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Biomedical subjects

A Lamontagne

Publications and source records attributed to A Lamontagne.

At least 19 recordsLinked to original sources
PubMed2002

Mechanisms of disturbed motor control in ankle weakness during gait after stroke.

This study investigated the role of paresis, excessive antagonist coactivation, increased muscle-tendon passive stiffness and spasticity in the reduced stance phase plantarflexor moment (Mmax) and swing phase dorsiflexion during gait (DFmax) in subjects with a recent (<6 months post-stroke) hemiparesis (patients). The gait pattern of the paretic and non-paretic sides was evaluated in 30 patients (aged 57.8+/-10.8 years), whereas only one side was evaluated in 15 healthy controls (aged 59.1+/-9.8 years) while walking at natural and very slow speeds. Peak plantarflexor moment (Mmax) and peak medial gastrocnemius (MG) activation during the stance phase, as well as peak dorsiflexion angle (Dfmax) and peak tibialis anterior (TA) activation during the swing phase, were retained for analysis. In addition, a coactivation index and a plantarflexor spasticity index were calculated for both the stance and the swing phase, and plantarflexor passive stiffness was evaluated on an isokinetic dynamometer. The results showed that Mmax on the paretic and non-paretic sides were both reduced compared with control values at natural speed. This reduction was combined to a low MG activation (paresis) on the paretic side. On the non-paretic side, the reduced plantarflexor moment was related to excessive coactivation levels. The swing phase Dfmax tended to be reduced (not significantly) on the paretic side of the patients compared with control values. This reduction was neither associated with excessive antagonist coactivation nor to plantarflexor hyperactive stretch reflexes, but rather to an increased plantarflexor passive stiffness. In some of the patients, however, an increased TA activation that overcame the plantarflexor passive stiffness allowed for normal DFmax values. The functional consequences of the disturbed mechanisms of motor control observed in both the paretic and non-paretic sides are discussed.

Adult↗
PubMed2001

Multiphase transfer processes in waste rock piles producing acid mine drainage 2. Applications of numerical simulation.

Acid mine drainage (AMD) results from the oxidation of sulfides, mainly pyrite, present in mine wastes, either mill tailings or waste rock. This is the second of two papers describing the coupled physical processes taking place in waste rock piles undergoing AMD production. Since the oxidation of pyrite involves the consumption of oxygen and the production of heat, the oxidation process initiates coupled processes of gas transfer by diffusion and convection as well as heat transfer. These processes influence the supply of oxygen that is required to sustain the oxidation process. This second paper describes a numerical simulator used to represent the interaction of these coupled transfer processes. Numerical simulations are applied to two large sites with extensive characterization programs and widely different properties and behavior that were described in the first paper. The South Dump of the Doyon mine in Canada is permeable and has a high pyrite oxidation rate, thus making temperature-driven air convection the main oxygen supply mechanism. The Nordhalde of the Ronnenberg mining district in Germany contains lower permeability material which is less reactive, thus leading to a more balanced contribution of gaseous diffusion and convection as oxygen supply mechanisms. Overall, simulations allow a coherent representation of the conditions monitored within the waste rock piles and the confirmation of their physical properties. Conceptual simulations are also carried out to illustrate the potential effect of border membranes and layered co-mingling as mitigation methods used to control AMD production in either active or future waste rock piles.

Chemical Phenomena↗
PubMed2001

Locomotor-specific measure of spasticity of plantarflexor muscles after stroke.

