HISTORY

Vertigo, strictly defined, refers to an hallucination of movement. When the symptom complex is of spinning or rotation, the cause is almost always the inner ear or peripheral vestibular system. Although it is true that some patients experience a definite sense of environmental spin or self-rotation, the majority do not present solely with true spinning vertigo. The most common complaint is one of dizziness, a term that represents a variety of symptoms (Table 1):

The examiner should elicit an exact description of what the patient is experiencing. Is it a spinning sensation that could be characterized as vertigo, pointing to the peripheral vestibular apparatus? Is it a sensation of falling without rotation? Is it a sensation of unsteadiness or imbalance? Is there a particular direction in which the patient tends to fall? When the patient's complaint is actually of incoordination or clumsiness, the cause may be cerebellar dysfunction or peripheral neuropathy. When the symptom complex is of "lightheadedness" or "swimmy-headedness," the examiner should think of presyncope or syncope and consider systemic factors such as postural hypotension, vasodepressor syncope, or cardiac arrhythmia.

After trying to define the true qualitative nature of the symptom complex, one must proceed to a consideration of temporal factors. Is the patient's experience a continuous one? Are there episodes of severe symptomatology with symptom-free intervals? If the symptoms are episodic, do they occur only when the patient is upright?

Patients often have difficulty describing their symptoms. Initially, it is important that patients provide their own description before the examiner biases the outcome by suggesting descriptive phrases. Some patients are asked to describe their symptoms without using the word dizziness cannot further characterize the symptoms.

In addition to determining whether the symptom complex is episodic, one should define duration, length of symptoms, and any associated complaints such as tinnitus, hearing loss, double vision, slurred speech, numbness, or paralysis. A history of episodic disequilibration accompanied by diplopia, slurred speech, perioral numbness, dimming of vision, and occasional drop attacks would suggest transient vertebrobasilar ischemia (Troost-1995, Bradley-Daroff Chapter 18). Are there associated symptoms such as headache, and have these occurred at earlier times in life? If the patient had experienced severe episodes of imbalance in early life, followed by occipital or generalized headaches, especially throbbing, the history would be suggestive of basilar artery migraine. Did the dizziness follow head trauma, a systemic illness accompanied by aminoglycoside antibiotic therapy, or a mild upper respiratory infection? Episodic positional vertigo with brief episodes of spinning while turning over in bed is suggestive of a common condition, benign paroxysmal positional vertigo (BPPV) (Troost & Patton, 1992). Did the symptom complex occur following ear surgery or infection, deep-sea diving, or a concussive blow to the ear? Such a history, with or without hearing loss, would suggest a perilymph fistula.

There are a significant number of patients whose balance disorder is aggravated or even caused by anxiety. If the symptom of disequilibration or dizziness is of long duration, it is often difficult to tell whether the symptom complex is caused by anxiety or depression or whether the anxiety or depression are secondary to the dizziness. One always tries to make a positive diagnosis of a neurosis or chronic anxiety disorder based upon other symptomology and historical information. There may be a history of previous episodes of serious depression or anxiety attacks, and these should be elucidated before arriving at the conclusion that dizziness is secondary to anxiety.

Neurologists and neuro-otologists follow a large number of patients with chronic vertiginous sensations who remain undiagnosed. These patients complain of constant or intermittent disequilibration, often aggravated by position change, as well as by visual stimuli such as moving traffic, patterned wallpaper, or by passing food displays in supermarkets. Many of these patients have become agoraphobic; they hesitate to leave their homes, and particularly fear driving a car that will be passed by other automobiles. Some of these persons have had a single attack of acute peripheral vestibulopathy but have never made appropriate central compensation or adapted to their peripheral abnormality. Although mechanisms for compensation remain unclear, the majority of patients, particularly those younger than 30, rapidly recover from an acute peripheral vestibulopathy. Elderly patients or patients with a previously existing intrinsic brainstem abnormality, will rarely make adequate compensation for an acute peripheral vestibulopathy. These patients continue to complain of severe disequilibration and have exacerbated symptoms with a variety of visual inputs. They often have completely normal examinations and vestibular tests.

Figures 1 and 2 illustrate what might happen following an acute peripheral vestibular abnormality.
Figure 1:
Figure 1 (Left) Vestibular afferent input during normal horizontal head rotation to the right. Increased firing rate from right peripheral vestibular apparatus. Ocular deviation shows slow phase deviation to the left. VN = vestibular nuclei. (Adapted from Baloh 1984 and Daroff 1977). (Right) Acute left peripheral vestibulopathy with resultant acute vertiginous sensation simulating head rotation to the right. Slow phase ocular deviation to the left (small arrow) and fast phase of nystagmus to the right (bold arrow) and away from the side of the peripheral vestibular injury.

Figure 2:

Figure 2 (Left) Normal adaptation for prior left peripheral vestibulopathy. Despite a reduced firing rate from the left side, the central nervous system (CNS) has compensated for the disparity and there is no nystagmus or vertigo. (Right) Abnormal compensation for prior left peripheral vestibulopathy. The patient continues to experience vertiginous sensations and may have nystagmus with a fast phase to the right (solid arrow).

In some individuals, as diagrammed in the right-hand panel of Figure 2, there is decreased ability to compensate for peripheral vestibular abnormality. One possibility would be a congenital inability to make CNS compensation, but others include: (1) an acquired central inability to compensate due to CNS lesions as from multiple sclerosis or previous brainstem stroke, (2) a fluctuating peripheral vestibular problem, as in Meniere's disease, (3) relative inactivity without much afferent input, and (4) a peripheral vestibular apparatus providing inaccurate, although non-fluctuating afferent information. Careful history taking may reveal childhood meningitis, a remote head injury, or particular susceptibility to motion sickness in childhood. An explicit search during history taking should be made to define these possibilities.