Parkinson Disease: Corcos DM

Prodoehl J, Corcos DM, Vaillancourt DE. · Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL 60612, USA. · Neurosci Biobehav Rev. · Pubmed #19428499 No free full text.

Abstract: The classic grasping network has been well studied but thus far the focus has been on cortical regions in the control of grasping. Sub-cortically, specific nuclei of the basal ganglia have been shown to be important in different aspects of precision grip force control but these findings have not been well integrated. In this review, we outline the evidence to support the hypothesis that key basal ganglia nuclei are involved in parameterizing specific properties of precision grip force. We review literature from different areas of human and animal work that converges to build a case for basal ganglia involvement in the control of precision gripping. Following on from literature showing anatomical connectivity between the basal ganglia nuclei and key nodes in the cortical grasping network, we suggest a conceptual framework for how the basal ganglia could function within the grasping network, particularly as it relates to the control of precision grip force.

Tisch S, Rothwell JC, Limousin P, Hariz MI, Corcos DM. · Unit of Functional Neurosurgery, Sobell Department of Motor Neuroscience, Institute of Neurology, London WC1N 3BG, UK. · IEEE Trans Neural Syst Rehabil Eng. · Pubmed #17601185 No free full text.

Abstract: Dystonia is an involuntary movement disorder characterized by muscle contractions causing abnormal postures and spasms, affecting part or all of the body. Dystonia may be primary where an abnormal gene, most commonly DYT1, may be identified, or secondary to structural brain lesions or heredodegenerative disorders. The underlying defect is believed to be abnormal basal ganglia modulation of cortical motor pathways, and various motor and sensory physiological abnormalities have been demonstrated. The failure of medical treatment in many patients with the more severe and generalized forms of dystonia has led to renewed interest in neurosurgical treatment approaches. In recent years, deep brain stimulation (DBS) of globus pallidus internus (GPi) has emerged as an effective treatment for dystonia, particularly patients with primary generalized dystonia, where remarkable improvement may occur. In contrast to Parkinson's disease, the beneficial effects of DBS in dystonia are not immediate but progressive over weeks to months. Physiological and imaging studies in dystonia patients with GPi DBS have demonstrated both short and long-term effects of GPi DBS on motor cortex and subcortical circuits including progressive normalization of spinal and brainstem excitability after GPi DBS which correlate with clinical improvement. These effects, in light of existing physiological data in dystonia, suggest that GPi DBS acts primarily by major modification of basal ganglia output to brainstem, thalamus, and cortex resulting in neural reorganization, which may explain the characteristic progressive improvement in dystonia after GPi DBS.

Prodoehl J, Corcos DM, Rothwell JC, Metman LV, Bakay RA, Vaillancourt DE. · Department of Movement Sciences, University of Illinois, Chicago, IL 60608, USA. · IEEE Trans Neural Syst Rehabil Eng. · Pubmed #17601184 links to  free full text

Abstract: This study examined the control of elbow force in nine patients with Parkinson's disease when visual feedback was available and when visual feedback was removed to determine how medication (Meds) and unilateral deep brain stimulation (DBS) of the subthalamic nucleus (STN) affect memory guided force control. Patients were examined in each of four treatment conditions: 1) off treatment; 2) Meds; 3) STN DBS; and 4) Meds plus STN DBS. With visual feedback available, there was no difference in force output across treatment conditions. When visual feedback was removed force output drifted under the target in both the off-treatment and the Meds conditions. However, when on STN DBS or Meds plus STN DBS force output drifted above the target. As such, only STN DBS had a significant effect on force output in the vision removed condition. Increased force output when on STN DBS may have occurred due to disruptions in the basal ganglia-thalamo-cortical circuitry. We suggest that modulation of output of the internal segment of the globus pallidus by STN DBS may drive the effect of STN DBS on memory guided force control.

Flament D, Shapiro MB, Pfann KD, Moore CG, Penn RD, Corcos DM. · Department of Physical Medicine and Rehabilitation, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA. · Mov Disord. · Pubmed #12112195 No free full text.

