Noise-induced duodenal lesions: a light and electron microscopy study of the lesions of the rat duodenal mucosa exposed to low frequency noise.

BACKGROUND AND AIMS: Non-auditory effects of noise, including digestive disorders have long being reported. Low frequency noise (LFN) is considered to be responsible to most of non-auditory effects of noise and is widely spread in modern societies. Only a few studies were designed to evaluate these noise-induced digestive alterations. The pathogenesis of duodenal ulcers and erosions is complex and noise may be an environmental co-factor. The aim of the present study was to investigate the morphological injury of LFN-exposed duodenal mucosa. MATERIALS AND METHODS: Five groups of Wistar rats were exposed to continuous LFN, during increasing periods, since 1 to 13 weeks. A control group was kept in silence. Duodenal specimens were studied using light microscopy (LM), scanning electron microscopy (SEM) and transmission electron microscopy (TEM). RESULTS: We disclosed several changes in LFN-exposed rats: on LM, mucosa showed superficial erosions of the epithelial layer, degeneration, picnosis and cell death, with no inflammation. On SEM, epithelium presented displacement of cells and unequal distribution of microvilli, with coalescence and fusion. On TEM, microvilli were irregularly distributed, damaged and fragmented. The terminal web was destroyed. Morphological alterations occurred early, after just 1 week of LFN-exposure, persisted with longer noise exposition and did not suffer any evolution. Changes were similar among all LFN-exposed groups. CONCLUSIONS: LFN-exposed duodenal mucosa develops destruction of microvilli and terminal web, leading to cellular death and development of superficial erosions. These lesions of cytoskeleton structures could explain why cells with actinic and tubulinic structures like cilia and microvilli present severe destruction after LFN-exposure. These erosions are similar to those seen in dyspeptic patients.

Noise-induced duodenal lesions

Vibroacoustic disease (VAD) is a systemic diseasethat results from long-term exposure tolow-frequency noise (LFN). VAD can cause lesionsin several organs. Noise-exposed individualsfrequently present digestive symptoms, butonly a few studies have attempted to evaluategastrointestinal lesions. The aim of this studywas to investigate the duodenal alterations inVAD, using an animal model of the disease.Adult Wistar rats were exposed to continuousLFN. After five, nine and thirteen weeks theywere sacrificed. The duodenums were studiedby light microscopy and scanning electron microscopy,and compared with those of animalskept in silence. Superficial erosions and widespreadcell death with microvilli coalescence andfusion were observed, by light and electronmicroscopy. Erosion, cellular degeneration anddeath, and microvilli destruction, reflect noise-inducedduodenal alterations in rats which may beequivalent to the ulcers and dyspeptic symptomsreported in human VAD patients (AU)

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Low frequency noise and whole-body vibration cause increased levels of sister chromatid exchange in splenocytes of exposed mice.

Chronic exposure to low frequency (LF) noise and whole-body vibration (WBV) induces both physiological and psychological alterations in man. Recently, we have shown that long-term occupational exposure to LF noise and WBV produces genotoxic effects in man expressed as an increase in sister chromatid exchange (SCE) levels in lymphocytes. The objectives of the present study were to investigate whether the observed effect could be reproduced in a murine model and, if so, which of the agents, LF noise alone or in combination with WBV, would be instrumental in the SCE induction. SCEs were analyzed in spleen lymphocytes of mice exposed to LF noise alone and in combination with WBV for 300 and 600 hr. An effect at the cell cycle kinetics level was also investigated. The results revealed significant increases in the mean SCE number per cell and in the proportion of cells with high frequency of SCEs (HFCs) in lymphocytes of mice submitted to combined noise and WBV over controls. No significant differences were found between single noise-exposed and control mice. A cell cycle delay was observed exclusively in the noise and WBV exposure groups. In conclusion, we demonstrated that, as in exposed workers, prolonged exposure to the combination of LF noise and WBV determines an increase in SCE level in mice while LF noise alone is not effective in SCE induction.

