Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Locomotion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

Avian locomotion activated by brainstem infusion of neurotransmitter agonists and antagonists. II. gamma-Aminobutyric acid.

The companion article (Sholomenko et al. 1991) described the brainstem locomoter regions in the bird where direct intracerebral injection of a number of putative excitatory neurochemicals, including cholinergic agonists, N-methyl-d-aspartate (NMDA) and Substance P, evoke locomotion. Using the same experimental protocol, this study focuses on the locomotor effects following discrete brainstem injections of the inhibitory neurotransmitter, gamma-aminobutyric acid (GABA), and some of GABA agonists and antagonists. Brainstem regions that were electrically and chemically stimulated included the ventromedial medullary reticular formation, the pontobulbar locomotor strip of the dorsolateral pons and medulla, the pontine reticular formation, and the mesencephalic reticular formation. Locomotion was evoked after the injection of the GABA antagonists picrotoxin (a GABAA receptor antagonist) and bicuculline (GABAA antagonist) into several brainstem locomoter regions. Brainstem stimulated locomotion (both chemically and electrically induced) could be transiently blocked by intracerebral infusion of GABA and irreversibly blocked by muscimol (GABAA agonist). Our avian results are similar to those described for mammals and provide support for the suggestion that motor circuitry, at least at brainstem levels, is similar in all vertebrates.

Animals↗

Dopamine and endogenous opioid regulation of picrotoxin-induced locomotion in the ventral pallidum after dopamine depletion in the nucleus accumbens.

Microinjection of picrotoxin or the mu-opioid agonist, Tyr-D-Ala-Gly-NmePhe-Gly-OH (DAMGO), into the ventral pallidum (VP) produces an increase in locomotor activity that is antagonized by dopamine receptor blockade. To investigate the regulation of VP-induced locomotion by the dopaminergic innervation of the nucleus accumbens (NA) and the role of opioid receptors in this regulation, dopamine innervation of the NA was bilaterally lesioned with 6-hydroxydopamine (6-OHDA). The lesions resulted in an 89-97% depletion of tissue dopamine levels in the nucleus accumbens compared with sham-lesioned rats. Dopamine depletion in the NA failed to significantly antagonize picrotoxin or DAMGO injected into the VP. However, the dopamine receptor antagonist, haloperidol (0.1 mg/kg, IP), blocked the picrotoxin-initiated increase in horizontal photocell counts in both sham- and 6-OHDA-lesioned rats. The opioid receptor antagonist, naloxone (1.0 mg/kg, SC), also blocked the picrotoxin-induced locomotion in 6-OHDA-lesioned rats but did not block locomotion in the sham-lesioned rats. At a higher dose (3.0 mg/kg, SC), naloxone blocked picrotoxin-induced locomotion in both sham- and 6-OHDA-lesioned rats. These results indicate that although dopamine depletion in the NA does not affect the permissive role of dopamine transmission on locomotion elicited from the VP, it results in an increased sensitivity to enkephalinergic transmission.

Animals↗

Modulation of polymorphonuclear leukocyte locomotion by synthetic amphiphiles: effect of saturated fatty acid esters (C2-C18) of poly(ethyleneglycol) 6000.

The capacity of synthetic amphiphiles poly(ethyleneglycol) 6000 (PEG) esterified with saturated fatty acids (C2-C18), to modify polymorphonuclear leukocyte (PMNL) locomotion has been investigated. It was noticed that PEG-myristate (M-PEG; C14) stimulated the random locomotion of PMNL populations in concentrations up to about 1 g/L. The esters with shorter aliphatic chains had negligible effects, whereas those with longer chains, PEG-palmitate (P-PEG; C16) and PEG-stearate (S-PEG; C18) reduced the locomotion, irrespectively of concentration. The ability of the PMNL to be stimulated by an attractant liberated from normal human serum was slightly impaired by M-PEG, but not by P-PEG. The response to M-PEG of individual PMNL was heterogeneous in that some cells were stimulated and others were inhibited. However, the average result was a reduction of the motility. This indicates that methods used for the study of the locomotion of cell populations may not always reflect the average behavior of the whole population. It was also concluded that the different effects of M-PEG and P-PEG owed to dissimilar effects on the membrane structure of the PMNL since (1) M-PEG perturbated the PMNL membrane more than P-PEG, as assayed by the release of superoxide anion (O2-), although the binding was smaller, and (2) M-PEG and P-PEG increased and decreased the membrane fluidity, respectively, as measured with fluorescent bleaching and recovery after bleaching of labeled PMNL. The results indicate a subtle coupling between membrane structure and PMNL locomotion.

