RIGHT BPPV- ANTERIOR OR POSTERIOR

This video shows Dix-Hallpike positioning done by Dr. Ajay Kumar Vats, D.M. (Neurology), Udaipur (Rajasthan), India, on a patient with right (posterior/anterior) semicircular canal BPPV. This patient had a closed head trauma four days prior to complaints of vertigo. This elicited nystagmus in the Hallpike position on right but the type of nystagmus could not be characterized as patient closed his eyes partially during Dix-Hallpike positioning (this is common because the severity of peripheral vertigo decreases with eye closure). Voluntary eye closure interferes with examination of the type of nystagmus which is important for identifying the involved canal. After lateralization of the diseased ear, the localization of the involved canal is important as far as diagnosis is concerned. However once lateralization of the diseased ear is established, for the treatment purpose it doesn't matter whether it is posterior or anterior canal which is affected as both anterior and posterior canal BPPV are treatable with Epley maneuver. Epley maneuver was done by Dr. A. K. Vats on this patient and he was free of vertigo after single time performed Epley maneuver.

Benign Paroxysmal Vertigo of Childhood

This entity was first described by Basser in 1964 (Basser LS. Benign paroxysmal vertigo of childhood. Brain 1964; 87:141-52), benign paroxysmal vertigo occurs in young children as episodes of unexplained fright/grotesque associated with disturbances in balance or even falls. The prevalence is 2-2.6% and the sex distribution is equal. Mostly the onset is sudden (95%) with an expression of anxiety and fear on the face of the child, who usually grasps any person standing nearby or any other object or else may sway or refuse to stand. The ataxia may remain unnoticed because some children refuse to leave their beds. Whereas the infants may cry but children with developed spoken language may complain of dizziness and nausea. A very attentive mother may also report nystagmus. The neuro-vegetative signs and symptoms like pallor, nausea, perspiration, photophobia, phonophobia, unusual head positions and vigorous vomiting are common. However, there is no loss of consciousness. In some children, the episode may evolve to syncope. The duration of episode is generally brief few seconds to < 5 minutes but sometimes lasts a few hours, with an utmost duration of 48 hours. The episode typically resolves with sleep but in few cases relief is obtained by lying or sitting down. The age of onset is between 2-4 years with range of 5 months to 8 years. The episode frequency varies from once every 1-3 months to once a day. Episodes tend to more frequent at first and become rarer with time and increasing age. The episodes may occur in clusters over several days and then subside for weeks or months. Triggers include roundabouts, swings, and seesaws, i.e., means of stimulating the labyrinth but may also include awakening, fever, tiredness, or stressful events. A positive family history of migraine, motion sickness and atopic disease is common. It is speculated that benign paroxysmal vertigo of childhood constitutes an early-onset variant of basilar-type migraine. It is suggested that benign paroxysmal vertigo of childhood consist of two entities - one would be a migraine equivalent with a family history of migraine and the other a more pure form without any relation to migraine. Benign paroxysmal vertigo is certainly under diagnosed because of the brief duration of attacks and their benign nature.Electroencephalogram tracings in waking and sleeping states, as well as during an episode, are normal. Audiologic examinations, including impedance measurement with stapedial reflex, always produce negative results. The vestibular examinations have failed to help explain the etiopathogenesis of the disorder considered by some authors  as a peripheral vestibular dysfunction, and by others as a central vestibular problem, with a deficiency of the vestibular nuclei or of the vestibular-cerebellar pathways. The differential diagnosis includes benign paroxysmal positional vertigo and episodic ataxia. Benign paroxysmal positional vertigo is the most common cause of vertigo in adults and is caused by a detachment of otoliths from the utricular macula and its inappropriate entry into semicircular canal but is rare in children. A diagnosis of episodic ataxia should prompt a trial of acetazolamide. The  tornado epilepsy, acoustic schwannoma and other tumors of the cerebellopontine angle, other posterior fossa tumours, Meniere’s disease and vestibular neuronitis are the other differentials that should be considered. Benign paroxysmal vertigo should also be differentiated from the idiopathic vertigo that may occur in association with migraine, because most children with migraine headache (typically older than in the age range when benign paroxysmal vertigo occurs) may report vertigo either just before or during a migraine headache. This is now a well defined entity called migraine associated dizziness. The benign paroxysmal vertigo of childhood disappears after a few months or a few years, usually by age 5 years (range, 2-16 years, i.e., after 3 months to 8 years) but evolution to migraine is frequent. In the short term, some children may develop a dysfunction classifiable as another childhood periodic syndrome, such as cyclic vomiting syndrome, or recurrent abdominal pain and motion sickness. In a single reported case, a woman manifested benign paroxysmal torticollis as a toddler, and then developed benign paroxysmal vertigo and finally migraine. Because attacks of benign paroxysmal vertigo are brief, no treatment is usually given. Treatment of an attack can include symptomatic medications such as antiemetics, although sleep will abort an attack in most patients. If attacks are frequent, one may consider prophylaxis with cyproheptadine.

