1.11 Vertigo ("Dizzy, lightheaded")

Presentation

This may be a nonspecific complaint which must be refined further into either an altered somatic sensation (giddiness, wooziness); orthostatic blood pressure changes (lightheadedness, sensation of fainting); or the sensation of the environment (or patient) spinning (true vertigo). In inner ear disease, vertigo is virtually always accompanied by nystagmus, which is the ocular compensation for the unreal sensation of spinning; but the nystagmus may be extinguished when the eyes are open and fixed on some point (by the same token, vertigo is usually worse with the eyes closed). Nausea and vomiting are common accompanying symptoms, but less common (depending on the underlying cause) are hearing changes, tinnitus, cerebellar or adjacent cranial nerve impairment.

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Discussion

In general, the more violent and spinning the sensation of vertigo, the more likely the lesion if peripheral. Central lesions tend to cause less intense vertigo and more vague symptoms. Peripheral etiologies of vertigo or nystagmus include irritation of the ear (utricle, saccule, semi- circular canals) or the vestibular division of the eighth cranial (acoustic) nerve by toxins otitis, viral infection, or cerumen or a foreign body against the tympanic membrane. The term "labyrinthitis" should be reserved for vertigo with hearing changes, and "vestibular neuronitis" for the common short-lived vertigo without hearing changes usually associated with viral upper respiratory infections. Paroxysmal positional vertigo may be related to dislocated otoconia in the utricle and saccule. If it occurs following trauma, suspect a basal skull fracture with leakage of endolymph or perilymph, and consider otolaryngologic referral for further evaluation and positional Central etiologies include multiple sclerosis, temporal lobe epilepsy, basilar migraine and hemorrhage in the posterior fossa. A slow-growing acoustic neuroma in the cerebellopontine angle usually does not present with acute vertigo but rather a progressive unilateral hearing loss with or without tinnitus. The earliest sign is usually a gradual loss of auditory discrimination.

Vertebrobasilar arterial insufficiency can cause vertigo, usually with associated nausea, vomiting and cranial nerve or cerebellar signs. It is commonly diagnosed in dizzy pateints who are older than 50, but more often than not the diagnosis is incorrect. The brainstem is a tightly-packed structure in which the vestibular nuclei are crowded in with the oculomotor nuclei, the medial longitudinal fasiculus, cerebellar, sensory and motor pathways. It would be unusual for ischmia to produce only vertigo without accompanying diplopia, ataxia, sensory or motor disturbance. Although vertigo may be the major symptom of an ischemic attack, careful questioning of the patient commonly uncovers symptoms implicating involvement of other brainstem structures. Objective neurologic signs should be present in frank infarction of the brainstem.

Either central or peripheral nystagmus can be due to toxins, most commonly alcohol, tobacco, aminoglycosides, minocycline, disopyramide, phencyclidine, phenytoin, benzodiazepines, quinine, quinidine, aspirin, salicylates, non- steroidal anti-inflammatories and carbon monoxide. Nystagmus occuring in central nervous system disease may be vertical and disconjugate, whereas inner ear nystagmus never is. Central nystagmus is gaze-directed (beats in the direction of gaze) whereas inner ear nystagmus is direction-fixed (beats in one direction regardless of the direction of gaze). Central nystagmus is brought out by visual fixation, which supressed inner ear nystagmus.

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