Physiologie und Klinik des vestibulären systems

Kornhuber, H. H.

doi:10.1007/bf02594460

Cited by 10 publications

(17 citation statements)

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“…Smith (1963), Jung andKornhuher (1964), andKornhuber (1966) report that the absence of vertical OKN may be most frequently ascribed to bilateral lesions of the mesodiencephalon. In addi tion, it has been ascertained that the cases with abnormalities in vertical gaze manifest defective vertical OKN (Davidoff et al, 1966).…”

Section: Discussionmentioning

confidence: 99%

Neurotological Studies upon Intoxication by Organic Mercury Compounds

Mizukoshi¹,

Nagaba²,

Ohno³

et al. 1975

ORL

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In 1965, a strange illness, which afterwards was diagnosed as the intoxication caused by organic mercury compounds, began to affect the inhabitants of the riverside areas of the Aganogawa River, Niigata, Japan. The authors have investigated the neurotological disturbances, which occurred in 144 cases intoxicated with organic mercurials. The results obtained are summarized as follows: Recruitment (in SISI and other tests) was negative in all the cases except for 32 with inner ear deafness, and Békèsy’s audiometry (TTS) showed type II: unsettled wide amplitude in 17 cases and severe abnormal adaptation characterizing the type III pattern in nine cases. Spontaneous and positional nystagmus were recorded with ENG in 94 of 144 cases. In 62 of 144 cases, pathological findings of horizontal optokinetic nystagmus were recorded, and those of vertical optokinetic nystagmus were frequently observed in 81 of the 118 cases tested (69 %). Judging from the authors’ observations, neurotological disturbances due to chronic mercurial intoxication may be considered mainly as lesions of the retrocochlea and of the oculomotor system in the brain stem and the cerebellum.

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Section: Discussionmentioning

confidence: 99%

Neurotological Studies upon Intoxication by Organic Mercury Compounds

Mizukoshi¹,

Nagaba²,

Ohno³

et al. 1975

ORL

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“…In order to find an explanation of this different procedure we need a better understanding of this phe nomenon termed central compensation. We have to distinguish clearly between two different mechanisms: The first one is a specific vestibular phenomenon, the second one a non-specific central mechanism, substituting the deficient vestibular functions by optic and somatosensory regulations [Kornhuber, 1966], The term central compensation may strictly speaking only be used for visual and somatosensory regulations, whereas the specific vesti bular mechanism ought to he termed as accommodation of the vestibular system to a state of dysfunction as it has been put forward already 20 years ago by Mittermaier [1049Mittermaier [ , 1950. The underlying neurophysiological mechanism is explained by Trincker [1966] as follows: Destruction of one labyrinth causes a con siderable loss of information at the level of the vestibular nuclei, which can only be compensated by a surplus of information from the remaining intact labyrinth.…”

Section: Discussion Of Resultsmentioning

confidence: 99%

Central Compensation of Vestibular Dysfunction

Pfaltz¹,

Kamath²

1970

ORL

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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.

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“…From the peripheral vestibular system, the stimulus spreads to the medulla oblongata (3), in particular to the vomiting centre, from which nausea and vomiting are elicited. But the inferior vermis of the cerebellum is also supposed to be of great significance in the origin of kinesia since, according to the results of animal experiments, the symptoms of kinesia are markedly reduced or can no longer be detected after removal of the inferior vermis, in spite of an intact vomiting centre (6). Wood and Graybiel (12) are of the opinion that there is a predominance of the cholinergic over the adrenergic system.…”

Section: Causes O F Kinesiamentioning

confidence: 99%

“…The most important factor in the origin of kinesia (e.g., sea-and air-sick ness) is the very powerful stimulus to the vestibular system, which leads to the most varied autonomic symptoms through stimulation of certain structures in the brain stem (6,11). Depending on the degree of severity of the kinesia, pallor, headaches, outbreak of sweating, salivation and even very intense nausea with sickness and vomiting have been observed (8).…”

Section: General Outlinementioning

confidence: 99%