Abstract: We studied the effect of high-frequency electrical stimulation of the ventral-intermediate nucleus of the thalamus (Vim) in four patients implanted with chronic stimulators to determine whether this procedure adversely affects reaction time to a proprioceptive stimulus. Two patients had undergone this surgery for treatment of tremor resulting from Parkinson's disease insufficiently responsive to levodopa therapy and two patients for treatment of essential tremor. Reaction times to auditory, visual, cutaneous, and proprioceptive stimuli were tested in a simple motor task requiring flexion of the elbow joint to a visual target in response to each stimulus. Reaction times were tested postoperatively with and without the stimulator turned on. We found that reaction time for all stimulus modalities was not increased when the stimulator was turned on; in fact, reaction times were, on average, slightly shorter during stimulation, but this difference was not statistically significant. We conclude that transmission of somatosensory inputs, necessary for initiating voluntary movement, from the periphery to the cortex is not significantly impaired by stimulation of the ventral-intermediate nucleus of the thalamus in patients with pathological tremor.

Vaillancourt DE, Spraker MB, Prodoehl J, Abraham I, Corcos DM, Zhou XJ, Comella CL, Little DM. · Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 West Taylor, 650 AHSB, MC 994, Chicago, IL 60612, USA. · Neurology. · Pubmed #19129507 No free full text.

Abstract: BACKGROUND: In the midbrain of patients with Parkinson disease (PD), there is a selective loss of dopaminergic neurons in the ventrolateral and caudal substantia nigra (SN). In a mouse model of PD, investigators have administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and found that measures derived using diffusion tensor imaging (DTI) were correlated with the number of dopamine neurons lost following intoxication. METHODS: Twenty-eight subjects (14 with early stage, untreated PD and 14 age- and gender-matched controls) were studied with a high-resolution DTI protocol at 3 Tesla using an eight-channel phase array coil and parallel imaging to study specific segments of degeneration in the SN. Regions of interest were drawn in the rostral, middle, and caudal SN by two blinded and independent raters. RESULTS: Fractional anisotropy (FA) was reduced in the SN of subjects with PD compared with controls (p < 0.001). Post hoc analysis identified that reduced FA for patients with PD was greater in the caudal compared with the rostral region of interest (p < 0.00001). A receiver operator characteristic analysis in the caudal SN revealed that sensitivity and specificity were 100% for distinguishing patients with PD from healthy subjects. Findings were consistent across both raters. CONCLUSIONS: These findings provide evidence that high resolution diffusion tensor imaging in the substantia nigra distinguishes early stage, de novo patients with Parkinson disease (PD) from healthy individuals on a patient by patient basis and has the potential to serve as a noninvasive early biomarker for PD.

Robichaud JA, Pfann KD, Leurgans S, Vaillancourt DE, Comella CL, Corcos DM. · Department of Kinesiology and Nutrition (M/C 994), University of Illinois at Chicago, 1919 West Taylor Street, 650 AHSB, MC 994, Chicago, IL 60612, USA. · Clin Neurophysiol. · Pubmed #19084473 No free full text.

Abstract: OBJECTIVE: This study evaluated whether changes in the electromygraphic (EMG) pattern during rapid point-to-point movements in individuals diagnosed with PD can: (1) distinguish PD subjects from healthy subjects and (2) determine if differences in the EMG pattern reflect disease severity in PD. METHODS: Three groups of 10 PD subjects and 10 age/sex-matched healthy subjects performed rapid 72 degree point-to-point elbow flexion movements. PD subjects were divided, a priori, into three groups based upon off medication motor UPDRS score. RESULTS: Measures related to the EMG pattern distinguished all PD subjects and 9 out of 10 healthy subjects, resulting in 100% sensitivity. Further, significant correlations were shown between EMG measures and the motor UPDRS score. After 30 months, the one healthy subject whose EMG pattern was abnormal was reexamined. The EMG measures remained abnormal and the motor UPDRS score went from 0 to 10. Parkinson's disease was diagnosed. CONCLUSION: Measures related to the variability of the EMG pattern during rapid point-to-point movements provide neurophysiological measures that objectively distinguish PD subjects from healthy subjects. These measures also correlate with disease severity. SIGNIFICANCE: EMG measures may provide a non-invasive measure that is sensitive and specific for identifying individuals with PD.