Cell Membrane↗

Effects of naltrexone on amphetamine-induced locomotion and rearing: acute and repeated injections.

The present experiment investigated the ability of the opiate receptor antagonist naltrexone to block the increased locomotion and rearing produced acutely by amphetamine as well as the sensitization of these responses produced when this drug is administered repeatedly. Rats in different groups received an injection of amphetamine (1.5 mg/kg, i.p.) or saline preceded 30 min earlier by an injection of naltrexone (0, 0.5, 1.0, 5.0 or 10.0 mg/kg, i.p.). Naltrexone dose-dependently reduced the rearing but had no effect on the locomotion produced by this dose of amphetamine. The locomotion and rearing observed following saline were not affected. This pattern of results was observed following each of six additional pairs of injections, one pair of injections given every third day. Once, soon (2-4 days) and once, long (9-12 days) after the last injection, all animals were injected with amphetamine (0.75 mg/kg, i.p.) in the absence of naltrexone (tests for sensitization). Animals having been pre-exposed to amphetamine preceded by naltrexone showed no evidence of sensitized rearing on either test, indicating that naltrexone blocked sensitization of this response to amphetamine. These animals, however, exhibited sensitized locomotion on both tests. These results suggest an important but complex role for dopamine-opioid interactions not only in the production of acute locomotor responding to amphetamine but also in the sensitization of locomotor responding when this drug is administered repeatedly. The present findings also suggest that amphetamine-induced rearing is more dependent than locomotion on neuronal mechanisms involving dopamine-opioid interactions.

Amphetamine↗

Exposure to a rotating virtual environment during treadmill locomotion causes adaptation in heading direction.

The objective of this study was to investigate the adaptive effects of variation in the direction of optic flow, experienced during linear treadmill walking, on modifying locomotor trajectory. Subjects (n=30) walked on a motorized linear treadmill at 4.0 km h(-1) for 24 min while viewing the interior of a 3D virtual scene projected on to a screen 1.5 m in front of them. The virtual scene depicted constant self-motion equivalent to either (1) walking around the perimeter of a room to one's left (Rotating Room group) or (2) walking down the center of a hallway (Infinite Corridor group). The scene was static for the first 4 min and then constant rate self-motion was simulated for the remaining 20 min. Before and after the treadmill locomotion adaptation period subjects performed five stepping trials. In each trial they marched in place to the beat of a metronome at 90 steps min(-1) for a total of 100 steps while blindfolded in a quiet room. The subject's final heading direction (deg) and final X (fore-aft, cm) and final Y (medio-lateral, cm) positions were measured for each trial. During the treadmill locomotion adaptation period subjects' 3D torso position was measured. We found that subjects in the Rotating Room group, as compared with the Infinite Hallway group: (1) showed significantly greater deviation during post-exposure testing in the heading direction and Y position opposite to the direction of optic flow experienced during treadmill walking; and (2) showed a significant monotonically increasing torso yaw angular rotation bias in the direction of optic flow during the treadmill adaptation exposure period. Subjects in both groups showed greater forward translation (in the +X direction) during the post-treadmill stepping task that differed significantly from their pre-exposure performance. Subjects in both groups reported no perceptual deviation in position during the stepping tasks. We infer that viewing simulated rotary self-motion during treadmill locomotion causes adaptive modification of sensorimotor integration in the control of position and trajectory during locomotion, which functionally reflects adaptive changes in the integration of visual, vestibular, and proprioceptive cues. Such an adaptation in the control of position and heading direction during locomotion, because of the congruence of sensory information, demonstrates the potential for adaptive transfer between sensorimotor systems and suggests a common neural site for processing and self-motion perception and concurrent adaptation in motor output.

Adaptation, Physiological↗

Visually induced gait deviations during different locomotion speeds.

