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Posturography is a method of measuring a patient's ability to control his balance. Currently available testing techniques may be useful to otologists, although they have not been shown to yield information beyond that obtained from other diagnostic procedures. More powerful techniques are under development, but methodologic problems remain, and none is yet ready for routine clinical use.
A selected review of the literature concerning different forms of pressure stimulation of the normal and abnormal vestibular labyrinth is presented. On the basis of this review, it can be stated that there are definite vestibular signs and symptoms associated with pressure stimulation. The exact mechanisms remain in doubt. The responses, however, appear to be mediated through the vestibular hair cells.
Perilymph fistulae present a diagnostic dilemma to the clinician. As yet, there is no readily available, widely accepted diagnostic test. Electrocochleography (ECoG), with the advent of extratympanic recording techniques, has become a clinically applicable probe of cochlear function. Clinical ECoG was used to study guinea pigs (n = 35) both before and after surgical fistulization (n = 18) or fistulization and repair (n = 17) of the round window membrane. The animals were killed, and histopathologic examination of the temporal bones was carried out 0, 1, 3, 4, 7, 10, 14, 21, and 28 days after surgery. Of the 33 animals that survived surgery, 30 demonstrated ECoG wave-forms. No significant difference between the preoperative and postoperative wave-forms could be detected. Histopathologic study showed rapid healing of the fistulae, with no evidence of hydrops. Although there appeared to be a relatively selective loss of the outer hair cells of the cochlear basal turn, autolysis precluded detailed analysis. ECoG, as performed clinically, does not appear to detect the presence, spontaneous healing, or repair of a round window membrane fistula in the guinea pig.
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Benign paroxysmal vertigo of childhood is a vestibular disorder characterized by multiple sudden brief episodes of true vertigo with nystagmus usually beginning after the age of 4. The diagnosis is based on the characteristic history, because the otologic and neurologic examinations, electronystagmogram, audiogram, and electroencephalogram are usually normal. The etiology of the disorder remains unknown, although a vascular disturbance of the posterior circulation with ischemia of the labyrinth or vestibular nuclei is most commonly postulated. A review of the literature and five new cases are used to acquaint otolaryngologists with this entity, review the characteristic clinical history, discuss differential diagnosis, and emphasize the usual clinical course.
The program of the electronystagmographic examinations in the pathology of the central nervous system contains 11 groups of tasks. Sixty signs of central impairments are listed, from which 26 nystagmic irregularities had a small diagnostic value. No sign occuring alone could be taken as pathognomonic, only a group of signs can be used for the impairment localization. Besides for the peripheral vestibular and the peripheral vestibulocochlear impairments, the authors succeeded to make a group containing pathogomonic signs for mixed vestibular impairments as well as for multiple sclerosis affecting vestibular structures.
Among 49 male workers, mean age 30 years, who had been working in conditions of extreme noise and vibration for between 6 months and 10 years vestibular disturbances could be shown (in the form of spontaneous nystagmus, lowered caloric excitability, or pathology in rotatory tests) in as high as 44.9%. The lesions were believed to have arisen in the peripheral vestibular organ as a consequence of the low frequency vibration.
In guinea pigs that had been treated with very large doses of the aminoglycoside amikacin (14 x 450 mg/kg/day, i.m.) clear, short-latency responses to various click stimuli could be recorded at the round window. When the same cochleas were examined histologically, no outer or inner hair cells could be found along the entire length of the basilar membrane, save for a very few outer hair cells remaining at the apex. The response patterns resembled that of the compound action potential, and various characteristics suggest that they were of neural origin. Vestibular function, investigated by electronystagmography during rotation, appeared normal, as did most of the saccular and utricular hair cells. Transmission electron microscopy revealed a significant number of cochlear nerve fibres still innervating the remnants of Corti's organ. In other cochleas with similarly extensive destruction induced by another aminoglycoside (sisomycin, 14 x 125 mg/kg/day, 15 days as well as 3 months post-Rx), no responses could be recorded from the round window. Cochleas that were less affected, with the upper turns preserved, gave only small, long-latency responses. These preliminary observations are confirmed by further experiments now in progress. They suggest that unless a considerable number of inner hair cells remained undetected in the lower basal turn, a possibility that appears highly unlikely, there was either a direct mechanical excitation of cochlear nerve fibres, or an acoustical stimulation of vestibular sense organs.
Assessment of postural control in vestibular deficient subjects with and without visual and ankle joint sway information permitted: 1) a quantitative assessment of the overall vestibular information used by the individual patient for control of upright posture; 2) an estimate of the extent to which the vestibular deficient subject can appropriately "select" and alternatively use visual and ankle joint somatosensory information for compensatory postural control and 3) quantification of adaptive changes in postural responses to visual and somatosensory inputs. Results from this study support the hypothesis that abnormal vestibular function disrupts the subject's reference to gravity (earth) vertical. This loss of an absolute spatial reference normally provided by vestibular input prevents the resolution of conflicting or inaccurate visual and somatosensory spatial references which may occur during active or passive body movements.
