1

Introduction

Vestibular neuritis (VN) is the second most common cause of peripheral vestibular vertigo . Recurrent episodes of vestibular disturbance, such as positional vertigo and unsteadiness, have been found to occur in approximately 50% of patients with VN . Recurrences of VN, however, have been significantly smaller, 2% to 17% . Viral inflammatory changes to the vestibular nerve have been presumed to be the cause of VN . Notably, 60% to 70% of documented patients with VN in autopsy were found to have Herpes simplex virus 1 in the vestibular ganglia . Recurrent episodes of vestibular disturbance are thought to be caused by viral reactivation, causing inflammation and neuronal damage . Success with antiviral therapies has varied. One large study of 141 patients with VN compared corticosteroid therapy with valacyclovir therapy, finding no significant effect using valacyclovir . Another study of 40 patients with VN found that its antiviral protocol (acyclovir) was effective in 75% of patients with a secondary antiviral therapy (intratympanic ganciclovir) bringing the success rate to 89% . In addition, a consensus has not been reached on the efficacy of corticosteroid use alone in recurrences of vestibular disturbance .

2

Case

A 57-year-old woman with a history of herpes simplex labialis was previously diagnosed with vestibular neuritis in October 2008. She had experienced recurrent attacks of vertigo, lasting up to 2 days, and disequilibrium lasting 2 to 3 weeks. These attacks were followed by periods of complete remission. The frequency of these attacks increased over time and is documented, beginning in 2009 ( Fig. 1 ). Initially, these attacks would follow an outbreak of oral herpes or an upper respiratory infection but later began spontaneously. The patient refused corticosteroid treatment and did not find relief using dimenhydrinate as needed.

Recurrences of prolonged continuous vestibular disturbances (>1 week) plotted against time rounded to the nearest month.

The patient had left beating nystagmus on positional maneuver and a 25% decrease in energy function on the right. A magnetic resonance imaging (MRI) performed after a recurrence of her disequilibrium had subsided did not show enhancement or abnormalities of the brain parenchyma or cochleovestibular nerves. Audiogram, acoustic reflex, tympanometry, and carotid artery ultrasound results were all normal. The patient began keeping a log of reoccurrences of vestibular disturbance in January 2009 to attempt to identify possible triggers, but she was unable to find any common factor.

In March 2011, the patient received oral valacyclovir at 500 mg a day prescribed by her primary care physician to prevent herpes labialis outbreaks. The patient did not have any outbreaks in 6 months while taking daily valacyclovir. Incidentally, she did not have a single recurrence of vestibular disturbance in this time either. At the time of this article’s preparation, the patient has had no recurrence of vestibular symptoms.

After beginning daily low dose prophylactic valacyclovir, the patient has demonstrated a significant decrease in the frequency of vestibular disturbances. Based on the plot of reoccurrences per month ( Fig. 1 ), prolonged vestibular disturbances were found to occur on average every 1.92 months. A standard deviation was calculated to be 0.82. If a recurrence were to occur just after the time of this article’s preparation, 6 months removed from a previous recurrence, the calculated Z score would equal 4.97 ( P < .0001).