Benign positional vertigo

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Benign positional vertigo

  1. 1. BENIGN POSTURAL/POSITIONAL VERTIGO What is BPPV? What is its natural history? What causes BPPV? How is BPPV diagnosed? What are the treatments for BPPV? Dr. Medical Officer, Dept. of Otolaryngology.
  2. 2. BENIGN POSTURAL/POSITIONAL VERTIGO  It is a common occurence. and one of the easiest to diagnose and treat.  As the name BPPV indicates that it is:  Benign or not a very serious or progressive condition;  Paroxysmal, meaning sudden and unpredictable in onset;  Positional, because it comes about in specific head positions.  “BPPV is a spinning dizziness that occurs in only one or two of a series of head positions and each attack is characterized by spinning vertigo, is short, usually severe and may be accompanied by geotropic nystagmus that occurs a few seconds after specific head movement.”
  3. 3. Natural History  Age: It occurs most frequently in the middle-aged, in the forties and fifties.It is rare or infrequent in childhood or youth and old age.  Sex: It shows no sex preference other than slightly greater representation of women in fifth decade.  Vertigo:  The symptoms are most often experienced when the patients lie down, which distinguishes it from Orthostatic hypotension. Movements like rolling over in bead, bending over, or looking upward usually initiate a attack of BPPV.  The vertigo usually lasts no more than a minute or two.
  4. 4.  Both the vertigo and nystagmus tend to lessen in severity with repititions of the evoking movement.  It may be accompanied by a slight feeling of nausea and vomiting in some patients.  Vertigo persists typically for only a few days or weeks, then declines and stops. The period of remissio that follows is usually prolonged from months to years. In the group of patients with reasonable antecedent cause such as head injury the period of activity may be long, but not in the idiopathic group.  It is not possible to quantify postural vertigo other than to note its presence or absence, and if present, its intensity.  Positional Nystagmus however, lends readily to classification.
  5. 5. TYPE NYSTAGMU S LESION VERGO I Persistent direction changing Peripheral Vestibular Or CNS Vertigo generally minor or absent. II Persistent direction fixed Same Same III Paroxysmal transient form (Barany Dix Hallpike type most common) Mainly inner ear abnormalities Prominent and terrifying. ASCHAN’S CLASSIFICATION
  6. 6. Persistent forms of positional nystagmus occur from static changes of head position relative to gravity (STATIC) Paroxysmal forms require in addition a certain brisk speed of movement from one position into the provocative position (DYNAMIC) The proposed classifiction Hugh o Barber’s, divides nystagmus into two types:  Type I (STATIC PERSISTENT)  Direction Changing  Direction fixed  Type II (DYNAMIC PAROXYSMAL)  Typical (Dix-Hallpike)  Atypical (others). While Paroxysmal Postional Nystagmus (PPN) is certainly nearly always due to non lethal (benign) inner ear abnormality, this is not always the case. Cases of PPN due to vertebrobasilar disease, tumors of posterior fossa, cerebellum and brain stem have been reported. However in these cases the nystagmus is more likely to be atypical than typical.
  7. 7. CAUSES  Another name of BPPV is cupulolithiasis, meaning “rocks in the cupula”  It has been discovered that the probable cause of BPPV is dislodgement of small calcium carbonate crystals that float through the inner ear fluid (endolymph) and strike against the sensitive nerve endings (the cupula) within the balance apparatus at the end of each semicircular canal (the ampulla)
  8. 8. DIAGNOSIS Assessment of any disorder of Equilibrium must be based on a multidisciplinary approach. A comprehensive careful medical history is imperative and can often indicate the direction to take in order to further investigate the cause of the complaints. Together with complete general medical examination, with particular attention to CVS, Locomotor System, CNS, Eyes and Ears. Although exclusion of otological pathology is essential in any balance disorder, many conditions will elude diagnosis if balance is equated purely with a disorder of vestibular function.
