________________________________________________________________________ Dizziness and Vertigo
SPONTANEOUS EPISODIC VESTIBULAR SYNDROMES
Dimenhydrinate, scopolamine, or diazepam may be required in severely symptomatic patients before CRP, patients who become severely symptomatic after CRP, or those who refuse CRP. Patients exceptionally prone to motion sickness should receive meclizine [15; 21; 115]. CRP plus betahistine more effectively reduced vertigo symptoms than CRP alone [149]. If prescribed, clinicians should educate patients that vestibular suppressants can increase risks of cognitive impairment, falls, drug interactions, and machinery or driving accidents [21]. BPPV and CNS Disorders Aside from migraine, BPPV in patients with pre-existing central neurologic disorders is rarely addressed in the literature. In one study of 93 patients with BPPV, 31.2% had a central neurologic disorder, with cerebrovascular disease and migraine the most common. The efficacy of repositioning therapy was excellent for BPPV with or without a pre-existing central neurologic disorder [150]. Post-CRP Residual Dizziness Residual dizziness following successful repositioning is com- mon in patients with BPPV, described as continuous or intermittent imbalance, lightheadedness, or unsteadiness without positional vertigo. The duration of vertigo before CRP is linked to residual dizziness and incomplete central adapta- tion. Residual dizziness is significantly associated with anxiety disorders, and subjects with high anxiety show more durable and disabling dizziness even after the resolution of acute vertigo in absence of otolithic or vestibular dysfunction [131; 151]. Anxiety is highly prevalent in elderly patients with BPPV, and the adverse impact of residual dizziness on psychologic, social, and daily functioning can be severe. Early recognition and treatment of BPPV and comorbid anxiety is recommended to decrease the incidence of residual dizziness [131]. Refractory BPPV If BPPV remains refractory despite a correct diagnosis and competently performed repositioning maneuvers, surgery may be indicated. The two surgical options are partial neurectomy of the vestibular nerve (singular nerve) or occlusion of the affected (mainly posterior) semicircular canal. Of the two, posterior canal occlusion is favored based on symptom reduc- tion and complications [152]. Superior Canal Dehiscence Syndrome In superior canal dehiscence syndrome, sound- or pressure- induced dizziness with auditory symptoms of autophony, hyperacusis, or tinnitus results from a bony dehiscence of the superior semicircular canal. Surgical repair of the canal is the recommended treatment [120].
For patients with vestibular migraine or Ménière disease, vertigo attacks are unpredictable and difficult to control or avoid. The unpredictable, distressing experience may elevate patient anxiety over the next attack sufficiently to induce a secondary panic-like disorder, substantially adding to the psychologic burden [50]. Migraine and anxiety disorders share common genetic and environmental risk factors, and an interaction between migraine and anxiety is established. Auditory center, limbic system, and vestibular system interconnections may account for high rates of anxiety in patients with persistent tinnitus, fluctuating hearing loss, and vertigo symptoms in vestibular migraine or Ménière disease [50; 153]. Ménière Disease and Endolymphatic Hydrops The episodic vertigo, hearing loss, and tinnitus in Ménière disease is associated with endolymphatic hydrops in the labyrin- thine system of the affected ear [128]. Ménière disease should be viewed and managed as a chronic condition, and treatment is tiered by disease stage and severity [154]. Acute symptomatic relief does not address the underlying pathophysiology, and the clinical goal is to minimize recurrent vertigo attacks and hearing symptoms to prevent new or additional damage to vestibular structures [155]. First Tier Patients with Ménière disease are vulnerable to dietary and environmental factors that can impact hearing and balance. Triggers for Ménière disease may include high salt intake, caf- feine, alcohol, nicotine, stress, monosodium glutamate, and allergies. Patients who identify and avoid triggers may greatly reduce their Ménière disease symptoms [155]. Therefore, lifestyle modification is the cornerstone of first-tier treatment. Caffeine and nicotine are vasoconstrictors that may reduce microvascular flow in the labyrinthine system. Alcohol also causes fluid and electrolyte shifts that can stress a fragile ear. Smoking cessation and limiting daily intake to one caffeinated or alcoholic beverage are typically recommended [155]. When dietary and environmental changes fail to control the episodes, combinations of diuretic and as-needed vestibular suppressant/antiemetic agents are effective to control vertigo episodes in many patients, but do not protect hearing loss. Off-label use of sublingual lorazepam (0.5–1 mg up to four times per day) is anecdotally effective in achieving relief from acute vertigo attacks [155].
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Book Code: ANCCTX2027
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