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Vestibular Migraine

Migraine can manifest as attacks of recurrent vertigo either spontaneous or positional, lasting seconds to days. Vestibular migraine is an evolving entity and therefore various terms like migraine-associated vertigo, migraine-associated dizziness, migraine-related vestibulopathy, migrainous vertigo, benign recurrent vertigo, and basilar migraine, are probably used to the same patient population. The term basilar migraine, however, should be restricted to patients who fulfill the diagnostic criteria of the International Headache Society (IHS) for basilar migraine.

Diagnostic criteria

In the current IHS classification, vertigo is not included as a migrainous symptom in adults except for the basilar migraine which considers vertigo as an aura symptom of basilar migraine that should last between 5 and 60 minutes and is followed by migrainous headache. Besides this, a second aura symptom from the posterior circulation should be reported. In fact, less than 10% of patients who have vestibular migraine in published case series fulfill the criteria for basilar migraine thus making basilar migraine an unclassifiable category for these patients. As a consequence, most adult patients who have vestibular migraine cannot be classified with the current IHS criteria.

Clinical features Demographic Aspects

Vestibular migraine may occur at any age and has female preponderance, with a reported female-to-male ratio between 1.5 and 5 to 1. It probably follows an autosomal dominant pattern of inheritance with decreased penetrance in men. In most patients, migraine begins earlier in life than vestibular migraine and some have been free from migraine attacks for years when vestibular migraine first manifests itself. In some women migraine headaches are replaced by vertigo attacks around the time of menopause. Vestibular migraine seems to occur more often in patients who have migraine without aura than in patients who have migraine with aura.

Vestibular migraine in Children

Benign paroxysmal vertigo of childhood is an early manifestation of vestibular migraine that is recognized by the IHS classification of headaches.

Clinical Presentation in adults

Patients with vestibular migraine typically report spontaneous or positional vertigo. In some patients there is a continuum of spontaneous vertigo transforming into positional vertigo after several hours or days. This positional vertigo is distinct from BPPV with regard to duration of individual attacks ( it lasts often as long as the head position is maintained in Dix-Hallpike position in vestibular migraine versus seconds only in BPPV), duration of symptomatic episodes (minutes to days in vestibular migraine versus weeks to months in BPPV), and nystagmus findings. Approximately 40-70% of patients experience positional vertigo in the course of the disease but not invariable with every attack. Head motion intolerance, quite similar to motion sickness (imbalance, illusory motion or nausea aggravated or provoked by head movements) and visual vertigo (vertigo provoked by moving visual scenes, such as traffic or cinema) are two other prominent feature of vestibular migraine. Nausea and imbalance are frequent but nonspecific accompaniments of acute vestibular migraine. The duration and frequency of attacks can vary between patients and in individual patients over time. The duration of vertigo ranges from seconds (approximately 10%) and minutes (30%) to hours (30%) and several days (30%). Some patients take weeks to recover fully from an attack. The attacks may occur days, months, or even years apart in an irregular fashion. Overall, only 10-30% of patients have vertigo with the typical duration of a migraine aura (5–60 minutes). Vestibular migraine often doesn’t fulfill the duration criterion for an aura as defined by the IHS but the temporal relationship to migraine headaches is also not maintained. The vertigo can precede headache, as would be typical for an aura; may begin with headache; or may appear late in the headache phase. Many patients may experience attacks with headache at one time and without headache at some other time. In some patients, vertigo and headache never occur together and in these cases, diagnosis is based on migrainous symptoms during the attack other than headache. Along with the vertigo, patients may experience photophobia, phonophobia, osmophobia, and visual or other auras. These epiphenomena are important to be clearly sought for during history taking because they may represent the only apparent connection of vertigo and patients often do not volunteer them. Hearing loss and tinnitus are not prominent symptoms of vestibular migraine but have been reported in individual patients who have vestibular migraine. Hearing loss is usually mild and transient, without progression in the course of the disorder. However, patients with severe fluctuating hearing loss suggestive of meniere's disease and migrainous features during the attack implying vestibular migraine have been reported. Asking for migraine-specific precipitants of vertigo attacks may provide valuable diagnostic information (menstruation,deficient or irregular sleep, excessive stress, specific foods such as matured cheese, red wine, monosodium glutamate and finally, sensory stimuli, such as bright or scintillating lights, intense smells, or noise). In some patients migrainous accompaniments and typical precipitants may be missing, but vestibular migraine is considered the most likely diagnosis after other potential causes have been investigated and ruled out. In such a situation, a favorable response to antimigraine drugs supports the suspicion of an underlying migraine mechanism. However, apparent efficacy of a drug cannot be regarded as an absolute confirmation of the diagnosis because spontaneous improvement, placebo response and co-prescribed drug effects (anxiolytic, antidepressant) have to be taken into account.