In utero and postnatal exposure of Wistar rats to low frequency/high intensity noise depletes the tracheal epithelium of ciliated cells.

Chronic exposure of men or rodents to low frequency/high intensity (LFHI) noise causes a number of systemic changes that make up the so-called vibroacoustic disease (VAD), a disorder that includes alterations of the respiratory system, namely, of its epithelial layer. We have investigated here the susceptibility of the tracheal epithelium of Wistar rats to in utero and postnatal exposure to LFHI noise by comparing its ultrastructure with that of the tracheal epithelium of control rats and of animals exposed to LFHI noise only after reaching adulthood (8 weeks of age). Scanning electron microscopy (SEM) of the inner surface of rat trachea was used to determine the relative areas covered by ciliated and non-ciliated cells. In rats that were exposed in utero and postnatally to LFHI noise, we observed that out of 100 microm(2) of tracheal epithelium only 31 +/- 14 microm(2) were covered by cilia, whereas in control rats; ciliated cells occupied an average of 60 +/- 18 microm(2) out of 100 microm(2) of the epithelium; this difference between the two groups was statistically significant (p <0.05). In rats that were exposed to LFHI noise only after reaching adulthood, cilia covered 55 +/- 22 microm(2) out of 100 microm(2) of the luminal surface of the trachea, a value that, although lower than that of controls, was not found to be statistically different. We conclude that (1) the tracheal ciliated cells are damaged by exposure of rats to LFHI noise if the animals are kept under this environmental aggression during in utero and postnatal periods; (2) tracheal ciliated cells from adult rats are more resistant to the deleterious effects of LFHI noise than pleura or lung alveolar cells that were shown before to undergo marked changes upon chronic exposure of rats to LFHI noise. These findings suggest a note of caution regarding pregnant women and young children: they should be prevented from areas where LFHI noise occurs, namely, in aircraft and textile industries where this type of environmental hazard is often present.

Increased levels of sister chromatid exchanges in military aircraft pilots.

Sister chromatid exchanges (SCEs) were scored in lymphocytes of nine high-performance pilots of alphajet aircrafts and of ten control individuals from the same air base. Statistical analysis of the mean SCE count per cell in the total number of cells analyzed as well as in those having 12 or more SCEs (high-frequency cells, HFCs) revealed a significant difference between pilots and controls, after adjusting for the effect of smoking. Analysis of the cell cycle kinetic data (replication and mitotic indices) revealed no significant differences either between pilots and controls or between smokers and nonsmokers. Previously, we reported an increase in the SCE levels in workers of the aeronautical industry exposed to noise and whole-body vibration. The present results corroborate those findings and indicate that noise and whole-body vibration may cause genotoxic effects in man.

The vibroacoustic disease--an emerging pathology.

Vibroacoustic disease (VAD) is the clinical manifestation of a systemic disease that develops after long-term exposure to noise (> or = 10 yr) which is characterized by large pressure amplitude (> or = 90 dB SPL) within the lower frequency bands (< or = 500 Hz). Noisy environments produce more widespread systemic effects than initially suspected. This paper describes the chronology, population studied, and the statistical treatment used in our studies of VAD over the past 20 yr. We also describe the motivation that led to the evaluation and assessment of the exposed employees. Future research aims are also discussed.

Noise assessment during aircraft run-up procedures.

BACKGROUND: A comprehensive noise survey was conducted at Oficinas Gerais de Material Aeronautico (OGMA), Alverca, Portugal, and at several Portuguese Air Force (PoAF) bases, as part of an ongoing occupational noise assessment program. The major objectives consisted of measuring and analyzing noise radiated by various types of military aircraft while undergoing maintenance, repair, or testing. METHODS: Amplitude, frequency, time history and statistical analysis were conducted on noise emitted by aircraft during run-up procedures. Analysis and evaluation used various noise indexes (Leq and Lmax), frequency spectra, and sound pressure time histories for the assessment of noise exposure on the employees during their working life span. RESULTS: The results show a predominance of large pressure amplitudes within the lower frequency bands. This was correlated with long-term clinical observations in these workers. This study corroborates the definition of vibroacoustic disease as a systemic, noise-induced occupational pathology caused by long-term (>10 yr) exposure to large pressure amplitude (> or = 90 dB SPL) and low frequency (< or = 500 Hz) noise.

