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PubMed1988

Physiologic, histopathologic, and cineradiographic characterization of a new fluid-percussion model of experimental brain injury in the rat.

The fluid-percussion technique produces experimental brain injury by rapid injection of a fluid volume into the closed cranial cavity. The experiments reported here characterize a new, more controlled technique for fluid-percussion brain injury in the rat and systematically examine systemic physiologic, histopathologic, and electroencephalographic responses in the rat at two levels of injury severity. The new technique was developed to permit independent variation of the fluid pressure pulse parameters and, thus, more accurately define the brain loading conditions associated with fluid-percussion injury. The new technique produced changes in mean arterial blood pressure similar to previous techniques; however, bradycardia was not observed. Significant increases in heart rate were produced by both injury levels and were more prolonged at the high level of injury severity. Both magnitudes of injury produced significant decreases in EEG amplitude immediately postinjury, but high severity injury produced a greater decrease in delta frequency band (1-4 Hz) activity than did low severity injury. Both levels produced hemorrhage at the site of injury, thalamus, corpus callosum, hippocampus, and fimbria hippocampus similar to previous techniques. Higher levels of injury produced more extensive cerebral hemorrhage and greater spinal involvement. In a separate group of animals, cineradiographic images were made at coronal, sagittal, and dorsal orientations during the fluid pressure pulse. Intracranial fluid movement was characterized by rapid radial movement within the epidural space. The data suggest that the distributed nature of fluid-percussion induces pathology, and dysfunction may reflect a diffuse mechanical loading of the brain surface. The model appears to give repeatable effects useful in the study of closed head injury.

Animals↗

PubMed1999

Percussion--a new way to diagnose a pneumothorax.

We describe a new clinical sign in a case series of three patients who developed pneumothoraces during mechanical ventilation in the intensive care unit. All three patients were in the supine position. Two patients had x-rays that were inconclusive before insertion of chest drains and the third had a pneumothorax diagnosed on clinical findings alone. On each occasion we were able to diagnose pneumothorax using sternal percussion and simultaneous auscultation. The method relies on percussion of the sternum while simultaneously ausculating the anterior (superior) chest on the side of the suspected pneumothorax. The stethoscope is then placed on the other side of the chest. The percussion sound on the affected side has an exaggerated, resonant and booming quality. The percussion note is exaggerated partly because a stethoscope is used and partly because, in the supine patient, air localizes upwards to the anterior thorax.

Female↗

PubMed1983

Effects of selected bronchial drainage positions and percussion on blood pressure of healthy human subjects.

The purpose of this experimental study was to examine blood pressure changes of healthy subjects in response to position changes (from supine to level and head-down side lying) and percussion. Twenty male and 20 female volunteers with a mean age of 25.9 years were divided randomly into four groups so that each group consisted of 5 men and 5 women. After resting supine for 20 minutes, subjects assumed a level or a head-down side-lying position (-10 degrees) for 6 minutes. During this 6 minutes, percussion was applied to two of the four groups. Systolic and diastolic blood pressures significantly decreased when subjects turned from a supine to a level or a head-down side-lying position. The decreases lasted the length of time the side-lying position was maintained. The blood pressure responses to head-down side lying did not significantly differ from the responses to level side lying. The blood pressure responses to the level and the head-down side-lying positions with percussion did not differ from the responses to these positions without percussion.

Adult↗

PubMed1990

Duration patterns of percussion sound in healthy and periodontally affected teeth.

Ten periodontally affected subjects and 10 healthy subjects were selected in order to examine the duration patterns of percussion sounds in all upper teeth, excluding the 8's. Probing depth, loss of attachment, tooth mobility by 'Periotest', bone loss and percussion sound duration via occlusal sound analyser were recorded during the pretreatment period. The following results were obtained from the study: (i) the normal duration of percussion sounds ranged from 4.40-5.33 ms; (ii) percussion sound values of periodontal patients were of longer duration than those of healthy subjects; (iii) a close correlation between duration and other individual parameters was found in all upper teeth, with the exception of molars.

Acoustics↗

PubMed1992

Mobility and percussion sound of healthy upper incisors and canines.

In order to evaluate the correlation between mobility and percussion sound, 126 upper incisors and canines in 21 student volunteers were measured by means of the Periotest (Siemens), by evaluating the percussion sound subjectively and by analyzing its spectrum. The attenuation time and frequency of the sound were measured for each tooth. A logical mobility and percussion sound existed in accordance with the sizes of the teeth. Spearman correlation coefficients close to 1.00 were noted in individual cases between the Periotest and the three other tests describing the percussion sounds.

Adult↗

PubMed1989

Clapping or percussion causes atelectasis in dogs and influences gas exchange.

