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This study examines the relation of hypoac tive labyrinths to the achievement of motor milestones such as sitting and walking. Two children with genetic sensorineural hearing losses with vestibular dysfunction who walked very late did not show any evidence to suggest a diffuse neurologic cause for this delay at follow-up examinations. A review of electronys tagmographic (ENG) vestibular tests of 353 children under age ten years discovered 17 children who had been tested twice or more. There was disagreement between the two tests in four (24%), suggesting less than adequate relia bility of ENG test results in infants and chil dren. Forty-nine children had hypoactive labyrinths. The records of 22 of these were suitable for surveying the relation of the vestibu lar dysfunction to age at walking. Ten of the 22 children walked at 18 months or later, indicating that some, but not all children with vestibular dysfunction will be late walkers. Some of the children who walked at a normal age were described as having "weak necks" or "floppy heads," and some sat late. Accordingly, counsel ing of parents of deaf children who walk late should be delayed until vestibular testing has been carried out to avoid false diagnoses of associated brain damage or mental retardation. It is urged that all deaf children undergo vestibular testing, and that those with abnormal tests be retested to make certain of the results. Procedures to test vestibular function in infants and children need to be standardized, as shown by personal observations and a survey of the pertinent literature.

Six weeks after cautery of the external endolymphatic duct orifice of elasmobranchs, histologic distention of the endolymphatic sac itself was produced. However, there was no demonstrable behavioral correlate in sharks or rays of associated vestibular dysfunction either immediately or up to six weeks postoperatively (documented by movies, including underwater). The unique anatomy of the endolymphatic system open to sea water via the external endolymphatic duct in elasmobranchs and ability to produce histologic evidence of hydrops indicate that this model system can be useful in study of inner ear fluid dynamics and of pathophysiology of hydrops. Paradoxically, this study strengthens conclusions made by Portmann in the 1920s about the importance of the endolymphatic sac and duct in inner ear fluid dynamics in elasmobranchs, even though we were unable to duplicate the behavioral effect.

Nystagmographic records from an unusual case of spontaneous nystagmus probably of the central vestibular type were presented, demonstrating that nystagmus under selected conditions reflects with exquisite sensitivity certain aspects of mental functioning. Something of the process or processes monitored seems to be communicated by what is popularly indicated by such terms as “concentration,” “mental activity,” and “mental effort” and are not adequately explained by such concepts as changes in “alertness” or “attention” and “release from a central inhibition.” The importance of these mental factors lies in the additional hazard they impose on the use of quantitative changes in nystagmus for neurological diagnosis. Studies using nystagmus to demonstrate vestibular dysfunction in patient groups characterized by less than optimal cooperation must be reassessed. The usefulness of this parameter in the future study of mental function is emphasized.

The clinical picture and the histological findings in a case of hydrops endolymphaticus cochleae is given. The case is remarkable because of an unusual degeneration of the first neurons in the apical turn of the right ear. There is also a beginning hydrops in the apical turn of the opposite ear. Neither clinically nor histologically could signs of a vestibular dysfunction be found. The findings are discussed.

The present study is based upon the results of repeated vestibular examinations under nystagmographic control, performed in a group of patients with strictly unilateral peripheral vestibular lesions. Central compensation of peripheral vestibular dysfunctions is relying upon two entirely different mechanisms. The first one is a specific vestibular phenomenon, depending on the integrity of the efferent vestibular system. It is termed ‘accommodation’, i.e. by means of the efferent fibers the responses from the remaining intact labyrinth are modulated, adjusting them to the functional deficiency (inhibition and facilitation). Accommodation is generally completed within a short time unless there is a lesion of the elements of the vestibular ganglion or an impairment of conductivity of the peripheral neuron. Functional disorders at the level of the vestibular ganglion or of the first neuron will implicate uncomplete and delayed accommodation. The second mechanism is a non specific central phenomenon, substituting the deficient vestibular functions by optic and somatosensory regulation. Hence the term centralcompensation should strictly speaking only be used for this particular phenomenon. It is depending upon the functional integrity of the central nervous system. For this reason traumatic and vascular lesions of the brain will delay the achievement of this compensatory mechanism according to the severity of the central disorder.