A unique case of vibroacoustic disease: a tribute to an extraordinary patient.

This paper describes the case of a patient, Mr. A, who died in 1987. The information provided by Mr. A in life, and his insistence on making a will demanding an autopsy on his death, has given us invaluable data on Vibroacoustic Disease (VAD). Mr. A was an intellectually curious man who researched the medical literature related to his condition, and compared it to his own experience. He would describe all his sensations during his many epileptic seizures. Solely because of the results of Mr. A's autopsy, new avenues of research were initiated. These have led to new concepts and exciting new perspectives on noise-induced extraaural pathology. VAD is today a well-established and easily diagnosed entity. This paper is a tribute to Mr. A, in whose honor we have an on-going commitment to establish VAD as an occupational disease, reimbursable by Worker's Compensation.

The clinical stages of vibroacoustic disease.

BACKGROUND: Vibroacoustic disease (VAD) is an occupational disease occurring in susceptible workers who have had long-term exposure (> or = 10 yr) to large pressure amplitude (> or =90 dB SPL) and low frequency noise (< or = 500 Hz). The clinical progression is insidious, and lesions are found in many systems throughout the body. Some of the findings, such as extracellular matrix changes, appear to be specific to this disease. Others, such as cognitive impairment, seem to be common in different types of stress-induced pathology. In 1956, Professor Eugenia Andreeva-Galanina developed a classification of hand-arm vibration-induced pathology. This has been further refined and has become an important tool in occupational medicine. Thus, it is also important now to define the clinical stages of VAD in accordance with the appearance of the most common signs and symptoms. METHODS: We analyzed the files of 140 patients with VAD, paying close attention to the chronology of the clinical findings, the registry of eventual and on-the-job accidents, and the evaluation of disabilities. RESULTS: We have classified VAD in function of the time it took for 50% of the population to acquire the relevant sign or symptom. Stage I, mild signs (behavioral and mood associated with repeated infections of the respiratory tract, e.g., bronchitis); Stage II, moderate signs (depression and aggressiveness, pericardial thickening and other extracellular matrix changes, light to moderate hearing impairment, and discrete neurovascular disorders); Stage III, severe signs (myocardial infarction, stroke, malignancy, epilepsy, and suicide). CONCLUSION: This classification should be capable of assessing work fitness, and is a primary approach to a complex and multidisciplinary problem with implications in diagnosis, prevention and disability compensation within VAD.

Sister chromatid exchange analysis in workers exposed to noise and vibration.

BACKGROUND: There has been a growing interest in the combined effects of noise and vibration. In a population of aeronautical workers diagnosed with vibroacoustic disease (VAD), a large incidence of malignancy was detected. These workers were exposed to large pressure amplitude (LPA) (> or = 90 dB SPL) noise, with energy content concentrated within the low frequency (LF) bands (< or = 500 Hz) and whole-body vibration (WBV). To our knowledge, there are no studies conducted in humans or animals that address the issue of the potential genotoxic effects of vibration combined with noise. In the present study, the levels of sister chromatid exchanges (SCE) and of cells with high frequencies of SCE (HFC) were analyzed in peripheral blood lymphocytes of workers employed in various occupations within the aeronautical industry. METHODS: SCE and HFC were analyzed in lymphocytes of 50 workers occupationally exposed to noise and vibration and of 34 office-worker controls (G0). The exposed group included: 10 hand-vibrating tool operators (G1), 15 engine test cell technicians (G2), 12 aircraft run-up technicians (G3) and 13 Portuguese Air Force helicopter pilots (G4). Groups 2-4 were exposed to WBV and LPALF noise; group 1 was exposed to LPA high frequency noise and local vibration. Statistical analysis of the mean SCE count per cell was carried out by multiple regression analysis comparing various predictor variables: type of exposure, duration of exposure, age, and cigarette consumption. RESULTS: Only cigarette consumption and type of exposure were found to be significantly correlated with the mean SCE frequency. After allowing for the effects of smoking, the analysis indicates that: 1) there was no significant difference between G1 and G0 (p > 0.05); 2) the differences between G2 and G0, G3 and G0, G4 and G0 were all highly significant (p < 0.001); 3) there was no significant difference between G2 and G3 (p > 0.05), nor between G2 and G3 combined and G4 (p > 0.05); and 4) G2 and G4 combined had a significantly elevated mean SCE frequency compared G0 (p < 0.001). Statistical analysis of the proportion of HFC was consistent with these results. CONCLUSION: Our data suggest that occupational exposure to LPALF noise and WBV may lead to increased levels of SCE in men. These results also suggest a reason for the high incidence of malignancy in VAD patients. The observed effects may not reflect a direct action of these physical agents on DNA. Alternative explanations may lie in the noise-, vibration-, and/or stress-induced pathophysiological changes.

