Treatment of Vertigo
Source: Department of Otolaryngology, UTMB, Grand Rounds
Date: November 26, 1997
Resident Physician: Ravi V. Pachigolla, MD
Faculty Physician: Jeffery T. Vrabec, MD
Series Editor: Francis B. Quinn, Jr., MD
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Vertigo is a complex symptom manifested in a host of disorders. A proper understanding of patient’s symptoms is essential to proper diagnosis and treatment. Patients may confuse vertigo with feelings of syncope, visual disturbances, confusion or slowed mentation. Vertigo usually refers to a true spinning sensation either experienced by the patient or the external world. Key components of a history include but are not limited to presence or absence of nystagmus, rotation of nystagmus, nausea or vomiting, hearing loss, severity, onset, duration, frequency of attacks, medication history, other otologic complaints, and other related questions. A physical may include but not be limited to an otologic exam, electronystagmography, evaluation for nystagmus (with Frenzel lenses), dix-hallpike testing, fistula testing with a politzer bag or other means, audiograms, cranial nerve exam, and other neurotologic testing. After an appropriate history and physical exam have been performed, further workup may include lab work and imaging studies. After a diagnosis has been made, treatment strategies can then be fashioned.
Vestibular Diseases and their Medical Management
Three senses are used to convey streams of sensation: visual, vestibular, and somatosenory. When there is a mismatch between information carried on two or more senses, vertigo is perceived. Drug treatment is aimed to manipulate neurotransmitters to lessen the symptoms of vertigo. Cholinergic, monoaminergic, and glutaminergic synapses have been demonstrated in these circuits. Refinement of medications to target these synapses exist for the future so that specific antagonists to muscarinic and histamine receptors can eventually be made without the adverse effects of broadly acting antagonists.
Agents aimed at sedating the vestibulobrainstem axis are particularly useful in aborting the acute attack and temporarily suppressing the acute symptoms caused by ablative surgical procedures. These vestibulosuppressants have a well established record of controlling vertigo.
Anticholinergics were the first drugs to be used in the treatment of vertigo. The most commonly used anticholinergics are homatropine and scopolamine. These agents are nonselective, and end up blocking all muscarinic receptors much like atropine. They do possess properties that allow treatment of motion sickness. They can also affect vestibular compensation leading to reversible overcompensation. Only agents that cross the blood-brain barrier are effective. Generally, the medications last only a few hours; however, transdermal scopolamine may last four days. Again, muscarinic blockade outside the CNS can lead to side effects of dry mouth, urinary retention, and constipation. Within the CNS, side effects include memory disturbances and confusion. Prostatic hypertrophy and closed-angle glaucoma contraindicate their prescription. The class of drugs used most commonly to treat acute attacks of vertigo are antihistamines. Agents in this class include Promethazine, Diphenhydramine, Prochlorperazine, Meclizine, and Cinnarizine. These agents vary in their ability to control the bouts of vertigo and have associated sedative and anticholinergic properties. The most antiemetic of these agents include Meclizine and Prochlorperazine. These two agents also have the lowest anticholinergic effects while Prochlorperazine is more sedating than Meclizine and Meclizine has a longer duration of action. Other agents like Promethazine and Diphenhydramine are too sedating and less antiemetic compared to the other agents. The mechanism of action is poorly understood but may involve central anti-histaminic effects. Histamine agonists like Betahistine are sometimes used to treat vertigo. The mechanism of action of these drugs is not exactly clear but may involve improved blood flow or facilitation of vestibular compensation. This agent in particular has been studied recently because of its specific effects on H2 and H3 receptors. It has been shown that it has agonistic effects at H2 and antagonistic effects at H3 receptors. Whether the agonism at H2 leading to increased firing of medial vestibular neurons or its antagonism at H3 receptors possibly leading to increased cochlear blood flow leads to decreased vertigo is unclear. These experiments have shown insight though that antagonism at H1 receptors, the key action of classic antihistamines does not appear to affect vertigo. Side