OBJECTIVES: To study the stretch reflex excitability (spasticity) of the plantarflexor muscles during gait in patients with hemiparesis and to study the relationships of spasticity during gait with spasticity at rest and gait speed. DESIGN: Cross-sectional, descriptive. SETTING: Rehabilitation center. PARTICIPANTS: Convenience sample of 30 patients (58 +/- 11yr) with hemiparesis (<6mo poststroke) and 15 healthy controls (59 +/- 8yr). INTERVENTIONS: Patients walked at natural speed, healthy subjects at very slow speed for 10 gait cycles. Electromyographic activation of the medial gastrocremius was recorded by using surface electrodes. A 2-dimensional video camera system with reflective markers was used to acquire kinematics of the lower limbs. MAIN OUTCOME MEASURES: Electromyography-lengthening velocity slopes, calculated from measures obtained during the lengthening periods of the medial gastrocnemius muscle during the stance and the swing phases. Measured spatisticity (Modified Ashworth Scale [MAS]), static strength (ankle clonus), and motor control (Fugl-Meyer test). RESULTS: Velocity-sensitive electromyographic responses, indicative of hyperactive stretch reflexes, were found on the paretic side during the stance phase of gait (in 66% of the patients), but not on the nonparetic side or in controls. In many patients, velocity-sensitive responses coexisted with low plantarflexor activation levels during the stance phase. No clear patterns of response were measured during the swing phase in either group. Spasticity during gait in the patients was found to be positively related (r = .47, p < .01; r = .57, p < .001) to spasticity at rest (MAS; ankle clonus), whereas it was found to be negatively related to gait speed (r = -.47 to -.53, p < .01). CONCLUSIONS: The validity of the present method is supported by the fact that it is locomotor-specific and that it allowed for a good discrimination between spastic and nonspastic limbs, as well as between stance and swing phases of the gait cycle. The results also support plantarflexor spasticity as a factor contributing to the poor locomotor performance after stroke.

Adult↗
PubMed2000

Contribution of passive stiffness to ankle plantarflexor moment during gait after stroke.

OBJECTIVE: To measure the contribution of passive stiffness to the ankle plantarflexor moment during gait in subjects with hemiparesis early after stroke. The relationship of passive stiffness with gait speed was also examined. DESIGN: Cross-sectional, descriptive. PATIENTS AND OTHER PARTICIPANTS: A sample of convenience of 14 patients (54.7+/-10.9 yrs) with a hemiparesis for less than 5 months and 11 healthy controls (50.6+/-11.6 yrs). MAIN OUTCOME MEASURES: The contribution of passive stiffness to the plantarflexor moment during gait was obtained using moment-angle slope (stiffness) values. Total plantarflexor stiffness was measured during gait, and passive stiffness was measured during passive dorsiflexion imposed by an isokinetic dynamometer at velocities and ranges of movement matched with values recorded during the plantarflexor lengthening period of the stance phase. The contribution of passive stiffness was obtained by dividing the passive stiffness (dynamometer) by the total plantarflexor stiffness (gait). RESULTS: On the paretic side, passive stiffness contributed more (16.8%; range 2.9% to 49.6%) to total plantarflexor stiffness during gait compared (p<.01) with both the nonparetic side (7.3%) and control values (5.9%). This increased contribution on the paretic side resulted from a large muscle-tendon passive stiffness, a decreased active muscle contribution, or both. Although in some patients the increased passive component led to the development of a total plantarflexor stiffness that was within normal values, it did not in others either because the active component was very small or because limited dorsiflexion during the stance phase prevented the passive component tension to develop. The contribution of passive stiffness was not significantly (p>.05) related to gait speed in both the patients and the controls. CONCLUSIONS: The increased contribution of passive stiffness to total plantarflexor moment during gait likely acts as an adaptation for a defective muscle active component, helping ankle push-off at the end of the stance phase. Although this mechanism is effective in most of the patients, it cannot come into action if the dorsiflexion movement during the stance phase is prevented, for instance, by enhanced stretch reflexes.

Adult↗
PubMed2000

Coactivation during gait as an adaptive behavior after stroke.

The aims of the present study were to quantify the impairment in ankle coactivation on the paretic and non-paretic sides of subjects with hemiparesis and to examine the relationship of ankle coactivation with postural instability, motor deficit of the paretic lower extremity and locomotor performance. Electromyography of the medial gastrocnemius (MG) and tibialis anterior (TA) muscles were recorded bilaterally during gait in 30 subjects (62.1+/-9.9 years) who had suffered a recent stroke (<6 months) as well as on one side of 17 healthy controls (59.3+/-9.1 years) walking at very slow speed. Ankle muscle coactivation was calculated by dividing the time of overlap between MG and TA signals (threshold of 20 microV) by the duration of the gait phases of interest: stance, swing, first and second double support sub-phases and single support sub-phase. The time spent in single support and the peak plantarflexor moment of force on the paretic side were used to measure, respectively, postural stability and dynamic strength of the paretic plantarflexors. The subjects with hemiparesis demonstrated less coactivation on the paretic side during the single support sub-phase (p<0.01) and more coactivation during first and second double support sub-phases on the non-paretic side (p<0.001) compared to control values. The patients with coactivation patterns that differed the most from controls were the patients with the more severe impairments and disabilities. While the reduced coactivation on the paretic side may contribute to poor postural stability and poor locomotor performance, the presence of excessive coactivation on the non-paretic side when both limbs were in ground contact may be an adaptation to help maintain postural stability during gait.