Echocardiographic evaluation in 485 aeronautical workers exposed to different noise environments.

INTRODUCTION: Vibroacoustic disease (VAD) is a heterogeneous and systemic entity, caused by long term (> or =10 yr) exposure to noise environments characterized by large pressure amplitude and low frequency (LPALF) (> or =90 dB SPL, < or = 500 Hz), and not explained by other possible etiologic agents. The goal of this study was to identify possible structural changes in hearts of men with suspected VAD. METHODS: A total of 485 men were divided into 3 noise groups: no noise exposure (< or =70 dB), n = 48 (Group I); moderate noise exposure, (>70dB and < 90 dB), n = 113 (Group II); and intense noise exposure (> or =90 dB), n = 324 (Group III). Echo-Doppler studies were performed (HP SONOS 1500) and recorded on coded videotapes. Three observers performed blinded evaluations of 26 echo-Doppler parameters. For the purpose of the present study only 12 morphological parameters were compared among the groups: thickening of the mitral, aortic, tricuspid, and pulmonary valves, pericardium and endocardium; mitral valve regurgitation, prolapse and ruptured chordae tendinae; and inflow velocities. Thickness and severity of the applicable parameters were scored in seven-grade scale (0,0.5,1, ...,3). RESULTS: All evaluated parameters were statistically significantly different in Group I vs. Group III, except flow velocity E. Comparison of Group I vs. Group II revealed statistically significant differences in mitral, aortic, tricuspid and pericardial thickening, with the strongest evidence for mitral and pericardial structures. CONCLUSIONS: This confirms the results of previous studies. Occupational exposure to noise environments characterized by LPALF noise causes structural changes in the heart. Mitral valve and pericardial thickening constitute the first signs of VAD.

Airway flow limitation in patients with vibroacoustic disease.

INTRODUCTION: Vibroacoustic disease (VAD) is a pathology caused by occupational exposure to large pressure amplitude and low frequency (LPALF) noise (> or =90 dB SPL, < or =500 Hz), and has been the object of study by this group for the past 20 yr. In a group of 140 VAD-diagnosed patients, 7 non-smoker aircraft technicians developed clinical signs of respiratory insufficiency at an early age. Previously, multi-focal fibrosis had been observed in the lung of Wistar rats exposed to occupationally simulated LPALF noise and with no possibility of contamination by fumes, dust or other chemical agents. The goal of this study is to compare pulmonary imaging and/or functional changes in two age- and exposure-time matched groups of VAD-diagnosed aircraft technicians, with and without airflow limitation symptoms. METHODS: In a population of 140 individuals occupationally exposed to LPALF noise and diagnosed with VAD, we excluded the smokers (45 cases) and selected 7 individuals with complaints of airway flow limitations, average age 42.3 yr (SD = 2.3). From the remaining non-smokers without respiratory complaints, we selected a group of 15, age-matched patients (average age 36 yr, SD = 6.5). All subjects received a high-resolution CT scan of the chest and respiratory function tests consisting of body plethysmography, spirometry and metacholine airway provocation. RESULTS: There is a significant relationship between the presence of symptoms and imaging of lung fibrosis through high-resolution CT scan (p = 0.03624). There are no significant differences when both groups are compared with respect to the percentage of predicted values of lung function: Vital Capacity (VC), Total Lung Capacity, Forced Expiratory Volume during the first second of expiration, Maximal Expiratory Flow at 50% VC, Total Airway Resistance, and Airway Reactivity after 25 mg of metacholine. CONCLUSION: High resolution CT scan is a valuable tool for diagnosis of lung fibrosis in VAD patients who have symptoms of airway flow limitations. The fact that lung ventilation tests did not present significant changes between both groups is in agreement with findings in Wistar rats. This strongly suggests that a process of focal pulmonary fibrosis may be induced by occupational noise exposure, and is a feature of VAD.

