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Evaluation of vinpocetine as a THERAPY in patients with sensorineural hearing loss: A phase II, open-label, single-center study
Abstract and Figures
The progressive degeneration of the excitable cells of the ear depends on the sustained excitation of the voltage-sensitive sodium channels, so the negative pharmacological modulation could be a rational therapeutic strategy against the damage of these cells. The objective was to demonstrate the effectiveness of Vinpocetine (VPC), a potent sodium channel blocker, as a treatment for acquired sensorineural hearing loss. A phase II, longitudinal and prospective open clinical study, was conducted over a period of 12 months with patients older than 18 years, to demonstrate the effectiveness of Vinpocetine (VPC) as a treatment for acquired sensorineural hearing loss, using evoked potentials, otoacoustic emissions, audiometry and logoaudiometry, analyzing the results at 6 and 12 months of treatment with Vinpocetine (30 mg/day in 3 doses). It was observed that from 0 to 6 months there was hearing impairment (which was already expected due to the age of the patients). From 6 to 12 months and from 0 to 12 months there were significant differences with a tendency towards improvement, indicating that the aforementioned deterioration not only stopped, but that with the use of vinpocetine, the hearing capacity improved. It is concluded that Vinpocetine helps to stop hearing impairment and even improve hearing.
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... Preliminary studies have examined the potential beneficial effects of vinpocetine against memory loss, cancer, and Alzheimer's disease [134,135]. A clinical study highlighted its effect in treating acquired sensorineural hearing loss and improving hearing . Further, several clinical studies have shown that ginseng reduces tinnitus symptoms and improves the hearing threshold in people with sensorineural hearing loss [137,138]. ...
Background: The world's age-related health concerns continue to rise. Audio-vestibular disorders, such as hearing loss, tinnitus, and vertigo, are common complaints in the elderly and are associated with social and public health burdens. Various preventative measures can ease their impact, including healthy food consumption, nutritional supplementation, and lifestyle modification. We aim to provide a comprehensive summary of current possible strategies for preventing the age-related audio-vestibular dysfunction. Methods: A PubMed, Embase, and Cochrane review databases search was conducted to identify the relationship between diet, lifestyle, and audio-vestibular dysfunction. "Diet", "nutritional supplement", "lifestyle", "exercise", "physical activity", "tinnitus", "vertigo" and "age-related hearing loss" were used as keywords. Results: Audio-vestibular dysfunction develops and progresses as a result of age-related inflammation and oxidative stress. Diets with anti-inflammatory and antioxidant effects have been proposed to alleviate this illness. A high-fat diet may induce oxidative stress and low protein intake is associated with hearing discomfort in the elderly. Increased carbohydrate and sugar intake positively correlate with the incidence of audio-vestibular dysfunction, whereas a Mediterranean-style diet can protect against the disease. Antioxidants in the form of vitamins A, C, and E; physical activity; good sleep quality; smoking cessation; moderate alcohol consumption; and avoiding noise exposure are also beneficial. Conclusions: Adequate diet or nutritional interventions with lifestyle modification may protect against developing audio-vestibular dysfunction in elderly individuals.
... As a vincamine alkaloid derivative, vinpocetine had been widely utilized to treat various conditions like cognitive impairment and cerebrovascular diseases for decades ago . It is indicated in such conditions since it reduces blood viscosity and subsequently improves cerebral circulation and metabolism; it acts as a Na-channel inhibitor and free radicals scavenger , . Furthermore, as a phosphodiesterase inhibitor, vinpocetine could improve spatial memory by modulating cholinergic activities and preventing neuronal cell damage through its antioxidant action . ...
Sepsis is a systemic inflammatory consequence resulting from microbial infection, it is assessed as a worldwide healthcare issue, and the main reason for death follows an infection. To explore the possible cardioprotective effects of vinpocetine during sepsis-induced cardiotoxicity. The current study was done with a total of forty male albino Swiss mice, aged 8-12 weeks, and weighing 25-30 gm. These animals had free access to food and water. After two weeks of adaptation, mice were divided into the following four groups (n = 10): (1) Normal group: apparently healthy mice. (2) CLP group: mice underwent CLP operation. (3) Vehicle group: mice received DMSO (4) Vinpocetine group: mice received vinpocetine 30 mg/kg intraperitoneally in 2 divided doses for 5 consecutive days. Vinpocetine group demonstrated a significant (p<0.05) decrease in the myocardial levels of cardiac troponin-I as compared to the CLP group. Furthermore, the vinpocetine group demonstrated a significant (p<0.05) decrease in the serum level of inflammatory cytokines (TNF-α, IL-6, & IL-1β) as compared to the CLP group. Additionally, the vinpocetine group showed a significant (p<0.05) elevation in the myocardial SOD activity and reduction of MDA level as compared to the CLP group. Histologically, All mice in the CLP group showed a significant (p<0.05) cardiac tissue injury, while the vinpocetine group showed a significant (p<0.05) reduced level of cardiac tissue injury. The anti-inflammatory effect through their ability to decrease serum levels of inflammatory cytokines (TNF-α, IL-1β, and IL-6). Also the anti-oxidant effect through their ability to decrease myocardial levels of MDA and increase the myocardial activity of SOD. This work is licensed under a Creative Commons Attribution Non-Commercial 4.0 International License.
