________________________________________________________________________ Dizziness and Vertigo
ANXIETY AND DIZZINESS The demonstrable interconnectivity between threat/anxiety, vestibular, visual, and somatosensory systems, and the interac- tions between anxiety disorders and vestibular morbidity point to the importance of a multimodality treatment approach for patients with anxiety and dizziness [72]. Studies have followed patients with dizziness over time and made several important findings [62; 72]. A highly anxious response to the acute dizziness/vertigo of new-onset vestibular neuritis or BPPV predicts continued dizziness 3, 6, and 12 months later. This initial psychologic response has a far greater impact on long-term outcomes than measurable vestibular dysfunction at baseline or follow-up. Patients with emerging symptoms of PPPD who receive cognitive-behavioral therapy within eight weeks of onset have marked reductions in dizzi- ness and avoidance of provocative situations six months later. A highly anxious response to a precipitating event may be the pivotal initiating pathophysiologic process in PPPD (the leading cause of long-term vestibular disability), and early symptom- specific interventions might counter this effect. Patients with poor recovery from acute vestibular neuritis have higher rates of visual dependence, autonomic arousal, anxiety, and fear of vestibular symptoms [139; 140]. Poor recovery is also unrelated to vestibular function, but significantly related to acute visual dependence and failure of sensory integration mechanisms to down-regulate visual contribution to central compensation processes. These data highlight the importance of [139; 140]: • Early identification of abnormal visual dependence and concurrent anxiety • Early treatment to improve long-term outcomes by reducing visual dependence with sensory re-weighting strategies • Combining pharmacotherapy and cognitive therapies to reduce anxiety and autonomic arousal In vestibular patients, successful treatment outcomes require the simultaneous assessment of vestibular, psychiatric (anxiety), and functional (phobic vertigo) disorders. Only when identi- fied can they be addressed by systematically applied treatment that incorporates patient education, vestibular rehabilitation, cognitive-behavioral therapies, and medications to control mor- bidity and increase the potential for sustained remission [73]. SPONTANEOUS ACUTE VESTIBULAR SYNDROMES Acute Unilateral Vestibulopathy/Vestibular Neuritis This acute, spontaneous, peripheral vestibular disorder is characterized by the rapid onset of severe vertigo with nausea, vomiting, and gait instability. The symptoms can be severe and disabling in the short term; patients may need to be hos- pitalized for intravenous fluids and medications [128; 141]. Panic disorder has been found to develop in 10% of patients followed for two years after the initial acute vestibular neuritis episode [142].
Vertigo, nausea, and vomiting can be treated with a combina- tion of vestibular suppressants, not exceeding seven days to avoid disrupting CNS adaptation and compensation [15; 128]. The vestibular nerve is selectively vulnerable to inflammation- related swelling and entrapment by its pathway in a narrow, bony canal [34]. Oral corticosteroids may help reduce the severity of vestibular neuritis if initiated in the first few days. The recommended agents are [15; 120]: • Methylprednisolone initiated at 100 mg/day and then reduced by 20 mg every fourth day, OR • Prednisone 60 mg/day for one week When acute symptoms subside, patients should begin vestibu- lar rehabilitation to promote CNS adaptation and sensory re-weighting [15; 128]. Labyrinthitis A presumed viral acute labyrinthitis is reasonable to treat with corticosteroid therapy, such as a 10-day course of prednisone with 60 mg/daily on days 1 through 5, reduced to 10 mg/daily on days 6 through 9, and 5 mg on day 10. Some evidence sug- gests corticosteroid therapy may hasten recovery but does not change the long-term prognosis [141]. Patients with bacterial labyrinthitis should be referred to an ENT specialist. Herpes Zoster Oticus Patients with herpes zoster oticus should be treated with corti- costeroids and a high-dose oral antiviral (acyclovir, famciclovir, or valacyclovir) when reactivation of latent varicella zoster virus is suspected. Carefully look for painful vesicles on the external ear and within the back of the external ear canal. Even in the absence of visible vesicles, treatment with an antiviral agent is probably prudent with significant localized ear pain and normal tympanic membrane [15]. TRIGGERED EPISODIC VESTIBULAR SYNDROMES Benign Paroxysmal Positional Vertigo Canalith repositioning procedures (CRPs) are the first-line therapy option and the most effective treatment for BPPV for patients with prolonged symptoms and/or frequent recur- rences. Vestibular suppressants are generally avoided, though a brief course of an antihistamine (e.g., meclizine) may be indicated for initial symptom control. This may be all that is needed for patients with mild, self-limited symptoms and infrequent recurrences. Rarely, BPPV can be refractory to CRPs and require surgical occlusion of the affected semicir- cular canal [15]. Outcome assessment within one month of initial observation or treatment is necessary to document symptom resolution or persistence. Patients with persistent symptoms should be evaluated for treatment failure. Referral to a specialist is recom- mended to identify unresolved BPPV and/or an underlying peripheral or central vestibular disorder.
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Book Code: ANCCTX2027
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