Brady Workman is back this week with an article about vibration induced nystagmus, and how they can be helpful in vestibular function testing:

 

 

 

In the area of vestibular assessment, our test findings can sometimes be a bit unclear, often leaving us with as many questions as answers. This is especially true in cases where patients’ vestibular function tests do not align with one another; or when all test measures are unable to be implemented, in which scenario, a cross check measure would be gladly welcomed. I was recently reading an article by Dumas et al that purported the skull vibration induced nystagmus test (SVINT) as a “vestibular Weber test”, the auditory version of which is frequently utilized to differentiate between unilateral sensorineural (inner ear or hearing nerve) vs. conductive (problem with ear canal or middle ear) hearing loss. So lets take a deeper look at the author’s review of the literature, description of the test and personal findings.

A bone-conducted vibration applied to the skull can evoke nystagmus (jerking eye movements) in patients with a unilateral peripheral vestibular loss (reduction in inner ear balance input on one side). This nystagmus is not present in individuals with normal vestibular function or in cases of bilateral vestibular loss (reduced inner ear balance function on both sides). Vibration of the skull simultaneously stimulates both ears by setting the inner ear fluids into motion. This fluid motion equally stimulates both inner ears in the case of normal, symmetric vestibular function. When an individual has reduced or altered vestibular input on one side, stimulation through bone conduction does not equally stimulate each ear and nystagmus can occur, as there is asymmetric input from the labyrinths being sent to the brain. The nystagmus, when evoked, is typically of low degree and can be observed utilizing frenzel or videonystamography goggles.

In cases of unilateral peripheral vestibular loss, skull vibration induced nystagmus ranges from 75%-98% sensitivity with a specificity of 94%. Skull vibration induced nystagmus is more often present when larger degrees of asymmetry exist between labyrinths (caloric hypofunction of >50%). It is also noteworthy that skull vibration induced nystagmus is much more sensitive at detecting peripheral vestibular disease than brainstem lesions (better for detecting ear abnormalities than brain abnormalities).

The observed nystagmus is primarily horizontal in nature, but may also exhibit vertical and torsional (twisting) components. With superior semicircular canal dehiscence, the nystagmus may exhibit a larger torsional component. In cases of unilateral peripheral vestibular loss the fast phase of the nystagmus tends to beat (jerk) toward the healthy labyrinth or away from the affected ear. This pattern is observed in 91-98% of patients with unilateral peripheral vestibular loss. Skull vibration induced nystagmus can also be found in 82 to 100% of cases of unilateral superior semicircular canal dehiscence, most frequently with fast phases beating (jerking) toward the affected ear, or away from the intact labyrinth. In superior semicircular canal dehiscence a labyrinthine hypofunction is not the cause of the nystagmus, instead the fluid dynamics of the vestibular system have been altered due to the dehiscent canal, leading to increased stimulation of the ear with the dehiscence and asymmetric labyrinthine input to the brain.

The necessary skull vibrations can be induced with a number of vibratory sources ranging from relatively affordable to very expensive, making this test a viable measure for many clinics. Lists of vibrators that can be utilized are available in the linked article above. With this measure, there are few adverse side effects and the test is typically well tolerated by patients, with only some instances of reported lateropulsion (feeling of being pulled to the side) and/or nausea. However, the authors do caution against this test’s use in certain patient groups such as: recently operated otosclerosis, retinal detachment, recent cerebral hematoma and/or those with poorly controlled anticoagulant therapy.  

The skull vibration induced nystagmus test is a minimally invasive and easily administered test that may be useful in cases of vestibular neuritis/labyrinthitis (inner ear and/or nerve inflammation), vestibular schwannoma (tumor of hearing/balance nerve), Meniere’s disease (fluctuating inner ear fluid abnormality), and in cases where caloric irrigations and/or head impulses cannot be performed. This measure may also be useful in differentiating otosclerosis (abnormal growth of middle ear bones) or other conductive hearing loss from superior semicircular canal dehiscence, as a conductive hearing loss alone should not cause one to have vibration induced nystagmus, whereas a dehiscent superior semicircular canal is likely to create a nystagmus pattern with fast phases beating toward the affected labyrinth. Therefore, the skull vibration induced nystagmus test is likely a useful complementary measure to include in ones vestibular assessment test battery. Readers interested in learning more or in the implementation of this test clinically are referred to the above linked text for more detailed information.