Sturman MM, Vaillancourt DE, Shapiro MB, Metman LV, Bakay RA, Corcos DM. · Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois, USA. · Mov Disord. · Pubmed #18311827 No free full text.

Abstract: Currently, no study of subthalamic nucleus (STN) stimulation has compared continuous stimulation with a period of short-term stimulation, which is frequently employed in the clinic and in research studies. Therefore, this study examined the effects of STN stimulation over 90 min (short) and greater than 3 months (long) on the cardinal signs of Parkinson's disease. The 90 min time period immediately followed a 12 hour withdrawal from both STN stimulation and medication. Ten PD patients who received STN stimulation were studied. Bradykinesia, rigidity, and tremor were evaluated using the UPDRS and motor control measures which included peak velocity (bradykinesia), work (rigidity), and amplitude (tremor). Results showed no difference between 90 min and greater than 3 months of STN stimulation for the UPDRS or motor control measures. This finding confirms that the treatment efficacy that is derived from a relatively short time course of stimulation generalizes to longer time periods of high frequency STN stimulation that patients experience in their daily lives. As such, it is reasonable to evaluate the effect of DBS after 90 min of stimulation in clinical trials and research studies.

Shapiro MB, Vaillancourt DE, Sturman MM, Metman LV, Bakay RA, Corcos DM. · University of Illinois, Chicago, IL 60612, USA. · IEEE Trans Neural Syst Rehabil Eng. · Pubmed #17601186 links to  free full text

Abstract: We quantified the effects of deep brain stimulation (DBS) of the subthalamic nucleus (STN) and medication on Parkinsonian rigidity using an objective measure of work about the elbow joint during a complete cycle of imposed 1-Hz sinusoidal oscillations. Resting and activated rigidity were analyzed in four experimental conditions: 1) off treatment; 2) on DBS; 3) on medication; and 4) on DBS plus medication. Rigidity at the elbow joint was also assessed using the Unified Parkinson's Disease Rating Scale (UPDRS). We tested ten patients who received STN DBS and ten age-matched neurologically healthy control subjects. The activated rigidity condition increased work in both Parkinson's disease (PD) patients and control subjects. In PD patients, STN DBS reduced both resting and activated rigidity as indicated by work and the UPDRS rigidity score. This is the first demonstration that STN stimulation reduces rigidity using an objective measure such as work. In contrast, the presurgery dose of antiparkinsonian medication did not significantly improve the UPDRS rigidity score and reduced work only in the activated rigidity condition. Our results suggest that STN DBS may be more effective in alleviating rigidity in the upper limb of PD patients than medications administered at presurgery dosage level.

Sturman MM, Vaillancourt DE, Metman LV, Sierens DK, Bakay RA, Corcos DM. · Department of Movement Sciences, University of Illinois at Chicago, Chicago, IL 60612, USA. · Mov Disord. · Pubmed #17469210 links to  free full text

Abstract: This study examined the efficacy of subthalamic nucleus (STN), deep brain stimulation (DBS), and medication for resting tremor during performance of secondary tasks. Hand tremor was recorded using accelerometry and electromyography (EMG) from 10 patients with Parkinson's disease (PD) and ten matched control subjects. The PD subjects were examined off treatment, on STN DBS, on medication, and on STN DBS plus medication. In the first experiment, tremor was recorded in a quiet condition and during a cognitive task designed to enhance tremor. In the second experiment, tremor was recorded in a quiet condition and during isometric finger flexion (motor task) with the contralateral limb at 5% of the maximal voluntary contraction (MVC) that was designed to suppress tremor. Results showed that: (1) STN DBS and medication reduced tremor during a cognitive task that exacerbated tremor, (2) STN DBS normalized tremor frequency in both the quiet and cognitive task conditions, whereas tremor amplitude was only normalized in the quiet condition, (3) a secondary motor task reduced tremor in a similar manner to STN DBS. These findings demonstrate that STN DBS still suppresses tremor in the presence of a cognitive task. Furthermore, a secondary motor task of the opposite limb suppresses tremor to levels comparable to STN DBS.

