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Physiotherapy in hospitalized medical patients.

Few data on exercise training in hospitalized patients are available, but because exercise may help and it unlikely to harm, some sort of early and maximal mobilization should be attempted. Breathing exercises as practiced currently have little apparent effect beyond the temporary benefit of inducing a slow, deep breathing pattern. New breathing exercises, based on data from physiology laboratories, should be formulated and evaluated. Postural drainage and percussion represent the physiotherapist's mainstay in dealing with exacerbations of chronic obstructive disease. In some patients, these maneuvers increase production of sputum and produce improvements in pulmonary function that, although not large, are significant. Other patients show no acute benefit. Current belief holds that patients with large sputum volumes, notably those with cystic fibrosis and bronchiectasis, are the most likely to be helped by postural drainage and percussion; but definitions vary as to what is a large sputum volume. Two studies have assessed the effect of postural drainage and percussion on the clinical course of patients with pneumonia and patients with exacerbations of chronic bronchitis, and both produced negative results.

Drainage↗

Physiological effects of vibration in subjects with cystic fibrosis.

The physiological mechanisms by which vibration and other physiotherapy interventions may clear secretions in subjects with cystic fibrosis are unknown. The main aim of this study was to compare the expiratory flow rates and frequencies of airflow oscillation of vibration to those of Acapella(R), Flutter(R), positive expiratory pressure and percussion. Respiratory flow rates were measured during interventions, the order of which was randomised. The oscillation of the airflow of the interventions was determined by frequency spectral analysis. In 18 young adult subjects with cystic fibrosis, the mean peak expiratory flow rate of vibration was greater than Flutter(R), percussion, Acapella(R) and positive expiratory pressure. The mean+/-sd of the oscillation of the airflow of vibration (8.4+/-0.4 Hz) was lower than Acapella(R) (13.5+/-1.7 Hz) and Flutter(R) (11.3+/-1.5 Hz) but similar to percussion (7.3+/-0.3 Hz). Theoretically, the higher peak expiratory flow rate of vibration compared to the other physiotherapy interventions may promote secretion clearance. In addition, the frequency of oscillation of vibration was within the range demonstrated to increase mucus transport. This study has provided some evidence for the physiological rationale for the use of vibration to aid secretion clearance.

Adult↗

Chest physical therapy. The immediate effect on oxygenation in acutely ill patients.

There is no documentation in the literature of the risk of hypoxemia after chest percussion in acutely ill adults with nonsurgical pulmonary disorders. We studied the immediate effect of postural drainage and chest percussion (PDP) on oxygenation in 22 hospitalized patients with a variety of acute, nonsurgical pulmonary disorders. Heart rate, respiratory rate, blood pressure, and arterial blood gas levels were measured at four points before, during, and after PDP. There was a significant fall in PaO2 after chest percussion in ten patients who produced no sputum or small amounts of mucoid sputum. The mean PaO2 fell 16.8 mm Hg (P < 0.05) immediately after PDP, when compared to the value obtained after postural drainage alone, and had fallen another 5.3 mm Hg (P < 0.01) 30 minutes after return to the pretreatment position. There was no significant change in PaO2 in 12 patients who produced moderate to large amounts of mucopurulent secretions. The fall in PaO2 was probably due to increased ventilation-perfusion mismatch since this fall was avoided in two patients restudied while receiving 100 percent oxygen. We concluded that all acutely ill patients receiving PDP should be carefully monitored and, if necessary, should receive increased levels of inspired oxygen to avoid hypoxemia. Our data suggest that the use of PDP in patients without sputum production is not indicated and is potentially dangerous.

Acute Disease↗

The usefulness of the Phalen test and the Hoffmann-Tinel sign in the diagnosis of carpal tunnel syndrome.

