Dizziness, which is one of the most common symptoms of patients referred for neurological evaluation, comprises a variety of symptoms. Even though each symptom may have a different pathophysiologic mechanism and significance, the description is often vague and intriguing. Accordingly, understanding what is meant by "dizziness", which can manifest as presyncope, disequilibrium, oscillopsia, and vertigo, should be the first step in evaluating dizzy patients.1

Lightheadedness or presyncope is a sensation of impending loss of consciousness due to a momentary decrease in the cerebral blood flow. Patients experience presyncopal dizziness when rapidly standing up from a relaxed supine or seated position. It may occur with multiple sensory disturbances, orthostatic hypotension, and cardiac arrhythmias as well as hyperventilation syndrome and panic attacks.

Disequilibrium is an imbalance or unsteadiness experienced while standing or walking. It is caused by various factors including diminished vision, loss of vestibular function, defects in proprioception, and motor dysfunction from the central or peripheral nervous system. It also relates to nonvestibular syndromes such as visual vertigo, presyncopal faintness, or somatoform phobic postural vertigo.

Oscillopsia is the subjective illusion of visual motion. While vertigo occurs with the eyes open or closed, oscillopsia only occurs when the eyes are open. Patients with acquired nystagmus report spontaneous oscillopsia due to apparent motion of the visual scene from retinal slip. Patients with bilateral loss of the vestibulo-ocular reflex (VOR) frequently experience oscillopsia during head movements. Defects in eye movements due to inappropriate VOR cause retinal image motion during head motion.

Vertigo is the illusion of movements of oneself or the environment due to an imbalance of tonic neural activity in the vestibular-cortical pathway. Although patients usually report rotational vertigo, occasionally they describe a sensation of linear displacement or tilt. Vertigo is commonly exacerbated by head movements and accompanied by nausea and vomiting. Vertigo may be due to unilateral injury to the peripheral vestibular organs such as the labyrinth or vestibular nerve. It also results from damage to the central vestibular structures including the vestibular nuclei, vestibular thalamic nuclei, vestibular cortex, and cerebellum. While peripheral vestibular disorders are always characterized by a combination of perceptual, ocular motor, and postural symptoms and signs, central vestibular lesions may give rise to only some of them.

The primary aim of the bedside evaluation of a dizzy patient is the detection of any vestibular deficits. While the vestibular impairments can be readily determined in patients with acute vertigo, meticulous examination is required in those with chronic dizziness. When the vertigo is induced in certain circumstances, reproduction of those situations is important during the evaluation. One of the most important aims of the bedside evaluation, especially in acute vertigo, is to differentiate the central from peripheral vestibular pathologies. Peripheral vestibular disorders resulting from damage to the labyrinth or vestibular nerve are usually benign, despite the possible presence of severe dizziness. Conversely, central vestibular disorders may be fatal without prompt and proper management. The bedside neurotological examination should include evaluation both for static and dynamic vestibular imbalances. Due to an anatomical proximity, patients with dizziness often also exhibit ocular motor impairments, and so a comprehensive neurotological examination should include an evaluation of the eye movements.2 Recent studies have indicated that simple bedside examinations such as tests for head impulse, gaze-evoked nystagmus (GEN), and skew deviation can reliably predict a central pathology in patients with isolated vertigo.3,4

Bedside examination of dizzy patients should begin with observation of the head posture (i.e., tilt or turn) and ocular alignment. Dysfunction of the pupil and eyelid may aid central localization of the vestibulopathy, as in lateral medullary infarction (Wallenberg syndrome) with Horner syndrome. Ocular misalignment is frequent in central vestibulopathy, and should be determined in nine cardinal positions of the gaze, along with the range of eye movements.

The ocular tilt reaction (OTR) refers to the triad of head tilt, ocular torsion, and skew deviation (Fig. 1).5 The OTR is known to reflect unilateral or asymmetric dysfunction of the graviceptive pathways from the utricle. Skew deviation indicates a vertical misalignment of the eyes due to a supranuclear pathology.2 The presence of skew deviation may be inferred by vertical diplopia and can be confirmed by the cover test. This involves covering one eye and detecting a corrective vertical movement of the other eye to fixate the target, which indicates the presence of skew deviation. As a rule, the head is tilted toward the side of the lower eye and the ocular torsion occurs in the same direction with the upper poles of the eyes rotating to the lower eye.6 Since the graviceptive pathway responsible for the OTR is known to cross the midline just above the abducens nucleus level and ascend in the contralateral medial longitudinal fasciculus (MLF),7,8 lesions below the lower pons cause ipsiversive OTR, and more rostral lesions induce contraversive OTR. Cerebellar lesions may give rise to ipsi- or contraversive OTR depending upon the structures involved.9 Although it can occur in peripheral vestibular disorders, skew deviation observed in acute isolated vertigo more commonly indicates a central vestibular lesion.3

A tilt of the subjective visual vertical (SVV) is the most sensitive sign of vestibular tone imbalance in the roll plane.6 It may occur in lesions involving either the central or peripheral vestibular pathways. The bucket method is a simple and reliable bedside test for measuring a tilt of SVV,10 in which patients indicate the position of a bucket where the line on the bottom inside the bucket is estimated to be truly vertical while they sit upright and look into a plastic bucket. The examiner then measures the SVV tilt using an external scale as the angle that the line is off the true vertical.