Optic flow is essential for the perception of self motion and the control of path integration during locomotion. Inverting prisms oriented 15 degrees off vertical in the roll plane were used to experimentally distort optic flow during locomotion. Depending on the direction in which the prisms were rotated, optic flow was diagonally upward to the right or upward to the left. A reproducible deviation of gait toward the direction of perceived optic flow was found in ten healthy subjects. This deviation is explained to be a gait deviation that compensates for misleading perceived self motion induced by optic flow. The amount of deviation was dependent on locomotion speed. When walking slowly (about 1 m/s), mean deviation was 0.22+/-0.08 m/s to the right and -0.18+/-0.08 m/s to the left for right and left, respectively, diagonal prism orientation. Deviation was significantly less when running (about 3 m/s) with mean deviations of 0.05+/-0.03 m/s and -0.06+/-0.03 m/s, respectively (ANOVA, P<0.01). It is assumed that path integration during running is largely achieved by highly automated spinal programs operating independently of sensory control. In contrast, walking is more dependent on afferent and reafferent visual control. Thus, the experiments show that visual control of locomotion is direction specific and dependent on optic-flow-induced vection. It becomes less influential with increasing speed of locomotion, e.g., when walking in contrast to running.

Adult↗

Comparative studies of the effects of chlorpromazine and 5,6-dihydroxytryptamine on locomotion, defensive reactions in the snail Helix lucorum, and command neuron excitability in long-term sensitization.

The actions of the neuroleptic chlorpromazine (CPZ) and the neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) on defensive reactions, locomotion, formation of long-term sensitization, and the electrical characteristics of command neurons in the common snail were compared. Prolonged (chronic) treatment with CPZ led to a significant increase in the pneumostoma closure time, as well as changes in motor behavior, with a decrease in the rate of locomotion. Administration of 5,6-DHT in small daily doses for one week was accompanied by gradual decreases in the rate of locomotion of the snails, which persisted for one week. A similar effect was seen after administration of the same total dose of neurotoxin, 30 mg/kg, as a single injection. Administration of CPZ prevented the formation of long-term sensitization, as did treatment with 5,6-DHT. The procedures of treatment with CPZ, long-term sensitization, long-term sensitization followed by CPZ, and acquisition of long-term sensitization on the background of treatment with CPZ gave a locomotion speed which was directly proportional to the length of the sole. No such relationship was seen during the acquisition of long-term sensitization on the background of treatment with 5,6-DHT. Electrophysiological studies showed that chronic CPZ led to a depolarization shift in the membrane potential and a decreased action potential generation threshold in command neurons, which also occurred on treatment with 5,6-DHT. It is concluded that the actions of the neuroleptic CPZ on defensive behavior and locomotion in the common snail, as well as on the electrical characteristics of identified neurons, were similar to the toxic actions of serotonin.

5,6-Dihydroxytryptamine↗

Locomotion in the cat: basic programmes of movement.

Observations in cats of flexion and extension movements of the 4 limbs have led to the conclusion that the different forms of alternative locomotion (e.g. walking, trotting, swimming) and in-phase locomotion (galloping, jumping) result from the interaction of 'programmes' for the coordination of (1) the homologous limbs (pair of hindlimbs or pair of forelimbs) and (2) the homolateral limbs (hind- and forelimb of the same side of the body). The movements of the homologous pairs of limbs are coupled out of phase in alternate locomotion and approximately in phase in the phase form of locomotion. The movements of the homolateral pairs of limbs occur approximately out of phase in the trotting type of coupling and approximately in phase in the pacing type of coupling. Transitions between the different forms of coupling occur abruptly over 1 or 2 steps. Therefore, for each type of coupling (homologous or homolateral) there are two distinct forms or 'programmes' of movement. The hypothesis is advanced that (a) all the characteristic patterns of locomotion in the cat result from different combinations of these 'programmes' of homologous and homolateral limb coupling; (b) the 'programmes' are mutually self reinforcing in the gaits in which the coordination of the movements of the 4 limbs is bilaterally symmetrical; (c) the 'programmes' act in competition in certain gaits which are not bilaterally symmetrical giving rise at times to a changing gait pattern, and (d) the temporary dominance of one 'programme' or another can determine the gait of the particular step.

5-Hydroxytryptophan↗

Localization of dopamine receptor subtypes occupied by intra-accumbens antagonists that reverse cocaine-induced locomotion.