Both the Phalen test and the percussion (Hoffmann-Tinel) test are considered to be the classic diagnostic tests for Carpal Tunnel Syndrome (CTS). Sensitivity of these tests, as given in the literature, ranges from 42 to 85% (Phalen) and from 38 to 100% (Hoffmann-Tinel), and specificity from 54 to 98% and from 55 to 100% respectively. The objective of this study was to evaluate sensitivity and specificity of both tests and to analyse the influence of such selected factors, such as patient's age and duration of symptoms. The clinical group consisted of 112 patients (147 hands) with CTS confirmed clinically and on nerve conduction studies. The control group of 50 patients (100 hands) was selected from hospital volunteers, who did not complain of any hand symptoms. Sensitivity and specificity of the Phalen test turned out to be respectively 85 and 89% and for the percussion test, 67 and 68%. There was no significant influence of patients' age upon the test results. Seventeen patients showed negative results for both tests, but in these individuals, the duration of symptoms was significantly longer than in the remaining group. These findings indicated essential diagnostic value for the Phalen test, but considerably smaller for the percussion test. In the diagnosis of long lasting syndromes, the usefulness of both tests is limited.

Adult↗

A clinical and roentgenographic correlation of diaphragmatic movement.

Diaphragmatic excursion was determined by percussion in 29 patients by two observers and then compared with measurements made from inspiration and expiration chest roentgenograms. The range of movement as determined by percussion was related to spirometric indices of ventilatory capacity. Our study showed wide interobserver variation in the clinical measurements and a poor correlation with diaphragmatic excursion measured roentgenographically. Although we were able to demonstrate a significant correlation between forced vital capacity (FVC) and clinically determined range of diaphragmatic movement, five patients had a reduced FVC despite the fact that the clinical determination of diaphragmatic movement was greater than 2 cm. Both observers missed paradoxical movement in the one patient in whom it was present. We conclude that percussion of th diaphragms for the purpose of estimating the range of movement is of limited clinical value and should no longer be recommended as part of the physical examination.

Adolescent↗

Rippling muscle disease: evidence for phenotypic and genetic heterogeneity.

We describe the clinical features of a family with rippling muscle disease. Muscle stiffness and myalgia were the most prominent symptoms. Muscle rippling, although distinctive, was present in only 6 of the 11 affected family members, whereas persistent muscle contraction to muscle percussion was present in all affected adults. Although this persistent contraction resembled percussion myotonia, it was electrically silent and is therefore more aptly called "percussion contracture." We also observed two clinical features not emphasized in previously reported kindreds: mild but asymptomatic weakness of face or proximal muscles was present in 5 of 11 affected members, and 5 individuals also complained of toe walking after a prolonged period of inactivity, reflecting the disproportionate involvement of the calf muscles. The pedigree suggested autosomal dominant inheritance. Our linkage analysis excluded the region on chromosome 1q identified in a previous linkage study.

Adolescent↗

Characteristics of hammer stones and anvils used by wild bearded capuchin monkeys (Cebus libidinosus) to crack open palm nuts.

Capuchins living in Boa Vista (Piauì, Brazil) crack open hard palm nuts on hard, level surfaces (anvils) using stones (hammers) as percussive tools. This activity leaves diagnostic physical remains: distinctive shallow depressions (pits) on the surface of the anvil, cracked shells, and stone hammers on the anvil. To initiate comparison of percussive stone tool use and interpretation of the artifacts it produces across capuchins, chimpanzees, and hominins, we describe a sample of the anvils and hammer stones used by capuchin monkeys at our site. Anvils (boulders and logs) were located predominantly in the transition zone between the flat open woodland and ridges, in locations that offered some overhead coverage, and with a tree nearby, but not necessarily near palm trees. Anvils contained shallow, hemispherical pits with smooth interiors. Hammers represent a diverse assemblage of ancient rocks that are much harder than the prevailing sedimentary rock out of which they eroded. Hard stones large enough to serve as hammers were more abundant on the anvils than in the surrounding area, indicating that capuchins transport them to the anvils. Capuchins use hammers weighing on average more than 1 kg, a weight that is equivalent to 25-40% of the average body weight for adult males and females. Our findings indicate that capuchins select stones to use as hammers and transport stones and nuts to anvil sites. Wild capuchins provide a new reference point for interpreting early percussive stone tool use in hominins, and a point of comparison with chimpanzees cracking nuts.

