ABSTRACT
RESUMO Objetivo Identificar as definições fisiopatológicas adotadas pelos estudos que investigaram a "sinaptopatia coclear" (SC) e "perda auditiva oculta" (PAO). Estratégia de pesquisa Utilizou-se a combinação de unitermos "Auditory Synaptopathy" or "Neuronal Synaptopathy" or "Hidden Hearing Loss" com "etiology" or "causality" or "diagnosis" nas bases de dados EMBASE, Pubmed (MEDLINE), CINAHL (EBSCO) e Web of Science. Critérios de seleção Incluiu-se estudos que investigaram a SC ou PAO em humanos com procedimentos comportamentais e/ou eletrofisiológicos. Análise dos dados Realizou-se a análise e extração de dados quanto a terminologia, definição e população estudada. Resultados Foram incluídos 49 artigos. Destes, 61,2% utilizaram a terminologia SC, 34,7% ambos os termos e 4,1% utilizaram PAO. As condições mais estudadas foram exposição ao ruído e zumbido. Conclusão A terminologia SC foi empregada na maioria dos estudos, com referência ao processo fisiopatológico de desaferenciação entre as fibras do nervo coclear e as células ciliadas internas
ABSTRACT Purpose To identify the pathophysiological definitions adopted by studies investigating "cochlear synaptopathy" (CS) and "hidden hearing loss" (HHL). Research strategies The combination of keywords "Auditory Synaptopathy" or "Neuronal Synaptopathy" or "Hidden Hearing Loss" with "etiology" or "causality" or "diagnosis" was used in the databases EMBASE, Pubmed (MEDLINE), CINAHL (EBSCO), and Web of Science. Selection criteria Studies that investigated CS or HHL in humans using behavioral and/or electrophysiological procedures were included. Data analysis Data analysis and extraction were performed with regard to terminology, definitions, and population. Results 49 articles were included. Of these, 61.2% used the CS terminology, 34.7% used both terms, and 4.1% used HHL. The most-studied conditions were exposure to noise and tinnitus. Conclusion CS terminology was used in most studies, referring to the pathophysiological process of deafferentiation between the cochlear nerve fibers and inner hair cells.
ABSTRACT
Non-steady state noise has become the main type of workplace noise. Compared with steady state noise, non-steady state noise may cause more serious hearing loss. This paper reviews the new situation of occupational hearing loss caused by non-steady state noise exposure, the overview of international noise exposure assessment standards and new challenges, and the new evidence of non-steady state noise induced hearing loss, so as to provide the basis for the future research of non-steady state noise induced hearing loss.
Subject(s)
Humans , Auditory Threshold , Hearing Loss, Noise-Induced , Noise , Noise, Occupational/adverse effects , Occupational Diseases/epidemiologyABSTRACT
SUMMARY: There is an increasing amount of evidence that supports the diabetic complications of the central nervous system structure and function. The cerebellum, which is one of the primary structure derived from the hindbrain, plays an important role in motor control, motor coordination, and non-motor functions, such as cognitive processing. The synapse is a critical structure that regulates neuronal communication, and well-defined afferent and efferent fibre connections in the cerebellum help in maintaining the proper working order. Thus, the present study sought to investigate the long-term effects of diabetes-induced synaptopathy in the cerebellum, using both histological and ultrastructural studies. Twenty Sprague-Dawley male rats were divided randomly into control and diabetic groups, and diabetes was then induced through a single intraperitoneal injection of streptozotocin (60 mg/kg body weight). Six month later, the rats were sacrificed and the cerebellum was removed. Light and electron microscopic examinations showed a degeneration of Purkinje cells (Neuron purkinjense) with shrunken cells, pyknotic nuclei, and synaptopathy, including the reduction in synapse density, number of synaptic vesicles, and maturation of synapses in the molecular layer of diabetic cerebellum. The disruptions in synaptic profiles, which observed in the diabetic condition, could be related to cerebellar dysfunction, thus leading to the defects in coordinated movement, balance, as well as cognitive learning and memory.
RESUMEN: Actualmente existe una creciente evidencia que apoya las complicaciones diabéticas de la estructura y función del sistema nervioso central. El cerebelo, una de las estructuras primarias del cerebro posterior, desempeña un papel importante en el control motor, la coordinación motora y las funciones no motoras, tanto como en el procesamiento cognitivo. La sinapsis es una estructura crítica que regula la comunicación neuronal y las conexiones de fibras aferentes y eferentes bien definidas en el cerebelo, ayudan a mantener el funcionamiento correcto. Por lo tanto, en el presente estudio se investigaron los efectos a largo plazo de la sinaptopatía inducida por la diabetes en el cerebelo, utilizando estudios histológicos y ultraestructurales. Veinte ratas SpragueDawley macho se dividieron al azar en grupos de control y diabetes, se indujó la diabetes a través de una inyección intraperitoneal única de estreptozotocina (60 mg / kg de peso corporal). Seis meses después, se sacrificaron las ratas y se extrajo el cerebelo. Los exámenes de microscopías óptica y electrónica mostraron una degeneración de las neuronas purkinjenses (células de Purkinje), con células reducidas, núcleos picnóticos y sinaptopatía, como también la densidad reducida de sinapsis, el número de vesículas sinápticas y la maduración de las sinapsis en la capa molecular del cerebelo de las ratas diabéticas. Las interrupciones en los perfiles sinápticos, que se observaron en la condición diabética, podrían estar relacionadas con la disfunción cerebelosa, lo que lleva a defectos en el movimiento coordinado, el equilibrio, así como al aprendizaje cognitivo y la memoria.