The human pericardium in vibroacoustic disease.

INTRODUCTION: One of the main features of vibroacoustic disease (VAD) is the proliferation of the extra-cellular matrix which induces cardiovascular morphological and dynamic changes, and has been evaluated through echo-Doppler. While all subjects exposed to large pressure amplitude (> or =90 dB SPL) and low frequency (< or =500 Hz) (LPALF) for at least 15 yr have thickening of some cardiac structure, most frequently the pericardium, no significant diastolic changes accompany these observations. Echocardiography has become the diagnostic method of choice for the VAD. However, there have been no studies relating the echo-images of pericardial thickening to gross anatomy. METHODS: We present the histology and ultrastructure of the pericardia of four patients who underwent cardiac surgery. RESULTS: The most important findings concern the real thickening of the pericardium (values: 1.11, 1.35, 2.19, and 2.33 mm vs. norm: < or = 0.5 mm), the dynamic arrangements of mesothelial cells in the serosa layer, and the plasticity of the cells found among the multifascicular waveform collagen fibers. We found that the fibrosa of VAD patients has three layers: sandwiched between two thickened layers of normal fibrosa there is a loose tissue layer with vascular, nervous, and adipose structures. CONCLUSION: These features may partially explain why no important diastolic changes are observed in VAD patients in spite of the pericardium thickening.

Morphological changes in rat lung parenchyma exposed to low frequency noise.

BACKGROUND: Airway flow limitation is has been identified in nonsmoker aeronautical technicians who are exposed to long term (> or =10 yr) large pressure amplitude and low frequency (LPALF) noise (> or =90 dB, < or =500 Hz). Considering this work environment, some kind of pulmonary impairment would be expected, given the probable, but not de facto, existence of fuel exhausts and vapors. In the course of morphofunctional studies of rat pleura exposed to LPALF noise environments, intense subpleural fibrosis was identified. Thus, we decided to study the deep lung parenchyma of these noise-exposed rodents. METHODS: One group of five Wistar rats was exposed to LPALF noise for a cumulative 4000 h, and another of five rats were exposed for a cumulative of 5000 h. The control group consisted of 10, age-matched, Wistar rats that were kept in the same conditions, but in silence. Fragments of lung parenchyma were extracted after sacrifice, and processed for light microscopy, and for scanning and transmission electron microscopy. RESULTS: Focal interstitial fibrosis of the deep lung parenchyma were identified as well as changes in the small bronchial cilia. The amount of brush cells was increased in the locations where microvilli were abnormal. An obvious increase of alveolar type II pneumocyte cells was observed with numerous, large and confluent lamellar bodies. DISCUSSION: In contrast with the normal lung morphology observed in the control group, changes in the extra-cellular matrix and epithelial cells were identified in the exposed rats. No fuel exhaust, vapors or dust were present in the environment of the noise-exposed rats. These results, linked with the respiratory disorders identified in noise-exposed humans, strongly suggest that LPALF noise is an agent of pulmonary fibrosis.

Morphofunctional study of rat pleural mesothelial cells exposed to low frequency noise.