Animals↗

The irrelevance of fusimotor activity to the Achilles tendon jerk of relaxed humans.

In two normal subjects the sciatic nerve was blocked completely using concentrated lidocaine. The muscle afferent and reflex electromyographic responses to reproducible percussion of the Achilles tendon were recorded while the blocks developed. The intensity of percussion was sufficient to produce an Achilles tendon jerk in one subject when at rest and in the other during reinforcement. The block did not alter the muscle afferent response to tendon percussion in either subject. It is concluded that background fusimotor activity is not a prerequisite for the tendon jerk and that, during complete relaxation, there may be no significant fusimotor drive directed to the triceps surae. The varying ease with which tendon jerks can be elicited in different normal subjects or in different muscles of the same subject appears to be related not to fusimotor activity but to differences in the "central excitability state."

Achilles Tendon↗

Postinjury administration of L-deprenyl improves cognitive function and enhances neuroplasticity after traumatic brain injury.

The rat model of combined central fluid percussion traumatic brain injury (TBI) and bilateral entorhinal cortical lesion (BEC) produces profound, persistent cognitive deficits, sequelae associated with human TBI. In contrast to percussive TBI alone, this combined injury induces maladaptive hippocampal plasticity. Recent reports suggest a potential role for dopamine in CNS plasticity after trauma. We have examined the effect of the dopamine enhancer l-deprenyl on cognitive function and neuroplasticity following TBI. Rats received fluid percussion TBI, BEC alone, or combined TBI + BEC lesion and were treated once daily for 7 days with l-deprenyl, beginning 24 h after TBI alone and 15 min after BEC or TBI + BEC. Postinjury motor assessment showed no effect of l-deprenyl treatment. Cognitive performance was assessed on days 11-15 postinjury and brains from the same cases examined for dopamine beta-hydroxylase immunoreactivity (DBH-IR) and acetylcholinesterase (AChE) histochemistry. Significant cognitive improvement relative to untreated injured cases was observed in both TBI groups following l-deprenyl treatment; however, no drug effects were seen with BEC alone. l-Deprenyl attenuated injury-induced loss in DBH-IR over CA1 and CA3 after TBI alone. However, after combined TBI + BEC, l-deprenyl was only effective in protecting CA1 DBH-IR. AChE histostaining in CA3 was significantly elevated with l-deprenyl in both injury models. After TBI + BEC, l-deprenyl also increased AChE in the dentate molecular layer relative to untreated injured cases. These results suggest that dopaminergic/noradrenergic enhancement facilitates cognitive recovery after brain injury and that noradrenergic fiber integrity is correlated with enhanced synaptic plasticity in the injured hippocampus.

Acetylcholinesterase↗

Blood-brain barrier breakdown occurs early after traumatic brain injury and is not related to white blood cell adherence.

The time course of blood-brain barrier (BBB) breakdown after traumatic brain injury (TBI) has important implications for therapy. This study was conducted in order to test post-traumatic BBB dysfunction in a model of fluid-percussion induced TBI in rabbits at 1 and 6 hours after TBI and relate it to white blood cell (WBC) activation. Ten anesthetized rabbits had chronic cranial windows implanted three weeks prior to experimentation. Fluid-percussion injury (3.5 atm.) was induced and animals were followed for 1 or 6 h. Intravital fluorescence videomicroscopy was used to assess BBB permeability and WBC adhesion to pial venules. Na(+)-fluorescein was infused continuously over 30 min at either 30 min (Group I, n = 5) or 5.5 h (Group II, n = 5) after TBI. Microvascular permeability in individual postcapillary venules was assessed qualitatively at 1 and 30 min after start of infusion. TBI led to a transient mean arterial blood pressure (MAP) surge after trauma and a progressive increase in the number of sticking WBCs per mm2 vessel wall. Na(+)-fluorescein extravasation was observed in 4 out of 5 Group I animals and in none of Group II. BBB breakdown was not associated with WBC sticking. We conclude that after fluid-percussion injury the BBB is damaged at 1 h post-trauma and that its function is restored 6 h later. Increased WBC sticking at 6 h is not associated with BBB breakdown. Whether WBCs may cause vascular permeability changes at a later point needs further investigation.