Observation of nystagmus is of great importance in the otoneurologic examination. By means of electronystagmography it is possible to examine the nystagmus under different visual conditions such as in darkness or with eyes closed. Physiological nystagmus is characterized by miniature eye movements with an amplitude of 4-5 minutes of one degree. With fixation, the amplitude decreases and the frequency increases. Vestibular nystagmus is a biphasic eye movement with slow and rapid phases of opposite directions. The intensity increases when the eye bulb is directed in the same direction as the fast phase or when fixation is hampered by darkness or eye closure. Nystagmus in which the fast phase changes direction according to the direction of gaze, i.e. gaze (paretic) nystagmus, can be congenital, but is often a result of paralysis of the eye muscles, of infection, intoxication or, if asymmetric in amplitude, of an acoustic neurinoma. Fixation nystagmus, miner's nystagmus, and nystagmus latens, is called optic nystagmus, and is thought to be caused by defects in the fixation mechanism. The main characteristic is that it changes direction if one or both eyes are closed and often interferes with the vestibular nystagmus. In the diagnosis of dizzy patients with optic nystagmus, the examination of the vestibular system must be carried out with other methods than nystagmus recordings.
The forward-backward and right-left sways in the upright standing posture were examined using stabilometry and analysis with a 5-dimensional feedback model. The forward-backward sway was found to have a fast, hidden periodicity, composed of sways due to a loss of the labyrinthine righting reflex upon the head and interaction between the head and knee sways. Furthermore, on the basis of our previous investigation, the forward-backward sway was found to depend on the increased spinal reflexes caused by a loss of labyrinthine inhibitory control upon the antigravity muscles. The right-left sway is slow and irregular, being mainly produced by disturbance of the head righting reflex.
In earlier studies of perilymphatic fistulae, we described their histologic criteria and the clinical criteria for the identification and prediction of patencies of the labyrinth capsule related to disorders of hearing and balance. These patencies were either of the fissula ante fenestram or of the round window niche-posterior canal ampulla fissure. The permeability of the fibrous core of a patent fissula ante fenestram has been questioned, authors of some earlier articles arguing that the tissue is loose, others that it is dense. This study demonstrates loose fibrous and cellular structure in the fissula's tract, dense collagen at the circumference. The loose arrangement of tissue suggests that fluid can pass through this patency, and it appears similar to that of the spiral ligament which has been shown to contain perilymph by way of intercellular communications with the perilymphatic space.
The effect of electric stimulation on vestibular compensation was studied in guinea pigs. Pharmacological labyrinthectomy was performed by injecting chloroform into the right middle ear under light ether anesthesia. The guinea pigs were divided into four groups: a control group which was not electrically stimulated after labyrinthectomy, a group stimulated with 0.6 mA square wave, a group stimulated with 0.3 mA square wave, and a group stimulated with 0.6 mA pulse wave. Electric stimulation, which started 1 h and 15 min after labyrinthectomy, was given through retroauricular electrodes. Nystagmus and head deviations were recorded and analyzed to assess the process of compensation at 1, 2, 3, 4, 5, 8, 12, 18 and 24 h after labyrinthectomy. Electrically stimulated groups, especially group 0.6 mA square wave and group 0.6 mA pulse wave, showed faster compensation in nystagmus and head-body deviation than the control group. Therefore, in this study, electric stimulation seemed to contribute favorably to vestibular compensation.
An extensive vestibular examination was carried out in a group of 29 noise-exposed technicians. A spontaneous nystagmus was found in 18 persons, and 24 had a positional nystagmus exceeding a velocity of the slow phase of 5 degrees/s in three or more positions. In 17 subjects a cervical nystagmus could be provoked, while a nystagmus preponderance of more than 20% in the rotation test was found in seven persons. A difference in excitability between the labyrinths of more than 20% was shown by seven subjects. None of the subjects showed pathology in the tests for central vestibular disorders. The technicians were divided into four groups, according to the severity of their hearing loss. No correlation was found between the grade of the hearing loss and the vestibular function disturbance. This can be explained in terms of the adaptive properties of the vestibular system. All subjects showed pathology in one or more of the vestibular tests. The medico-legal aspects of vestibular involvement in noise-induced hearing loss can be of some importance. Hearing loss itself does not affect work capability directly; however, a vestibular disorder might well do so. In consequence, noise-exposed individuals could be disabled because of vertigo or balance disorder--an important and perhaps neglected aspect of noise-induced hearing damage.
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