effects include headache and nausea and this agent should not be used in patients with duodenal ulcer or pheochromocytoma. The fact that histamine agonists and antagonists can be used to treat vertigo underscores the fact that the mechanism for vertiginous attacks has not been clearly elucidated. Antidopaminergics can also be used to control vertigo, most specifically, nausea and vomiting. These agents act at the chemoreceptor trigger zone and thus basically alleviate the nausea and vomiting. Agents such as chlorpromazine can be used to reduce the neurovegetative symptoms that parallel vertigo and may improve the psychoaffective symptoms. Side effects include orthostatic arterial hypotension, and extrapyramidal side effects. Benzodiazepines affect acute vertiginous episodes by modulating GABA receptors. They allow sedation, hypnosis, decreased anxiety, and muscle relaxation. Side effects include memory disturbace, addiction, and extreme sedation. Ca channel antagonists are used in Europe for treatment of vertigo. Two of the most commonly used are Cinnarizine and flunarizine. Cinnarizine has been shown to suppress post-rotatory dizziness and nystagmus and have equal efficacy compared to prochloperazine. Side effects were uncommon apart from occasional drowsiness. The mechanism of action is not entirely clear. Perhaps calcium antagonists may be vestibular suppressants because vestibular hair cells are endowed with calcium channels. Side effects include sedation and weight gain and over longer periods may lead to Parkinsonism.
Both medical and surgical treatment for hydrops report improvement in patient symptoms in up to 80% of cases. Without treatment, symptoms may also resolve in a significant number of cases. No cure currently exists for hydrops and current therapy is to specifically control the number of attacks, progressive hearing loss, and allow functional daily living. Medical treatment of hydrops should begin by relieving this hydrops. Therefore, salt restriction (2 gm Na diet), and diuretics are often the first line therapy. This therapy is used to reduce endolymph volume. This therapy often results in control of symptoms in up to 60% of patients; however, long term control of progressive hearing loss is less certain. Recent reevaluation of studies have disputed their beneficial effects and as such a clear mandate cannot be given to using to diuretics. Diuretics have become the mainstay for treatment of hydrops. Osmotic diuretics such as glycerol have been shown to reduce hydrops especially in patients with fluctuant symptoms though effects only last a few hours. Oral urea may produce more sustained benefit however revolting tastes prevent their routine use, glycerol being very sweet and urea almost unbearably bitter. Another therapy involves carbonic anhydrase inhibitors (acetazolamide). Carbonic anhydrase is located in the stria where endolymph is produced so by affecting this enzyme, theoretically, endolymph production should decrease. When given intravenously, exacerbation of hearing loss and an increase in hydrops as measured by electrocochleography occurred. However, a discrepancy between intravenous and oral administration has been noted with acetazolamide; nonetheless, preliminary trials have shown this drug to be ineffective with the possibility of unpleasant side effects such as metabolic acidosis. One particular mild diuretic combination of triamterene and hydrochlorothiazide may reduce the frequency of attacks of vertigo. Agents such as Praxilene (enhances aerobic metabolism) have also been used with equivocal results. Immunologic therapy is still under scientific investigation.
Vertigo may be a manifestation of Meniere’s but also of other autoimmune diseases. The evidence in favor of autoimmunity in Meniere’s is not great and thus steroid use in Meniere’s is not as effective as in other autoimmune inner ear disorders associated with vertigo such as Cogan’s. Therefore, it is crucial to distinguish between presumably autoimmune disorders as steroid use is crucial in alleviating the progressive nature of these conditions whereas in Meniere’s it is not as crucial. Steroids have been shown to even have a local effect in the inner ear affecting the sodium-potassium pump and possibly leading to decreased endolymph volume. They, of course, have their systemic effects which must be taken into account when prescribing these drugs. Other immunosuppressives such as methotrexate and cyclophosphamide have been occasionally used for autoimmune ear dysfunction although both have serious side effects. Methotrexate can lead to myelosuppression, stomatitis and renal failure while cyclophosphamide can lead to hemorrhagic cystitis.