BACKGROUND: Vibroacoustic disease (VAD) is a noise-induced pathology occurring in workers occupationally exposed to large pressure amplitude (> or =90 dB SPL) and low frequency (< or = 500 Hz) (LPALF) noise, over long periods of time (> or = 10 yr). Patient complaints frequently involve the respiratory tract. There have been three cases of pleural effusion of unknown etiology and with unusually long recovery times. To better understand what may be occurring we studied the effects of LPALF noise on the morphological and functional characteristics of pleural mesothelial cells of Wistar rats. METHODS: The animals were exposed to LPALF noise for periods ranging from 24-600 h. An intrapleural instillation of calcium tungstate was performed, and after sacrifice the pleural visceral and parietal leaflets were studied by scanning electron microscopy. RESULTS: Acute exposure to LPALF noise caused a temporary decrease in the number of mesothelial microvilli, and prolonged exposure resulted in a definite decrease in their number as well as an impairment of their capacity to absorb particles within in the pleural space. CONCLUSION: These results explain the pleural pathology found in human patients with VAD and confirm the deleterious effect of LPALF noise on the respiratory system.

The effect of chronic exposure to low frequency noise on rat tracheal epithelia.

INTRODUCTION: Vibroacoustic Disease (VAD) is a multi-systemic entity caused by occupational or chronic exposure to large pressure amplitude and low frequency (LPALF) noise (> or = 90 dB SPL, < or = 500 Hz). The clinical picture involves extra-auditory pathology, such as neurological disturbances, respiratory disorders and cardiovascular problems. Among the first complaints of VAD patients are coughing, bronchitis, and inflammation or infection of the oral cavity and the upper respiratory pathways. The goal of ths study was to investigate the effects of occupationally simulated LPALF noise exposure on rat tracheal epithelium to determine if they could explain the symptoms found in VAD patients. METHODS: We exposed 20 Wistar rats to occupationally simulated (8 h x d(-1), 5d x wk(-1)) LPALF noise for an accumulated total of 1236 h. The control group consisted of 10 age-matched rats, kept in equal conditions but in silence. Histological and ultrastructural studies were performed on the tracheal epithelia of both populations. RESULTS: The most dramatic changes were identified in the ciliated cells of the exposed rats. There were frequent images of shaggy or necrotic cilia as well as regularly to partially sheared cilia. Also, there were frequent images of different stages of cilia recovery. CONCLUSION: Occupationally simulated exposure to LPALF noise can cause important changes in ciliated cells rat tracheal epithelia. This may partially explain the clinical findings observed in VAD patients.

Neurological aspects of vibroacoustic disease.

INTRODUCTION: Mood and behavioral abnormalities are the most common early findings related to vibroacoustic disease (VAD). Other signs and symptoms have been observed in VAD patients. Brain MRI discloses small multifocal lesions in about 50% of subjects with more than 10 yr of occupational exposure to large pressure amplitude (> or = 90 dB SPL) and low frequency (< or = 500 Hz) (LPALF) noise. However, to date, there have been no studies globally integrating all the neurological, imaging and neurophysiological data of VAD patients. This is the main goal of this study. METHODS: The 60 male Caucasians diagnosed with VAD were neurologically evaluated in extreme detail in order to systematically identify the most common and significant neurological disturbances in VAD. RESULTS: This population demonstrates cognitive changes (identified through psychological and neurophysiological studies (ERP P300)), vertigo and auditory changes, visual impairment, epilepsy, and cerebrovascular diseases. Neurological examination reveals pathological signs and reflexes, most commonly the palmo-mental reflex. CONCLUSIONS: A vascular pattern underlying the multifocal hyperintensities in T2 MR imaging, with predominant involvement of the small arteries of the white matter, is probably the visible organic substratum of the neurological picture. However, other pathophyisological mechanisms are involved in epileptic symptomatology.

Balance disturbances in individuals with vibroacoustic disease.