Yu H, Sternad D, Corcos DM, Vaillancourt DE. · Department of Movement Sciences, University of Illinois at Chicago, Chicago, IL 60612, USA. · Neuroimage. · Pubmed #17223579 links to  free full text

Abstract: Previous neuroimaging studies have found hyperactivation in the cerebellum and motor cortex and hypoactivation in the basal ganglia in patients with Parkinson's disease (PD) but the relationship between the two has not been established. This study examined whether cerebellar and motor cortex hyperactivation is a compensatory mechanism for hypoactivation in the basal ganglia or is a pathophysiological response that is related to the signs of the disease. Using a BOLD contrast fMRI paradigm PD patients and healthy controls performed automatic and cognitively controlled thumb pressing movements. Regions of interest analysis quantified the BOLD activation in motor areas, and correlations between the hyperactive and hypoactive regions were performed, along with correlations between the severity of upper limb rigidity and BOLD activation. There were three main findings. First, the putamen, supplementary motor area (SMA) and pre-SMA were hypoactive in PD patients. The left and right cerebellum and the contralateral motor cortex were hyperactive in PD patients. Second, PD patients had a significant negative correlation between the BOLD activation in the ipsilateral cerebellum and the contralateral putamen. The correlation between the putamen and motor cortex was not significant. Third, the BOLD activation in the motor cortex was positively correlated with the severity of upper limb rigidity, but the BOLD activation in the cerebellum was not correlated with rigidity. Further, the activation in the motor cortex was not correlated with upper extremity bradykinesia. These findings provide new evidence supporting the hypothesis that hyperactivation in the ipsilateral cerebellum is a compensatory mechanism for the defective basal ganglia. Our findings also provide the first evidence from neuroimaging that hyperactivation in the contralateral primary motor cortex is not a compensatory response but is directly related to upper limb rigidity.

Vaillancourt DE, Prodoehl J, Sturman MM, Bakay RA, Metman LV, Corcos DM. · Department of Movement Science, University of Illinois, Chicago, Illinois 60612, USA. · Mov Disord. · Pubmed #16124011 links to  free full text

Abstract: We investigated the control of movement in 12 patients with Parkinson's disease (PD) after they received surgically implanted high-frequency stimulating electrodes in the subthalamic nucleus (STN). The experiment studied ankle strength, movement velocity, and the associated electromyographic patterns in PD patients, six of whom had tremor at the ankle. The patients were studied off treatment, ON STN deep brain stimulation (DBS), on medication, and on medication plus STN DBS. Twelve matched control subjects were also examined. Medication alone and STN DBS alone increased patients' ankle strength, ankle velocity, agonist muscle burst amplitude, and agonist burst duration, while reducing the number of agonist bursts during movement. These findings were similar for PD patients with and without tremor. The combination of medication plus STN DBS normalized maximal strength at the ankle joint, but ankle movement velocity and electromyographic patterns were not normalized. The findings are the first to demonstrate that STN DBS and medication increase strength and movement velocity at the ankle joint.

Sturman MM, Vaillancourt DE, Corcos DM. · Department of Movement Sciences (M/C 994 University of Illinois at Chicago, 808 South Wood, 690 CMET, Chicago, IL 60612, USA. · J Neurophysiol. · Pubmed #15716367 links to  free full text

