Biomedical subjects

Julie A Robichaud

Publications and source records attributed to Julie A Robichaud.

4 recordsLinked to original sources

PubMed2005

Force control and disease severity in Parkinson's disease.

Several measures of isometric contractions reflect motor impairments in subjects with Parkinson's disease (PD), including long relaxation times and greater power in the 5 to 15 Hz electromyographic (EMG) bandwidth during the holding phase of contractions compared to those measures in healthy subjects. We sought to determine whether the impairments observed in subjects with PD in the performance of isometric contractions reflect disease severity. Twenty-eight subjects with PD performed isometric contractions at a torque level equal to 50% of the torque generated during a maximum voluntary contraction while off medication. Subjects were instructed to reach the target torque as fast as possible upon hearing the auditory "go" signal and to relax their muscles when a second auditory cue signaled the end of the hold phase. There was a significant positive correlation between torque relaxation time and Unified Parkinson's Disease Rating Scale (UPDRS)-Motor score. A significant positive correlation was also observed between the proportion of power in the 5 to 15 Hz frequency bin of the agonist EMG signal and UPDRS-Motor score, and a significant negative correlation between the proportion of power in the 15 to 30 Hz frequency bin and UPDRS-Motor score. These measures provide objective quantification of the severity of motor impairment that can be used to investigate the efficacy of different interventions in individuals with PD.

Acoustic Stimulation↗

PubMed2004

Greater impairment of extension movements as compared to flexion movements in Parkinson's disease.

Research on isometric contractions in subjects with Parkinson's disease (PD) has shown that anti-parkinsonian medication results in a greater increase in extensor strength than flexor strength. This finding is consistent with the hypothesis that there is a greater impairment in neural activation of extensor muscles as compared to flexor muscles in subjects with PD. Such a hypothesis is physiologically feasible given the known differences in the neural control of flexor and extensor muscles. If the above hypothesis is true for both phasic and tonic muscle activation, then differences between performance of rapid single-joint flexion and extension movements should exist in subjects with PD. Twelve subjects with PD, "off" and "on" medication, and 12 age-and sex-matched healthy control subjects performed rapid single-joint movements in flexion and extension over three distances. For neurologically healthy subjects, we did not identify any significant differences in either kinematic or EMG parameters between flexion and extension movements. In contrast, in the PD subjects extension movements were slower and associated with more agonist bursts when compared to flexion movements. The results are consistent with the hypothesis that there is a differential impairment of neural activation of extensor muscles of the arm as compared to flexor muscles in subjects with PD.

Aged↗

PubMed2002

Spinal cord modulation associated with isometric contractions.

OBJECTIVE: The dual-strategy hypothesis explains single-joint voluntary movement by dividing movements into two different strategies and suggesting that different excitation pulses modulate these movements. The existence of this excitation pulse was evaluated by quantifying magnitude and timing changes in the H-reflex (changes in spinal excitability) prior to a voluntary contraction. These changes in spinal excitability were assessed during a ballistic plantar flexion isometric contraction, where both the target size and force level was manipulated. METHODS AND MATERIALS: Subjects were seated in a modified chair with a force transducer placed under the metatarsal heads to measure ankle force output. Following a visual stimulus subjects were trained to produce a plantar flexion force of 25% and 50% of a maximum voluntary contraction, within target sizes of 5% and 15% of the selected force level. Soleus motor neuron reflex excitability was analyzed by measuring changes in the H/M ratio. The H-reflex was randomly elicited by tibial nerve stimulations at 15, 30, 45, 60, 75 and 90 ms prior to the recorded average soleus premotor time for each of the force and target size conditions. RESULTS: A two-way repeated-measures analysis of variance indicated a significant effect among target sizes for the time of change in spinal excitability, slope of facilitation (rate of rise of spinal excitability), and peak facilitation. A significant difference was also established between force levels for the slope and peak facilitation, but there was no difference with time of facilitation. CONCLUSIONS: These results indicate that changes in both target size and force level can influence slope and peak of facilitation. However, only target size appears to affect the time of facilitation. Results clearly support the existence of an excitation pulse that is regulated by the type of movement.

Adult↗

PubMed2002

Effect of medication on EMG patterns in individuals with Parkinson's disease.

Individuals with Parkinson's disease show dramatic improvements in their ability to move when medicated. However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while off and on antiparkinsonian medication. When the subjects were off medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. These results show that medication does not alter the temporal profile of EMG activation.

Aged↗