  9. 9.  Patient should describe in his own words what the complaint of “dizziness” or “vertigo” actually involves for him. From this description it usually immediately becomes clear whether the pateint means dizziness in the medical sense of vertigo or whether it’s a matter of visual disturbance, light- headedness , orthostatic hypotension etc.  It it really is “vertigo” then it is necessary to ask:  What type is it History:
  10. 10.  In case of attacks one has to know the frequency and duration, or any vegetative symptoms.  Influencing circumstances if any.  Secondary Symptoms e.g., tinnitus, reduced hearing, headache, neurologic abnromalities(parasthesias), visual and speech disturbances, or diminished awareness etc.
  11. 11.  GENERAL & SYSTEMIC EXAMINATION:  Patient’s temperature, blood pressure and pulses  Pallor, cyanosis, jaundice.  Assessment of Cardiovascular / Neurological / Psychiatric status is important. DIAGNOSIS Examination
  12. 12.  E.N.T EXAMINATION:  HEARING TEST:  A simple hearing test using wispering voice can give an estimate of Hearing loss if any.
  13. 13. • TUNNING FORK TESTS • Gives a more accurate idea of hearing loss and determining the type of hearing loss. • Following tests can be performed: • Rinne’s • Weber’s • Abc
  14. 14. DIAGNOSIS • VESTIBULAR EXAMINATION STANCE & GAIT (Vestibulospinal function assessment): (1) Romberg (Romberg 1846) Assess ability to stand, feet together, hands by the side, with eyes open and closed for 20-30 sec.If required clasp his hands together and pull t divert his attention. In presence of a uncompensated unilateral, peripheral vest. Lesion , lesion of posterior white column orunilat. Cerebellar lesion patient tends to sway towards the affected side. Quantitative assessment of body sway may be achieved by using a balance platform.
  15. 15. (2) Gait Testing: May provide information about many systems which give rise to imbalance. Although vestibular, visual and proprioceptive activity are all vital for maintenance of perfect balance, spatial orientation can be controlled by any two of these mechanisms (Joughees 1953). This physiological principle is admirably demonstrated on gait testing of a patient with bilateral vestibular failure.  Unilateral cerebellar hemisphere pathology like unilateral vestibular pathology cause a tendenmcy to veer to affected side.  Medline cerebellar dysfunction tends to give broad based ataxic gait.  Loss of proprioception results in high stepping foot slapping gait. Etc.
  16. 16. Unterberger Test: Patient has to walk with knees raised high, on a spot for 1 minute with his eyes closed and his arms stretched out horizontally in front. Turning to one side by more than 45 deg. In the course of 50 steps is pathological and points to a compensated vestibular disorder.
  17. 17. Babinski-Weill Test: Patient is made to walk five paces forward and five paces backward with eyes shut for 30 seconds. In a unilateral vestibular lesion patient walks in a star shape.
  18. 18. EYE MOVEMENT TESTS: Careful examination of eye movements and nystagmus provides a wealth of information regarding vestibular disorders.(Bedside assessment may provide much information, but quantitative data may be more accurately interpreted by using precise visual targets and recording the eye movt.s by electronystagmography. (1) NYSTAGMUS TESTS: • Involves carefully observing and interpreting involuntary eye movements. • Nystagmus has a slow (vestibular) phase and a fast (central) recovery phase. Because this fast recovery phase can be seen best, the type of nystagmus is named after the direction of this phase. Nystagmus towards the right generally indicates pathology on the left hand side. • Nystagmus can be divided in a number of ways:
  19. 19. •Spontaneous Nystagmus: Nystagmus which occurs With head in normal upright postion. This is not necessarily pathological •Induced Nystagmus: Nystagmus which occurs when •Head is held in a certain position – positional nys. •Head is brought into a certain position – Positioning nystagmus
  20. 20. Positional/ positioning nystagmus  Positional Nystagmus  When head is in a position other than a normal upright position  Wait for 10 seconds in a particular head position to give any positioning nystagmus a chance to die away.  Any nystagmus which persists as long as patient is lying in a particular position is permanent postional nystagmus Central Cause.  Nystagmus which occurs both when the patient islying on his left and right side is known as symmetrical nystagmus Central Cause.  Positioning Nystagmus:  The nystagmus occurs when there is a change of head position and provided it is of short duration has no significance.  In case of BPPV, a specific positioning nystagmus can be elicited which is pathological.