Abstract: The purpose of this investigation was to determine the effects of healthy aging on the regularity of physiological tremor under rest and postural conditions. Additionally, we examined the contribution of mechanical reflex factors to age-related changes in postural physiological tremor. Tremor regularity, tremor-electromyographic (EMG) coherence, tremor amplitude, and tremor modal frequency were calculated for 4 age groups (young: 20-30 yr, young-old: 60-69 yr, old: 70-79 yr, and old-old: 80-94 yr) under resting and loaded postural conditions. There were 6 important findings from this study: 1) there were no differences between the young and elderly subjects for any of the dependent variables measured under the rest condition; 2) postural physiological tremor regularity was increased in the elderly; 3) postural physiological tremor-EMG coherence was also increased in the elderly, and there was a strong linear relation between peak tremor-EMG coherence in the 1- to 8-Hz frequency band and regularity of tremor. This relation was primarily driven by the increased magnitude of tremor-EMG coherence at 5.85 and 6.83 Hz; 4) enhanced mechanical reflex properties were not responsible for the increased magnitude of tremor-EMG coherence in the elderly subjects; 5) tremor amplitude was not different between the 4 age groups, but there was a slight decline in tremor modal frequency in the oldest age group in the unloaded condition; and 6) despite the increases in postural physiological tremor regularity and the magnitude of low frequency tremor-EMG coherence with age, there was a clear demarcation between healthy aging and previously published findings related to tremor pathology.

Robichaud JA, Pfann KD, Vaillancourt DE, Comella CL, Corcos DM. · Department of Physical Therapy, School of Health and Rehabilitation Sciences, Indiana University, Indianapolis, Indiana 46202, USA. · Mov Disord. · Pubmed #15593316 No free full text.

Abstract: 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.

Sturman MM, Vaillancourt DE, Metman LV, Bakay RA, Corcos DM. · Department of Movement Sciences (M/C 994), College of Applied Health Sciences, University of Illinois at Chicago, 808 S. Wood Street, 690 CME, Chicago, IL 60612, USA. · Brain. · Pubmed #15240437 links to  free full text

Abstract: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and antiparkinsonian medication have proved to be effective treatments for tremor in Parkinson's disease. To date it is not known how and to what extent STN DBS alone and in combination with antiparkinsonian medication alters the pathophysiology of resting and postural tremor in idiopathic Parkinson's disease. The purpose of this study was to examine the effects of STN DBS and antiparkinsonian medication on the neurophysiological characteristics of resting and postural hand tremor in Parkinson's disease. Resting and postural hand tremor were recorded using accelerometry and surface electromyography (EMG) from 10 Parkinson's disease patients and 10 matched control subjects. The Parkinson's disease subjects were examined under four treatment conditions: (i) off treatment; (ii) STN DBS; (iii) medication; and (iv) medication plus STN DBS. The amplitude, EMG frequency, regularity, and 1-8 Hz tremor-EMG coherence were analysed. Both STN DBS and medication reduced the amplitude, regularity and tremor-EMG coherence, and increased the EMG frequency of resting and postural tremor in Parkinson's disease. STN DBS was more effective than medication in reducing the amplitude and increasing the frequency of resting and postural tremor to healthy physiological levels. These findings provide strong evidence that effective STN DBS normalizes the amplitude and frequency of tremor. The findings suggest that neural activity in the STN is an important modulator of the neural network(s) responsible for both resting and postural tremor genesis in Parkinson's disease.

Pfann KD, Robichaud JA, Gottlieb GL, Comella CL, Brandabur M, Corcos DM. · The Department of Movement Science (M/C 194), University of Illinois at Chicago, 901 West Roosevelt Road, Chicago, IL 60608, USA. · Exp Brain Res. · Pubmed #14991213 No free full text.

