Control Nerves (control + nerve)

Distribution by Scientific Domains


Selected Abstracts


Diameter of the Cochlear Nerve in Endolymphatic Hydrops: Implications for the Etiology of Hearing Loss in Ménière's Disease,

THE LARYNGOSCOPE, Issue 9 2005
Cliff A. Megerian MD
Abstract Objective/Hypothesis: Endolymphatic hydrops (ELH) is an important histopathological hallmark of Ménière's disease. Experimental data from human temporal bones as well as animal models of the disorder have generally failed to determine the mechanism by which ELH or related pathology causes hearing loss. Hair cell and spiral ganglion cell counts in both human and animal case studies have not, for the most part, shown severe enough deterioration to explain associated severe sensorineural hearing loss. However a limited number of detailed ultrastructural studies have demonstrated significant reductions in dendritic innervation densities, raising the possibility that neurotoxicity plays an important role in the pathology of Ménière's disease (MD) as well as experimental endolymphatic hydrops (ELH). This study tests the hypothesis that neurotoxicity is an important primary mediator of injury to the hydropic ear and is reflected in measurable deterioration of the cochlear nerve in the animal model of ELH. This study also explores the previously presented hypothesis that cochlear injury in ELH is mediated through the actions of nitric oxide (NO) by evaluating whether hearing loss or various measures of cochlear damage can be ameliorated by administration of an agent that limits excess production of NO. Study Design: Part one of the project involves the surgical induction of endolymphatic hydrops and correlation of long term hearing loss with histological parameters of ELH severity as well as cochlear nerve and eighth cranial nerve diameter measurements. In part two, aminoguanidine is administered orally to a separate set of hydropic animals in an attempt to limit cochlear injury presumably mediated by NO. Methods: Guinea pigs are subjected to surgical induction of unilateral endolymphatic hydrops after establishing baseline ABR thresholds at 2, 4, 8, 16, and 32 kHz. Threshold shifts are established prior to sacrifice at 4 to 6 months and temporal bones processed for light microscopy. Measurements of cochlear nerve and eighth cranial nerve maximal diameters as well as average maximal diameters are carried out and correlated to hearing loss and a semi-quantitative measure of hydrops severity. The identical experiments are carried out in animals treated with aminoguanidine, an inhibitor of inducible nitric oxide synthase. Results: The mean maximal diameter (n = 14) of the hydropic cochlear nerve was significantly reduced (432.14 ± 43.18 vs. 479.28 ± 49.22 microns, P = .0025) as compared to the control nerve. This was also seen in measures of the eighth cranial nerve (855.71 ± 108.82 vs. 929 ± 81.53 microns, P = 0.0003). Correlation studies failed to show correlation between hydrops severity and a cochlear nerve deterioration index (r = -0.0614, P = .8348). Similarly, hearing loss severity failed to correlate with cochlear nerve deterioration (r = 0.1300, P = .6577). There was a significant correlation between hearing loss and hydrops severity (r = 0.6148, P = .0193). Aminoguanidine treated animals (n = 5) also sustained nerve deterioration to the same degree as non-treated animals and there appeared to be no protective effect (at the dosage administered) against ELH related hearing loss, hydrops formation, or nerve deterioration. Conclusion: ELH results in significant deterioration of cochlear nerve and eighth cranial nerve maximal diameters in the guinea pig model. These findings are in accord with previous studies which detected ultrastructural evidence of dendritic damage and indicate that neural injury is of sufficient severity to result in light microscopic evidence of cochlear nerve and eighth cranial nerve deterioration. These data support the concept that the principle pathological insult in ELH is a form of neurotoxicity, especially in light of previous studies which indicate relative preservation of hair cells at similar points in time. The lack of correlation between the severity of hydrops and nerve deterioration suggests that nerve deterioration is independent of hydrops severity. [source]


Demyelination secondary to chronic nerve compression injury alters Schmidt,Lanterman incisures

JOURNAL OF ANATOMY, Issue 1 2006
Brent L. Berger
Abstract The role of Schmidt,Lanterman incisures (SLIs) within the myelin sheath remains the subject of much debate. Previous studies have shown a positive correlation between the number of SLIs per internode and internodal width for both normal and pathological myelin internodes. As chronic nerve compression (CNC) injury induces demyelination, we sought to evaluate if CNC injury altered the occurrence of SLIs using nerve-teasing techniques and light microscopy. Rigorous examination of the teased axons from nerves subjected to CNC injury for 1 month, 2 months or 8 months revealed that there is indeed a positive correlation between the number of SLIs per internode and the internodal width. However, unlike previous studies, the degree of positive correlation between these two parameters was greater in the internodes that had undergone remyelination in response to CNC injury as compared with the internodes from control nerves. These findings support the theory that SLIs are likely to assist in the metabolic processes of the myelin sheath, including growth and maintenance of the myelin sheath. [source]


