VERTIGO: CAUSES & MANAGEMENT

VERTIGO: CAUSES & MANAGEMENT

1. VERTIGO: CAUSES & MANAGEMENT Dr Harjitpal Singh Assistant Professor(ENT), Dr RKGMC, Hamirpur .

2. DEFINITION SUBJECTIVE SENSE OF IMBALANCE “Sensation as if the external world is revolving around the patient or as if he himself is revolving in space”

3. VESTIBULAR SYSTEM Peripheral vestibular system:-include the vestibular apparatus( 3 SCC , Utricle & Saccule ) and vestibular nerve Five Vestibular Receptor organs are present in the Vestibular Labyrinth. Two Maculae in utricle and saccule ( otolith organs) --- Linear Acceleration. Three Cristae Ampullares of SSC --- Angular Accleration . Central vestibular system(within CNS):starts from vestibular nuclei in the Pons and its central connection(including cerebellum)

4. PATHOPHYSIOLOGY Balance requires – Normal functioning vestibular system Input from visual system ( vestibulo -ocular) Input from proprioceptive system ( vestibulo -spinal) Central causes compromise central circuits that mediate vestibular influences on posture, gaze control, autonomic function Disruption of balance between inputs results in vertigo Goal of treatment: restore balance between different inputs

5. PATHOPHYSIOLOGY( cont ) Vestibular system influences autonomic system Intimate linkage in brainstem pathways between vestibular and visceral inputs Alteration of vestibular inputs results in: Nausea, vomiting Pallor Respiratory/circulatory changes

6. Causes of peripheral vestibular system Like any organ in the body, the vestibular system can be affect by:- A) Congenital malformation:-but it is a symptomatic as central compensation occur early in infancy B) Acquired:- 1.Infections:- bacterial or viral ;acute or chronic e.g labrynthitis , vestibular neuritis, syphilis 2.Tumour:-like acoustic neuroma (vestibular schwannoma ) 3.Trauma:-temporal bone fracture, perilymph fistula 4.Autoimmune:- autoimmune inner ear diseases 5.Vascular:- labyrinthine apoplexy 6.Degenerative:- Dysequilibrium of ageing ( presbyastasis ) 7.Miscillaneous:- Meniere's disease, benign paroxysmal positional vertigo(BPPV)

7. CLASSIFICATION ANATOMICAL DURATION OF VERTIGO NATURE OF VERTIGO

8. ANATOMICAL A) PERIPHERAL VESTIBULAR DISORDERS BPPV Meneir’s disease Vestibular neuronitis Labyrinthitis Vestibulotoxic drugs Head trauma Perilymph fistula Syphilis Acoustic neuroma

9. ANATOMICAL( cont ) B) CENTRAL VESTIBULAR DISORDERS Vertebrobasilar insufficiency Posterior inferior cerebellar artery syndrome Basilar migraine Cerebellar disease Multiple sclerosis Tumors of brainstem Epilepsy

10. DURATION OF VERTIGO

11. NATURE OF VERTIGO ROTATIONAL UNSTEADINESS

12. ROTATIONAL BPPV Labyrinth fistula Vertebrobasilar insufficincey Meniere’s disease Vestibular neuronitis Trauma Labyrinthitis Metastatic deposits in CP angle

13. UNSTEADINESS Drugs Travel sickness Perilymph fistula Hyperventillation Vestibular insufficiency CNS lesions

14. BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV) Most common cause Dysfunction of posterior SCC Cupulolithiasis vs. Canalithiasis Cupulolithiasis Calcium deposits embedded on cupula PSCC becomes dependent on gravity Canalithiasis Calcium debris ( otoconia ) displaced into PSCC Does not adhere to cupula

15. BPPV( cont ) Head movements Looking up Lying down Rolling onto affected ear Result in displacement of “sludge” / otoconia Vertigo lasting a few seconds Treatment approaches Laboratory maneuvers Particle repositioning Habituation exercises

16. MENIERE’S DISEASE Is an inner ear disease characterized by :- Episodic vertigo ,hearing loss ,tinnitus and ear fullness lasting for minutes –days. The disease affect cochlea and SCC and vestibule(whole membranous labyrinth) which reflect its symptoms

17. MENIERE’S DISEASE ( cont ) Pathogenesis Distension of the membranous labyrinth or endolymphatic hydrops is postulated as a cause of this condition either due to excessive production or impair absorption of endolymph The attack occurs due to small ruptures in Reissner membrane leading to mixing of the endolymph and perilymph .