Adaptation, Physiological↗
PubMed2000

The hepatitis B virus core promoter is strongly activated by the liver nuclear receptor fetoprotein transcription factor or by ectopically expressed steroidogenic factor 1.

Orphan nuclear receptor fetoprotein transcription factor (FTF) was previously identified as a specific regulator of the alpha(1)-fetoprotein gene during early liver development and in response to hormonal signals (L. Galarneau, J.-F. Paré, D. Allard, D. Hamel, L. Lévesque, J. D. Tugwood, S. Green, and L. Bélanger, Mol. Cell. Biol. 16:3853-3865, 1996). Here we report a functional analysis of FTF interactions with the hepatitis B virus (HBV) nucleocapsid promoter. DNA-protein-binding assays show that the HBV core promoter contains two high-affinity FTF-binding sites and a third, lower-affinity site shared with other receptors. Transfections in HepG2, Hep3B, and PLC/PRF/5 hepatoma cells using chloramphenicol acetyltransferase reporter genes with the nucleocapsid promoter linked or not linked to enhancer I indicate that FTF is a potent activator of the HBV core promoter, more efficient than HNF4alpha, HNF3alpha, HNF3beta, or C/EBPalpha. Steroidogenic factor 1, a close FTF homolog which binds to the same DNA motif and is expressed ectopically in HepG2 cells, seems to be an even stronger inducer than FTF. Point mutations of the FTF-binding sites indicate direct FTF activatory effects on the core promoter and the use of both high-affinity sites for productive interaction between the core promoter and enhancer I. Coexpression assays further indicate that FTF and HNF4alpha are the most efficient partners for coactivation of the pregenomic core promoter, which may largely account for the hepatic tropism and the early amplification of HBV infection. Carboxy terminus-truncated FTF behaves as a dominant negative mutant to compete all three FTF sites and strongly deactivate core promoter interactions with enhancer I; this suggests possible new ways to interfere with HBV infection.

Base Sequence↗
PubMed1999

From genotype to phenotype: a clinical pathological, and biochemical investigation of frontotemporal dementia and parkinsonism (FTDP-17) caused by the P301L tau mutation.

Frontotemporal dementia is a heterogeneous, often inherited disorder that typically presents with the insidious onset of behavioral and personality changes. Two genetic loci have been identified and mutations in tau have been causally implicated in a subset of families linked to one of these loci on chromosome 17q21-22. In this study, linkage analysis was performed in a large pedigree, the MN family, suggesting chromosome 17q21-22 linkage. Mutational analysis of the tau coding region identified a C-to-T change in exon 10 that resulted in the conversion of proline to a leucine (P301L) that segregated with frontotemporal dementia in this family. The clinical and pathological findings in the MN family emphasize the significant overlap between Pick's disease, corticobasal degeneration, and frontotemporal dementia and challenge some of the current dogma surrounding this condition. Pathological studies of two brains from affected members of Family MN obtained at autopsy demonstrate numerous tau-positive inclusions that were most prominent in the frontal lobes, anterior temporal lobes, and brainstem structures, as well as Pick-like bodies and associated granulovacuolar degeneration. These Pick-like bodies were observed in 1 patient with motor neuron disease. Because exon 10 is present only in tau mRNA coding for a protein with four microtubule binding repeats (4R), this mutation should selectively affect 4Rtau isoforms. Indeed, immunoblotting demonstrated that insoluble 4Rtau is selectively aggregated in both gray and white matter of affected individuals. Although there was significant pathological similarity between the 2 cases, the pattern of degenerative changes and tau-positive inclusions was not identical, suggesting that other genetic or epigenetic factors can significantly modify the regional topology of neurodegeneration in this condition.

Brain↗
PubMed1998

Evaluation of reflex- and nonreflex-induced muscle resistance to stretch in adults with spinal cord injury using hand-held and isokinetic dynamometry.