Clinical and Neurotologic Findings in Patients who have Vestibular migraine

In most patients, the general neurologic and otologic examination is normal in the symptom-free period. Approximately 10-20% of patients with vestibular migraine have unilateral hypoexcitability to caloric stimulation and approximately 10% have directional preponderance of nystagmus responses. These findings are not specific for vestibular migraine because they can be found in migraine patients who do not have vestibular symptoms and in many other vestibular syndromes. Neuro-ophthalmologic examination during attack-free period reveals that more than 60% of vestibular migraineurs show slight central ocular motor disorders e.g. gaze-evoked nystagmus, saccadic smooth pursuit,  horizontal or vertical spontaneous nystagmus or central positional nystagmus. The latter is always persistent as long as the provoking position is maintained and was usually do not beat in the plane of positioning, unlike the benign paroxysmal positional nystagmus. In clinical practice, history usually provides more clues for the diagnosis than vestibular testing, because there are no abnormalities that are specific for vestibular migraine. Therefore, in patients with a clear-cut history, no additional vestibular tests are required.

Treatment

In many patients, vestibular migraine attacks are severe, long, and frequent enough to warrant acute or prophylactic treatment. Unfortunately, current treatment recommendations are based on expert opinion rather than on solid data from randomized placebo-controlled trials. It is suggested that medications used for migraine prophylaxis may be effective, including propranolol, metoprolol, tricyclic antidepressants, divalproex sodium, topiramate and flunarizine. The carboanhydrase inhibitors acetazolamide and dichlorphenamide, which are not normally used for migraine prophylaxis, have also been used successfully. Expected side effects, such as orthostatic hypotension with beta-blockers or weight gain with divalproex sodium, influence the selection of the drug. The patients with vestibular migraine are advised to monitor the frequency and severity of their attacks in a diary. Treatment response should be evaluated after 3 months. A greater than 50% reduction in attack frequency is a reasonable goal. Treatment of acute vestibular migraine with acute migraine medication can be attempted with triptans and vestibular suppressants, such as promethazine, dimenhydrinate, and meclizine. Nonpharmaceutic approaches in the treatment of vestibular migraine should not be neglected and may be even more effective than drugs in individual patients. A thorough explanation of the migrainous nature of the attacks can relieve unnecessary fears. Avoidance of identified triggers, regular sleep and meals and regular exercise has a definite role in migraine prophylaxis.

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Benign Paroxysmal Positional Vertigo

What is Benign Paroxysmal Positional Vertigo? 