18. MENIERE’S DISEASE ( cont ) Clinical features The duration of the vertigo last usually for 30 minutes to 4 hours The vertigo is often disabling and very acute in onset Associated with nausea and vomiting The patient feels tired for the next few days after the attack.

19. MENIERE’S DISEASE ( cont ) Hearing loss is sensorineural in type and in early stage of the disease affects the lower frequencies and return to normal after the attack (fluctuating hearing loss ) Tinnitus and a feeling of fullness or pressure in the affected ear may precedes the attack Over the course of the disease hearing loss and tinnitus become permanent The disease is usually unilateral initially but can become bilateral Sign:- spontaneous rotatory nystagmus Investigations:- P.T.A. , brain MRI may be needed to role out central causes

20. ACOUSTIC NEUROMA Vestibular symptoms are variable and tinnitus is common. Diagnosis is made on the basis of radiological investigations. Treatment depends upon size of tumour . Various modalities are surgery, steriotactic surgery.

21. VESTIBULAR NEURITIS Etiology Most likely due to viral infection supported by polymerase chain reaction to detect viral DNA In postmortem study mostly Herpes simplex virus type one Symptoms Acute spontaneous vertigo associated with nausea and vomiting lasting from days –weeks, No cochlear & CNS involvement, no The symptoms subside over the following days but many patients have residual imbalance that last for months . Hearing is normal Sign Acute attack there is nystagmus (horizontal towards the unaffected side ) After acute stage passed, nystagmus disappear but patient characteristically rotate towards the affected side when attempt to march on a spot with their eyes closed positive Unterberger test PTA ,brain MRI may be needed if central vertigo cannot be excluded easily

22. TRAUMATIC INNER EAR DISEASE Non-Operative: Labyrinthine concussion or fracture of temporal bone. Post-Operative: A perilymph fistula may occur after ear surgery esp. ` stapedectomy Temporal bone fractures Longitudinal fractures 80 -90 % , Usually spare the labyrinth and facial nerve Transverse fractures 10- 20% , Transverse fracture usually involve the labyrinth and thus lead to sensorineural hearing loss with profound vertigo. This vertigo will settle with time as central compensation occurs .

23. TRAUMATIC INNER EAR DISEASE( cont ) Management For fracture itself--conservative plus broad spectrum antibiotic Vertigo---vestibular sedative Haemotympanum ----conservative treatment usually resolves within 3-4 weeks Tympanic membrane perforation----usually heals within 3 months if persists then myringoplasty Facial nerve paralysis: Immediate paralysis treated by surgical exploration with attempt to repair the nerve. Delayed paralysis : usually treated conservatively CSF leak : Medical treatment : bed rest ,head elevation, stool softener , lumbar drain and antibiotics to prevent meningitis Surgical closure of the defect if medical treatment fail

24. LABYRINTHITIS Inflammation of labyrinth due to any cause. May be viral or bacterial. Viral may occur during course of an exanthematous disease like mumps/measles or influenza type illness. Bacterial labyrinthitis may be circumscribed, serous or suppurative in a case of otorrhoea . It may also occur during course of meningitis.

25. SUPERIOR SEMICIRCULAR CANAL DEHISCENCE SYNDROME Syndrome of vertigo and oscillopsia induced by loud noises or by stimuli that change middle ear or intracranial pressure Tullio phenomenon - eye movement - loud noise Hennebert's sign “Third mobile window

26. MIGRAINE Concomitant vertigo and disequilibrium Headache control improves vertigo Diagnostic criteria Personal/family history Motion intolerance Vestibular symptoms - do not fit other causes Theories - vascular origin, abnormal neural activity (brainstem), abnormal voltage-gated calcium channel genes.

27. VERTEBROBASILAR INSUFFICIENCY Vertigo, diplopia, dysarthria, gait ataxia and bilateral sensory & motor disturbance Transient ischemia - low stroke risk Antiplatelet therapy - aspirin 325mg qD Ticlid Platelet aggregate inhibitor Risk of life-threatening neutropenia Only in patients unable to tolerate aspirin

28. CNS NEOPLASM Tumors involving brainstem, cerebellum or midbrain Other signs of intracranial disease are found On ENG nystagmus is found to be irregular and enhanced on eye opening.

29. POSTERIOR INFERIOR CEREBELLAR ARTERY THROMBOSIS (LATERAL MEDULLARY SYNDROME Onset is with severe vertigo with contralateral hemianalgesia .