BACKGROUND AND PURPOSE: In this study, we compared the intertrial reliability of resistive torque measurements obtained with hand-held and isokinetic dynamometers and examined the validity of the hand-held dynamometers for the assessment of spastic hypertonia, defined as reflex- and nonreflex-induced resistance to stretch. SUBJECTS: Nine subjects (mean age = 40.6 years) with a chronic (1-5 years) spinal cord injury participated. METHODS: The plantar flexors were stretched at 5 degrees /s (low velocity [LV]) and 180 degrees /s (high velocity [HV]) with an isokinetic dynamometer while the evaluator attempted to match these velocities with a hand-held dynamometer. Electromyographic activity of the soleus and tibialis anterior muscles as well as ankle displacements were recorded. Resistive torque and velocity, measured at -5 degrees of dorsiflexion, were averaged (n = 4). RESULTS: High intraclass correlation coefficients (ICCs) were found at LV and HV for both the hand-held (ICC = .93 and .84) and isokinetic (ICC = .99 and .93) dynamometers. With the hand-held dynamometer, lower resistive torques were found at LV (0.8 N.m) and HV (1.2 N.m), whereas higher velocities were attained at HV. CONCLUSION AND DISCUSSION: The results indicate that the reproducibility of resistive torques obtained with hand-held dynamometry compares with that obtained with isokinetic dynamometry and allows testing of velocities that can be adjusted to the specific level of resistance to stretch. Electromyography confirmed the validity of hand-held dynamometry for assessing reflex and nonreflex components of SH. [Lamontagne A, Malouin F, Richards CL, Dumas F. Evaluation of reflex- and nonreflex-induced muscle resistance to stretch in adults with spinal cord injury using hand-held and isokinetic dynamometry.

Adult↗
PubMed1997

Viscoelastic behavior of plantar flexor muscle-tendon unit at rest.

Muscle stretching as an exercise routine is widely used in orthopaedic and neurological rehabilitation. However, the muscle response to specific stretching parameters is still unclear. The aim of this study was to investigate the effect parameters, such as stretch velocity, stretch extent, and initial muscle-tendon resistance, on the plantar flexor response to passive movement. Eighteen healthy subjects (23-41 years) participated in this study. Five passive ankle dorsiflexions were randomly imposed at various velocities from 5 degrees/sec to 180 degrees/sec using a Kin-Com dynamometer, while unwanted activations of the soleus and tibialis anterior muscles were detected with surface electrodes. The resistive torque was averaged at -10 degrees and 0 degree of dorsiflexion. As shown by analyses of variance followed by Scheffé post hoc procedures, the resistive torque was significantly increased (p < 0.01) between 5 degrees/sec and higher velocities (60 degrees/sec or 120 degrees/sec and higher). A strong linear resistive torque-velocity relationship was also observed, as indicated by Pearson correlation coefficients of 0.92 (-10 degrees) and 0.91 (0 degree). The absolute resistive torque increment, calculated at 180 degrees/sec, was larger at 0 degree of dorsiflexion than at the -10 degrees of dorsiflexion position. Finally, subjects with larger initial plantar flexor resistance had a higher resistive torque increment (p < 0.05) at a high velocity of stretch (180 degrees/sec) than those with less initial muscle-tendon resistance. These results indicate that 1) the nonreflex resistive torque response to stretch is velocity-sensitive and 2) both a larger stretch extent and muscle initial resistance lead to greater resistive torque increments at high velocity. These observations suggest that slow and gradual stretching procedures, rather than rapid or ballistic movements, should be used, especially with stiff muscles to reduce the chance of injury from excessively high tension.

Adult↗
PubMed1990

Tetrahydroaminoacridine-lecithin combination treatment in patients with intermediate-stage Alzheimer's disease. Results of a Canadian double-blind, crossover, multicenter study.