Animals↗

Quantitative analysis of blood-brain barrier damage in two models of experimental head injury in the rat.

The integrity of the blood-brain barrier was studied in a new model of closed head injury, and in an established model of fluid percussion injury, in the rat. Brain injury in this new model is induced by impact and acceleration of the protected rat skull. Severe hypertension is not a characteristic of this new model as compared to the tremendous surge following direct dural percussion. This is important because of the well known sensitivity of the cerebral microvasculature for acute hypertension. Using a radioactive tracer technique the dysfunction of the barrier was quantified. It is shown that the BBB is temporarily damaged due to trauma, subsequent arterial pressure surge, as seen in the percussed animals, deteriorates the dysfunction of the barrier even further. This study indicates that vascular damage is a key event following head injury. Yet the concomitant basic pathophysiological sequelae of different models must be considered when studying barrier damage and cerebral edema following brain injury. Time window studies of the barrier indicate that the barrier seals within a few hours following severe concussive head injury, and in the absence of a hypertensive surge.

Animals↗

Autonomic control of the heart and renal vascular bed during autonomic dysreflexia in high spinal cord injury.

Autonomic function and hemodynamics were studied in nine spinal cord injured (SCI) subjects, at rest and during peripheral afferent stimulation, bladder percussion. Nine able-bodied subjects were studied for comparison during unstimulated conditions. Spontaneous baroreceptor reflex sensitivity was calculated from recordings of ECG and intraarterial blood pressure. An index of sympathetic activity was provided by measuring total body noradrenaline (NA) spillover by isotope dilution technique. Renal vascular resistance was calculated from PAH-clearance.SCI subjects had lower total body NA spillover (1011 +/- 193 vs 2261 +/- 328 pmol/min, P < 0.01), but similar baroreceptor reflex sensitivity and hemodynamics compared to able-bodied subjects at rest. In SCI group, during bladder percussion, mean arterial pressure increased (79 +/- 5 vs 113 +/- 8 mm Hg, P < 0.01), whereas heart rate was reduced during the first minute of the manoeuvre (62 +/- 2 vs 56 +/- 2 bpm, P < 0.05). Baroreceptor reflex sensitivity remained unchanged. Total body NA spillover and renal vascular resistance increased by 332 % (from 1004 +/- 218 pmol/min, P < 0.05) and 55 % (from 0.078 +/- 0.011 mmHg/ml/min, P < 0.05), respectively.SCI subjects demonstrated lower total body sympathetic outflow but normal baroreceptor reflex sensitivity at rest, suggesting a balanced autonomic output to the heart. Bladder percussion caused a substantial increase in renal vascular resistance and blood pressure, which was partly due to marked generalised sympathetic activation. This activation was counterbalanced by an increased vagal activity as evidenced by reduction of the heart rate.

Adult↗

The effect of acetylcholine depletion on behavior following traumatic brain injury.

Rats were injected with either saline; A-4 (40 mg/kg, i.p.), a bis tertiary amine derivative of hemicholinium-3; or A-5 (50 micrograms/kg, i.p.), a bis quaternary amine derivative of hemicholinium-3, 1 h prior to moderate fluid percussion brain injury. A variety of reflexes and responses were measured up to 60 min following injury, and body weight and several neurological measures were taken daily up to 10 days following injury. Pretreatment with either A-4 or A-5 significantly attenuated components of transient behavioral suppression, as well as more enduring deficits in body weight and beam walk and beam balance performance. A-4 administered prior to fluid percussion was found to reduce striatal, but not pontine, acetylcholine content. A-5 did not significantly reduce acetylcholine content in either area. Both A-4 and A-5 pretreatment prevented a significant increase in acetylcholine content in the cerebrospinal fluid following fluid percussion injury; however, only A-5 significantly reduced plasma acetylcholine content. These results confirm cholinergic involvement in the production of both transient and longer-lasting behavioral deficits following traumatic brain injury. Furthermore, traumatic brain injury may allow plasma constituents to gain access to the central nervous system.

