Use and Misuse of Medications in the Treatment of Dizziness

This reviewdiscusses the pharmacological treatment of dizziness, focusing particularly on the vertigo subtype of dizziness. Classes of medications useful in the treatment of vertigo include anticholinergics, antihistamines, benzodiazepines, calcium channel blockers, and dopamine blockers. These medications often have multiple actions. They may modify the intensity of symptoms (eg, vestibular suppressants) or they may affect the underlying disease process (eg, calcium channel blockers in the case of vestibular migraine). Most of these agents, particularly those that are sedating, also have a potential tomodulate the rate of compensation for damage. This consideration has becomemore relevant in recent years, as vestibular rehabilitation physical therapy is now often recommended in an attempt to improve compensation. Accordingly, therapy of vertigo is optimized when the prescriber has detailed knowledge of the pharmacology of medications being administered as well as the precise actions being sought. Specific regimens of drug therapy can be tailored for four major etiological classes of vertigo. Otological vertigo includes disorders of the inner ear such as Ménière’s disease, vestibular neuritis, benign paroxysmal positional vertigo (BPPV) and bilateral vestibular paresis. In both Ménière’s disease and vestibular neuritis, vestibular suppressants such as anticholinergics and benzodiazepines are used. In Ménière’s disease, salt restriction and diuretics are prescribed in an attempt to prevent flare-ups. In vestibular neuritis, shorter durations of vestibular suppressants are now recommended in an attempt to promote compensation. Drug treatments are used as an adjunct to physical therapy for BPPV and bilateral vestibular paresis. Central vertigo includes entities such as migraine and stroke. Prophylactic agents (L-channel calcium channel blockers, tricyclic antidepressants, betablockers, anticonvulsants) are the mainstay of treatment for migraineassociated vertigo. In persons with stroke or other structural lesions of the brain stem or cerebellum, an eclectic approach incorporating trials of vestibular suppressants and physical therapy is recommended. Psychogenic vertigo includes disorders such as panic, anxiety disorder, and agoraphobia. Benzodiazepines and antidepressants are the most useful agents for this condition. Undetermined and ill-defined causes of vertigo make up a large remainder. An empirical approach to treating these patients involves incorporating trials of medications of general utility such as benzodiazepines, physical therapy, and trials of medication withdrawal. When 168 Copyright @ American Academy of Neurology. Unauthorized reproduction of this article is prohibited. appropriate, physical therapy and psychiatric consultation are suggested. NEUROPHYSIOLOGY OF DIZZINESS AND VERTIGO Dizziness is a general term that may encompass symptoms caused by diverse etiologies such as low blood pressure and drug side effect. This chapter will more specifically address vertigo, a common subtype of dizziness, defined as the illusion of rotational motion. Most vertigo is otological and is caused by dysfunction of the rotational velocity sensors of the inner ear, the semicircular canals. Other types of vertigo exist, however, and in this regard it is helpful to consider how the brain processes motion signals. Normal persons continuously process three types of sensory input: vestibular (inner ear), visual, and somatosensory. These three streams of information are combined in the brain to form an estimate of orientation and motion of the head and body. The three streams are also compared centrally, and when a mismatch between two or more senses occurs, vertigo can be perceived. From this systems-physiology perspective, sources of vertigo include all possible combinations of sensory disturbances related to motion as well as central malfunction of the comparison mechanism. Practically, however, because the visual and somatosensory senses mainly produce position-coded signals, vertigo is only rarely a consequence of visual or somatosensory malfunction. An example of ‘‘visual vertigo’’ might be vertigo that is associated with an oculomotor disturbance accompanied by nystagmus. Nevertheless, the common varieties of visual disturbance, diminished vision, double vision, or disorders of the accommodation system usually do not create vertigo. Similarly, vertigo is only occasionally associated with somatosensory dysfunction as in cervical vertigo. Central vertigo is more frequent but still uncommon with respect to otological vertigo, as will be later discussed in more detail. When treating vertigo, one must also consider motion sickness, which is the malaise and nausea that may follow real or illusory sensations of motion. Vertigo and motion sickness are not synonymous. For example, carnival rides frequently elicit illusory rotational sensations, but motion sickness can often be avoided. Also, the symptoms of motion sickness usually persist longer and tend to be more disturbing than the inciting vertigo. While vertigo is reliably experienced by normal persons experiencing similar sensory disturbances, susceptibility to motion sickness varies remarkably. The pharmacology of vertigo and motion sickness are clearly distinct. Finally, when planning treatment one must consider recovery and compensation. Every vestibular stimulus, whether the result of natural motion or disease, has the potential to initiate a process of compensatory adaptation. The pharmacology of compensation is distinct from that of vertigo and motion sickness and, in fact, agents that relieve vertigo, nausea, or motion sickness may block compensation. Two key concepts regarding compensation need to be considered when planning therapy of vertigo: (1) Promotion of central compensation is desirable during the process of recovery from persistent vestibular imbalance such as after a severe bout of vestibular neuritis. (2) Prevention of unneeded and counterproductive compensation may be desirable after a transient vestibular imbalance such as might be caused by Ménière’s disease. NEUROCHEMISTRY OF VERTIGO At least four major neurotransmitters of the vestibular system are involved in the three-neuron arc between the vestibular hair cells and the oculomotor nuclei that drives the vestibulo-ocular reflex. A host of other neurotransmitters also 169 KEY POINT: