Chapter 022. Dizziness and Vertigo (Part 3)

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Recurrent unilateral labyrinthine dysfunction, in association with signs and symptoms of cochlear disease (progressive hearing loss and tinnitus), is usually due to Ménière's disease (Chap. 30). When auditory manifestations are absent, the term vestibular neuronitis denotes recurrent monosymptomatic vertigo. Transient ischemic attacks of the posterior cerebral circulation (vertebrobasilar insufficiency) only infrequently cause recurrent vertigo without concomitant motor, sensory, visual, cranial nerve, or cerebellar signs (Chap. 364). Positional vertigo is precipitated by a recumbent head position, either to the right or to the left. Benign paroxysmal positional (or positioning) vertigo (BPPV) of the posterior semicircular canal is particularly common. Although the condition...

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Chapter 022. Dizziness and Vertigo (Part 3) Recurrent unilateral labyrinthine dysfunction, in association with signs and symptoms of cochlear disease (progressive hearing loss and tinnitus), is usually due to Ménière's disease (Chap. 30). When auditory manifestations are absent, the term vestibular neuronitis denotes recurrent monosymptomatic vertigo. Transient ischemic attacks of the posterior cerebral circulation (vertebrobasilar insufficiency) only infrequently cause recurrent vertigo without concomitant motor, sensory, visual, cranial nerve, or cerebellar signs (Chap. 364). Positional vertigo is precipitated by a recumbent head position, either to the right or to the left. Benign paroxysmal positional (or positioning) vertigo (BPPV) of the posterior semicircular canal is particularly common. Although the condition may be due to head trauma, usually no precipitating factors are identified. It generally abates spontaneously after weeks or months. The vertigo and accompanying nystagmus have a distinct pattern of latency, fatigability, and
habituation that differs from the less common central positional vertigo (Table 22- 1) due to lesions in and around the fourth ventricle. Moreover, the pattern of nystagmus in posterior canal BPPV is distinctive. When supine, with the head turned to the side of the offending ear (bad ear down), the lower eye displays a large-amplitude torsional nystagmus, and the upper eye has a lesser degree of torsion combined with upbeating nystagmus. If the eyes are directed to the upper ear, the vertical nystagmus in the upper eye increases in amplitude. Mild dysequilibrium when upright may also be present. Table 22-1 Benign Paroxysmal Positional Vertigo and Central Positional Vertigo Features BPPV Central Latencya 3–40 s None: immediate vertigo and nystagmus Fatigabilityb Yes No Habituationc Yes No
Intensity of vertigo Severe Mild Reproducibilityd Variable Good a Time between attaining head position and onset of symptoms. b Disappearance of symptoms with maintenance of offending position. c Lessening of symptoms with repeated trials. d Likelihood of symptom production during any examination session.A perilymphatic fistula should be suspected when episodic vertigo is precipitated by Valsalva or exertion, particularly upon a background of a stepwise progressive sensory-neural hearing loss. The condition is usually caused by head trauma or barotrauma or occurs after middle ear surgery. Vertigo of Vestibular Nerve Origin This occurs with diseases that involve the nerve in the petrous bone or the cerebellopontine angle. Although less severe and less frequently paroxysmal, it has many of the characteristics of labyrinthine vertigo. The adjacent auditory division of the eighth cranial nerve is usually affected, which explains the frequent association of vertigo with unilateral tinnitus and hearing loss. The most common cause of eighth cranial nerve dysfunction is a tumor, usually a schwannoma
(acoustic neuroma) or a meningioma. These tumors grow slowly and produce such a gradual reduction of labyrinthine output that central compensatory mechanisms can prevent or minimize the vertigo; auditory symptoms are the most common manifestations. Central Vertigo Lesions of the brainstem or cerebellum can cause acute vertigo, but associated signs and symptoms usually permit distinction from a labyrinthine etiology (Table 22-2). Occasionally, an acute lesion of the vestibulocerebellum may present with monosymptomatic vertigo indistinguishable from a labyrinthopathy.Table 22-2 Features of Peripheral and Central Vertigo Sign or Peripheral Central Symptom (Labyrinth) (Brainstem or Cerebellum) Direction of Unidirectional; fast Bidirectional or associated nystagmus phase opposite lesiona unidirectional Purely Uncommon Common horizontal nystagmus
without torsional component Vertical or Never present May be present purely torsional nystagmus Visual fixation Inhibits nystagmus No inhibition and vertigo Severity of Marked Often mild vertigo Direction of Toward fast phase Variable spin Direction of fall Toward slow phase Variable Duration of Finite (minutes, days, May be chronic symptoms weeks) but recurrent
Tinnitus and/or Often present Usually absent deafness Associated None Extremely common CNS abnormalities (e.g., diplopia, hiccups, cranial neuropathies, dysarthria) Common BPPV, infection Vascular, causes (labyrinthitis), Ménière's, demyelinating, neoplasm neuronitis, ischemia, trauma, toxin