  21. 21. Dix-Hallpike Test  Dix & hallpike used the term “benign postural vertigo” to denote the symptoms & “postional nystagmus of benign paroxysmal type” to denote the nystagmus.  They also considered the lesion was peripheral and located in the utricle of the ear, which, when undermost released the nystagmus.
  22. 22.  DIX-HALLPIKE TEST: Barany-Dix-Hallpike nystagmus is diagnostic of BPPV It occurs when the head is moved into a provocative position (head hanging Rt. Or Lt. or head hanging sagittal) quickly but not slowly. Latent period of 1- 10 sec. When nystagmus appears , it quickly reaches peak then declines more slowly and stops within 30 seconds, and on repeating the test the nystagmus and vertigo can be exhausted.
  23. 23.  GAZE TEST Have the patient look at a point 30 deg away from midline to the right and left in succession.  Latent nystagmus becoming stronger when looking in one direction and not dying away Cause is peripheral vest. Disorder.  Nystagmus appearing exclusively when looking to one side: Unilateral gaze nystagmus. Cause is central.  Bilateral gaze nystagmus points to a central CNS disorder.
  24. 24. (2) EYE MOVEMENT TESTS: (1) Saccadic Eye Movements: Assessed by asking the patient to look back and forth, between two targets directly in front of him and note (latency, velocity and accuracy. • No abnormality – Peripheral labyrinthine disorders • Prolonged Latecny – Damage to the supranuclear control of the brain stem saccade-generating centres eg., basal ganglion disorders. • Impaired saccadic accuray (over and undershooting) – Cerebellar pathology. • Slowing of saccadic movts. – lesion at any level from pretectal and parapontine saccade-generating centres to the extraocular muscles.
  25. 25. (2) Smooth Pursuit System: Smooth pursuit system may be examined clinically by moving a finger slowly backwards and forwards in front of the patient’s eyes.  Bilateral impaired persuit – Tired or inattentive patient, psychotropic medication, alcohol etc.  Unilateral derangement – Organic disease of cerebellar hemispheres, the brainstem or parieto- occipital dysfunction.
  26. 26. Compensation from a Vestibular Lesion  The rate at which a patient compensates depends upon four factors:  Age: The younger the patient the faster the compensation  Patient compensates quicker from a peripheral lesion e.g.,labyrinthitis, than from a central one, e.g., brain stem vascular thrombosis.  Compensates quicker from unilateral than from bilateral lesion.  Compensates from a static lesion, e.g., labyrinthectomy, than from a variable one eg., Menier’s disease.
  27. 27. TREATMENT Medical  Spontaneous Resolution:In most cases  In others symptoms persist ( It is found that these latter individuals have studiously avoided head positions that precipitate their symptoms – Hugh.O.Barber).  Medications: Most patients who report to physicians/ surgeons are prescribed medications such as  Meclizine or Diazepam  Betasec  Cinnarizine  flunarizine (There is no good evidence that medications are of value in BPV-HOB)
  28. 28. Exercises  A variety of types of physical therapy have been recommended for BPV.  How do these exercises work?  One possibility is that habituation of the abnormal vestibular signals is enhanced when the patient is repeatedly put in the offending position.  An alternative hypothesis (Brandt and Daroff) is that exercises shake free otlithic debris from the cupula and entered them into a safer position.  Whatever the mechanism, these exercises or similar protocols are almost always successful provided patient adheres to them  When symptoms donot respond to the exercises, it is worthwhile reconsidering the diagnosis and carrying out CT scanning.