Enhanced B7 Costimulatory Molecule Expression In Inflammatory Human Sural Nerve Biopsies

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2001
R Kiefer
Objectives-To define the role of the costimulatory molecules B7-1 and B7-2 in inflammatory disorders of the peripheral nervous system. B7 molecules are essential for effective antigen presentation and may determine the differentiation of T cells into a Th-1 or Th-2 phenotype, thus modulating immune response and disease course. Methods-Forty nine sural nerve biopsies from patients with neuroborreliosis, Guillain-Barre syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), CIDP variants and hereditary neuropathies, and those with no detectable abnormality were investigated. The expression of B7-1 and B7-2 mRNA and protein was investigated by polymerase chain reaction (PCR) and immunocytochemistry. Results-B7-1 mRNA was strongly upregulated in both cases of neuroborreliosis, in two cases of GBS and one case of variant CIDP. Moderate to low levels were detected in the remaining GBS and CIDP biopsies and were rarely found in a noninflammatory control group consisting of hereditary neuropathy and normal nerves. At the immunocytochemical level, strong expression of B7-1 protein was found in both neuroborreliosis cases, and moderate or low expression in six of eight GBS cases and seven of 17 CIDP cases investigated, whereas only one of five non-inflammatory control nerves showed staining, which was very weak. In neuroborreliosis, B7-1 protein was found very pronounced in epineurial infiltrates, whereas in CBS and CIDP, labelling was predominantly endoneurial and localised to putative macrophages. B7-2 mRNA and protein were expressed only at low levels in neuroborreliosis and selected autoimmune neuropathy cases, and were essentially absent from noninflammatory controls. Conclusions-B7 molecules are expressed in the peripheral nervous system and regulated during disease, and their presence in macrophages underlines the putative function of endoneurial macrophages as local antigen presenting cells in the immunopathology of peripheral nerve. B7-1 rather than B7-2 is preferentially upregulated, possibly promoting the induction of a Th-1-type T cell response within the nerve. [source]


Morphologic, functional and behavioral effects of titanium dioxide exposure on nerves