We examined the effects of 10 min of lower lateral chest wall percussion with a mechanical percussor or hand clapping in groups of anesthetized, paralyzed, and ventilated supine dogs. Mechanical percussion was applied at 10-16 Hz and caused an esophageal pressure swing (delta Pes) of 10-17 cmH2O. Hand clapping was applied at 4-7 Hz and caused a delta Pes of 6-17 cmH2O. At necropsy there were large reddened areas on the lateral surface of the underlying lung as well as smaller reddened areas on the hilar surfaces of both lungs and on the lateral surface of the opposite lung. These reddened regions were demonstrated to be atelectatic by postmortem lung inflation (which caused the reddened areas to disappear) and by microscopic examination. Despite the atelectasis, gas exchange improved toward the end of the percussion or clapping period. In four dogs that were ventilated for an additional 20 min after percussion, there was a tendency for gas exchange initially to worsen and then to gradually improve.

Animals↗

PubMed1995

Chest percussion.

The direct method of chest percussion, first described by Auenbrugger but disseminated by Corvisart, has rapidly been replaced by the indirect or digitodigital method. Chest percussion has not been evaluated by modern acoustic means, so that our present knowledge of the method does not consistently differ from the 19th century approach. Auscultatory percussion is not superior to conventional percussion.

Auscultation↗

PubMed1991

[Effect of lateral position and chest percussion on pulmonary gas exchange in patients with decreased level of consciousness].

The purpose of this study is to verify the effect of lateral position and chest percussion on gas exchange in the decreased level of conscious patients. The Subjects for this study were 21 patients 'admitted in ICU of CNUH from Dec 18th, 1989 to Aug 4th, 1990. The Data was analyzed by paired t-test. The results of this study as follows: 1) In comparison of supine position, good-lung dependent position and good-lung dependent with chest percussion, the difference of PaO. was statistically significant (P less than 0.05). 2) In comparison of supine position, good-lung dependent position and good-lung dependent with chest percussion, the difference of A-a Do. was statistically significant (p less than 0.05). In conclusion, the use of good-lung dependent position and chest percussion was effective nursing intervention on decreased level of conscious patients in ICU.

Consciousness↗

PubMed1999

[Physical examination--percussion of the thorax].

Percussion of the chest cannot detect small lesions (< 3 cm in diameter) and lesions situated deep in the lung (5-7 cm away from the outside of the thoracic wall). The value of percussion as a test to detect a pathological pulmonary situation in comparison with chest radiography is evaluated in only a few studies. Chest percussion appears to be of limited value; especially the sensitivity is very low. Moreover, the inter- and intra-observer errors are high. The value of percussion to detect cardiomegaly is only investigated in one recent study in a selected patient population. In this study the predictive values as well as the reproducibility appear to be moderate.

Cardiomegaly↗

PubMed2001

[History of chest percussion].

Although percussion of the abdomen was already known to the Greek physician Galenos (2nd century A. D.) who used it to distinguish between ascites and meteorism, the Viennese physician Leopold Auenbrugger (1722-1809) started to use, the percussion of the chest as a diagnostic tool. In 1761 he published his experience in a treatise called "New Method for Detecting Hidden Ailments of the Chest by Percussion of the Thorax" (Inventum novum ex percussione thoracis hummani ut signo abstruso interni pectoris morbos detergendi). However, this method was introduced into practice only 50 years later by Jean Nicolas Corvisart, who translated Auenbrugger's book in 1808 into French. The famous Vinnese internist of Czech origin Joseph Skoda (1805-1881) set the teaching about percussion and auscultation on a firm physical basis. Skoda confronted the physical findings with dissection materials in close cooperation with the renowned Vinnese pathologist Karl Rokitansky (1804-1878), who was born in Hradec Králové. The Medical School in Prague became famous for its excellent command of methods based on physical examination and surpassed even the Viennese School.

History, 15th Century↗

PubMed1985

Inefficiency of chest percussion in the physical therapy of chronic bronchitis.

The effect of manual chest percussion was studied in 10 patients recovering from an acute exacerbation of chronic bronchitis. All patients were studied on 2 consecutive days. Physiotherapy consisting of postural drainage and instructed coughing was given on both days. Chest percussion was included in a randomized way on either day. Percussion was associated with a small but statistically significant increase in airflow obstruction, measured as a reduction in FEV1 after the treatment. There were no differences in the deposition or clearance of inhaled radiolabelled particles between the 2 forms of treatment. Changes in oxygen saturation were small and insignificant during both forms of treatment. The study indicates that manual chest percussion is of little value as an adjunct to postural drainage and instructed coughing in the treatment of patients with chronic bronchitis.

Aged↗

PubMed1996

Changes in lCBF, morphology and related parameters by fluid percussion injury.

