Dizziness and Vertigo _________________________________________________________________________
Head Injury Blunt head trauma, blast injuries, whiplash, or barotrauma may lead to direct vestibular nerve injury, labyrinthine concussion, or mechanical disruption of inner ear membranes to result in an AVS presentation. Basal skull fracture and traumatic ver- tebral artery dissection should always be considered. TBI may cause post-concussion syndrome, typically with a combination of dizziness, headache, fatigue, and minor cognitive impair- ment, with dizziness the most common symptom in the first
Skew deviation is a vertical misalignment of the eyes due to imbalance in gravity-sensing vestibular pathways. Alternate eye cover testing checks for ability to maintain vertical alignment of the eyes. Have the patient gaze directly on a midline target (e.g., the examiner’s nose), then cover one eye, and the other, alternating back and forth every one to two seconds. Skew is shown by slight upward vertical correction on one side, and downward on the other side, appearing the moment the eye is uncovered. Horizontal movements are irrelevant; no vertical misalignment equals no skew. This test is very specific for central etiologies. The timing-and-trigger syndrome should be identified before targeting the exam, because the same clinical feature can predict a benign condition in one syndrome and a dangerous condition in another syndrome [6; 36]. ACUTE VESTIBULAR SYNDROME AVS is defined by acute-onset, persistent dizziness lasting days to weeks, sometimes with lingering sequelae. The temporal evolution at onset and progression during the first week is more important diagnostically than total illness duration. Many patients have an early peak in symptom severity, rapid symptom improvement over the first week, and gradual recov- ery over weeks to months. Unusual cases resolve in less than 48 to 72 hours [36]. Triggered AVS For diagnostic purposes, AVS is classified into acquired (postexposure/triggered) and spontaneous forms. Triggers in t-AVS refer to behavior or exposures that precipitate dizziness. Patients with AVS typically experience worsening of dizziness (exacerbation) with head movement. This feature can be con- fusing or misleading, as for example when triggered dizziness in a patient with vestibular neuritis or stroke is misdiagnosed as BPPV [8]. Triggered AVS results from trauma or toxic exposure and is typically diagnosed largely based on exposure history, which is usually obvious. The most common causes are blunt head injury or ingestion of prescribed or illicit drugs affecting the brainstem, cerebellum, or peripheral vestibular apparatus. Carbon monoxide exposure and acute toxicity is a rare but important consideration [36]. Most patients experience a single, acute attack resolving gradually over days to weeks following the exposure. Depend- ing on the nature of trauma or toxin, other symptoms (e.g., headache, altered mental status) may predominate. Rotatory vertigo, spontaneous nystagmus (when looking straight ahead), and head-motion intolerance may be absent or unimpressive if the pathologic effects are bilateral and relatively symmetric (as with most toxins) [36].
two post-injury weeks [36]. Drug Side Effects/Toxicity
Anticonvulsant side effects or toxicity are a frequent cause of dizziness and vertigo seen in the ED. As mentioned, ami- noglycoside toxicity is an established cause of acute bilateral vestibular failure. Gentamicin can cause profound, permanent loss of vestibular function with relatively spared hearing; toxic- ity may occur after just a single antibiotic dose. Patients usually show gait unsteadiness and oscillopsia (bouncing vision) while walking [36]. Spontaneous AVS Spontaneous AVS is defined as acute onset of persistent diz- ziness and vertigo associated with nausea or vomiting, gait instability, nystagmus, or head motion intolerance. A focused physical exam is often diagnostic, because patients are usually symptomatic at presentation [8]. Prototype causes include vestibular neuritis and labyrinthitis [10]. Possible dangerous causes include posterior circulation stroke of the cerebellum or brainstem (the most frequent), bacterial labyrinthitis, and labyrinthine stroke (much less frequent) [8; 36]. Peripheral causes of s-AVS are more common, but central causes are not infrequent and can be fatal if missed, especially with vertebro-basilar ischemia [18]. This would not be as con- cerning if patients with posterior circulation TIA or stroke presented with classical focal neurologic signs along with the vestibular symptoms of AVS, as the diagnosis would be straightforward [56; 106]. However, this is often not the case. The 1975 National Institutes of Health (NIH) recommenda- tion that isolated dizziness or vertigo not be considered a TIA persists as a standard teaching [107]. This has contributed to missed diagnoses of TIA and stroke, because many patients with posterior circulation TIA or stroke present with isolated dizziness or vertigo without focal neurologic signs [36; 106; 108]. Patients with s-AVS presenting to the ED with dizziness are at high risk (25%) for stroke. Of nearly 800,000 annual strokes in the United States, 18% are strokes in the posterior fossa (within the brainstem or cerebellum) and up to 70% present with dizziness [8; 18].
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