CLINICAL ORAL IMPLANTS RESEARCH, Issue 5 2004
An experimental study on rats
Abstract Objectives: The purpose of this study was to explore morphologic, functional, and behavioral effects of titanium dioxide (TiO2) on nerves. Material and methods: A total of 17 albino rats were used for nerve conduction experiments, hot-plate tests, and histological evaluation. TiO2 was implanted unilaterally on the sciatic nerves of five rats. Ten days after surgery, test and control nerves were dissected and their signal transduction speeds were quantified by suction electrodes in a bath containing a Tyrode solution. Twelve rats were divided into three equal groups resulting in equal number of nerves (n=8) for TiO2 implantation, surgical exposure of the nerves, and for use as controls. One week after surgery, hot-plate tests were undertaken for 10 consecutive days to determine response latencies of the nerves. At the termination of the experiments, the nerves were harvested, processed, and examined under a microscope. Results: The signal transduction speeds of TiO2 -implanted nerves was similar to control specimens (P>0.05). The avoidance responses of TiO2 -implanted, surgically exposed, and control nerves were comparable (P>0.05). At the cellular level, TiO2 did not lead to any signs of adverse reactions on nerves. Conclusions: TiO2, the main oxide surrounding endosseous titanium implants, does not alter the structure and the function of myelinated nerves. Résumé Le but de cette étude a été d'explorer les effets morphologiques, du comportement, de la fonction du dioxide de titane (TiO2) sur les nerfs. Dix-sept rats albinos ont été utilisés pour ces expériences de comportement nerveux, des tests en culture et l'évaluation histologique. Le TiO2 a été implanté unilatéralement sur les nerfs sciatiques de cinq rats. Dix jours après la chirurgie, les nerfs tests et contrôles ont été disséqués et leur vitesse de transduction du signal ont été quantifiée par des électrodes de succion dans un bain contenant une solution de thyrode. Douze rats ont été répartis en trois groupes égaux résultant en un nombre égal de nerfs (n=8) pour l'implantation de TiO2, l'exposition chirurgicale des nerfs et pour l'utilisation comme contrôle. Une semaine après la chirurgie, des tests de culture ont été effectués durant dix jours d'affilée pour déterminer les temps de latence de réponse des nerfs. A la fin des expériences, les nerfs ont été prélevés et examinés sous microscope. Les vitesses de transduction du signal des nerfs où il y avait implantation de TiO2 étaient semblables aux contrôles (P>0.05). Les réponses de manquement des nerfs contrôles, chirurgicalement exposés et implantés TiO2 étaient semblables (P>0.05). Au niveau cellulaire, le TiO2 n'entraînait pas d'effets secondaires sur les nerfs. Le dioxyde de titane, l'oxyde principal entourant les implants titane endoosseux n'altère ni la structure ni la fonction des nerfs myélinisés. Zusammenfassung Ziel: Es war das Ziel dieser Studie, morphologische und funktionelle Verhaltensänderungen eines Nerven als direkte Reaktion auf Titandioxid (TiO2) zu untersuchen. Material und Methode: Man verwendete für Versuche bezüglich Reizleitung der Nerven, für den Kochplattentest und für histologische Untersuchungen insgesamt 17 Albinoratten. Zuerst implantierte man bei fünf Ratten einseitig TiO2 direkt auf den Ischiasnerven. 10 Tage nach der Chirurgie resezierte man die Test- und die Kontrollnerven, legte sie in ein Bad mit Tyrodelösung und mass mit Saugelektroden die Leitgeschwindigkeit eines Signals. Die 12 übrigen Ratten teilte man auf drei gleichgrosse Gruppen auf und erhielt somit je acht Nerven (n=8) für die Implantation von TiO2, die chirugische Entblössung oder für die Kontrollgruppe. Eine Woche nach der Chirurgie führte man an 10 aufeinanderfolgenden Tagen den Kochplattentest durch, um Verzögerungen der Nervenreaktion zu messen. Nach Abschluss dieser Untersuchung entnahm man die Nerven, bereitete sie histologisch auf und untersuchte sie anschliessend unter dem Mikroskop. Resultate: Die Leitgeschwindigkeit eines Signals beim Nerven mit implantiertem TiO2 war ganz ähnlich wie bei den Kontrollnerven (P>0.05). Die Abwehrreaktion von Nerven mit implantiertem TiO2, von chirurgisch entblössten Nerven und von Kontrollnerven war vergleichbar (P>0.05). Auf zellulärer Ebene führte TiO2 zu keiner Abwehrreaktion der Nerven. Zusammenfassung: Titandioxid, anteilsmässig das häufigste Oxid auf enossalen Implantaten, verändert weder Struktur noch Funktion von myelinisierten Nerven. Resumen Objetivos: El propósito de este estudio fue explorar los efectos morfológicos, funcionales y de comportamiento del dióxido de titanio (TiO2) sobre los nervios. Material y métodos: Se usaron un total de 17 ratas albinas para experimentos de conducción nerviosa, pruebas de plato caliente, y evaluación histológica. Se implantó TiO2 unilateralmente en los nervios ciáticos de cinco ratas. 10 días tras la cirugía, se disecaron los nervios de prueba y de control y se cuantificaron sus velocidades de transducción de señales por electrodos de succión en un baño conteniendo solución tiroidea. Se dividió a 12 ratas en tres grupos iguales resultando en igual numero de nervios (n=8) para implantación de TiO2, exposición quirúrgica de los nervios y para usarlos de control. Una semana tras la cirugía, se llevaron a cabo pruebas de plato caliente durante 10 días consecutivos para determinar las latencias de respuesta de los nervios. A la terminación de los experimentos, los nervios se recolectaron, se procesaron y se examinaron bajo el microscopio. Resultados: Las velocidades de transducción de señales de los nervios implantados de TiO2 fueron similares a las de los especímenes de control (P>0.05). Las respuestas de huida de los nervios implantados de TiO2, expuestos quirúrgicamente, y los nervios de control fueron comparables (P>0.05). A nivel celular, el TiO2 no condujo a ningún signo de reacciones adversas en los nervios. Conclusiones: El dióxido de titanio, el óxido principal que rodea a los implantes endoóseos de titanio, no altera la estructura ni la función de los nervios mielínicos. [source]