30. Management

31. HISTORY DESCRIPTION Ask the patient to describe the problem True rotatory vertigo or dizziness. Severity Number of attacks Temporal pattern (continuous vs. episodic / short vs. prolonged) If associated with turning the head, lying supine, or sitting upright. Vestibular & cochlear symptoms (hearing loss either fluctuating or progressive, tinnitus, ear pressure, nausea and vomiting) Degree of impairment during the attack Syncope:Transient loss of consciousness with loss of postural tone Presyncope : Lightheadedness-an impending loss of consciousness Psychiatric dizziness: Dizziness not related to vestibular dysfunction Disequilibrium: Feeling of unsteadiness, imbalance or sensation of “floating” while walking

32. SECONDARY SYMPTOMS Tinnitis Hearing impairment Headache or visual symptoms. Neurological abnormalities Brainstem symptoms ( diplopoia , dysarthria , facial paraesthesia , extremity numbness or weakness.)

33. PREVIOUS HISTORY Injuries: Head trauma in the past (post traumatic hydrops ) History Of prior ear surgery (labyrinthine fistula, perilymphatic fistula.) Drugs : Aminoglycosides , cisplatin , miocycline Stress situations Family illness Systemic Diseases: History of DM (causes visual, proprioceptive , vascular problems) HTN, cardiovascular and cerebrovascular diseases

34. GPE Cardiovascular, BP (including orthostatic) in both arms, pulse Neurologic ENT HEAD AND NECK EXAMINATION Detailed ENT Examination Tympanic membrane for retraction, perforation, Infection, cholesteatoma,valsalva Assess hearing on both sides Cranial nerves Bruits in the neck

35. SPECIFIC VESTIBULAR SYSTEM EXAMINATION (Balance tests need not be performed in acute vertigo) Nystagmus Corneal test Fistula test Romberg test Gait Past-pointing and falling Hallpike-manoeuvre (positional test) Caloric tests Electronystagmography Test of cerebellar dysfunction

36. Nystagmus Defined as involuntary, rhythmical, oscillatory movement of eyes It is an important sign in evaluation of vestibular system It can be either horizontal /vertical/ rotatory nystagmus It has 2 components : SLOW & FAST The direction of fast component indicates the direction of the nystagmus Slow component usually ipsilateral to diseased structure Fast component due to cortical correction

37. Intensity of nystagmus is indicated by its degree. AS PER ALEXANDER’S LAW 1 st DEGREE It is weak nystagmus and is present when patient looks in the direction of fast component 2 nd DEGREE It is stronger than 1st degree and is present when patient looks straight ahead 3rd DEGREE It is stronger than the 2nd degree and is present when the patient looks in the direction of the slow component This law may not hold true in case of nystagmus of central region

38. PRESENCE of spontaneous nystagmus is indicative of ORGANIC LESIONS - Tone of imbalance of vestibulo -ocular reflux Peripheral nystagmus – is suppressed by optic fixation Enhanced by darkness and use of FRENZEL GLASS Central nystagmus is not supressed by optic fixation TORSIONAL NYSTAGMUS – Indicates lesion of brainstem/vestibular nuclei e.g. SYRINGOMYELIA VERTICAL DOWNBEAT NYSTAGMUS – Lesion is at cranio -cervical region e.g. Arnold- chiari malformation/degenerative lesion of cerebellum VERTICAL UPBEAT NYSTAGMUS – Lesion at the junction of pons and medulla/ pons and midbrain PENDULAR NYSTAGMUS – congenital/acquired e.g. Multiple sclerosis May also be disconjugate Via., vertical in one eye and horizontal in other.

39. Central Peripheral Spontaneous nystagmus that cannot be Suppressed by fixation suppressed by fixation. Changes direction with gaze Doesn’t change direction with gaze. Purely vertical, Horizontal, rotatory , horizontal, or torsional Never vertical Paroxysmal but Not fatigable Paroxysmal but fatigable in in Dix- hallpike test, Dix- hallpike test, has latency, no latency, Lasting lasts less than a minute, longer than 60 sec. and doesn't change direction with often vertical, may different head positions. change direction with different head positions.

40. CORNEAL TEST Loss of corneal reflex -- Cerrebelopontine Angle Lesion

41. FISTULA TEST Apply intermittent pressure on tragus OR By using Siegel's speculum IN NORMAL PERSON: NEGATIVE Because pressure changes in external auditory canal can’t be transmitted to labyrinth ABNORMALITY: POSITIVE Erosion of horizontal semi-circular canal- cholesteatoma Surgically created window in horizontal canal- fenestration operation Abnormal opening in oval window- post stapedectomy fistula Abnormal opening in round window- rupture of round window membrane ALSO INDICATES THAT LABYRINTH IS STILL FUNCTIONAL

42. FALSE NEGATIVE FISTULA TEST : IN CHOLESTEATOMA: it covers the site of fistula and it doesn’t allow pressure changes to be transmitted to the labyrinth IN LABYRINTH DEAD FALSE POSITIVE FISTULA TEST : Means + ve test without presence of fistula It is seen in two conditions : 1.congenital syphilis 2.Meniere’s disease. Congenital syphilis: stapes footplate is hypermobile Meniere’s disease: due to fibrous bands connecting utricular macula to the stapes footplate.

