Chapter 022. Dizziness and Vertigo (Part 2)

Physiologic Vertigo This occurs in normal individuals when (1) the brain is confronted with an intersensory mismatch among the three stabilizing sensory systems; (2) the vestibular system is subjected to unfamiliar head movements to which it is unadapted, such as in seasickness; (3) unusual head/neck positions, such as the extreme extension when painting a ceiling; or (4) following a spin. Intersensory mismatch explains carsickness, height vertigo, and the visual vertigo most commonly experienced during motion picture chase scenes; in the latter, the visual sensation of environmental movement is unaccompanied by concomitant vestibular and somatosensory movement cues. Space sickness, a...
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Chapter 022. Dizziness and Vertigo (Part 2) Chapter 022. Dizziness and Vertigo (Part 2) Physiologic Vertigo This occurs in normal individuals when (1) the brain is confronted with anintersensory mismatch among the three stabilizing sensory systems; (2) thevestibular system is subjected to unfamiliar head movements to which it isunadapted, such as in seasickness; (3) unusual head/neck positions, such as theextreme extension when painting a ceiling; or (4) following a spin. Intersensorymismatch explains carsickness, height vertigo, and the visual vertigo mostcommonly experienced during motion picture chase scenes; in the latter, the visualsensation of environmental movement is unaccompanied by concomitantvestibular and somatosensory movement cues. Space sickness, a frequent transienteffect of active head movement in the weightless zero-gravity environment, isanother example of physiologic vertigo. Pathologic Vertigo This results from lesions of the visual, somatosensory, or vestibularsystems. Visual vertigo is caused by new or incorrect eyeglasses or by the suddenonset of an extraocular muscle paresis with diplopia; in either instance, centralnervous system (CNS) compensation rapidly counteracts the vertigo.Somatosensory vertigo, rare in isolation, is usually due to a peripheral neuropathyor myelopathy that reduces the sensory input necessary for central compensationwhen there is dysfunction of the vestibular or visual systems. The most common cause of pathologic vertigo is vestibular dysfunctioninvolving either its end organ (labyrinth), nerve, or central connections. Thevertigo is associated with jerk nystagmus and is frequently accompanied bynausea, postural unsteadiness, and gait ataxia. Since vertigo increases with rapidhead movements, patients tend to hold their heads still. Labyrinthine Dysfunction This causes severe rotational or linear vertigo. When rotational, thehallucination of movement, whether of environment or self, is directed away fromthe side of the lesion. The fast phases of nystagmus beat away from the lesionside, and the tendency to fall is toward the side of the lesion, particularly indarkness or with the eyes closed. Under normal circumstances, when the head is straight and immobile, thevestibular end organs generate a tonic resting firing frequency that is equal fromthe two sides. With any rotational acceleration, the anatomic positions of thesemicircular canals on each side necessitate an increased firing rate from one and acommensurate decrease from the other. This change in neural activity is ultimatelyprojected to the cerebral cortex, where it is summed with inputs from the visualand somatosensory systems to produce the appropriate conscious sense ofrotational movement. After cessation of prolonged rotation, the firing frequenciesof the two end organs reverse; the side with the initially increased rate decreases,and the other side increases. A sense of rotation in the opposite direction isexperienced; since there is no actual head movement, this hallucinatory sensationis physiologic postrotational vertigo. Any disease state that changes the firing frequency of an end organ,producing unequal neural input to the brainstem and ultimately the cerebral cortex,causes vertigo. The symptom can be conceptualized as the cortex inappropriatelyinterpreting the abnormal neural input as indicating actual head rotation. Transientabnormalities produce short-lived symptoms. With a fixed unilateral deficit,central compensatory mechanisms ultimately diminish the vertigo. Sincecompensation depends on the plasticity of connections between the vestibularnuclei and the cerebellum, patients with brainstem or cerebellar disease havediminished adaptive capacity, and symptoms may persist indefinitely.Compensation is always inadequate for severe fixed bilateral lesions despitenormal cerebellar connections; these patients are permanently symptomatic whenthey move their heads. Acute unilateral labyrinthine dysfunction is caused by infection, trauma,and ischemia. Often, no specific etiology is uncovered, and the nonspecific termsacute labyrinthitis, acute peripheral vestibulopathy, or vestibular neuritis are usedto describe the event. The vertiginous attacks are brief and leave the patient withmild vertigo for several days. Infection with herpes simplex virus type 1 has beenimplicated. It is impossible to predict whether a patient recovering from the firstbout of vertigo will have recurrent episodes. Labyrinthine ischemia, presumably due to occlusion of the labyrinthinebranch of the internal auditory artery, may be the sole manifestation ofvertebrobasilar insufficiency (Chap. 364); patie ...