The purpose of this study was to examine whether blockade of either dopamine D1-like or D2-like receptors by selective antagonist administration into the nucleus accumbens (NAc) is sufficient to reverse cocaine-induced locomotion, and to develop a new technique that enables the population of receptors occupied by the antagonists to be quantified. Locomotor activity was assessed in rats that had received bilateral intra-accumbens injections of the D1-selective antagonist SCH-23390 (0-3.0 micrograms/0.5 microliters/side) or the D2/D3-selective antagonist sulpiride (0-1.0 micrograms/0.5 microliters/side), followed 15 min later by injections of saline or cocaine (15 mg/kg, i.p.). To assess receptor occupancy by the antagonists, 105 min prior to sacrifice the rats received intra-accumbens injections of the antagonist, followed 15 min later by an injection of the non-selective irreversible antagonist, N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ; 10 mg/kg, i.p.). Receptors were labeled with [3H]SCH-23390 or [3H]sulpiride in sections containing the NAc, and the autoradiograms allowed quantitation of receptors occupied (i.e. protected from EEDQ) by the antagonist given in vivo. Only a dose of 3 micrograms/side SCH-23390 reversed cocaine-induced locomotion, whereas a dose of 0.5 microgram/side did not alter cocaine-induced locomotion despite occupying the same amount of [3H]SCH-23390 binding sites in the NAc. Intermediate doses of 0.1 and 0.3 microgram/side sulpiride reversed cocaine-induced locomotion, and also occupied the greatest number of [3H]sulpiride binding sites in the NAc. The results suggest that blockade of D2-like, but not D1-like, receptors in the NAc is sufficient to reverse cocaine-induced locomotion, and also demonstrate the importance of quantifying receptors occupied by drugs administered intracranially.

Animals↗

In vivo effects of indomethacin and flurbiprofen on the locomotion of neutrophils elicited by immune and non-immune inflammation in the rat.

The in vivo effects of indomethacin (3 mg/kg) and flurbiprofen (1.5 mg/kg) were investigated on the development of three different pleural inflammations in the rat and on in vitro locomotion of elicited neutrophils (PMN). Indomethacin and flurbiprofen similarly reduced the development of non-immune pleurisy induced by decomplemented isologous rat serum (DIRS) to a similar degree but had no effect in the delayed hypersensitivity reaction (DHR) model. Flurbiprofen was less effective than indomethacin in the immediate hypersensitivity reaction (IHR) model. PMN elicited by the two immune reactions (IHR and DHR) displayed lower random and directed locomotion than DIRS-elicited PMN. Neither drug interfered with DIRS-elicited PMN locomotion. They inhibited both random migration and directed locomotion of unwashed PMN (i.e. suspended in their original exudate) elicited by IHR or DHR and stimulated by the peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) or isologous rat serum (IRS). Locomotion of washed IHR-elicited PMN stimulated with IRS was also inhibited by the two drugs. The data suggest that these drugs could impair PMN movement at inflammatory sites.

Animals↗

Control of cell shape and locomotion by external calcium.

Dependence of locomotion of Xenopus laevis epidermal cells on calcium influx from the external medium was investigated. Inhibition of Ca2+ influx by 2 mM La3+ or 4 mM Tb3+ in the culture medium causes an immediate stop to locomotion and a loss of motion at the outer margin of the lamella; microcolliculi disappear and the entire lamella becomes flat and very thin. The cell body region enlarges by spreading into the lamella to an extent approximately coincident with the distribution of myosin. The increase in thickness of this area is the result. The cytoskeletal elements actin, alpha-actinin and myosin become homogeneously distributed throughout the cell and a great number of straight microtubules extend to the margin after 20 min in La3+-containing media. Prekeratin distribution does not change. Reduction of calcium concentration in the external medium by EGTA leads to cessation of cell locomotion. Sr2+ (1-4 mM) is also able to replace calcium for triggering locomotion. These findings point to a control of Ca2+-activated contractions of actomyosin by influx of external Ca2+. According to our model of cell locomotion [14] the contractions generate a hydrostatic pressure extending the lamella by flow of hyaloplasm towards the margin. Small swellings (microcolliculi) appearing thereby will be dislocated by a calcium-dependent sol-gel transformation in this area, which contains actin but not myosin.

Animals↗

Ketamine-induced locomotion in rats in an open-field.

The effects of ketamine on locomotion in an open-field were determined in hooded rats. Animals were given intraperitoneal injections of saline, or of 1, 10, 50 or 100 mg ketamine/kg body weight on separate days. Open-field behavior was examined for 60 min following injection. The 50 mg/kg dose of ketamine produced an increase in locomotion which peaked approximately 30 min after injection. A cataleptic immobility produced by the 100 mg/kg dose was followed by postanesthetic locomotion. The ketamine-induced locomotion consisted largely of ambulation about the perimeter of the field and was accompanied by ataxia, but included relatively little tight circling (rotation) during the peak of activity. Comparisons with the results of past research suggests that test-chamber design influences the type of locomotion induced by ketamine.