The effects of vinpocetine on internal Na+ (Na(i)), cAMP accumulation, internal Ca2+ (Ca(i)) and excitatory amino acid neurotransmitters release, under resting and under depolarized conditions, was investigated in rat striatum synaptosomes. Veratridine (20 microM) or high K+ (30 mM) were used as depolarizing agents. Results show that vinpocetine in the low microM range inhibits the elevation of Na(i), the elevation of Ca(i) and the release of glutamate and aspartate induced by veratridine depolarization. In contrast, vinpocetine fails to inhibit the rise of Ca(i) and the neurotransmitter release induced by high K+, which are both TTX insensitive responses. Results also show that the inhibition exerted by vinpocetine on all the above veratridine-induced responses is not reflected in PDE activity. Our interpretation of these results is that vinpocetine inhibits neurotransmitter release triggered by veratridine activation of voltage sensitive Na+ channels, but not that triggered by a direct activation of VSCC. Thus, the main mechanism involved in the neuroprotective action of vinpocetine in the CNS is unlikely to be due to a direct inhibition of Ca2+ channels or PDE enzymes, but rather the inhibition of presynaptic Na+ channel-activation unchained responses.
Hemispheric asymmetries in the processing of elemental speech sounds appear to be critical for normal speech perception. This study investigated the effects of age on hemispheric asymmetry observed in the neurophysiological responses to speech stimuli in three groups of normal hearing, right-handed subjects: children (ages, 8–11 years), young adults (ages, 20–25 years), and older adults (ages > 55 years). Peak-to-peak response amplitudes of the auditory cortical P1–N1 complex obtained over right and left temporal lobes were examined to determine the degree of left/right asymmetry in the neurophysiological responses elicited by synthetic speech syllables in each of the three subject groups. In addition, mismatch negativity (MMN) responses, which are elicited by acoustic change, were obtained. Whereas children and young adults demonstrated larger P1–N1-evoked response amplitudes over the left temporal lobe than over the right, responses from elderly subjects were symmetrical. In contrast, MMN responses, which reflect an echoic memory process, were symmetrical in all subject groups. The differences observed in the neurophysiological responses were accompanied by a finding of significantly poorer ability to discriminate speech syllables involving rapid spectrotemporal changes in the older adult group. This study demonstrates a biological, age-related change in the neural representation of basic speech sounds and suggests one possible underlying mechanism for the speech perception difficulties exhibited by aging adults. Furthermore, results of this study support previous findings suggesting a dissociation between neural mechanisms underlying those processes that reflect the basic representation of sound structure and those that represent auditory echoic memory and stimulus change.
Introduction and objectives Speech perception that takes place in the cochlea is involved in the process of language. The objective was to describe the findings in transient otoacoustic emissions in children with language problems before and after 6 months of speech therapy. Methods There were 17 children with language problems between 3 and 6 years of age diagnosed with anarthric language delay (expressive and mixed language disorder). They underwent medical history, otoscopy, intelligence level testing, initial language test, tympanometry of 226 Hz, audiometry and transient otoacoustic emission test. Results We evaluated the 17 patients again after 6 months of attending speech therapy. The percentage of overall reproducibility of transient otoacoustic emissions in both ears was adequate to perform frequency analysis. We found a statistically significant difference (P≤0.01) in the frequency of 1 kHz reproducibility when comparing results before and after therapy in the right ear. There was a significant difference (P≤0.05) when comparing the results of audiometry at frequencies of 0.5, 1.5, 2, 4 and 8 kHz in the right ear and a highly significant difference (P = 0.001) in the frequency of 3 kHz in the left ear. Conclusions The analysis of sound through the cochlea is involved in the process of language acquisition. A poor processing of speech sounds in the peripheral system could result in poor processing at the central level. Consequently, it is important to consider our results when making a diagnosis and carrying out rehabilitation treatment in children with language disorders.
Introduction and objective To identify the auditory or clinical test that has the best correlation with the ear in which we apply the monaural hearing aid in symmetric bilateral hearing loss. Material and method A total of 37 adult patients with symmetric bilateral hearing loss were examined regarding the correlation between the best score in speech discrimination test, corporal laterality, auditory laterality with dichotic digits in Spanish and score for filtered words with monaural hearing aid. Results The best correlation was obtained between auditory laterality and gain with hearing aid (0.940). Conclusions The dichotic test for auditory laterality is a good tool for identifying the best ear in which to apply a monaural hearing aid. The results of this paper suggest the necessity to apply this test in patients before a hearing aid is indicated.