Abstract: When young, healthy subjects perform rapid point-to-point and reversal movements over a range of distances, the patterns of muscle activation associated with accelerating the limb toward the target are modulated in the same way for both movement tasks. Differences in patterns of muscle activation for these two movement types are not observed until the deceleration phase of the movements. In this study, we first test the hypothesis that healthy, older subjects and subjects with Parkinson's disease will modulate the pattern of muscle activation in the same way during the acceleration phase of point-to-point and reversal elbow movements. Second, we test the hypothesis that healthy, older subjects and subjects with Parkinson's disease exhibit the same relationship in muscle activation patterns between the two movement types that have been observed for the young in the deceleration phase of the movements. Subjects performed point-to-point and reversal movements initiated in the direction of flexion over three distances (36, 54 and 72 degrees) "as fast as possible". Angle, velocity, acceleration and surface EMGs from biceps and triceps were recorded. With respect to the first hypothesis, the EMG, kinetic, and kinematic measures related to the acceleration phase of the movements were modulated in the same way for both movement types in the healthy older subjects. In the Parkinson's disease group, the kinematic and kinetic measures during the acceleration phase of the movements were the same in both movement types; however, the flexor and extensor EMG activation was smaller during reversal movements than during point-to-point movements. With respect to the second hypothesis, in contrast to that found in young subjects, in healthy older subjects, there was no significant difference between the movement types in the flexor EMG activity immediately after the time of peak velocity. This difference between younger and older subjects may be attributed to the fact that older subjects perform both movement types more slowly than do younger subjects. Although subjects with Parkinson's disease also move slowly, the flexor EMG shuts off more abruptly and more completely just after the time of peak velocity during reversal movements than during point-to-point movements. These results show that (1) for healthy subjects, when the task requirements are the same for the two movement types (acceleration phase), muscle activation patterns are modulated in the same way, and (2) both age and disease alter the relationship of muscle activation, kinetics and kinematics between point-to-point and reversal movements.

Robichaud JA, Pfann KD, Comella CL, Brandabur M, Corcos DM. · Department of Human Movement Sciences (M/C 194), University of Illinois at Chicago, 901 West Roosevelt Road, Chicago, IL 60608, USA. · Exp Brain Res. · Pubmed #14747885 No free full text.

Abstract: 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.

Vaillancourt DE, Prodoehl J, Verhagen Metman L, Bakay RA, Corcos DM. · Department of Movement Science, University of Illinois at Chicago, 901 West Roosevelt Road, Chicago, IL 60608, USA. · Brain. · Pubmed #14662520 links to  free full text

Abstract: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and antiparkinsonian medication (Meds) have proved to be effective therapies for treating bradykinesia in Parkinson's disease. However, it is not currently known how or to what extent STN stimulation alters the control signals to agonist and antagonist muscles to change movement speed. Our objective was to investigate movement speed along with the amplitude and temporal features of EMG activity to determine how and to what extent these parameters are changed by DBS and medication. Nine patients with Parkinson's disease were studied following neurosurgery that implanted high-frequency stimulating electrodes in the STN. The experiments for the patients were performed in each of four treatment conditions: (i) OFF treatment; (ii) STN DBS; (iii) Meds; and (iv) Meds plus STN DBS. Also, a group of age- and gender-matched control subjects were examined. Medication and DBS had similar effects in that both treatments increased movement speed, increased the amplitude of the first agonist burst, increased burst duration, reduced the number of agonist bursts, reduced cocontraction, increased the size of the antagonist EMG, and reduced the centroid time of the antagonist EMG. When DBS and medication were combined, only temporal measures of burst duration and the number of agonist bursts were different from the medication alone condition. There was a positive association between the level of bradykinesia OFF treatment and the level of bradykinesia following DBS and medication. The movement speed of neurologically normal control subjects' was over 40% higher during both flexion and extension movements when compared with the patients during Meds plus STN DBS. The changes in the muscle activation patterns provide a mechanism of action for the pharmacological and surgical interventions used to treat bradykinesia in Parkinson's disease. However, despite the success of medication and DBS at improving bradykinesia in patients with Parkinson's disease, patients' movement speed was not restored to normal due to limitations in the amplitude and temporal scaling of the agonist and antagonist bursting pattern. These findings suggest a link between basal ganglia function in scaling both the amplitude and temporal parameters of the input to the motor neuron pool.

Flament D, Vaillancourt DE, Kempf T, Shannon K, Corcos DM. · Department of Physical Medicine and Rehabilitation, Rush Presbyterian-St. Luke's Medical Center, Chicago, IL 60612, USA. · Clin Neurophysiol. · Pubmed #14652099 No free full text.