Acetylcholine↗

Prevention by eliprodil (SL 82.0715) of traumatic brain damage in the rat. Existence of a large (18 h) therapeutic window.

The neuroprotective potential of eliprodil (SL 82.0715), an N-methyl-D-aspartate (NMDA) receptor antagonist acting at the polyamine modulatory site, in brain trauma was examined in a rat model of lateral fluid-percussion brain injury. The volume of the lesion was assessed histologically by measuring, at 7 days post-injury, the area of brain damage at 10 coronal planes. Eliprodil (10 mg/kg i.p.) when given 15 min, 6 h and 24 h after fluid percussion (1.6 atm) and then b.i.d. for the following 6 days, reduced by 60% the volume of cortical damage. A similar neuroprotection was obtained when the first administration of eliprodil was delayed by up to 12 h after the brain insult. Moreover, when the treatment with this compound was started at 18 h post-injury, cortical damage was still significantly reduced by 33%. Autoradiographic studies showed that eliprodil treatment (10 mg/kg, i.p.), initiated 15 min after the trauma, also caused a marked reduction of the loss of the neuronal marker omega 1-2 (central benzodiazepine) binding sites and of the increase in the glial/macrophage marker peripheral type benzodiazepine binding sites in the cerebral cortex. In contrast, dizocilpine (a blocker of the cationic channel coupled to the NMDA receptor) when administered 6 h and 24 h after fluid percussion and then b.i.d. for the following 6 days induced a non significant reduction of the volume of the lesion at the highest tolerated dose (0.6 mg/kg i.p.). These results demonstrate the neuroprotective activity of eliprodil in experimental brain trauma using neuropathology as an endpoint and indicate that there is a very large time window for therapeutic intervention, consistent with the delayed nature of the neuronal loss, in this condition.

Animals↗

Traumatic brain injury produces impairments in long-term and recent memory.

Traumatic brain injury (TBI) in humans typically produces neurological suppression and a longer lasting impairment of memory clinically defined as post-traumatic amnesia. An animal model that reliably reproduces the physiological changes associated with TBI was used to assess the memory deficits following brain injury. Prior to TBI, rats were trained to perform one of four tasks that assessed either motor performance, long-term or recent memory. Rats were randomly assigned to one of three groups (anesthesia only, sham operation or fluid percussion). Following fluid percussion, used to produce TBI, rats were tested for 6 test sessions. The first session occurred 1-2 min after the experimental manipulation. The next 5 sessions followed the training schedule maintained prior to experimental manipulation. Differences in long-term memory occurred only in the first post-operative test session. Differences in recent memory performance were found across all 6 test sessions. The memory deficits were clearly dissociated from motor deficits. The similar memory deficits observed following human head injury and the experimentally produced TBI injury demonstrate that fluid percussion is a useful approach to examine underlying neurobiological mechanisms involved in head injury and possible clinical interventions.

Animals↗

Effects of mu opioid agonist and antagonist on neurological outcome following traumatic brain injury in the rat.

We examined the effects of an exogenous mu opioid agonist and antagonist on systemic physiology and neurological outcome following TBI in the rat. Experiment I: [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) (0.1 nMol or 0.3 nMol in 5 microliters) (n = 10) or artificial CSF (n = 10) was administered 5 min prior to fluid-percussion brain injury (2.1 atmospheres). Motor performance was assessed on days 1-5 after TBI. The mu receptor agonist, DAMGO significantly reduced both beam-walking latency and body weight loss after injury (p < 0.05). DAMGO-treated rats (n = 5) did not differ from CSF-treated rats (n = 5) on either systemic arterial blood pressure or heart rate responses to injury. Experiment II: Beta-funaltrexamine (beta-FNA) (20.0 nMol in 5.0 microliters) (n = 10) or artificial CSF (n = 10) was administered (icv) to rats 5 min prior to fluid-percussion brain injury (1.8 atmospheres). Motor performance was assessed on days 1-5 after TBI. The mu receptor antagonist, beta-FNA, significantly increased beam-walking latency after injury (p < 0.05). beta-FNA-treated rats (n = 5) did not differ from CSF-treated rats (n = 5) on either systemic arterial blood pressure or heart rate responses to injury. Experiment III: Neither beta-FNA nor DAMGO affected motor performance in uninjured rats. These results suggest that activation of mu opioid receptors by exogenous agonists may provide protection against deficits in motor performance produced by fluid percussion brain injury.