The efficacy and tolerance of orally administered vinpocetine was investigated in patients suffering from mild to moderate organic psychosyndromes including primary dementia. Two hundred and three patients were included in a placebo-controlled, randomized double-blind, multicentre trial and received every day for 16 weeks either: 3 x 10 mg doses of vinpocetine, 3 x 20 mg doses of vinpocetine, or 3 x placebo. Patients were assessed on ratings of clinical global impression, cognitive performance and on measures of the quality of life including depressive illness. There were no clinically relevant side-effects reported and the frequencies of adverse events between patients treated with vinpocetine (30 mg or 60 mg) and placebo were comparable. Statistically significant improvements were found in favour of both active treatment groups compared to placebo in both confirmatory evaluations of efficacy of treatment: the "Global Improvement" (on the CGI scale) and cognitive performance (SKT). Vinpocetine was also superior to placebo in ratings of the "severity of illness". This study demonstrates the usefulness and efficacy of vinpocetine in the management of patients with moderate organic psychosyndromes. An apparently greater therapeutic efficacy of 3 x 10 mg vinpocetine compared with the higher vinpocetine dosage is statistically not significant.
The effects of three vinca derivatives on [3H]batrachotoxin binding in rat cortical synaptosomes, on the inhibition of whole-cell Na+ currents evoked in voltage-clamped cortical neurones of the rat, on the protection against veratridine-induced cell death in cortical cultures and on the maximal electroshock-induced seizures in mice were compared. Vinpocetine, vincamine and vincanol reduced [3H]batrachotoxin binding with IC50 values of 0.34, 1.9 and 10.7 microM, blocked Na+ currents with IC50 values of 44.72 and 40 microM, and protected cortical against veratridine-induced cell death with IC50 values of 0.49, 26 and 33 microM, respectively. Upon i.p. administration, vinpocetine, vincamine and vincanol attenuated maximal electric shock-induced convulsions in a dose-dependent manner with ED50 values of 27, 15.4 and 14.6 mg/kg, respectively. The present findings indicate that the three vinca derivatives are potent blockers of voltage-gated Na+ channels, a mechanism that may contribute at least in part to the pharmacological/therapeutic benefit of these drugs.
The principal objective of this study is to explore the hypothesis that a blockade of Na(+) channels can prevent some of the mechanisms involved in ototoxicity. For this purpose, the potential action of the voltage sensitive Na(+) channel antagonist, vinpocetine, on the ototoxicity induced by the representative aminoglycoside antibiotic, amikacin, in guinea pigs was tested for almost half a year. Amikacin (450 mg/kg) administered daily (i.m.) for 5 days increases the thresholds of the auditory brainstem response (ABR) to the two frequencies tested (4 and 8 kHz). These threshold increases are permanent or at least long-lived, as after 40 days they are already established and are maintained until the end of the experiment (160 days after the antibiotic administration). Amikacin decreases the amplitude of ABR waves, particularly P1, and after 160 days increases the latency of ABR waves, particularly at the higher frequency tested (8 kHz). When the above amikacin regimen is followed by a daily (i.p.) vinpocetine (2 mg/kg) administration for 13 days the increase in ABR threshold and latency caused by amikacin alone is prevented. Moreover, the animals treated with amikacin alone show a decreased weight gain and a remarkable increased mortality in comparison with the group of animals post-treated with vinpocetine. We hope that the multiple beneficial effects exerted by the Na(+) channel blocker, vinpocetine, against aminoglycoside antibiotics-induced side effects could help to solve the serious limitations of the use of this type of antibiotic.
The effect of vinpocetine, a nootropic drug with anti-ischemic potential, on the release of DA and its main metabolite, DOPAC, was investigated in striatum isolated nerve endings under resting and depolarized conditions. Vinpocetine does not modify the baseline release of DA or the exocytotic release of DA evoked by high K(+), but inhibits the release of DA evoked by veratridine reversal of the DA transporter. In addition to these results, which confirm the vinpocetine selective blockade of voltage-sensitive presynaptic Na(+) channels (VSSC) previously reported [Neurochem. Res. 24 (1999) 1585], vinpocetine increases DOPAC release either under resting, veratridine or high K(+) depolarized conditions. This latter effect, which does not involve VSSC, was characterized. The parallel determination of the released and retained catecholamine concentrations revealed that vinpocetine increases DOPAC release at the expense of internal DA in a dose-dependent manner (low microM range). In contrast to vinpocetine, the selective MAO-A inhibitor, clorgyline, increases DA and decreases DOPAC formation. The combined action of vinpocetine and clorgyline does not indicate, however, that the activation of MAO is the mechanism responsible for the increase in DOPAC caused by vinpocetine. Reserpine, although more potent and efficient than vinpocetine, qualitatively exerts the same pattern of changes on DA and DOPAC concentrations. It is concluded that, in addition to the inhibition of presynaptic VSSC permeability, which selectively inhibits the transporter-mediated release of all neurotransmitters, vinpocetine increases DOPAC by impairing the vesicular storage of DA. Our results indicate that the cytoplasm extravesicular DA is metabolized by MAO to DOPAC. Most of the DOPAC formed is exported to the extracellular medium.