Benign Paroxysmal Positional Vertigo (BPPV) is a condition in which a patient has brief, sometimes severe attacks of rotatory vertigo with and without nausea, which are caused by rapid changes in head position relative to gravity. Typical triggers of BPPV include lying down or sitting up in bed, turning around in bed, getting in and out of bed and also bending over to tie the shoelaces, or extending the head in order to look up. Patients suffering from BPPV can be treated with certain well established exercises/maneuvers and relief is obtained in ninety percent of such cases in a week’s time.

What is pathophysiology of BPPV?

The Otoliths become detached from hair cells in utricle, inappropriately and most commonly enter the posterior semicircular canal owing to its gravity dependent position. In the normal situation as one turns head, for example, to the right the endolymph moves and SCC receptors fire. The nerve impulses generated in the vestibular nerve reach the vestibular nuclei and through medial longitudinal fasciculus impulses reach the subnuclei of oculomotor nerves carrying the information that "head is turning to the right". These oculomotor subnuclei turn the eyes in the same plane to the same degree but in the opposite direction so that the target of fixation falls on fovea. When the head stops turning, the endolymph stops moving and the SCC receptors stop firing and previously generated nerve impulses in the vestibular nerve cease. This information also reaches through the vestibular nuclei and medial longitudinal fasciculus to the subnuclei of oculomotor nerves informing that "head has stopped turning to right" so that the corrective eye movements induced as a consequence of disruptive head movements stop.In BPPV even after the head has stopped moving, the otoliths keep moving and drag the endolymph. As a result the  receptors continue  to fire inappropriately  giving a false information to the oculomotor subnuclei that "head is still moving". Since the eyes know that “head is not moving”, this leads to visual-vestibular mismatch and this is interpreted by the brain as “surrounding must be spinning in the opposite direction.

”What is cupulithiasis?

In 1962, Dr Harold Schuknecht proposed the cupulolithiasis (heavy cupula) theory. Via photomicrographs, he discovered basophilic particles or densities that were adherent to the cupula. He postulated that the PSC was rendered sensitive to gravity by these abnormal dense particles attached to, or impinging on, the cupula. This is analogous to the situation of a heavy object attached to the top of a pole. The extra weight makes the pole unstable and thus harder to keep in the neutral position. This produces persistent nystagmus and also explains the dizziness when a patient tilts the head backward.

What is canalithiasis theory?

In 1980 Epley published his canalithiasis theory. He believed that the symptoms of BPPV were more consistent with free-moving densities (canaliths) in the PSC rather than fixed densities attached to the cupula. While the head is upright, the particles sit in the PSC at the most gravity-dependent position. When the head is tilted back supine, the particles are rotated up to about 90 degrees along the arc of the PSC. After a momentary (inertial) lag, gravity pulls the particles down the arc. This causes the endolymph to flow away from the ampulla and causes the cupula to be deflected. The cupular deflection produces nystagmus.

What is Epley maneuver?

The Epley maneuver (also called canalith repositioning procedure or CRP) is a technique which is used to treat benign paroxysmal positional vertigo (BPPV). The maneuver consists of moving the patient through a series of positions which are designed to dislodge the debris (also called canaliths or otoconia made up of calcium carbonate) that has inappropriately entered the semicircular canal (mostly posterior semicircular canal) to the utricle where they are normally present in the form of calcium carbonate. In around 70% of cases, the Epley maneuver is very effective and the patient may require no further follow up treatment. Epley maneuver may be carried out by a doctor or a physical therapist and even by the patient himself. The diagnosis of BPPV is established on the basis of clinical history and Dix-Hallpike test (also called Nylen Barany test). It is important to lateralize the disorder to right or left and to localize it to the involved canal (posterior/anterior/horizontal) which can be done most of the times with the help of performing the Dix-Hallpike testing and observing the positional nystagmus. In most of the cases by practice, the treating doctor is able to lateralize the side (left or right) and localize the involved canal by observing the nystagmus elicited by Dix-Hallpike testing.
How is Dix-Hallpike testing done and what is expected to be seen and interpreted?

The video below shows Dix-Hallpike testing done by Dr. Ajay Kumar Vats, D.M. (Neurology), Udaipur, Rajasthan on a patient with left posterior semicircular canal BPPV, which is the most common variant of positional vertigo. This elicits an ageotropic upbeat nystagmus in the Hallpike position (diseased ear undermost).

