Test method-1.Patient sits on a couch. Examiners holds the patient’s head ,turns it 45° to the right2.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 andiv. fatigability Dix video
  24. 24. Interpretations of Nystagmus in HallpikeFinding Peripheral Central ( ?King )Latency Yes 3-10 sec. NoFatigability Yes NoNystagmus direction Fixed, typically mixed Changing, variable and pure rotational vertical or pure horizontalSuppression by Yes Novisual fixationSeverity Marked severe Mild to moderate But patient can not walk easilyConsistency Less consistent More consistentPast pointing In direction of slow In direction of fast phase phase
  25. 25. 6.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
  26. 26. 7.Lab investigations.1. Routine lab test include complete blood count, electrolytes, glucose and creatinine levels2. 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 test4. Electronystagmography (ENG )5. Optokinetic test6. Imaging (CT and MRI)
  27. 27. Neuroimaging1. 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
  28. 28. CT / MRI findings
  29. 29. 8.Treatment1. 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 treatment3. Exercise4. Surgery
  30. 30. 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.
  31. 31. 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
  32. 32. Drug treatment -Labyrinthine suppressants - mainly used in acute attack (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.
  33. 33. Drug treatment -Labyrinthine suppressants - mainly used in acute attackiii) Anticholinergics• Meclizine 12 5mgTDS. SE- Drowsiness . in acute attacks; acts onvomiting 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 oftreatment of 3-8 weeks and with daily doses of 32 to 36 mg
  34. 34. 3. Exercises (i)Epley’s maneuver (CRP)- first identify the side of lesionby neck extensionThe 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 flatfor 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 avibrator placed on the skull in order to better dislodge the otoconia.
  35. 35. ii)Brandt- Duroff exercises 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.
  36. 36. (iv) SurgeryThree 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.
  37. 37. 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.
  38. 38. Take home message 1. 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- Albert Einstein

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