We studied the efficacy and safety of oral tetrahydroaminoacridine (THA) combined with lecithin in 52 patients with Alzheimer's disease. The maximal tolerated dose of THA (up to 100 mg per day) was determined during an eight-week titration period, after which the tolerated dose of THA or placebo was given during two sequential randomized periods of treatment lasting eight weeks each. Highly purified lecithin (4.7 g per day) was administered during all phases of the study. Efficacy was expressed in terms of scores on the Mini-Mental State (MMS) test, the modified MMS test, the Hierarchic Dementia Scale, the Rapid Disability Rating Scale-II, and the behavioral scale of Reisberg et al. Safety was assessed by careful clinical monitoring as well as serial measurements of liver aminotransferases. Forty-six patients completed the titration period, and 39 completed the double-blind period, during which only the MMS score showed a small but significant increase (P less than 0.05) after four weeks of treatment with THA. Autonomic side effects of THA were common but mild. Reversible elevations of serum aspartate and alanine aminotransferase levels to three or more times the upper limit of normal occurred in 17 percent of patients; most of the patients affected were women. A liver biopsy performed in one patient showed resolving focal liver-cell necrosis. These studies fail to demonstrate a significant clinical benefit of THA given orally in a maximal dose of 100 mg per day over a period of eight weeks in combination with lecithin.

Administration, Oral↗
PubMed1984

Density-dependent regulation of growth in somatic hybrids between normal Chinese hamster fibroblasts and V79-8 (G1-) cells.

The purpose of this work was to determine the relationship between the presence of a G1 period in the mitotic cycle and a cell's ability to respond to density-dependent regulation of growth (DDR). Somatic hybrids were obtained between normal fibroblasts from newborn Chinese hamsters, which show a strong response to DDR, and V79-8 Chinese hamster cells, which are insensitive to DDR. Two variant V79-8 sublines were used, one reported to lack a G1 period (G1-) and the other with a G1 period (G1+). Fourteen hybrid clones were isolated in selective medium and analysed for growth properties and cell cycle parameters; their hybrid nature was supported by chromosome counts. All hybrid clones, irrespective of whether a V79-8 G1- or G1+ cell was one of the parents, showed pronounced DDR and had G1 periods of various lengths. Previous experiments had shown the absence of G1 to be dominant in somatic hybrids between V79-8 G1- and G1+ cell lines. Our results may mean that the G1- property provided by V79-8 is unable to overcome the very long G1 of normal fibroblasts, or in cells that can be arrested in G1 in response to DDR, some function prevents the dominant effect of the G1- cell on at least part of the G1 period.

Animals↗
PubMed1976

Nerve conduction studies and electromyography in Friedreich's ataxia.

Twenty-six of 50 patients were investigated with nerve conduction studies and electromyography using a standard protocol and were compared to the findings in 50 normal control subjects. Almost all cases of typical Friedreich's ataxia had absent sensory action potentials (SAP) in the digital (92%) or sural (96%) nerves. The others had markedly decreased S.A.P's. In these same patients motor conduction velocities were either normal or only slightly decreased. In the second, atypical group of 9 patients, the motor conduction velocities were considerably decreased. Because of the absence of sensory action potentials in Friedreich's ataxia, and that the absence was noted in our very mild cases, it is proposed that this measure be used to facilitate early diagnosis.

Action Potentials↗
PubMed1970

Electrophysiological studies in diabetic neuropathy.

In 30 patients with diabetic neuropathy sensory potentials in the median nerve, motor conduction in the lateral popliteal and median nerves, and electromyographic findings in distal and proximal muscles were compared with the severity of symptoms and signs. All patients had abnormalities in at least one of the electrophysiological parameters. The sensory potentials were the most sensitive indicator of subclinical involvement; abnormalities were found in 24 patients, 12 of whom had no sensory symptoms or signs and five of whom had no other clinical or electrophysiological evidence of neuropathy in the upper extremities. This indicates that sensory nerve fibres may be affected before motor. The next most sensitive parameter was the presence of fibrillation potentials, found in more than half the distal muscles examined. Slowing in motor conduction in the lateral popliteal nerve was the only electrophysiological change correlated to the severity of the neuropathy, and no other electrophysiological parameter was correlated to the duration or the severity of the neuropathy or the diabetes. An onset of neuropathy before or simultaneously with the manifestations of the diabetes, as well as the frequent occurrence of asymptomatic changes in sensory conduction, support the evidence at hand that the neuropathy develops concomitantly with and as an integral part of the metabolic disturbance rather than as a consequence of the vascular complications of diabetes. Of three patients with clinical signs or symptoms of a diabetic amyotrophy, two had asymptomatic electrophysiological abnormalities in distal nerves and muscles, consistent with widespread involvement of the peripheral nerves. The third patient had electromyographic changes in the medial vastus muscles suggestive of a myopathy. Motor and sensory conduction in distal and proximal nerves were normal.

Adult↗