We investigated the pathophysiological and morphological responses of anaesthetized rats to fluid percussion brain injury generated by an original midline fluid percussion injury device. Following different grades of trauma, lCBF was measured continuously in the right parietal cortex through a burr hole using laser Doppler flowmeter, and physiological parameters were monitored. Pathological changes also were evaluated microscopically. During the first 2 hours following trauma, we found four patterns of cerebral circulatory responses. Little measurable pathophysiological response occurred after percussion pulses of less than 1.33 atmospheres (atm). In animals subjected to pulses of greater than 4.30 atm, lCBF increased synchronously with blood pressure, and then both parameters decreased continuously until death. In animals subjected to pulses of 1.53 to 2.33 atm, trauma produced a transient increase in lCBF with no synchronous rise in blood pressure. In animals subjected to pulses of 2.70 to 3.87 atm, lCBF increased synchronously with blood pressure immediately following the injury, but had decreased markedly by 60 seconds and remained below the pre-injury baseline. Blood pressure recovered to baseline within 4 minutes of the injury. The transient increase in lCBF occurred within 5 seconds following percussion pulses of greater than 1.53 atm and appeared to be independent of the rise in systemic blood pressure. Apnoea occurred in animals subjected to pulses of greater than 1.53 atm, and the duration of apnoea and mortality rate correlated with the magnitude of the applied injury. A power decrease in the electroencephalogram post-injury and a delay in its recovery, both depended on the magnitude of the injury with few regional differences in the beta-2 band power. The distribution and extent of blood-brain barrier disruption and small haemorrhages also correlated with the magnitude of the injury. The number of neurons decreased significantly in both hippocampi by 2 weeks following moderate trauma. The four patterns of lCBF changes demonstrated in the present study, as well as the other responses to injury, may be useful for studying graded models of various diffuse brain injuries.

Animals↗

PubMed1989

Traumatic brain injury in the rat: characterization of a lateral fluid-percussion model.

Experimental fluid-percussion models produce brain injury by rapidly injecting saline into the closed cranium. In the present study we characterize the physiological, histopathological and neurological responses to mechanical brain injury in the rat produced by lateral fluid-percussion injury of graded severity. Physiological experiments (n = 105) demonstrated that all levels of injury produced an acute and transient systemic hypertension and bradycardia. Acute hypertension followed by significant hypotension occurred at higher magnitudes of injury. Post-injury suppression of electroencephalographic amplitude was related to the severity of injury. An increase in slow wave (delta/theta) electroencephalographic activity with a concomitant decrease in alpha/beta electroencephalographic activity were observed only at moderate and high magnitude of injury and were correlated with a worsened neurological outcome (r = 0.84; P less than 0.05) and increased mortality (r = 0.66; P less than 0.05). Alterations in brainstem auditory-evoked potentials were also observed only at the higher levels of injury. Histopathological analysis revealed that the extent of post-injury hemorrhage, cavitation and vascular disruption (as measured by extravasation of Evans Blue dye) was greater at the higher magnitudes of injury. Neurological scoring performed over a 4-week post-injury period demonstrated that lateral fluid-percussion brain injury produces a chronic neurological deficit that is directly related to the severity of injury. Survival was also significantly reduced at the higher magnitudes of injury. These data demonstrate that the lateral model of fluid-percussion injury in the rat reproduces many of the features of head injury observed in other models and species and may therefore be a useful experimental model for the study of the pathophysiology of traumatic brain injury.

Animals↗

PubMed1998

Rate and force of application of manual chest percussion by physiotherapists.

The rate and force of manual chest percussion as applied by 35 physiotherapists was investigated. The influence of gender, body weight, body mass index (BMI), rate and frequency of usage on force were examined. Percussion was applied to a healthy male for 35 seconds and the rate and force were measured using a force platform. The rate and force varied among subjects. The mean (SD) rate and force of percussion were 6.60 (1.00) Hertz and 58.10 (15.32) Newtons respectively. There was no relationship between force and 1) gender, 2) body weight, 3) BMI or 4) frequency of usage of percussion. A weak relationship was found between rate and force (r = -0.358, p = 0.034). Thirty-two subjects demonstrated a hand dominance.

Journal Article↗

PubMed2002

Percussion chemistry and muscle function.

A hypothesis is presented concerning the origin of the action of muscles in the human and animal bodies It is advanced that muscle action originates with very rapid chemical reactions known as percussion reactions. These give rise to the temporary precipitation of solids in muscle cells. The accompanying volume change gives rise to muscle contraction. The redissolving of these solids restarts the cycle. The percussion reaction also gives rise to percussion waves which travel along nerve fibres to cells in the brain and activate percussion reactions in the connected brain cells. The reverse also occurs and indicates the means whereby brain cells induce muscular action. It is shown that this mechanism is compatible with observations of muscle action.

