Inner Ear Blood Flow Research Articles

Pharmacotherapy of Vestibular Disorders and Nystagmus

Vertigo and dizziness are with a life-time prevalence of ~30% among the most common symptoms and are often associated with nystagmus or other oculomotor disorders. The prerequisite for a successful treatment is a precise diagnosis of the underlying disorder. In this overview, the current pharmacological treatment options for peripheral and central vestibular, cerebellar, and oculomotor disorders including nystagmus are described. There are basically seven groups of drugs that can be used (the "7 As"): antiemetics; anti-inflammatory, anti-Menière's, and antimigraine medications; antidepressants, anticonvulsants, and aminopyridines. In acute vestibular neuritis, recovery of the peripheral vestibular function can be improved by treatment with oral corticosteroids. In Menière's disease, a long-term high-dose treatment with betahistine-dihydrochloride (at least 48 mg three times daily) had a significant effect on the frequency of the attacks; the underlying mode of action is evidently an increase in inner-ear blood flow. The use of aminopyridines is a well-established therapeutic principle in the treatment of downbeat and upbeat nystagmus as well as episodic ataxia type 2 and cerebellar gait disorders. As was shown in animal experiments, these potassium channel blockers increase the activity and excitability and normalize irregular firing of cerebellar Purkinje cells. They evidently augment the inhibitory influence of these cells on vestibular and deep cerebellar nuclei. A few studies showed that baclofen improves periodic alternating nystagmus; gabapentin and memantine improve pendular and infantile nystagmus. However, many other eye-movement disorders such as ocular flutter, opsoclonus, central positioning, and see-saw nystagmus are still difficult to treat. Although substantial progress has been made, further state-of-the-art trials must still be performed on many vestibular and oculomotor disorders, namely Menière's disease, vestibular paroxysmia, vestibular migraine, and many forms of central eye-movement disorders.

Peripheral vestibular disorders

First, to update the diagnosis, pathophysiology, and treatment of the most frequent peripheral vestibular disorders. Second, to identify those disorders for which the diagnostic criteria are still deficient and treatment trials are still lacking. Bilateral vestibulopathy can be reliably diagnosed by the head-impulse test, caloric irrigation, and vestibular-evoked myogenic potentials. A new frequent subtype has been described: cerebellar ataxia, neuropathy, and vestibular areflexia syndrome. Benign paroxysmal positioning vertigo can be easily diagnosed and effectively treated. Vestibular neuritis is most likely caused by the reactivation of a herpes simplex type 1 infection; the inferior vestibular nerve subtype is now well established. More evidence is needed that the recovery can be improved by corticosteroids. Endolymphatic hydrops in Menière's disease can be depicted by high-resolution MRI after transtympanic gadolinium injection; a high-dosage and long-term prophylactic treatment with betahistine is evidently effective. Its mechanism of action is most likely an increase in the inner-ear blood flow. Vestibular paroxysmia is now a well established entity; carbamazepine is the treatment of first choice. Superior canal dehiscence syndrome can be reliably diagnosed; the best current treatment option is canal plugging. Although progress has been made in the diagnosis and treatment of most peripheral vestibular disorders, more state-of-the-art trials are needed on the treatment of bilateral vestibulopathy to prove the efficacy of balance training, of vestibular neuritis (in terms of recovery of peripheral vestibular function and central compensation), of vestibular paroxysmia to prove the effects of carbamazepine, and of Menière's disease to find the optimal dosage of betahistine.