A Place Called Vertigo
contact lens management
A Place Called Vertigo
Stop the world from spinning with contact lenses.
Susan Kovacich, O.D., F.A.A.O.
A 53-year-old Caucasian female presented complaining that her flat top bifocals triggered vertigo, especially when she used the stairs. As a result, she expressed an interest in a distance-only contact lens OD (her “good” eye) to alleviate her severe dizziness. I educated her that this would require readers. She said she was fine with that, and that she planned to use readers only when she was stationary reading or at the computer. (Of note: Progressive bifocals weren't an option here, as in the past, they made the patient feel “dizzy” as well.)
The patient's systemic history was positive for Ménière's disease (MD), for which she'd been diagnosed two years prior and took a “mild form” of hydrochlorothiazide/triamterene (Dyazide, GlaxoSmithKline) (dose unknown) to control her MD-induced vertigo. Her past ocular history revealed she was “essentially one-eyed since birth” because she “had so much astigmatism in her left eye, her brain shut it off.”
The patient's distance vision with her habitual flat top bifocals was 20/20 OD and Count Fingers (CF) @ 5' (PH 20/400) OS. Her near vision was 20/25 OD and 20/400 OS. With a refraction of +1.00-0.50 X 090 OD, her best-corrected visual acuity (BCVA) was 20/20, and with +3.75-2.75 X 180 OS, her BCVA was 20/100. A new ADD power of +2.50 improved her near vision to 20/20 OD. Her cover test was ortho at distance and near. Her slit lamp exam, intraocular pressures and internal ocular exam was within normal limits.
Based on these findings, I diagnosed the patient as having anisometropic hyperopic astigmatism OS > OD, with amblyopia OS and presbyopia OU.
MD is named for French physician Prosper Ménière (1799-1862), who first described this syndrome in 1861.1 Specifically, the condition is an inner ear disorder, which causes episodic vertigo, tinnitus, a feeling of fullness in the affected ear, hearing loss that may fluctuate initially, then become permanent through time and includes occasional headaches, abdominal discomfort and is associated with nausea and vomiting. MD patients usually describe the vertigo as a severe, intense whirling or spinning sensation. The frequency of the vertigo is highly variable and can cause anxiety, as the next episode can occur without warning. Horizontal rotary nystagmus has been observed during acute vertigo episodes. Patients are usually incapacitated during an acute event, preferring to keep still or lie down. The disease tends to lead to hearing loss, but the vertigo may subside with age.2
Researchers believe that MD symptoms result either from vascular compression (e.g. microvascular compression syndrome) or the buildup of fluid in the compartments of the inner ear (e.g. the labyrinth).3,4 The labyrinth contains the organs of balance (the semicircular canals and otolithic organs) and of hearing (the cochlea) and has two sections: the bony labyrinth and the membranous labyrinth. The membranous labyrinth contains endolymph, a fluid that stimulates receptors as the body moves. These receptors deliver signals to the brain regarding the body's position and movement. In the cochlea, fluid is compressed in response to sound vibrations. This stimulates sensory cells that send signals to the brain. In MD, some researchers believe that the endolymph buildup in the labyrinth hampers the normal balance as well as hearing signals between the inner ear and the brain, resulting in the symptoms described above.3 Others believe that with the dilation of the endolymphatic system, a small rupture of the delicate membranes results in the mixing of endolymph with perilymph (fluid in the cochlea), leading to the severe vertigo and other symptoms. The rupture quickly heals, resolving the symptoms.2
Approximately 615,000 individuals in the United States currently have MD, and 45,500 cases are newly diagnosed each year, according to the National Institute on Deafness and Other Communication Disorders. The disease usually manifests during the fourth and fifth decades. It is slightly more prevalent in females and occurs more commonly in those of northern European descent. A strong genetic component exists in as many as one fifth of patients. The cause of the disease is unknown, but acoustic trauma, autoimmune and inflammatory disease, syphilis, metabolic disorders and neoplasms should be ruled out.2
No cure currently exists for MD, and no one treatment works for everyone, though the following are examples of some successful treatments. (For a more extensive list, visit www.menieresinfo.com/treatment.html#which-treatments-work.)
MD patients usually describe their vertigo as a severe, intense whirling or spinning sensation.