  29. 29.  THE EPLEY OR SEMONT REPOSITIONING MANEUVER.  Principle: Reposition the crystals(otoconia) away from the nerve endings using gravity and moving them into an area of the inner ear that won’t cause any problems. To achieve this, the patient’s head is moved into various positions of the apley maneuver, the posterior semicircular canal is rotated in such a way as to deposit the displaced otoconia back into the vestibule.  Procedure:  Turn the patient’s head 45 degees to the side with most prominent symptoms during Hallpike test.
  30. 30.  With both hands holding the patient’s head, gently lay the patient down in the supine position with the head hanging over the edge of the couch, by 45 deg. Keep the postiion for at least 30 sec. or until nystagmus resolves.  Examiner now comes to the head end of the bed so as to be able to rotate patient’s head easily
  31. 31. •Turn the patients head 90 deg. In the opposite direction and observe for observe till the nystagmus disappears or for at least 30 seconds. •Ask patient to turn onto his shoulder.
  32. 32. •Guide the patient’s head down so that he is looking at the ground and wait for at least 30 secs. •The patient’s head is regripped and patient is made to sit up with the legs hanging over the side of the couch.
  33. 33. •The patient is now in sitting upright positon. • Move the patient’s head slightly forward. •This completes the procedure.
  34. 34. SURGICAL TREATMENT  Rarely required, when medical treatment and otolith repositioning techniques have failed.  Procedures which may be considered:  Singular Neurectomy (or Posterior Ampullar Nerve Section): This tiny branch of the balance (vestibular)nerve travels through a bony canal before it reaches the nerve endings of the balance canal. In experienced hands it is a safe surgery and relieves the symptoms permanently. In a small percentage of cases the nerve is unreachable. In a few cases hearing loss, dizziness , tinnitus can result from surgery.  Posterior Canal Plugging Procedure: This recently developed procedure has nearly replaced singular neurectomy due to its ease and effectiveness. In this procedure, a mastoidectom,y is performed and posterior semicircular canal is opened, exposing the delicate membranous channel and is firmly packed, so that the otolith can no longer move. The acute vertigo of BPPV is cured in most cases. The exact percentage of patients with some permanent hearing loss has not
  35. 35.  Vestibular Nerve Section : In some cases, when positional vertigo is quite severe and hearing normal, testing reveals that this is not due to crystalline debris floating in the canal, but due to a damaged nerve. In such ases , the balance nerve is cut to stop its distorted information. In successful cases, after an initial period of several weeks, dizziness gradually disappears. In this operation neurosurgeon exposes the nerve as it crosses from the ear to the brain and sections it under direct vision using a microscope. In some cases, high frequency hearing loss can occur because the balance nerve fibres and hearing fibres mix together along the borders of the nerves. Risks include hearing loss, tinnitus, facial nerve weakness, spinal fluid leakage, and meningitis.
  36. 36. Overview of Vertigo Treatment Journal of Audiological Medicine - 2000  Almost half a century has passed since Dix and Hallpike published their landmark paper describing the clinical profile of the three most common causes of peripheral vertigo:Benign paroxysmal postional , Meniere’s disease and Vestibular neuronitis.  Cupulo-canalolithiasis is by far the most frequent cause of rotatory vertigo; although the diagnosis can be easily carried out at the bedside and a ‘liberatory’ manoeuvre effected in a few minutes is curative, it is being performed only by a minority of physicians.  A sstandard pharmacological cure for Meniere’s disease has yet to be found, since its pathogenesis is multifactorial. Salt restriction diet and diuretics are sometimes effective, and chemical labyrinthectomy by intratympanic delivery of vestibulotoxic drugs or selective vestibular nerve section can stop the vertigo attacks but do not solve the underlying endolymphatic hydrops.  An isolated viral infection of the Scarpa’s ganglion and vestibular nerve are thought to be the cause of vestibular neuronitis.

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