43. ROMBERG TEST Patient is asked to stand with feet together and arms by side with eyes first open and then closed. With eyes open : patient can still compensates the balance With eyes closed : patient cant compensate –Here vestibular system is at more disadvantage Central: instability Peripheral: Patient sways to side of lesion If patient perform this test without sway then SHARPENED ROMBERG TEST is performed. Patient is asked to stand with one heel in front of toes and arms folded across the chest. Inability to perform this test indicates vestibular impairment

44. GAIT Patient walks along a straight line to a fixed point first with eyes opened and then closed. In the case of uncompensated lesion of peripheral vestibular system, with eyes closed Patient deviates to affected side

45. HALLPIKE MANOEUVRE (POSITIONAL TEST) USES When patient complains of vertigo in head position Helps to differentiate a peripheral from a central lesion. METHOD Patient sits in the couch Examiner holds the patient’s head, turns it 45˚ to the right and then places the patient in a supine position so that his head hangs 30˚ below the horizontal. Patient’s eyes are observed for nystagmus The test is repeated with head turned to left and then again in straight head- hanging position . Four parameters are observed: 1. Latency 2. Duration 3. Direction 4. Fatiguability

46. Dix- Hallpike manoeuvre

47. In benign paroxysmal positional vertigo Nystagmus appears after latency : 2-20s Duration : less than 1 min Direction : towards the ear that is under most On repetition : Nystagmus may be elicited but lasts for a shorter period. On subsequent repetition : Nystagmus disappears altogether NYSTAGMUS IS FATIGUABLE

48. IN CENTRAL LESIONS Tumours of 4th ventricle Cerebellum Temporal lobe Multiple sclerosis Vertibrobasilar insufficiency Raised intracranial tension Nystagmus is produced immediately as soon as the head is in critical position No latency Duration: lasts as long as head is in that critical position Direction: changes Fatiguability : nonfatiguable

49. TEST OF CEREBELLAR DYSFUNCTION For cerebellar diseases – all cases of giddiness should be tested. CEREBELLAR HEMISPHERE CAUSES: 1. Asynergia ( abn finger-nose test) 2. Dysmetria (inability to control range of motion) 3. Adiadochokinesia (inability to perform rapid alternating movements) 4. Rebound phenomenon (inability to control movement of extremity when opposing forceful restraint is suddenly released) MIDLINE DISEASE OF CEREBELLUM CAUSES: 1. Wide base gait 2. Falling in any direction 3. Inability to make sudden turns while walking 4. Truncal ataxia

50. Nystagmus observed in cerebellar diseases either in hemisphere or midline diseases include GAZE EVOKED NYSTAGMUS REBOUND NYSTAGMUS ABNORMAL OPTOKINETIC NYSTAGMUS

51. Caloric test Patient 45 degrees on couch Water 33degrees or 45 degrees Normal nystagmus COLD: OPPOSITE WARM: SAME

52. 1.CANAL PARESIS: Decreased duration of nystagmus Both hot and cold 2.DEAD LABYRINTH: No nystagmoid response 3.DIRECTION PREPONDERANCE: BY Both Hot and Cold CENTRAL/PERIPHERAL lesion

53. Electronystagmography Now a routine investigation in Vertigo ADVANTAGES: Closed eyes nystagmus recorded Small amplitude Nystagmus

54. Treatment

55. Medical Treatment Symptomatic Specific therapy Vestibular rehabilitation

56. Symptomatic Pharmacotherapy Predominant targeted vestibular neurotransmitters: Cholinergic Histaminergic GABA neurotransmitters - negative inhibition Vomiting center transmitters: Dopaminergic (D2) Histaminergic (H1) Seratonergic Multiple classes of drugs effective

57. Antihistaminergic – dimenhydrinate Anticholinergics - scopolamine, meclizine Anti- dopaminergic - droperidol Gamma- aminobutyric acid enhancing (GABA- ergic ) agents - lorazepam , valium

58. Some drugs of the antihistamine class are useful for symptomatic control of vertigo Have anti-motion sickness properties in large part due to inhibition of vestibular system H1 histaminergic neurotransmitters Examples include dimenhydrinate (Dramamine) and promethazine ( Phenergan ) Also suppress the vomiting center