                                                                                                                                  

What are contraindications of Epley maneuver?

Rheumatoid arthritis with atlanto-axial instability, severe degenerative cervical spinal disease including atlanto-axial instability from any cause, high grade carotid stenosis, unstable heart disease, ongoing CNS disease (TIA/stroke) and pregnancy beyond 24 weeks are contraindications to Epley maneuver.

Who should be doing Epley maneuver?

Ideally it should be done by the doctor (or a physical therapist in supervision of the treating doctor) who has diagnosed BPPV, and has lateralized as well as localized the involved semicircular canal. If the treating doctor is satisfied with the fact that the patient will be able to correctly perform the Epley maneuver self, this can be taught to the patient who can do it.

Is a single time Epley maneuver enough?

According to one study (Gustavo Polacow Korn et al.Repeated Epley’s maneuver in the same session in benign positional paroxysmal vertigo.Brazilian Journal of Otorhinolaryngology 2007; 73 (4): 533-539) repeated Epley maneuvers in less sessions rendered more positional nystagmus-free patients when compared to those submitted to more sessions of single maneuvers.

What is Semont maneuver?

The Semont maneuver (also called the Liberatory maneuver or brisk treatment) is effective in get ridding of the symptoms of benign paroxysmal positional vertigo (BPPV) with a cure rate of 53% after one treatment and 76% to 90% after two treatments in patients with canalithiasis. The Semont maneuver involves the patient rapidly moved from lying on one side to lying on the other. A single 10 - 15 minute session is usually all that is required. The Semont maneuver is performed as per the following five steps: 1. The patient is asked to sit on a sturdy examination couch in such a way that his both lower limbs are dangling down the free edge of the couch and the treating doctor (or the physical therapist) is on the other side of the couch so that the back of the patient is towards the front of the doctor (or the physical therapist).2. In this position the patient’s head is turned 45 degrees horizontally towards the unaffected ear.3. The patient’s torso with the patient’s head is turned 45 degrees horizontally toward the unaffected ear  is tilted to 105 degrees so that he is lying on the side of the affected ear with his head hanging and nose pointed upwards. Patient remains in this position for around 3 minutes - allowing debris to move to the apex of the ear canal.4. The patient is then quickly moved from this tilted half supine position, holding patient’s head in place to the opposite side through a 180 degree sweep until he is lying on the side of the unaffected ear with his nose pointed towards the ground. Patient remains in this position for 3 minutes allowing the debris to move toward the common crus.5. The patient is then slowly lifted back to the seated position. The debris/otoconia is presumed to fall into the utricle of the canal with this where it will no longer causes recurrent positional vertigo although a very severe vertigo with retropulsion often occurs when the patient is lifted to sit. The latter usually signifies a successful repositioning of the otoconia.

What is Brandt-Daroff treatment?

This form of treatment, invented by Professor Thomas Brandt and Professor Robert B. Daroff is a series of repetitive exercises. The patient sits on a bed in such a way that his both lower limbs are dangling down the free edge of the bed. The patient turns his head 45° horizontally to one side and then rapidly lies to the opposite side. The patient remains in this position for about 20 seconds and then slowly sits up and waits for 20 seconds. The same movement with same head positioning is repeated on the opposite side. The whole sequence is done five times in each direction and is performed one to three times a day for up to two weeks. The exercises are continued till the patient has two consecutive days without any symptoms. The purpose of this treatment is to move the otoconia/debris in the SCC back and forth. The individual otoconia particles dissolve in the endolymph in hundred hours as per the studies carried out in the guinea pigs. Brandt-Daroff treatment is, therefore, believed to work by breaking up the otoconia to allow its dissolution rather than repositioning the otoconia in the utricle. Brandt-Daroff treatment is the optimal treatment for mild canalithiasis of the posterior or anterior SCC. This situation occurs when the patient still has symptoms but no signs of BPPV (absence of inducible nystagmus on the Dix-Hallpike testing) after a single treatment. This treatment can be used in patients with severe BPPV caused by canalithiasis or cupulolithiasis, but it is not the first choice because it causes vertigo during the maneuver and may takes up to two weeks for success.

