vertebrobasilar insufficiency/hypoxia

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Cerebral evoked potentials in the chronic vertebrobasilar insufficiency.

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The syndrome of chronic vertebrobasilar insufficiency (VBI) consists in a complex of symptoms, often mild and transient, and lacks a complementary system of objective paraclinical investigations able to certify its existence. The study of somato-sensory, auditory and visual evoked potentials in VBI

Effect of a glutamate blocker, ipenoxazone hydrochloride on the hypoxia-induced firing in the medial vestibular nucleus.

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To elucidate the effectiveness of the drug in the treatment of vertebrobasilar insufficiency (VBI), we performed an electrophysiological study to examine the effects of ipenoxazone hydrochloride, a glutamate blocker, on hypoxia-induced firing in the medial vestibular nucleus (MVN) neuron, using

[Vertebrobasilar insufficiency and obstructive sleep apnea].

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The aim of this article is to point to correlation between vertebrobasilar insufficiency (VBI) and obstructive sleep apnea (OSA) that has not been perceived sufficiently till now. Namely, in the voluminous literature about sleep-disordered breathing, VBI has been cited only as one of the possible

[The effect of percutaneous transluminal stenting for vertebrobasilar ischemia on sleep apnea hypopnea syndrome].

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OBJECTIVE To evaluate the relationship between vertebrobasilar ischemia (VBI) and sleep apnea hypopnea syndrome (SAHS) and the effect of percutaneous transluminal stenting for VBI on the clinical parameters of SAHS. METHODS Twenty patients with VBI were included for clinical history, physical

Ondine's curse in association with diabetes insipidus following transient vertebrobasilar ischemia.

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Ischemic lesions of the brainstem can lead to complex neurologic deficits. Failure of the automatic control of ventilation (Ondine's curse syndrome) is a possible but rare syndrome following localized brainstem dysfunction. We report on a 49-year-old man with intermittent bradycardia, cranial

Decreased calcium-activated potassium channels by hypoxia causes abnormal firing in the spontaneous firing medial vestibular nuclei neurons.

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Vertebrobasilar insufficiency (VBI) presents complex varied clinical symptoms, including vertigo and hearing loss. Little is known, however, about how Ca(2+)-activated K(+) channel attributes to the medial vestibular nucleus (MVN) neural activity in VBI. To address this issue, we performed

[Vertebrobasilar insufficiency of prenatal origin: a case report].

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The case of a newborn presenting from birth with arthrogryposis multiplex congenita resting mainly on the legs, severe hypotonia, consciousness anomalies, clonic fits, recurrent apnea and bradycardia, absent sucking and swallowing is described. At the age 4 months a further episode of apnea and

Respiratory patterns in anesthetised rats before and after anemic decerebration.

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Experiments were undertaken to test the comparability of changes in respiratory frequency and tidal volume during hypoxia and hypercapnia in rats with and without intact peripheral chemoreceptors and with intact vagi. Neural organisation of respiratory control was perturbed by anemic decerebration,

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