Bedside evaluation of dizzy patients

Abstract

In recent decades there has been marked progress in the imaging and laboratory evaluation of dizzy patients. However, detailed history taking and comprehensive bedside neurotological evaluation remain crucial for a diagnosis of dizziness. Bedside neurotological evaluation should include examinations for ocular alignment, spontaneous and gaze-evoked nystagmus, the vestibulo-ocular reflex, saccades, smooth pursuit, and balance. In patients with acute spontaneous vertigo, negative head impulse test, direction-changing nystagmus, and skew deviation mostly indicate central vestibular disorders. In contrast, patients with unilateral peripheral deafferentation invariably have a positive head impulse test and mixed horizontal-torsional nystagmus beating away from the lesion side. Since suppression by visual fixation is the rule in peripheral nystagmus and is frequent even in central nystagmus, removal of visual fixation using Frenzel glasses is required for the proper evaluation of central as well as peripheral nystagmus. Head-shaking, cranial vibration, hyperventilation, pressure to the external auditory canal, and loud sounds may disclose underlying vestibular dysfunction by inducing nystagmus or modulating the spontaneous nystagmus. In patients with positional vertigo, the diagnosis can be made by determining patterns of the nystagmus induced during various positional maneuvers that include straight head hanging, the Dix-Hallpike maneuver, supine head roll, and head turning and bending while sitting. Abnormal smooth pursuit and saccades, and severe imbalance also indicate central pathologies. Physicians should be familiar with bedside neurotological examinations and be aware of the clinical implications of the findings when evaluating dizzy patients.

Keywords: bedside examination; dizziness; head impulse test; nystagmus.

Fig. 1

The ocular tilt reaction (OTR). The OTR refers to the head tilt, ocular torsion, and skew deviation that are ascribed to asymmetry in the otolithic pathway from the utricle. The head tilt and ocular torsion occur toward the hypotropic eye.

Fig. 2

Nystagmus in left peripheral vestibulopathy. In unilateral peripheral vestibular deafferentation, mixed torsional-horizontal nystagmus beating occurs toward the intact side. The nystagmus typically increases during the gaze in the direction of nystagmus and decreases during the gaze in the opposite direction (Alexander's law), but never changes direction.

Fig. 3

Frenzel glasses remove visual fixation using 20-diopter convex lenses, and facilitate the detection of nystagmus by magnifying the eyes.

Fig. 4

The Dix-Hallpike maneuver for benign paroxysmal positional vertigo involving the right posterior semicircular canal (PC). After seating the patient upright (A), the head is turned 45° in the direction of the involved ear (B: right ear in this figure). The patient is then moved from the sitting to the supine position, ending with the head hanging at 20° off the end of the examination table (C). The corresponding illustrations demonstrate the orientation of the semicircular canals and location of the otolithic debris in the PC (viewed from the patient's right side).

Fig. 5

Side-lying test for diagnosis of right posterior canal benign paroxysmal positional vertigo. After seating the patient on the examination table (A), the head is turned 45° away from the involved ear (B). The patient then lies on the side of the involved ear (C). The corresponding illustrations demonstrate the orientation of the semicircular canals and location of the otolithic debris in the posterior canal (viewed from the front).

Fig. 6

Supine roll test in geotropic benign paroxysmal positional vertigo involving the right horizontal canal. The head is turned about 90° to each side while supine. The corresponding illustrations demonstrate the migration of the otolithic debris in the horizontal canal in each position (arrows), and the direction of the induced nystagmus.

Fig. 7

Supine roll test in apogeotropic benign paroxysmal positional vertigo involving the right horizontal canal. When the head is turned about 90° to each side while supine, deflection of the cupula due to attached otolithic debris induces apogeotropic nystagmus (arrows).

Fig. 8

Head impulse test. A: In healthy subjects, a head impulse (arrow) normally induces a rapid compensatory eye movement in the opposite direction, and steady fixation is attained. B: In patients with unilateral peripheral vestibular hypofunction, a head impulse toward the affected side (large arrow) produces a corrective saccade (small arrows) after head rotation since the eyes move with the head due to a defective vestibulo-ocular reflex, and lose the target with the head rotation.