59. Common drugs used for vertigo

60. Specific Pharmacotherapy Vestibular Neuritis Meniere’s Disease Benign Paroxysmal Positional Vertigo Otosyphilis Vertebrobasilar Insufficiency Migraine (with vertigo)

61. Vestibular Neuritis Acute stage Bed rest , vestibular sedative, steroids can be used to shorten the course of the disease Antiviral?? Resolution stage After vertigo subsides (vestibular rehabilitation exercise) will enhance central compensation(as it is a paretic pathology)

62. Meniere's ‘s disease In acute phase :- treatment consists of vestibular sedative( stugerone , anti-emetics), Betahistine ( betaserc ) ,diuretics In long term :-avoidance of caffeine and salt and reassurance can reduce the number of the attacks and increase the patient ability to cope with the attacks

63. Surgical Treatment:- rarely needed Endolymphatic sac surgery: By transmastoid approachch the endolymaphatic sac either decompressed or a shunt is placed in the sac that communicates with the subarachnoid space or mastoid cavity Vestibular nerve section:- in patients with serviceable hearing Labyrinthectomy : - in patients with unilateral Meniere’s disease and poor hearing

64. Ablation therapy Gentamycin is given through the tympanic membrane will be absorbed through the round window and selectively damage the vestibular cells relative to the cochlear cells

65. BPPV Treatment approaches Liberatory maneuvers Particle repositioning Habituation exercises

66. The Epley and Semont Maneuvers Are both intended to move debris out of the sensitive part of the ear (posterior canal) to a less sensitive location. Each maneuver takes about 15 minutes to complete. Semont maneuver: It involves a procedure whereby the patient is rapidly moved from lying on one side to lying on the other. Epley Maneuver: It involves sequential movement of the head into four positions, staying in each position for roughly 30 seconds

67. Modified Epley Maneuver

68. Semont maneuver

69. Home Treatment Of BPPV: Brandt- Daroff Exercises The Brandt- Daroff Exercises is a method of treating BPPV, usually used when the office treatment fails. They succeed in 95% of cases.

70. Selective posterior canal plugging offers a reasonable surgical approach to intractable symptoms. Singular neurectomy , an older procedure, is less popular because it produces hearing loss in 7 to 17% of patients and fails in 8 to 12%.

71. Otosyphilis Penicillin established treatment IM and IV routes acceptable IM - 2.4 million units benzathine PCN weekly x 3 consecutive weeks is minimal treatment (some advocate up to 1 year) IV - 10 million units PCN G qD in divided doses x 10 days, followed by 2.4 million units benzathine PCN x 2 weeks

72. Vertebrobasilar insufficiency Vertigo, diplopia , dysarthria , gait ataxia and bilateral sensory & motor disturbance Transient ischemia - low stroke risk Antiplatelet therapy - aspirin Ticlid Platelet aggregate inhibitor Risk of life-threatening neutropenia Only in patients unable to tolerate aspirin

73. Migraine Treatment Modifying risk factors Exercise and diet Avoid nicotine, caffeine, red wine and chocolate Abortive medical therapy Ergots Sumatriptin Midrin Prophylactic medical therapy B blockers, Ca channel blockers, NSAIDs, amitryptiline , and lithium

74. Vestibular Rehabilitation Promoting vestibular compensation Habituation Enhancing adaptation of VOR & VSR May have initial exacerbation

75. Cawthorne Cooksey Exercises: Sitting Eye movements and head movements Shoulder shrugging and circling Bending forward and picking up objects from the ground Standing Eye, head and shoulder movements as before Changing form sitting to standing position with eyes open and shut Throwing a small ball from hand to hand (above eye level) Throwing a ball from hand to hand under knee Changing from sitting to standing and turning around in between Moving about (in class) Circle around center person who will throw a large ball and to whom it will be returned Walk across room with eyes open and then closed Walk up and down slope with eyes open and then closed Walk up and down steps with eyes open and then closed Any game involving stooping and stretching and aiming such as bowling and basketball

76. Habituation of pathologic responses Postural control exercises Visual-vestibular interaction Conditioning activities B.I.D., most improve after 4-6 weeks VRT - Elderly Multifactorial causes of balance difficulty Need 2 of 3 systems functional : vestibular, visual, proprioceptive Good outcome measures with longer time Impact on complications of falls

77. Conclusions Vestibular complaints common to ENT Thorough evaluation and understanding Dx and treat acute symptoms Wean vestibular suppressants Specific pharmacotherapy instituted Chronic, uncompensated disease benefits from early VRT

78. THANKS