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Flammer syndrome: a response to the unknown aspects of acute inner ear troubles?
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Semicircular canal dehiscence: a possible direct cause of benign paroxysmal positional vertigo?
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Pulse-wave velocity and benign paroxysmal positional vertigo (BPPV)
Background: The aetiology of the BPPV is still uncertain. Some factors have been individualized that could explain partly the onset or the tendency to the recurrence, among which traumas, osteoporosis, viral infections and cardiovascular factors of risk. With particular reference to the influence that the cardiovascular factors of risk can practice on the genesis and persistence of the BPPV, it needs to keep in mind that, despite these introduces a role largely sustained in literature, it concerns considerations that hear again of very controversial interpretations however. Purpose: The objective of the study is to try to furnish a good definition of the existing relationship between the VPPB and the rigidity of the arterial tree, reliable expression of the conditions of the vascular circle and easily measurable with the appeal to recent technologies. Primary objective: the definition of possible differences of the profile of rigidity of the vascular system among subjects affections from BPPV and subjects without otologic diseases. Objective secondary: the definition of possible relationships between recidivist of BPPV and profile of vascular rigidity in a population of adults and elderly. Results: The results allow to affirm that an association exists among BPPV and increase of the arterial vascular rigidity, shown from the presence of more elevated values both of cfPWV (carotido-femoral Pulse Wave Velocity) that of differential arterial pressure or pulsatry pressure (PP) in the patients with BPPV in comparison to those measured in the healthy subjects of the same age. Moreover, an association exists between recurrence of the episodes of BPPV and increase of the arterial vascular rigidity in the patients of superior age to 60, shown by the presence of more elevated values of cfPWV in the patients with recurring BPPV in comparison to those measured in the subjects
MICROINJECTIONS OF ALPHA-1-NORADRENERGIC AND ALPHA-2-NORADRENERGIC SUBSTANCES IN THE CEREBELLAR VERMIS OF DECEREBRATE CATS AFFECT THE GAIN OF THE VESTIBULOSPINAL REFLEXES
Microinjections of alpha 1- and alpha 2-noradrenergic substances in the cerebellar vermis of decerebrate cats affect the gain of the vestibulospinal reflexes
1. In addition to mossy and climbing fibers, the Purkinje (P)-cells of the cerebellar cortex receive noradrenergic (NA) afferents which originate mainly from the locus coeruleus. Since these fibers impinge also on the vermal cortex of the cerebellar anterior lobe, which receives a labyrinth input and projects to the lateral vestibular nucleus, experiments were performed in precollicular decerebrate cats to find out whether unilateral injection of alpha-adrenergic substances into the vermal cortex of the cerebellar anterior lobe exerted some influence on posture as well as on the dynamic characteristics of vestibulospinal (VS) reflexes evaluated by recording the multiunit EMG responses of the forelimb extensor triceps brachii of both sides to roll tilt of the animal at 0.15 Hz, +/- 10 degrees. 2. Unilateral injection into the vermal cortex of the culmen of the alpha 1-adrenergic agonist metoxamine or the alpha 2-adrenergic agonist clonidine (0.25 microliters at the concentration of 4 micrograms/microliters of saline) produced a postural asymmetry, characterized mainly by a slight decrease of the extensor tonus in the ipsilateral forelimb and an increased tonus in the contralateral forelimb. The same substances significantly increased the gain (imp./sec/deg) of the first harmonic component of the EMG responses of the ipsilateral and the contralateral triceps brachii to animal tilt. The crossed effects were more prominent for the alpha 2- than for the alpha 1-agonist. However, no significant changes in the phase angle of the responses were observed in both instances. The effects described above occurred within 5-10 min after the injection, reached the peak values after 15-20 min, and disappeared within 2 hours. 3. The postural and reflex changes described above were not due to irritative events following the injection, since they were not observed in control experiments after injection of 0.25 microliter of saline into the same corticocerebellar area prior to the administration of the alpha 1- or the alpha 2-adrenergic agonist. Moreover, the resulting effect were dose-dependent. 4. Both the ipsilateral as well as the contralateral effects induced by the alpha 1- or the alpha 2-adrenergic agonist metoxamine or clonidine were impaired by previous injection into the same corticocerebellar area of the corresponding alpha 1- or alpha 2-adrenergic antagonist prazosin or yohimbine, respectively (0.25 microliter at the concentration of 8-16 micrograms/microliters in both cases).(ABSTRACT TRUNCATED AT 400 WORDS
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