What are the recommendations of report of the quality standards subcommittee of the American Academy of Neurology (AAN) on the practice parameters for the optimal treatment of posterior semicircular canal BPPV?

Canalith repositioning procedure has been established as an effective and safe therapy that should be offered to patients of all ages with posterior semicircular canal BPPV. Recommendations have been rated as Level A as per the published Class I studies. The Semont maneuver is possibly effective for PSCCBPPV but receives only a Level C recommendation based on a single Class II study. There are many experts who believe that the Semont maneuver is as effective as canalith repositioning procedure, based on currently published articles but according to AAN practice parameters committee, the Semont maneuver can only be classified as “possibly effective.” There is insufficient evidence to establish the relative efficacy of the Semont maneuver to CRP (Level U).

What is horizontal canal BPPV?

The posterior semicircular canal owing to its gravity dependent position is the most commonly affected canal as the otoconia have the ease to enter this canal when the patient lies down. This is the reason why the posterior semicircular canal BPPV is the most common form accounting for approximately 85 to 90% of the cases of BPPV. Therefore unless otherwise qualified BPPV refers to posterior canal BPPV with the side (right or left) specifically lateralized. However 5 to 10% of patients of BPPV as per the different series of published scientific data have the horizontal canal BPPV.The Pagnini-McClure maneuver (also called the supine head turn maneuver or Roll test) is used to elicit the horizontal nystagmus. In this, the head is quickly rolled to one side, and nystagmus is looked for and the patient is asked to report any vertigo. The head is then slowly rolled back to a supine position. The head is then quickly rolled to the other side, and nystagmus is looked for and the patient is asked to report any vertigo. Whether it is canalithiasis or cupulolithiasis, the patient would have nystagmus and vertigo when they are rolled to either side but the type of nystagmus would differ in these two types of BPPV. For canalithiasis, the nystagmus is transient and the direction of the quick phases is toward the earth (geotropic). This is because the cupula bends up as the otoconia moves through the SCC, which transiently increases the firing rate in the nerve from horizontal SCC. For cupulolithiasis, the nystagmus is sustained and the direction of the quick phases is away from earth (ageotropic). This is because the cupula bends down caused by the weight of the otoconia, which causes a sustained decrease in the firing rate in the nerve from the horizontal SCC. Thus a horizontal canal BPPV also has two variants- a canalithiasis caused variant and another cupulithiasis caused variant.Barbeque roll over maneuver or Lempert’s maneuver has been found to be an optimal form of treatment is for severe forms of horizontal SCC BPPV caused by canalithiasis.  It can be used as an alternative treatment for horizontal SCC BPPV caused by mild canalithiasis. In the Barbeque roll over maneuver, the patient lies on his or her back on the examination bed with the affected ear down (the affected ear is being identified as the side that causes the most nystagmus and vertigo during the roll test.) The patient's head is then slowly rolled away from the affected ear until the nose is pointing up; the patient stays in this position for about 15 seconds or until the dizziness stops, whichever is more. The patient then continues to rolls the head in the same direction until the affected ear is up and remains in that position for 15 seconds or until the dizziness stops whichever is more. The patient then rolls the head and body in the same direction until the nose is down and remains there for 15 seconds. Finally, the head and body are rolled in the same direction to the original position with the affected ear down. After 15 seconds the patient then slowly sits up keeping his or her head level or pitched down 30°. The Barbeque roll over maneuver is more or less same for canalithiasis or cupulithiasis variant of the horizontal canal BPPV but each head turn is performed as quickly as possible in the latter variant as per some authorities in this subject.The video below shows Bar-be-que roll over maneuver or Lempert's maneuver being performed by Dr. Ajay Kumar Vats, D.M. (Neurology), Udaipur (Rajasthan), on a patient with left horizontal semicircular canal BPPV, which is a relatively uncommon form of positional vertigo. This elicits an ageotropic horizontal nystagmus in the first position (i.e.the fast component of nystagmus away from earth with the diseased ear undermost). This patient had a closed head trauma three days prior to complaints of vertigo. The first position of this maneuver is equivalent to Pagnini-McClure maneuver (also called the supine head turn maneuver or Roll test). The Bar-be-que 360 degree roll over maneuver or Lempert's maneuver performed in this patient coincides with reversal of ageotropic horizontal nystagmus in the first position (i.e. the fast component of nystagmus away from earth with the diseased ear undermost) to geotropic horizontal nystagmus in the fifth position (i.e. the fast component of nystagmus towards the earth with the diseased ear undermost), disappearance of vertigo and successful repositioning of otoconial particles from horizontal canal to the utriculus.