Animals↗

Opposite effects of acute versus chronic naltrexone administration on ethanol-induced locomotion.

Several studies have pointed out that the mu opioid receptor (MOR) can play a key role in some of the behavioural effects of ethanol. In the present study, the implication of the MOR in ethanol-induced locomotion in mice was assessed. First, the effects of the administration of different naltrexone doses (0.001-1.000 mg/kg) on the locomotor changes produced by ethanol (2.5 g/kg) were evaluated. In a second set of experiments, the ability of repeated naltrexone (6 mg/kg) administrations to modify the effects of ethanol was also assessed on mice locomotion. The results of the present study revealed that an acute naltrexone administration reduced dose-dependently ethanol-induced locomotion. Conversely, after repeated naltrexone injections, a transient boost of ethanol induced locomotor activity was observed. Thus, the results of the present study revealed that the effects of these naltrexone pretreatments on ethanol-induced locomotion are similar to the previously described changes on MOR activity. Moreover, the same (acute and chronic) naltrexone pretreatments produced similar changes on the locomotion of mice after a challenge with morphine (a MOR agonist), but not after tert-butanol (an alcohol which does not release beta-endorphins) administration. Therefore, our results are discussed in terms of the proved ability of ethanol to promote the release of beta-endorphins and, consequently, to activate the MOR.

Analysis of Variance↗

Effect of a hyaluronan synthase suppressor, 4-methylumbelliferone, on B16F-10 melanoma cell adhesion and locomotion.

Hyaluronan (HA) is a ubiquitous, major component of the extracellular matrix. It is involved in cell adhesion and locomotion, and hence in tumor metastasis. We have previously reported that 4-methylumbelliferone (MU) inhibits HA synthesis and may be a useful tool for examining the functions of HA. We here demonstrate that the formation of cell surface HA by melanoma cells and its release into the culture medium are inhibited by MU. Adhesion and locomotion assays revealed that the adhesion and locomotion of melanoma cells were dose-dependently inhibited by MU. Conversely, treatment with exogenous HA enhanced both adhesion and locomotion. Thus, preventing the formation of cell surface HA reduced both the adhesion and locomotion of melanoma cells, suggesting that MU may act as an inhibitor of tumor metastasis.

Animals↗

Bone mineral density of the proximal femur is not related to dynamic joint loading during locomotion in young women.

We characterized the extent to which body mass influences the relationship between hip joint moments during locomotion and bone mineral density (BMD) of the proximal femur in healthy young women (n = 24). There is some evidence of a direct relationship between hip joint moments during locomotion and BMD of the proximal femur in patients with osteoarthritis. Nevertheless, based on expected simultaneous influences of body mass on BMD and joint moments during locomotion, we hypothesized that BMD would not be significantly associated with hip joint moments during locomotion independently of body mass. BMD of the nondominant proximal femur was determined using DXA. The hip joint moments were determined by gait analysis. The correlation between peak internal rotation moment and BMD of the intertrochanteric region was significant (r = 0.48; P = 0.019). However, body mass was significantly correlated to both BMD and the internal rotation moment (r = 0.59 and 0.70; P = 0.002 and <0.001, respectively). After accounting for the relationship between body mass and hip joint moment, the internal rotation moment was not significantly correlated to BMD of the proximal femur (r = 0.04, P = 0.34) indicating that BMD is not significantly associated with hip joint moments during locomotion independent of body mass in young healthy women.

Absorptiometry, Photon↗

Postural and respiratory activation of the trunk muscles changes with mode and speed of locomotion.

Despite the importance of the deep intrinsic spinal muscles for trunk control, few studies have investigated their activity during human locomotion or how this may change with speed and mode of locomotion. Furthermore, it has not been determined whether the postural and respiratory functions, of which these muscles take part, can be coordinated when locomotor demands are increased. EMG recordings of abdominal and paraspinal muscles were made in seven healthy subjects using fine-wire and surface electrodes. Measurements were also made of respiration and gait parameters. Recordings were made for 10s as subjects walked on a treadmill at 1 and 2 ms(-1) and ran at 2, 3, 4 and 5 ms(-1). Unlike the superficial muscles, transversus abdominis was active tonically throughout the gait cycle with all tasks, except running at speeds of 3 ms(-1) and greater. All other muscles were recruited in a phasic manner. The relative duration of these bursts of activity was influenced by speed and/or mode of locomotion. Activity of all abdominal muscles, except rectus abdominis (RA), was modulated both for respiration and locomotor-related functions but this activity was affected by the speed and mode of locomotion. This study provides evidence that the deep abdominal muscles are controlled independently of the other trunk muscles. Furthermore, the pattern of recruitment of the trunk muscles and their respiratory and postural coordination is dependent on the speed and mode of locomotion.