Animals↗

PubMed1997

Production of tumor necrosis factor-alpha and interleukin-1beta by human cerebral microvascular endothelium after percussive trauma.

Intracerebral cytokine production is thought to be partially responsible for the brain edema and increased leukocyte adhesion seen after head injury by both a direct effect on vascular permeability and by causing leukocyte activation. Cerebrospinal fluid concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 are elevated after traumatic brain injury. The cerebral endothelium has not been investigated as a de novo source of cytokines after injury. We have found that conditioned media from cultured human cerebral microvascular endothelium (HCME) subjected to percussion trauma increases neutrophil chemotaxis. To test the hypothesis that percussive trauma increases the production of TNF-alpha and IL-1beta by HCME, serial supernatant samples from passage 2 HCME were collected for 24 hours and analyzed for TNF-alpha and IL-1beta concentration by enzyme-linked immunosorbent assay after trauma. HCME subjected to percussion injury secreted significantly more TNF-alpha at 8 and 24 hours and significantly more IL-1beta at 4 and 24 hours compared with uninjured controls (p < 0.05, Student's t test). These data suggest that HCME production of inflammatory cytokines occurs after traumatic brain injury independent of systemic influences. In situ cytokine production by HCME after percussion trauma may mediate the increased cerebral leukocyte accumulation and cerebrovascular dysfunction observed after focal brain injury.

Brain Injuries↗

PubMed2004

Effect of mild hypothermia on brain dialysate lactate after fluid percussion brain injury in rodents.

OBJECTIVE: To investigate the effects of mild hypothermia on brain microdialysate lactate after fluid percussion traumatic brain injury (TBI) in rats. METHODS: Brain dialysate lactate before and after fluid percussion brain injury (2.1 +/- 0.2 atm) was measured in rats with preinjury mild hypothermia (32 degrees C), postinjury mild hypothermia (32 degrees C), injury normothermia (37 degrees C), and the sham control group. Mild hypothermia (32 degrees C) was induced by partial immersion in a water bath (0 degrees C) under general anesthesia and maintained for 2 hours. RESULTS: In the normothermia TBI group, brain extracellular fluid lactate increased from 0.311 +/- 0.03 to 1.275 +/- 0.08 mmol/L within 30 minutes after TBI (P < 0.01) and remained at a high level (0.546 +/- 0.05 mmol/L) (P < 0.01) at 2 hours after injury. In the postinjury mild hypothermic group, brain extracellular fluid lactate increased from 0.303 +/- 0.03 to 0.875 +/- 0.05 mmol/L at 15 minutes after TBI (P < 0.01) and then gradually decreased to 0.316 +/- 0.04 mmol/L at 2 hours after TBI (P > 0.05). In the preinjury mild hypothermic group, brain extracellular fluid lactate remained at normal levels after injury (P > 0.05). CONCLUSION: The cerebral extracellular fluid lactate level increases significantly after fluid percussion brain injury. Preinjury mild hypothermia completely inhibits the cerebral lactate accumulation, and early postinjury mild hypothermia significantly blunts the increase of cerebral lactate level after fluid percussion injury.

Animals↗

PubMed1987

A fluid percussion model of experimental brain injury in the rat.

Fluid percussion models produce brain injury by rapidly injecting fluid volumes into the cranial cavity. The authors have systematically examined the effects of varying magnitudes of fluid percussion injury in the rat on neurological, systemic physiological, and histopathological changes. Acute neurological experiments showed that fluid percussion injury in 53 rats produced either irreversible apnea and death or transient apnea (lasting 54 seconds or less) and reversible suppression of postural and nonpostural function (lasting 60 minutes or less). As the magnitude if injury increased, the mortality rate and the duration of suppression of somatomotor reflexes increased. Unlike other rat models in which concussive brain injury is produced by impact, convulsions were observed in only 13% of survivors. Transient apnea was probably not associated with a significant hypoxic insult to animals that survived. Ten rats that sustained a moderate magnitude of injury (2.9 atm) exhibited chronic locomotor deficits that persisted for 4 to 8 days. Systemic physiological experiments in 20 rats demonstrated that all levels of injury studied produced acute systemic hypertension, bradycardia, and increased plasma glucose levels. Hypertension with subsequent hypotension resulted from higher magnitudes of injury. The durations of hypertension and suppression of amplitude on electroencephalography were related to the magnitudes of injury. While low levels of injury produced no significant histopathological alterations, higher magnitudes produced subarachnoid and intraparenchymal hemorrhage and, with increasing survival, necrotic change and cavitation. These data demonstrate that fluid percussion injury in the rat reproduces many of the features of head injury observed in other models and species. Thus, this animal model could represent a useful experimental approach to studies of pathological changes similar to those seen in human head injury.

Animals↗