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This article reviews the basic concepts underlying the balance system, describes the information provided by dynamic posturography, and explains how the technique complements and expands on the information provided by traditional tests of vestibular function.
Vestibular compensation is an excellent model for the study of plasticity of the adult central nervous system. Therefore it has been the subject of several studies in humans and animals, which will be briefly summed up by the authors. Lesions of the labyrinth or vestibular neurectomy are immediately followed of postural and oculomotor disorders, as well as by dynamic deficits of the various vestibular reflexes (vestibulo-ocular and vestibulonucal reflexes). While the former problems always recede in all species, the restoration of the dynamic properties of vestibular reflexes largely depends upon the species considered, in particular for the vestibulo-ocular reflex. However, this function seems to recover the gain and phase it had prior to the lesion in both humans and monkeys. What is the neuronal substrate of these various deficits? Electrophysiological studies have demonstrated at the acute stage a symmetrical activity between the two vestibular nuclei: on the side of the lesion, the nucleus becomes inactive, while the resting discharge of the contralateral vestibular neurons is increased. Following compensation, symmetric activity is restored between both nuclei due to the regeneration of a new basic discharge in the deafferented neurons. The matter of vestibular compensation can therefore be formulated as follows: which mechanisms enable a central neuron inactivated du to the suppression of most of its excitatory afferences to recover a normal spontaneous activity? Several hypotheses, either pre- or postsynaptic, are currently put forward. Presynaptic hypotheses consider the role of the various afferences of the vestibular nuclei, ie. visual, proprioceptive, commissural, cerebellar and other afferences. In fact, the vestibular nuclei are not merely relays between the labyrinthine receptors and the nuclei of the oculomotor nerves, but actually form real sensorimotor integration centers. Besides the afferences from the vestibular nerve, they receive several other sorts of information, including visual and spinal proprioceptive inputs. An increase in the activity of these afferences, a sprouting of their axon collaterals, may favor the return to a normal basic discharge of the central vestibular neurons. The postsynaptic hypotheses involve either a change in the intrinsic membrane properties of the central vestibular neurons following the lesion, or an increase in the number of receptors located on their surface. More specifically, denervation supersensitivity of the glutamatergic receptors has been put forward as the possible origin of vestibular compensation.
Vascular compression of the vestibulocochlear (VIIIth) nerve may cause constant or recurrent positional vertigo, tinnitus, and/or hearing loss. At present the diagnosis is based upon history, physical findings, audiologic assessment, vestibular function testing, and auditory brainstem evoked responses. Delineation of the vascular and neural anatomy within the cerebellopontine angle (CPA) has not been part of the preoperative assessment. We recently treated a patient demonstrating the clinical features of this syndrome. A magnetic resonance imaging (MRI) study revealed a vascular loop of the anterior inferior cerebellar artery intimately associated with the VIIIth nerve at the porus acusticus. To better define the significance of this finding, we retrospectively reviewed the CPA neurovascular anatomy of 100 (200 sides) otherwise normal MRI scans performed for unrelated disorders. Vessels were identified on 59.9 percent of sides while nerves were seen on 40 percent of sides. Contact between vessel and nerve occurred on 12.5 percent of sides and when both nerve and vessels were seen concurrently, they were in contact 50 percent of the time. These findings may preclude the use of MRI as the definitive diagnostic test in the preoperative assessment of vascular VIIIth nerve compression.
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This article reports the results of a four-year follow-up study initiated in 1970 on the long-term effects of gentamicin and kanamycin use in newborn infants. Audiometric, vestibular, and psychometric evaluations were performed on gentamicin-treated, kanamycin-treated, and untreated, matched control infants and children. No substantial sensorineural hearing loss or vestibular dysfunction was identified in these patients that could be attributed to aminoglycoside therapy. Performances on the Illinois Test of Psycholinguistic Abilities, Beery Test of Visual Motor Integration, the Peabody Picture Vocabulary Test, and on fine and gross motor examinations were comparable for the three study groups.
The authors report on a series of 18 patients operated through the posterior fossa approach for selective vestibular neurectomy. The indication for surgery consisted of intractable vertigo in cases of Ménière's disease. Results were excellent with a 94% cure of vertigo and 100% improvement. Postoperative hearing results were good with 78% of patients maintaining their discrimination score and 94% their pure tone average threshold. The results and the advantages of this approach are discussed and compared with the known procedures as reported in the literature.
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The dramatic symptomatology of sudden loss of vestibular function alarms the patient and the physician who is consulted in an emergency situation. The continuous vertigo is often accompanied by marked autonomic symptomatology, so that heart and cerebral diseases as well as acute intoxication are often primarily diagnosed. The differential diagnosis, clinical features, course of the disease and treatment are presented in this study of 54 patients treated in our department between 1980 and 1985. Aetiology and pathogenesis are discussed on the basis of the literature.