Animals↗

Selective cognitive impairment following traumatic brain injury in rats.

Impairment of cognitive abilities is a frequent and significant sequelae of traumatic brain injury (TBI). The purpose of this experiment was to examine the generality of the cognitive deficits observed after TBI. The performance of three tasks was evaluated. Two of the tasks (passive avoidance and a constant-start version of the Morris water maze) were chosen because they do not depend on hippocampal processing. The third task examined was the standard version of the Morris water maze which is known to rely on hippocampal processing. Rats were either injured at a moderate level (2.1 atm) of fluid percussion brain injury or surgically prepared but not injured (sham-injured control group). Nine days after fluid percussion injury, injured (n = 9) and sham-injured rats (n = 8) were trained on the one-trial passive avoidance task with retention assessed 24 h later. On days 11-15 following injury, injured (n = 9) and sham-injured (n = 8) rats were trained on a constant-start version of the Morris water maze that has the animals begin the maze from a fixed start position on each trial. Additional injured (n = 8) and sham-injured (n = 8) animals were trained on days 11-15 after injury on the standard (i.e. using variable start positions) version of the Morris water maze. The results of this experiment revealed that performance of the passive avoidance and the constant-start version of the Morris water maze were not impaired by fluid percussion TBI.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Experimental brain injury induces differential expression of tumor necrosis factor-alpha mRNA in the CNS.

In the present study, we examined the expression of tumor necrosis factor-alpha (TNF-alpha) mRNA i specific brain regions following experimental lateral fluid percussion traumatic brain injury (TBI) in rats. Adult Sprague-Dawley rats (n = 42) were anesthetized with sodium pentobarbital (60 mg/kg, i.p.) and subjected to lateral fluid percussion brain injury of moderate severity (2.4 atm.) centered over the left temporoparietal cortex, or 'sham' treatment (anesthesia and surgery without injury). Animals were killed by decapitation at 1, 6 or 24 h post injury, brains removed, and tissue samples of left (injured) parietal cortex (LC), right parietal cortex (RC), left adjacent cortex (LA), right adjacent cortex (RA), left hippocampus (LH) and right hippocampus (RH) were prepared. Total RNA was isolated and Northern blot hybridization was performed. TNF-alpha mRNA is expressed as the percent relative radioactivity of macrophage (positive control) RNA. In sham or naive animals, no consistent changes in expression of TNF-alpha mRNA were observed in any of the six brain areas at any times (less than 5%). A marked increase of TNF-alpha mRNA expression was observed in LH (104 +/- 17, P < 0.05 compared with sham), LC (105 +/- 21, P < 0.05) and LA (69 +/- 8, P < 0.01) in the traumatized hemisphere 1 h following injury. An increased TNF-alpha mRNA expression was also observed in LH (46 +/- 8, P < 0.05), LC(30 +/- 3, P < 0.01) and LA(32 +/- 3, P < 0.01) at 6 h which resolved by 24 h following injury. In the contralateral hemisphere, expression of TNF-alpha mRNA was increased in RH (46 +/- 2, P < 0.01) at 1 h and in RA (26 +/- 6%, P < 0.05) at 6 h. These results indicate that following parasagittal fluid percussion brain injury, the temporal expression of TNF-alpha mRNA is altered in specific brain regions, including those of the non-traumatized hemisphere. Post-traumatic alteration in gene expression of TNF-alpha might play an important role in both the acute and regenerative response to CNS trauma.

Animals↗