 

Photo courtesy of Frontiers in Neurology

This is a mildly updated version of my most read post regarding the use of meclizine. It is only mildly updated because there is still very little new information available.

Most patients complaining of dizziness or vertigo have been prescribed meclizine at some point. For a medication that is so widely used, there is very little solid information, creating potential for confusion regarding application and potential side effects. Meclizine is also packaged under the names Antivert, Bonine, and Dramamine II. So many patients come in to our balance clinic having received a prescription for meclizine, I am in the habit of asking them about perceived benefit. After listening to their symptoms (some of which include vertigo, nausea or motion sickness, but just as many do not), I ask them “What is it that the meclizine is treating?” The most common answer is “the dizziness.”

The term “dizziness” is very vague and can mean many different things.  Some types of dizziness can be helped by a temporary prescription of meclizine, many won’t be affected at all, and some could be made worse. In acute inner ear disease (such as Vestibular Neuritis/ Labyrinthitis or a Meniere’s episode), what is making you spin and nauseous is the brain trying to resolve the conflict between a healthy ear and an unhealthy ear sending different signals to the brain. The brain would rather receive no information from the inner ears than to receive conflicting information. Meclizine can help reduce this conflict and reduce vertigo and nausea. Medication taken to suppress vestibular symptoms ideally should be used only during the acute stage following vestibular insult, typically lasting three to five days. In order for maximal recovery to take place, the brain eventually must be made aware that a conflict exists, so meclizine must be withdrawn.

Meclizine and BPPV: A therapeutic dosage of meclizine creates a lasting sedating effect only to minimally reduce the intensity of symptoms of BPPV, which last only a few seconds. Canalith Repositioning procedures (AKA Epley maneuvers) are extremely effective in relieving the symptoms of positional vertigo. BPPV does not resolve any faster, and likelihood of future episodes is not affected, by meclizine. The AAO-HNS Clinical Practice Guideline for BPPV released in 2008 recommends against the use of vestibular suppressants for BPPV.

What is Meclizine?

Meclizine is an antihistamine with anticholinergic properties. According to Drugs.com, the mechanism of action is described as: “Antiemetic; antivertigo agent—Exhibits CNS depressant, anticholinergic, antiemetic, antispasmodic, and local anesthetic effects in addition to antihistaminic activity.a

·        Depresses labyrinth excitability and conduction in vestibular-cerebellar pathways.a

·        Antiemetic and antimotion-sickness actions result, at least in part, from central anticholinergic and CNS depressant properties.

The Physicians Desk Reference lists potential adverse reactions for meclizine, noting that “Drowsiness, dry mouth and, on rare occasions, blurred vision have been reported.” But what about functional impact? Could meclizine potentially make your symptoms worse, or have other undesirable side effects?

Manning et al. explored the central nervous system effects of meclizine and dimenhydrate (Dramamine I). Their results “demonstrate that both dimenhydrate and meclizine, in recommended doses, produce drowsiness and impaired mental performance greater than placebo.” These authors attempt to “interpret the meaning of the observed decrement in test scores” by comparing their results to the effects of ethanol (alcohol): “Ethanol serves as a unique drug to reference degree of impairment because there are epidemiologic data that relate to blood alcohol concentrations with a known risk (.07 percent) for being involved in a traffic accident.” Comparison of the data demonstrates that the effect of dimenhydrate and meclizine on mental reaction time is equal to that observed while blood alcohol levels were .04 percent to .06 percent. (In most states, .08 is legally drunk). A more recent study found that long term use of anticholinergics has been associated with higher than average rates of cognitive deficit and dementia. A more recent 2014 study found that meclizine had a negative effect on short term memory, but overall had less negative impact than other medications used for motion sickness such as promethazine and baclofen.

 The use of centrally sedating medication may impede the benefits of vestibular rehabilitation therapy. Vestibular patients taking vestibular suppressants, antidepressants, tranquilizers and anticonvulsants ultimately achieve the same level of recovery as patients not taking similar medications, but the length of therapy needed tends to be longer.

The Bottom Line?

Meclizine is helpful for vertigo associated with sudden acute vestibular asymmetry due to Menieres disease or Vestibular Neuritis/Labyrinthitis, but should be withdrawn once the acute symptoms have diminished. It is not recommended for complaints of lightheadedness, unsteadiness, loss of balance, or dysequilibrium, whether of vestibular origin or not. Vertigo related to BPPV is better treated through canalith repositioning techniques.