Dizziness is common, as reflected by the cost of assessing dizziness in U.S. emergency rooms, which reportedly exceeds $4 billion per year.1, 2 For many patients, the pathophysiology of dizziness will not be fully demonstrable by diagnostic tests. However, a systematic clinical approach allows for the identification of common forms of dizziness. Recognizing common patterns of dizziness helps narrow the differential diagnosis and identify which interventions for dizziness are most likely to succeed.
History and Physical Examination
Given a chief complaint of dizziness, significant effort must be made to determine what the patient’s experience actually is. The term dizziness is imprecise. It may signify vertigo, lightheadedness, disorientation, presyncope, mental confusion, generalized weakness, or postural instability. Complaints of dizziness generally have in common some disturbance in sense of position or motion. Almost invariably, such disturbances impact postural stability and gait, although the extent to which gait is involved varies.
Patients should be asked about their vision. The inner ear contributes to the control of eye position. In particular, the vestibular system keeps images stable on the retina. Failure of peripheral vestibular function causes instability of images during head motion (eg, while looking out the window of a moving vehicle or while walking), called oscillopsia.
It has been reported that improvements in the examination of dizzy patients would be expected to increase the safety and accuracy of the diagnostic process and reduce unnecessary use of expensive diagnostic tests.3
The clinician should look for spontaneous, unidirectional, predominantly horizontal nystagmus. If present, this suggests acute peripheral vestibulopathy, as described below. Posterior fossa brain lesions, in contrast, typically cause gaze-holding nystagmus or pure vertical nystagmus.
The head impulse test4 probes the vestibulo-ocular reflex, which is abnormal in multiple vestibular disorders. To perform this test, the patient fixates on the examiner’s nose with the patient’s head turned about 10° to the right or left of midline. The examiner then suddenly turns the patient’s head to 1 side or the other, through about 20°, exercising reasonable caution to avoid injury. Head impulses toward a damaged peripheral vestibular system cause passive movement of the eyes with the head followed by a corrective saccade away from the weak ear and back toward the intended direction of fixation.
In the dynamic visual acuity test of the vestibulo-ocular reflex, the examiner passively oscillates the head in the yaw/axial plane at about 2 Hz. If near vision worsens from baseline by more than 2 lines of vision, the test is abnormal.
Central nervous system lesions cause disturbances of gait and balance that frequently include excessively variable step length. In contrast, peripheral nerve lesions in the limbs, such as entrapment neuropathy, may cause abnormalities that repeat, machine like, from 1 gait cycle to the next.
The Romberg sign is a well-known sign of myelopathy with posterior column involvement.5 It is nonspecific and best viewed as evidence of visual dependence indicating functionally significant loss of proprioceptive or peripheral vestibular function.
Additional disorder-specific signs are discussed in greater detail below. The eye movement abnormalities discussed in this section are best learned by seeing them, which can be facilitated by online educational resources, such as the David Newman-Toker Neuro-Ophthalmology Collection within the Neuro-Ophthalmology Virtual Education Library.6
Clinical vestibular laboratory testing is beyond the scope of this review. The most widely available vestibular test is videonystagmography,7 which includes oculomotor testing, and the binaural, bithermal caloric test. A finding of significant caloric paresis is an indicator of vestibular hypofunction.
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-Gregory T. Whitman, MD
This article originally appeared in the December issue of The American Journal of Medicine.
