Medical Excellence- Issue 1

nose and to keep their head and neck loose. Then the examiner very quickly turns the patient’s head about 10–20 °, using a lateral to center motion. The normal (individuals with normal vestibu- lar function) response is that the patient’s focus will stay locked on the examiner’s nose. The presence of a corrective saccade (the eyes move with the head and then snap back in a fast corrective movement to the examiner’s nose) is a “positive” test (abnormal VOR), which generally indicates a peripheral process, usually vestibular neuritis. The absence of a corrective saccade in AVS is consistent with a stroke. It may seem counterintuitive that a normal finding predicts a dangerous disease. This is why the HIT is only useful in patients with the AVS and nystagmus. If an acutely dizzy patient with an AVS does not have nystagmus, it’s very unlikely to be vestibular, and therefore the HIT (which is meant to distinguish neuritis from stroke) becomes far less useful and usually misleading. Similarly, if the HIT were done in a patient with dizziness from urosepsis or dehydration, the test will be negative, i.e., worrisome for a stroke. Patients with cerebellar stroke have a negative (normal) HIT [30, 62]. This is because the circuit of the VOR does not loop through the cerebellum. On the other hand, occasional patients with posterior circulation stroke will have a falsely “positive” (abnormal) HIT, usually from a lateral brainstem infarct involv- ing the location where the vestibular nerve enters the brainstem. These strokes are uncommon and involve the anterior inferior cerebellar artery stroke (AICA) territory or an infarction directly involving the inner ear (labyrinthine stroke) itself. In both situ- ations, acute hearing loss usually occurs. Adding a bedside test of hearing (“HINTS plus”) will help to pick up the occasional AICA stroke [63]. This last point is important because traditional teaching is that if both hearing and dizziness coexist, the problem is peripheral (in the labyrinth). However, the blood supply to the labyrinth is due to ischemia of branches of the AICA, so this co-involvement of hearing and dizziness can occur from a stroke [64–66]. The relative frequency of this occurring from a periph- eral cause (true labyrinthitis) as opposed to stroke (AICA terri- tory) is unknown. A recent article with attached video clips reviews these phys- ical examination findings [27]. Because HINTS testing has not been fully validated when done by nonspecialists, I recommend adding two additional components of the HINTS testing—brain- stem and cerebellar testing and gait testing. Key elements include testing for pupillary function, facial motor and sensory symme- try, and dysarthria. Lateral medullary stroke (Wallenberg’s syn- drome), an important cause of the AVS, merits special attention. These patients have dysarthria, dysphagia, or hoarseness due to lower cranial neuropathy and may have Horner’s syndrome with mild ptosis and anisocoria that may only be evident in dim light (so that the normal larger pupil fully dilates, making the difference in pupil size more apparent) [67]. Common physical examination findings are hemifacial decreased pain and tem- perature sensation. Routine testing of only light touch can miss this finding. Finally, if all four initial components of the exam (nystag- mus, skew deviation, HIT, and general neurological exam) are nondiagnostic, gait testing must be performed. Ideally have the patient walk unassisted, but for patients too symptomatic to walk, test for truncal ataxia by asking the patient to sit upright in the stretcher without holding onto the side rails. A patient who cannot walk or sit up unassisted is unsafe for discharge, and an AVS patient who is unable to walk is more likely to have had a stroke than vestibular neuritis [30]. Imaging is not very useful in patients with the AVS. CT is a poor test for posterior circulation stroke [52–54]. MRI, even with DWI, misses 10–20% of strokes in AVS during the first 24–48 h [42, 55, 56]. In small brainstem strokes, MRI, with DWI, can still miss upward of 50% when tested within 48 h [56]. Table 4: Acute vestibular syndrome oculomotor physical findings. Oculomotor exam component Peripheral (usually vestibular neuritis) Central (usually posterior circulation stroke) Nystagmus (neutral gaze and gaze to the right and left) Dominantly horizontal and direction-fixed, beating away from the affected side Direction-changing horizontal or dominantly vertical and/or torsional and then central b (often mimics peripheral) Test of skew (alternate cover test) Normal vertical eye alignment (i.e., no skew deviation) Often mimics peripheral; if skew deviation is present, then central c Head impulse test (HIT) Unilaterally abnormal toward the affected side (presence of a corrective saccade) a Usually bilaterally normal (no corrective saccade) a Strokes in the anterior inferior cerebellar artery (AICA) territory may produce a unilaterally abnormal head impulse test that mimics vestibular neuritis, but hearing loss is usually present as a clue. If a patient has bilaterally abnormal HIT, this is also suspicious for a central lesion if nystagmus is present (AICA stroke or Wernicke’s syndrome) b Inferior branch vestibular neuritis will present with downbeat-torsional nystagmus, but this is a rare disorder. From the emergency medicine perspective, vertical nystagmus in a patient with an AVS patient should be considered to be central (a stroke) c Skew deviation, demonstrated by the bedside alternate cover testing, is very rare in peripheral vestibular cases; its presence should be considered to be central (a stroke, often in the brainstem) 8  |  Issue-1 MEDICAL EXCELLENCE