The patterns of spontaneous nystagmus (when present) are most informative for evaluating patients with dizziness/vertigo.11 The proper evaluation of the spontaneous nystagmus requires observation of the direction and the effects of gaze on the intensity and direction of the nystagmus. In unilateral peripheral deafferentation, the spontaneous nystagmus is mixed horizontal-torsional beating away from the lesion side (Fig. 2).12 The nystagmus typically increases during the gaze in the direction of the spontaneous nystagmus, and decreases during the gaze in the opposite direction (Alexander's law) (Fig. 2).13 Since the peripheral vestibular nystagmus is markedly suppressed by visual fixation, proper observation of the nystagmus requires the removal of visual fixation using Frenzel glasses14 that have 20-diopter convex lenses to prevent fixation and to magnify eye motion, allowing a better observation of the eyes (Fig. 3). When Frenzel glasses are unavailable, an ophthalmoscope can be used to observe nystagmus without fixation. By observing the optic disc with a direct ophthalmoscope while the other eye is covered, the nystagmus can be examined without fixation.15 However, when determining the direction of the nystagmus, it should be borne in mind that the retina (optic disc) moves in the direction opposite to the cornea for horizontal and vertical nystagmus. Since the disc also moves vertically in torsional nystagmus, motion of the surrounding retinal vessels should be considered when determining the direction of the nystagmus. In torsional nystagmus the discs move in opposing directions vertically. The distinguishing features of peripheral and central nystagmus are summarized in Table 1.

In contrast, the direction and fixation effects are variable in central vestibular nystagmus. Accordingly, when the characteristics of nystagmus do not conform to those of peripheral vestibular nystagmus, it should be considered central.16-19 However, even unidirectional horizontal-torsional nystagmus suppressed by visual fixation should not be simply regarded as peripheral unless other findings, such as a positive head impulse test or caloric paresis, are indicative of peripheral vestibular lesions.

Various bedside maneuvers may induce nystagmus or modulate the preexisting spontaneous nystagmus. Even in patients with spontaneous nystagmus, the modulation pattern may disclose an underlying pathology or aid in diagnosis. In patients with compensated vestibulopathy, the induction of nystagmus by various maneuvers is crucial in disclosing the underlying vestibular imbalance.20

Unilateral loss of vestibular function leads to static imbalance due to a difference in the tonic discharges between the vestibular nuclei on the two sides, and decreased dynamic sensitivity during rotation due to deficits in the push-pull combination of the responses. Loss of dynamic sensitivity results in reduced VOR gain, which can be identified using bedside tests.

Saccades are rapid eye movements that shift the line of sight between successive points of fixation. The patient is instructed to fixate alternatively on two targets, such as the tip of a pen and the examiner's nose. Saccades can be examined in both the horizontal and vertical planes. The velocity, accuracy, and conjugacy of the saccades should be determined at the bedside. Peripheral vestibular lesions do not impair saccades. Horizontal saccadic slowing is generally caused by dysfunction of the paramedian pontine reticular formation or the structures located more distally in the neural circuits for horizontal saccades,62 while vertical saccadic slowing is often due to lesions involving the rostral interstitial nucleus of the MLF or more distal structures.63 In general, lesions involving the pons cause horizontal saccadic slowing, whereas lesions affecting the rostral midbrain cause vertical saccadic slowing. Internuclear ophthalmoplegia can also cause slow saccades and lagging of the adducting eye during attempted contraversive saccades. The slow adducting saccades can be easily detected by having the patient follow an optokinetic drum or tape. Rapid phases made by the eye on the lesion side are smaller and slower. Saccades may overshoot (hypermetria) or undershoot (hypometria) the target, and corrective saccades would follow. These saccadic dysmetria are often caused by lesions involving the cerebellum (especially the dorsal vermis) or its connections.64,65 A unilateral lesion in the dorsal cerebellar vermis mostly induces contralateral saccadic hypermetria and ipsilateral hypometria, while lesions involving the fastigial nucleus generate contralateral saccadic hypometria and ipsilateral hypermetria.64,65 Patients with Wallenberg syndrome make hypermetric saccades to the lesion side (ipsipulsion) due to lesions affecting the inferior cerebellar peduncle.66

Smooth pursuit is a slow eye movement that holds the image of a small moving target on the fovea. The patient is asked to track a small target moving slowly in the horizontal or vertical direction with the head still. Corrective catch-up saccades occur if the pursuit movement does not match the target velocity. Since many neural structures are involved generating a smooth pursuit, and various factors including age, medications, and alertness can influence pursuit eye movements, impaired pursuit generally does not allow either topographical or etiological classification.62 However, marked asymmetry of pursuit eye movements suggests a unilateral lesion along the pursuit pathway. Since patients with horizontal nystagmus may exhibit impaired smooth pursuit in the direction of the nystagmus, the evaluation of vertical smooth pursuit may be helpful in determining smooth pursuit deficits in acute vestibulopathy.67,68

The severity of imbalance and falling direction may provide important clues as to the underlying vestibular impairments.

A crucial aspect in the management of dizzy patients is differentiating central vestibular disorders from the more benign peripheral vestibular disorders. A thorough bedside examination and careful history taking remain the most important diagnostic tools for dizziness/vertigo. Subtle ocular signs such as GEN, skew deviation, and a normal head impulse test are useful for determining the occurrence of acute stroke in patients with acute dizziness/vertigo.