Abstract: OBJECTIVE: We studied the ability of patients with Parkinson's disease to improve their performance in a motor task requiring both speed and accuracy in the execution of elbow flexion movements. Our goal was to investigate the changes in electromyographic activity associated with the changes in movement performance. METHODS: Eleven patients on anti-Parkinsonian medication were tested. The patients were selected for being bradykinetic, having little or no resting tremor or dyskinesias, and being in stages II or III of the Hoehn and Yahr rating scale. RESULTS: The untrained patients displayed multiple bursts of agonist activity, characteristic of Parkinsonian EMG recordings. All patients improved their performance by increasing peak velocity while maintaining movement accuracy within strict boundaries. With practice, the patients' performance changed in a manner similar to that which has been previously observed for performance curves in neurologically normal subjects. As movement duration decreased (i.e. peak velocity increased), we observed a slight decrease in the number of agonist bursts and an increase in the average burst duration. However, the patients continued to generate a fractionated, multi-burst agonist pattern. CONCLUSIONS: We conclude that Parkinsonian patients benefit from practice by improving their performance but remain fundamentally impaired in the generation of muscle activation patterns. This study has shown that the generation of fractionated, multiple short bursts of EMG activity that is characteristic of movements made by Parkinsonian patients is not normalized by practice.

Robichaud JA, Pfann KD, Comella CL, Corcos DM. · School of Kinesiology, University of Illinois at Chicago, Chicago, Illinois 60608, USA. · Mov Disord. · Pubmed #12360544 No free full text.

Abstract: 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.

Pfann KD, Buchman AS, Comella CL, Corcos DM. · School of Kinesiology, University of Illinois at Chicago, 60608-1516, USA. · Mov Disord. · Pubmed #11748736 No free full text.

Abstract: Studies of electromyographic (EMG) patterns during movements in Parkinson's disease (PD) have often yielded contradictory results, making it impossible to derive a set of rules to explain how muscles are activated to perform different movement tasks. We sought to clarify the changes in modulation of EMG parameters associated with control of movement distance during fast movements in patients with PD. Specifically, we studied surface EMG activity during rapid elbow flexion movements over a wide range of distances (5-72 degrees) in 14 patients with relatively mild symptoms of PD and 14 control subjects of similar age, sex, height, and weight. The PD group exhibited several changes in EMG modulation including impaired modulation of agonist burst duration; increased number of agonist bursts; reduced scaling of agonist EMG magnitude in the more severely impaired subjects; and increased temporal overlap of the antagonist and agonist signals in the most severely impaired subjects. These findings suggest that progressive motor dysfunction in PD is accompanied by increasing deficits in modulating muscle activation. These results help clarify previous disparate and sometimes contradictory results of EMG patterns in subjects with PD.

McAuley JH, Corcos DM, Rothwell JC, Quinn NP, Marsden CD. · MRC Human Movement and Balance Unit, Institute of Neurology, 23 Queen Square, London WC1N 3BG, UK. · J Neurol Neurosurg Psychiatry. · Pubmed #11254769 links to  free full text

Abstract: OBJECTIVES: Although Parkinson's disease is typically characterised by bradykinesia, rigidity, and rest tremor, the possibility that two additional motor deficits are manifest during small hand muscle activity was explored-namely, weakness and abnormal physiological tremor. METHODS: A paradigm previously used in normal subjects reliably records the strength, tremor and surface EMG of index finger abducting contractions against a compliant (elastic) resistance. In addition to the well known physiological tremor at around 10 Hz, there are other co existing peak tremor frequencies at around 20 and 40 Hz; the last of these frequencies corresponds to the range of EMG Piper rhythm. The same technique was used to study parkinsonian patients while on and off dopaminergic medication. RESULTS: The maximum strength of finger abduction produced by first dorsal interosseous contraction was considerably lower when patients were off medication (mean (SD) 6.27 (1.49) N when off v 12.33 (3.64) N when on). There was also a marked reduction in the power of Piper frequency finger tremor (p<0.0005) and EMG (p<0.0005) oscillations that did not simply result from weaker contraction. CONCLUSION: As the components of physiological tremor at higher frequencies are thought to derive from CNS oscillations important in motor control, their loss in parkinsonism in association with severe off symptoms may represent an important pathophysiological link between dopaminergic depletion and parkinsonian motor deficits.