The diagnosis of retrocochlear hearing impairment is mainly based on threshold tone decay, absence of the stapedius reflex, abnormal dichotic speech discrimination and ERA findings. A relatively poor discrimination for monosyllables with regressive understanding at high intensities can also indicate a neural or central lesion provided that the unaffected side has been correctly masked. ERA results mainly show a synchronisation disorder within the brain-stem, i.e. the J V-response is prolonged or cannot be recorded at all. The cortical response N1, however, corresponds to the subjective threshold except that in impairments of the cortex, the N1-response is worse than expected from the pure tone threshold. Representative examples are given.
Some vertiginous lesions producing nystagmus (e.g. acute vestibulopathy, benign paroxysmal postural vertigo and Ménière's disease) are well-defined diseases of purely labyrinthine origin. The possible place of a functional disorder of the vertebral joints on their etiology and pathogenesis, has been discussed, but is purely hypothetical. Since the lesion almost always reaches with reduced function of the vestibular apparatus, the course of the disease depends crucially on central compensation of the peripheral disorder of vestibular function. Investigations of the effect of a functional disorder of the vertebral joints on the central compensation of vestibular functional disorders have not been described previously. Our own observations show that a functional disorder of the vertebral joints can crucially impair central compensation of peripheral vestibular vertigo. The pathological mechanism of the impaired compensation is discussed, and diagnostic and therapeutic consequences explained.
After stapedectomy otoliths were displaced from the endolymphatic space to the cupula of the posterior semicircular canal and caused a paroxysmal benign positional nystagmus which lasted 18 months. The positional nystagmus demonstrated a rotatory component during the Hallpike manoeuvre. The paroxysmal benign nystagmus disappeared after transtympanic nerve neurectomy of the inferior branch of the vestibular nerve (Gacek 1974). This procedure is only recommended for vertigo lasting longer than 1 year. The current findings support the theory that cupulolithiasis is the cause of paroxysmal benign positional nystagmus which can occur after stapedectomy. The rotatory nystagmus is generated in the posterior semicircular canal.
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A critical review of neurophysiological literature is given about the part played by the neck proprioceptors in the regulation of vestibular functions. In comparison with vestibular and optokinetic influences the neck proprioceptors are of secondary importance. A critical review of the publications by the supporters of a cervical genesis of vertigo leads to the conclusion that "cervical nystagmus" must be proven before the concept of neck-triggered vertigo can be accepted. In relation to all forms of vertigo, vertigo induced by cervical disorder represents a very low percentage only.
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Pathological nystagmus may be spontaneous, positional, or gaze-evoked. Peripheral vestibular nystagmus is usually rotatory, the horizontal component being most prominent. It is - in contrast to a central vestibular nystagmus - strongly inhibited by fixation. Spontaneous congenital nystagmus is also prominent with fixation, but it can usually be distinguished from acquired fixation nystagmus based on its long duration, atypical waveforms and high frequency. Two general types of positional nystagmus can be identified on the basis of nystagmus regularity: static and paroxysmal. The most common variety of positional nystagmus is the so-called benign paroxysmal positional nystagmus, which in the majority of cases occurs as an isolated symptom of unknown cause. Gaze-evoked nystagmus, prominent with fixation, includes dissociated, rebound and gaze-paretic nystagmus forms. Symmetrical gaze-evoked nystagmus is most commonly produced by ingestion of certain drugs. Phenomena related to nystagmus include: amblyopic, voluntary, and convergence-retraction nystagmus, ocular dysmetria, ocular flutter, opsoclonus, ocular bobbing, and ocular myoclonus.
Prominent loops of the anterior inferior cerebellar artery in the cerebellopontine angle are found frequently during anatomic studies of this region. These vascular loops are suspected of causing hearing loss, tinnitus, and vertigo, and surgery has been advocated to separate the vascular loop from the eighth cranial nerve. Previous reports have described pathologic anatomy, surgical approaches, and results of treatment. In this study, we report the results of a uniform battery of audiometric and vestibular system test results administered to fifteen patients with prominent vascular loops in the internal auditory canal diagnosed by pneumo-CT. All patients were tumor suspects before CT because of unilateral (or asymmetric) tinnitus or hearing loss. Hearing losses ranged from mild to profound, and most were of a cochlear type with excellent speech discrimination. Only one-third of the patients had abnormal caloric tests, but spontaneous nystagmus was detected in all but one of the patients by photoelectric nystagmography. The wide range of audiometric and vestibular system test results probably reflects the complex interaction between the vascular loop and eighth cranial nerve, in which the loop exerts pressure on the nerve, and the nerve compromises inner ear circulation. Eighth nerve tumors and vascular loops produce similar symptoms, but a cochlear type of hearing loss with good speech discrimination and normal caloric testing should raise suspicion of a vascular loop. Pneumo-CT is an effective means of diagnosing vascular loops and differentiating them from other lesions of the cerebellopontine angle.
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