► Sodium restriction/diuretic therapy. Limiting salt intake to 2,000 mg a day and taking water pills reduces the amount of fluid the body retains, which may help decrease fluid volume and inner ear pressure, lowering episodes of dizziness.2,3
► Lifestyle modifications. Not smoking, limiting caffeine, chocolate and alcohol intake, as well as exercising and reducing stress are associated with decreasing symptoms.2,3
► Drugs. Diuretics, such as hydrochlorothiazide/triamterene (Dyazide), prescribed for this patient, or 25 mg hydrochlorothiazide/ 37.5 mg triamterene (Maxide 25, Mylan Bertech Pharmaceuticals, Inc.) are often used to manage MD. Other medications, such as diazepam (Valium, Hoffmann-La Roche Ltd.), glycopyrrolate (Robinul Forte, Shionogi Pharma, Inc.), lorazepam (Ativan, Pfizer) and meclizine have been shown effective in both relieving and limiting vertigo.3 Also, the injection of the ototoxic antibiotic, gentamicin directly into the middle ear space has gained worldwide popularity for vertigo control. However, this method significantly raises hearing loss risk, as it can damage the microscopic hair cells in the inner ear that aid in hearing.3 Further, some doctors use a corticosteroid delivered to the inner ear via intratym-panic injection to decrease vertigo — a safer alternative to gentamicin administration.2,3,5
► Pressure pulse device. These devices send air pressure pulses through the tympanostomy tube into the middle ear. The middle ear contains a structure comprised of two membranes that separate the middle ear from the inner ear: the oval window and the round window. It is theorized that the air pressure pulses are somehow sent by virtue of the two membranes to the inner ear, and that the endolymphatic fluid in the inner ear may, in turn, be affected in some positive way that provides MD-symptom relief. The exact mechanism of how this works, however, is not known.4
► Surgery. Endolymphatic sac decompression (ESD) is a procedure in which the bony cavity that surrounds the endolymphatic sac is enlarged by drilling away bone, and excess endolymph is drained. The reduction in excess fluid and pressure can provide the patient with temporary vertigo relief. Since endolymph can build up again following ESD, an endolymphatic sac shunt (ESS) may be implanted to continuously drain the excess endolymph. These procedures are controversial, as the effects may not be long-lasting. However, both ESD and ESS spare hearing.4 Other surgical procedures tend to be ablative and hearing function is sacrificed to control the vertigo. A labyrinthec-tomy, results in loss of hearing (although the patient may have already suffered hearing loss in that ear from the disease).1 In a vestibular neurectomy, the vestibular portion of the 8th cranial nerve (vestibulocochlear nerve) is severed from the affected inner ear organ (vestibule). The risks of this procedure include compromised hearing and cerebral-spinal fluid leak, among others.4
► Cochlear implant. In June 2010, the FDA approved a cochlear implant that alleviates vertigo. Specifically, the patient wears a processor behind his affected ear and activates it as an attack begins. The processor then wirelessly signals the implant, which is imbedded almost directly underneath in a small well created in the temporal bone. The implant transmits electrical impulses through three electrodes inserted into the canals of the inner ear's bony labyrinth, overriding the MD symptoms, simultaneously replacing the function of the ear until it recovers. Currently, a clinical trial is underway to assess the usefulness of cochlear implants in the treatment of MD.5
I fit the patient with a +0.75D sphere soft contact lens, which provided her with 20/20 distance vision. She had a pair of +2.50 readers at home that she would use for her near vision until it was determined the contact lens trial was successful.
At her one-week follow-up visit, the patient reported she was extremely happy with her vision OD and requested a contact lens in her amblyopic eye, even if it “only improved vision a little bit.” I informed the patient that becoming more aware of her poor vision OS might aggravate her MD, but she elected to be fit regardless. So, I chose a soft toric 8.7/+3.00-2.25 X 180/14.5 lens. This provided her left eye with 20/100 vision, with no improvement upon over-refraction.
At her next follow-up visit one week later, the patient said she was elated with her improved peripheral vision OS, even though her BCVA was only 20/100. She also said she experienced no episodes of vertigo with the contact lenses. Glasses were ordered for the patient with a trifocal spectacle (plano/+2.50 ADD, 50% intermediate) for stationary near tasks. The patient was scheduled for a one-year annual exam, for which she has not yet been seen.
Every so often, a patient presents unable to wear spectacles for some reason. I've had patients who have extremely narrow or flat nasal bridges, which were difficult-to-impossible to fit, and some patients so sensitive to any pressure on the sides of their head, that the temples of even the lightest frame were painful for them. Some patients have large differences in prescriptions (anisometropia) between the eyes, making the image difference (anisokonia) too large for the brain to fuse. Others, such as the patient described above, have issues with balance and vertigo. Since the extreme vertigo can be debilitating in these cases, any reduction in the triggers that cause the motion sickness or spinning sensation can vastly improve these patient's quality of life. Many people with motion sickness experience a “swimming” sensation associated with plus lenses or bifocal spectacles, particularly progressive addition lenses. When examining these patients, ask specific questions about visual activities that make the patient uncomfortable, and explore other refractive options, such as single vision glasses for distance and/or near, lined bifocals/trifocals and contact lenses.
When a patient has a refractive error and cannot wear glasses, contact lenses can often be employed to manage these challenging patients.
A practitioner who makes it a point to offer contact lenses in special cases like these not only instills patient loyalty, but attracts several referrals as well.
By being aware of MD and how we, as eyecare practitioners, can help these patients, we become a valuable member of these patients' healthcare team. OM
Special thanks to Steven M. Parnes, MD, of University Ear, Nose & Throat, Albany, NY for reviewing the MD portion of this case study.
1. Deafness Research Foundation. Ménière's Disease. www.drf.org/Menieres+ Disease. Accessed 1/7/11.
2. Williamson R. Ménière's Disease. Conn's Current Therapy 2010. Philadelphia: Saunders; 2010:214-216
3. National Institutes of Health. National Institute on Deafness and Other Communication Disorders. Ménière's Disease. www.nidcd.nih.gov/health/balance/meniere.html#2. Accessed 1/7/11
4. Ménière's Disease Information Center. MDIC www.menieresinfo.com/treatment.html#treatment-devices. Accessed 1/7/11
5. University of Washington News. Guiden M, Donohue B. Researchers develop first implanted device to treat balance disorder. http://uwnews.org/article.asp?articleID=60951 Accessed 1/7/11.
DR. KOVACICH IS AN ASSOCIATE CLINICAL PROFESSOR IN THE CORNEA AND CONTACT LENS CLINIC AT THE INDIANA UNIVERSITY SCHOOL OF OPTOMETRY AND A FELLOW IN THE AMERICAN ACADEMY OF OPTOMETRY. E-MAIL HER AT SKOVACH@INDIANA.EDU, OR SEND COMMENTS TO OPTOMETRICMANAGEMENT@GMAIL.COM.
Optometric Management, Issue: February 2011