Inner ear barotrauma results from rapid shifts in middle and inner ear pressure during diving causing shearing of vestibular membranes. Occasionally, it results in vertigo, most of the time sensorineural hearing loss. Basic treatment involves bed rest and avoidance of activities that may increase intracranial pressure. This usually results in resolution of vertigo however a small percentage may continue to have symptoms and require further surgical therapy. Inner ear decompression sickness differs from inner ear barotrauma. This usually results from rapid ascent during a deep dive which leads to bubbles forming in the intralabyrinthine region. These bubbles distort membranes and often cause severe vertigo usually during the ascent. Treatment consists of immediate hyperbaric oxygen treatment to recompress the bubbles.
Chronic vertigo usually results from undercompensation of acute vertiginous attacks. Not usually amenable to vestibular suppressants, other modalities are needed to deal with this condition. Vestibular rehabilitation exercises, introduced earlier this century have only recently become popular in alleviating chronic vertigo. The premise behind these exercises is to allow adaptation and habituation between the vestibuloocular and vestibulospinal tracts and allow for mobilization and relief of vertigo. Often, this involves patients aggravating the positions and movements that cause vertigo and repeating them to allow adaptation. Other methods involve dynamic therapy where patients walk backwards, sideways, and in the dark on thick carpet. The last maneuver forces patients to rely on non-ocular and non-proprioceptive mechanisms to maintain balance. Obviously, care should be taken when prescribing these exercises and should be undertaken with the aid of a therapist.
Treatment for BPPV varies. A majority of patients experience spontaneous resolution of symptoms within months of onset. The canalith repositioning maneuver has become the basis for non-surgical treatment of BPPV. Instituted at Portland Otologic Clinic in 1979, it has become the standard therapy. Various refinements with or without vibratory enhancement has been used widely with a high degree of success. Up to 80% of patients may have resolution of their symptoms following one treatment session. 95% may have resolution after several treatments. The idea is that the canaliths are shifted to the nonampullated end of the canal where they no longer affect semicircular dynamics. The plane of the particular canal you wish to affect should be kept in the plane with gravity while slowly maneuvering the otoconia in an ampullopetal direction. Vibration of the skull facilitates migration by minimizing adherence - this also improves the results. Complications are few and rare but precautions should be taken in those patients who have back and neck problems, hypertension and so forth. Contraindication to vibration (perilymph fistula, retinal detachment) also should be taken into account. Occasionally a canalith jam may occur provoking a severe vertiginous episode not relieved by head position. Low frequency vibration and repositioning of the head is used to unjam the canaliths and allow for a retry.
Chemical labyrinthectomy is one last aspect for treatment of vertigo I’d like to discuss. Ever since it has been known that aminoglycosides were ototoxic, their potential in treating intractable, severe vertigo has assumed prominence. Originally, streptomycin was given intravenously until patients reported effects of lightheadedness or unsteadiness at which point therapy was stopped. The therapy was quite effective however severe hearing loss and oscillopsia prevented its widespread use. It was noted that Streptomycin was quite cochleotoxic therefore other newer aminoglycosides were developed with the hope that they be less cochleotoxic yet still vestibulotoxic. Gentamycin administered intratympanically has resulted from these endeavors. Given in various concentrations, using transmeatal and endaural techniques and given over a period of days, transtympanic gentamycin has shown upwards of 90% relief of vertigo without hearing loss and some improvement in tinnitus and aural pressure. It is usually given until patients complain of dizziness or have nystagmus. Cold water calorics can also be used to measure response. And generally speaking, if length of treatments is kept under six days, hearing loss should not develop.
The non-surgical treatment for vertigo depends on many criteria including the specific disease entity, patient tolerances and other factors. An appropriate regimen should be fashioned to each particular disease and patient preferences with the general understanding that medications do not necessarily cure the disease but instead can control symptoms and prevent unnecessary surgery.
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