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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...
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...
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