The authors reported a case of a 60-yearold female with cancer of petous pyra- mide which was metastatic from colon.She had a gastreintestinal trouble for about two pears.Several months ago she started to have deafness, vestibular dysfunction, facial nerve paralysis and trigeminal neuralgia.Operation was performed because of teh pyramide.The patient died on the 13th day after the operation Histological study revealed adenocarcinoma

Publisher Summary This chapter discusses the loss of auditory or vestibular function during or after decompression, which is an old and continuing concern in the diving community. It discusses the problem of vestibular dysfunction caused by decompression, possible causes of such malfunctions, and possible avenues of research. Most reports of vestibular problems in diving involve middle-ear squeeze during compression. The controlling half-time tissues and the pressure-time relationships in the caisson exposures are similar to those in our own deep dives, suggesting that these factors might conceivably account for the appearance of decompression-related vestibular and hearing symptoms in both instances. The sudden onset of vestibular symptoms during or after decompression naturally leads to the assumption that the etiology is decompression-related, and the odds favor such an assumption. Definitive knowledge about the pathophysiology of vestibular derangement will help to avoid and treat it more effectively when it does occur.

Studies by various workers over the last several decades have established the existence of many physiological changes in adult schizophrenia.1-4It has not been demonstrated that these changes are primary, however, or that they are of prognostic value. In this study we have investigated vestibular functioning in schizophrenic children. This area was chosen for several reasons. First, hyporeactivity and paradoxical vestibular reactions were reported in adult schizophrenics by Angyal.5In commenting on that study, Paul Schilder seemed convinced that organic changes in vestibular functioning were present in some adult schizophrenics.6 Second, there is a good deal of presumptive evidence that childhood schizophrenics have some problem in the area of vestibular functioning. Loretta Bender7has demonstrated space, time, and motion preoccupation in some schizophrenic children. A more recent study8has confirmed this. The importance of spontaneous whirling and toe

A series of 29 patients with the Arnold-Chiari malformation who had signs and symptoms related to the auditory and vestibular systems are analyzed, and four illustrative case reports are detailed. Although no consistent pattern emerged, these abnormalities may simulate other lesions, including acoustic neuromas. This disease should be considered in the neuro-otologic differential diagnosis. Hypotheses on the pathogenesis of the auditory and vestibular dysfunction include further stretching of the congenitally elongated nerves, bending of the eighth cranial nerve over the bony edge of the porus acusticus, and compression of brain-stem nuclei by displaced cerebellar tonsils.

SUMMARY Five epileptic patients who experienced vertiginous or showed rotatory phenomena during epileptic attacks were described. Peripheral vestibular stimulation was used as an activating EEG procedure. The observations described here, supported by data from the literature, led the author to the following conclusions: 1 Different abnormal EEG patterns, focal or generalized, besides temporal foci, may be found in connection with vertiginous and other epileptic manifestations of vestibular dysfunction. 2 In the observed cases with vertiginous and gyratory epileptic attacks no other EEG responses to the stimulation of the horizontal semicircular canals were seen, than otherwise occasionally observed in epileptic patients. The term “vestibulogenic seizures” therefore should be used with caution only in the sense of a reflex induction of an epileptic phenomenon. RESUME Cinq malades epileptiques qui presentaient des sensations vertigineuses ou des mouvements giratoires pendant leurs crises ont subi une “activation” par la stimulation vestibulaire peripherique. Les resultats obtenus s'accordent avec ceux de la litterature et permettent les conclusions suivantes: 1 Differentes anomalies EEGraphiques, focalisees ou generalisees, peuvent etre rencontrees en dehors des foyers temporaux chez ces malades. 2 La stimulation des canaux semi-circulaires horizontaux ne provoque chez ces malades aucune autre reponse EEGraphique que celle qui est provoquee de temps en temps chez d'autres malades epileptiques. Le terme de “crise vestibulogene” ne peut done etre utilise avec precaution que dans le but de designer la production reflexe d'un phenomene epileptique.

A toxic optic neuritis or a toxic neuritis of any other nerve has not previously been reported as occurring as a result of the administration of sulfanilamide or of any of the related drugs in man. Likewise manifestations of involvement of the central nervous system have been limited to the observation of mental confusion by Paton and Eaton, 1 and to the unamplified statement by Whitby 2 that he is familiar with one human case in which symptoms of involvement of the nervous system, such as occur in mice developed. In mice, according to Long and Bliss, 3 symptoms of vestibular dysfunction and spastic paralysis develop as a result of the administration of sulfanilamide. The majority of toxic manifestations that have resulted in human cases from the use of these drugs are concerned with the blood. They are cyanosis, 4 sulfhemoglobinemia (especially when some sulfate has been administered simultaneously 5