The multisensory physiological and pathological vertigo syndromes

Abstract

Vertigo occurs with either physiological stimulation or pathological dysfunction of any of the three stabilizing sensory systems: vestibular, visual, and somatosensory. The physiological syndromes, induced by intersensory or intrasensory mismatches, include motion sickness and space sickness as well as height, visual, somatosensory, auditory, head-extension, and bending-over vertigo. This review emphasizes the relationship between these physiological forms of vertigo and the pathological clinical vertigo syndromes.Brandt T, Daroff RB: The multisensory physiological and pathological vertigo syndromes.Ann Neurol 7:195-203, 1980 Vertigo is usually defined as a hallucination of movement secondary to a vestibular disturbance. Such a definition is, in our judgment, too restrictive, and we believe that a more useful and comprehensive definition is displeasing distortion of static gravitational orientation or erroneous perception of either self or object motion. Physiological vertigo usually implies a mismatch among inputs from the sensory systems subserving static and dynamic spatial orientation as well as posture: vestibular, visual, and somatosensory. These systems are mutually interactive and redundant, in that posture and locomotion are guided by simultaneous reafferent vestibular, visual, and somatosensory cues [23]. The functional ranges of the individual systems overlap, enabling them to compensate partially for each other's deficiencies.The intensity of vertigo is a function of the magnitude of the mismatch and is increased if the intact sensory systems are eliminated, such as with eye closure during pathological vestibular vertigo.Vertigo may thus be induced by physiological stimulation or pathological dysfunction of any of the stabilizing sensory systems. The symptoms of vertigo include sensory qualities identified as vestibular, visual, and somatosensory. As distinct from one's perception of self motion during natural locomotion, the vertigo experience is linked to impaired perception of a stationary environment; this perception is mediated by central nervous system processes known as "space constancy mechanisms." Loss of the outside stationary reference system required for orientation and postural regulation contributes to the distressing admixture of both self and surround motion.We review vertigo in this paper, emphasizing the parallelism between the physiological and pathological syndromes. Readers are referred to several recent reviews for fuller discussion of the specific pathological vestibular disorders [ 2 , 4 , 24, 33, 401. Physiological and clinical vertigo syndromes are commonly characterized by a combination of phenomena involving perceptual, oculomotor, postural, and vegetative manifestations: vertigo, nystugmus, ataxia, and nausea (Fig 1). These four manifestations correlate with different aspects of vestibular function and emanate from different sites within the central nervous system. The vertigo itself is consequent to a disturbance of cortical spatial orientation. Nystagmus is seconda...

Neuronal Mechanisms and the Treatment of Motion Sickness

“…Motion sickness is caused by certain types of motion and is induced during passive locomotion in vehicles, generated by unfamiliar body accelerations, to which the person has not adapted, or by an intersensory conflict between vestibular and visual stimuli [1]. Motion sickness indiscriminately affects air, sea, road and space travelers.…”

Acute Isolated Uvular Infarction

“…Acute unilateral vestibular paralysis causes mixed horizontal and torsional nystagmus beating to the contralesional side, and perception of apparent body motion directed away from the side of the lesion. These result in falling toward the lesional side due to the compensatory vestibulospinal reaction [8]. Disturbed otolithic signals and a loss of spatial orientation with respect to gravity due to damage to the uvula may have contributed to the severe postural imbalance in our patient.…”

Deficient high-acceleration vestibular function in patients with polyneuropathy

“…Average ages of patients with predominantly axonal (66 Ϯ 10 y; n ϭ 18, 8 women) and patients with predominantly demyelinating PNP (65 Ϯ 13 y; n ϭ 19, 4 women) were similar. Average duration of symptoms, as recorded in the medical histories, was 6.7 Ϯ 5.5 years (range [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Abnormal clinical findings on patients with PNP included the following: 1) unilaterally (n ϭ 12) or bilaterally (n ϭ 10) abnormal bedside headimpulse tests; 2) stand and gait ataxia (n ϭ 29); 3) sensory deficits (touch: n ϭ 37; pain: n ϭ 33; temperature; n ϭ 33; position: n ϭ 19; vibration: n ϭ 25); and 4) abnormal motor signs (muscle atrophy: n ϭ 20; muscle weakness: n ϭ 19; hyporeflexia or areflexia: n ϭ 33 patients).…”

“…1 Additional vestibular impairment, however, could also play a role, i.e., imbalance in patients with PNP may be multisensory. 2 From a therapeutic perspective, the recognition of such an additional vestibular impairment is pivotal, because therapeutic strategies focusing on vestibular rehabilitation are able to improve postural stability. [3][4][5] So far, a concomitance of peripheral neuropathy and vestibular impairment as determined by caloric irrigation has been described in two populations of patients with PNP.…”