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Vestibular Neuronitis and Labyrinthitis

What is vestibular neuronitis?

Vestibular neuronitis is an acute peripheral vestibulopathy and the second most common cause of peripheral vestibular vertigo after benign paroxysmal positional vertigo. The signs and symptoms of vestibular neuronitis are acute onset of sustained rotatory vertigo, horizontal spontaneous nystagmus toward the unaffected ear with a torsional component, lateropulsion i.e. falls with the eyes closed toward the affected ear and nausea & vomiting. The caloric testing (usually not required for clinical diagnosis) invariably shows ipsilateral canal paresis but the latter can be interpreted with a carefully performed Halmagyi head thrust test. The video shown below illustrates that on thrusting this pateint's head to his right while he fixates on examiner's face, a catch-up saccade to his left is seen implying right canal paresis.

There is no catch-up saccade on thrusting this pateint's head to his left while he fixates on examiner's face, indicating that the left sided canals are normally functioning. This is illustrated in the video below.

 Herpes simplex virus type 1 (HSV-1) DNA has been detected on autopsy with the use of polymerase chain reaction in human vestibular ganglia. It is speculated that after primary infection of the epithelium (apthous stomatitis), HSV-1 enters the axon terminals and is carried by axonal transport to sensory neurons of the human trigeminal ganglia and geniculate ganglia. In these ganglia it remains latent until certain stimuli reactivate HSV-1 by switching its viral state from latent to lytic. During reactivation in the trigeminal ganglion, virus particles can be transported back to the entry site, causing herpes labialis. In contrast, when reactivated in the geniculate ganglion, the virus may spread via the faciovestibular anastomosis to the vestibular ganglia (Scarpa's ganglion) causing vestibular neuronitis. Vestibular neuronitis affects only a part of the vestibular trunk, usually the superior division (horizontal saccular canal paresis), which travels separately and has its own ganglion whereas the inferior part (the posterior semicircular canal) is mostly spared. A very occasional patient may have a combined superior and inferior vestibular neuronitis. Most patients recover well from vestibular neuritis, even without treatment. Nonetheless, studies suggest that a course of oral steroids in the form of oral methylprednisolone (100 mg/day, doses tapered by 20 mg every third day) for three weeks accelerates the recovery of vestibular function but whether steroids influence long-term outcome is less certain. Thus, until more data become available, it is reasonable to treat otherwise healthy individuals who present within 3 days of onset with steroids and to withhold steroids from those who are at higher risk of complications. Antiemetics and vestibular suppressants are useful acutely but should not be given for more than three days because their prolonged use impedes the process of central vestibular compensation. In evaluating a patient with an acute vestibular syndrome, it is important not to miss a central cause, such as a brainstem or cerebellar infarct or hemorrhage, which could be life-threatening and the definitive central signs may not always be present. Thus, any patient thought to have vestibular neuritis but has significant vascular risk factors should be evaluated for a possible posterior circulation stroke by getting a magnetic resonance imaging on a 1.5 Tesla machine with instructions to get thin three millimeter axial as well coronal cuts of medulla oblongata on diffusion weighted and apparent diffusion coefficient imaging sequences. Early resumption of normal activity should be encouraged, to promote compensation. Cawthorne Cooksey exercises for vestibular rehabilitation therapy can further promote this process. A retrospective study on 148 patients by D. Huppert et al (Low recurrence rate of vestibular neuritis: A long-term follow-up. Neurology 2006; 67:1870–1871), the long-term recurrence rate of vestibular neuronitis for the entire follow-up period was 1.9% ( 2 out of 148 patients) and in both patients, the second occurrence of vestibular neuronitis affected the contralateral ear with respect to the initial manifestation. Thus, for all practical purposes, vestibular neuronitis is a monophasic illness.http://www.dizziness.webs.com/