Abdominal Muscles↗

Effects of MPEP on locomotion, sensitization and conditioned reward induced by cocaine or morphine.

Exposure to environmental cues is considered a major cause of relapse in detoxified addicts. Recent findings showed an involvement of glutamate in cue-induced relapse and suggest that subtype 5 of metabotropic glutamate receptors (mGluR5) is involved in conditioned drug-reward. The present study applied the conditioned place preference (CPP) paradigm to examine the involvement of mGluR5 in cocaine- and morphine-induced behaviours. Results of previous mice-studies were extended into rats by using the selective mGluR5 antagonist 2-methyl-6-(phenylethynyl)pyridine (MPEP). As a result, the evaluated behavioural parameters were dose-relatedly affected by MPEP. Low-dosed MPEP (10 mg/kg, i.p.) did not affect spontaneous locomotion, reduced cocaine-induced hyperlocomotion and produced sensitized locomotion, while showing no effect on sensitized locomotion induced by repeated cocaine or morphine. Low-dosed MPEP did not genuinely block development of cocaine- and morphine-CPP, but rendered CPP expression state-dependent. The medium MPEP-dose (30 mg/kg) was most effective in reducing spontaneous locomotion. The high MPEP-dose (50 mg/kg) was most effective in reducing both body-weight and morphine-CPP expression. Cocaine-CPP expression was not affected by any MPEP-dose. In conclusion, mGluR5 are involved in modulation of spontaneous and cocaine-induced locomotion, in state-dependent learning and in expression of morphine-CPP. Thus, MPEP may be beneficial for relapse prevention in morphine-addicts.

Animals↗

Seat interface pressures of individuals with paraplegia: influence of dynamic wheelchair locomotion compared with static seated measurements.

OBJECTIVE: To provide a comparison of the seat interface pressures between static seating and dynamic seating during wheelchair locomotion of individuals with paraplegia. DESIGN: Repeated measures multivariate analysis of variance (MANOVA) comparing two conditions: static seat and dynamic seat interface pressures. SETTING: University campus and clinic. PARTICIPANTS: Fifteen participants, each of whom propelled a manual wheelchair for at least 5 hours per week over the previous 6 months and functioned with a spinal cord injury/ disability level of T1 or below. MAIN OUTCOME MEASURES: Peak pressure (PP) and pressure time integral (PTI) as measured by the Novel Pliance System, which consists of a flexible 32 x 32 capacitive sensor mat (each sensor 1.5 cm2) interfaced with a PC, was sampled at 10Hz. The participants were measured in their own wheelchair with a new Jay Active seat cushion. RESULTS: The repeated measures MANOVA showed a difference in the PP and PTI between the static and dynamic measurements (Wilk's = .00, p < .05). Follow-up dependent t tests yielded a difference in PP (t = 5.40, p < 0.025) and no difference in the PTI between static and dynamic conditions (t = 1.45, p > 0.025). The PP during static seating (mean = 16.2 +/- 5.0 kPa [121 +/- 37.5 mmHg]) was less than during dynamic seat interface pressures during wheelchair locomotion (20.03 +/- 6.6 kPa [152.3 +/- 49.5 mmHg]). PP varied by up to 42% during the wheelchair locomotion cycle. The PTI was similar between static (30.1 +/- 9.3 kPa [225.75 +/- 69 mmHg]) and dynamic conditions (36.2 +/- 18.1 kPa [271 +/- 135.7 mmHg]). CONCLUSIONS: The results from this study are consistent with some of the previous work on the nondisabled and a single case study, but with greater external validity because of the nature of the sample chosen and the methodology employed. PPs were greater during dynamic wheelchair locomotion compared with static seating interface pressures, with the peak varying up to 42% during the wheelchair locomotion cycle. The PTI indicates that the cumulative effect of the loading was comparable between conditions. The question that remains is whether this dynamic loading, resulting in a change in PP throughout the cycle, has a significant effect on tissue health.

Adult↗