INTRODUCTION: In previous studies, patients with vibroacoustic disease (VAD) presented hyperintense foci in T2 of the cerebral white matter, brainstem and basal nuclei. The most probable etiology is ischemia. One of the most frequent complaints of these patients is balance disturbances which, in two cases, has threatened the patients' ability to maintain their jobs. The purpose of this study was to compare two methods, one neurophysiological (auditory evoked potentials - AEP) and the other structural imaging (brain MRI), in order to determine to what extent the changes detected with these methods may be related to each other in this pathology. METHODS: Twenty individuals occupationally exposed to large pressure amplitude (> or = 90 dB SPL) and low frequency (< or = 500 Hz) noise, received neurological and otorhinolaryngological examinations. All of them had previously received audiograms, tympanograms and electronystagmograms. All 20 patients also received brain MRI and AEP studies. RESULTS: The individuals with vertigo and changes of the AEP present the greater number of changes in the brain MRI. CONCLUSION: This could be an indication that in many VAD cases vertigo may have a central origin.

The palmo-mental reflex in vibroacoustic disease.

BACKGROUND: Vibroacoustic disease (VAD), is a multisystemic nosological entity, caused by occupational exposure to large pressure amplitude (> or = 90 dB SPL) and low frequency (< or = 500 Hz) (LPALF) noise. The most common neurological finding in patients with VAD is the palmomental reflex (PMR). The aim of this study is to evaluate the frequency and characteristics of this primitive reflex in a population of VAD patients. METHODS: Sixty individuals, occupationally exposed to LPALF noise underwent a neurological examination. In each one, unilateral contraction of the chin muscles was triggered through the stimulation of the thenar eminence. When a response habituation was observed, or when there was no response except previously existing skin retraction and small dimples, an EMG was performed. All these subjects also received brain MRI and measurement of endogenous evoked potentials. RESULTS: Thirty individuals presented unilateral or bilateral PMR; 26 of these presented changes in the brain MRI. EMG measurement evidenced continuous contraction of the chin muscles, without visible PMR, triggered by the stimulation of the thenar eminence. CONCLUSION: PMR is present in 50% of the patients with VAD. In the VAD patients, the frequency of abnormal chin muscle activity is higher than the frequency of PMR and represents a loss of the cortical control over the brainstem structures.

Effects of occupational exposure to low frequency noise on cognition.

INTRODUCTION: Previous studies performed on groups of workers employed in the aeronautical industry revealed morphological vascular changes of the central nervous system (CNS) and some difficulty in attention and memory retention. The goal of this study is, therefore, to determine whether prolonged occupational exposure to large pressure amplitude (> or = 90 dB SPL) and low frequency (< or = 500 Hz) (LPALF) noise leads to cognitive deterioration. METHODS: We observed 40 male workers employed as aircraft technicians, with average age of 43.3 yr (range 35-56, SD = 4.82) occupationally exposed to LPALF noise for a long period of time, average 22 yr (range 13-30, SD = 4.90), and 30 educationally- and age-matched male controls. None of the subjects had a history of alcoholism, and all were drug-free. The P300 event-related brain potential elicited with an auditory discrimination task was recorded and psychological tests (the Wechsler memory scale and the Toulouse-Piéron test) were performed. RESULTS: The P300 latency was significantly longer (328.5 vs. 307.5 ms, F = 11.7, deg. signif.=0.001) and the amplitude significantly smaller (10.9 vs. 12.6, F = 4.3, deg. signif.=0.04) in the exposed group than in the controls. No significant differences were found in the results of the Toulouse-Piéron test. The different subscales of the Wechsler memory scale did not show any significant difference except in the immediate verbal memory, where the exposed workers were found to have poorer results than the controls (10.0 vs. 11.3, F = 5.6, deg. signif.=0.02). However, the memory quotient obtained from the Wechsler memory scale indicated a significant difference between both groups (101.8 vs. 108.3, F = 10.1, deg. signif.=0.002); exposed subjects presented lower results. CONCLUSION: These findings suggest that prolonged exposure to LPALF noise might contribute to cognitive impairment and that the P300 event-related brain potential recording may be a valuable diagnostic tool.