Objective measurement of muscle rigidity in parkinsonian patients treated with subthalamic stimulation

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) has been shown to be an effective treatment for Parkinson's disease (PD). The intraoperative positioning of DBS electrodes and postoperative adjustment of the stimulation parameters, however, require continuous, precise evaluation. Moreover, ambulatory measurements of the symptoms would also help to evaluate changes in the progression of PD in these patients. To this aim, we objectified rigidity measurements via surface EMG recordings of the Mm. biceps (bic) and triceps brachii (tric) in patients treated with chronic stimulation of the STN. We show that cessation and initiation of DBS have effects on the EMG profile during standardized extension and flexion movements in the elbow joint. These data correlate significantly with clinical ratings. Thus, EMG recordings of the Mm. bic and tric during this standardized extension‐flexion movement can be used to objectively measure rigidity and to monitor its course over time. In view of its low technical requirements, this technique lends itself to use during DBS implantation surgery and in the clinical environment. © 2008 Movement Disorder Society     

Electromyography and mechanomyography of elbow agonists and antagonists in Parkinson disease

The purpose of this study was to assess the electromyographic (EMG) and mechanomyographic (MMG) activities of agonist and antagonist muscles in Parkinson disease patients during maximal isometric elbow contraction in flexion and extension. Ten elderly females with Parkinson disease (average age 75 years) and 10 age‐matched healthy females were tested. The torque and the EMG and MMG signals from biceps brachii and triceps brachii were recorded during sustained maximal voluntary isometric contraction of the elbow flexors and extensors. There were no intergroup differences in the EMG and MMG activities of agonist and antagonist muscles or in torque. This might be because the Parkinson subjects were tested during their medication “ON” phase, or perhaps maximal isometric contraction (MVC) induced greater active muscle stiffness that affected the MMG signal. Muscle Nerve 40: 240–248, 2009     

Was Sherrington right about co-contractions?

Differences in electromyographic (EMG) activity between brief isometric maximum voluntary contractions under conditions of agonist contraction and agonist-antagonist co-contractions were assessed for elbow flexors (biceps brachii) and elbow extensors (triceps, long head). Expressing maximum EMG co-contraction activity as a ratio of agonist maximum EMG activity of the same muscle yielded EMG ratios consistently below 1.0 (mean = 0.48 for flexion and 0.76 for extension). Flexor EMG ratios did not co-vary with elbow position but extensor EMG ratios approached 1.0 or sometimes greater at shorter muscle lengths (elbow extension). Findings were in general accord with Sherrington's original proposal of 'double reciprocal innervation'. Neural circuitry designed to limit full muscle activation during co-contractions may serve to protect the joint against excessive tangential or compressive forces.     

Coactivation of the elbow antagonist muscles is not affected by the speed of movement in isokinetic exercise

Since muscle coactivation increases the stiffness and stability of a joint, greater coactivation is likely during faster than slower movements. Very few studies, though, have been conducted to verify this hypothesis. Moreover, a large number of studies have examined coactivation of muscles surrounding the knee joint whereas there are few reports on the elbow joint. The aim of this study was therefore to compare the antagonist activation of the elbow flexors and extensors during isokinetic concentric exercises and to investigate the influence of angular velocity on their activation. Twelve men participated in the study. The surface electromyographic signals (sEMG) were recorded from the biceps brachii (BB) and triceps brachii (TB) muscles during three maximal voluntary isometric contractions (MVC) of elbow flexors and extensors and a set of three maximal elbow flexions and extensions each at 15 degrees, 30 degrees , 60 degrees, 120 degrees, 180 degrees, and 240 degrees.s(-1). Normalized root mean square (RMS) of sEMG was calculated during the isokinetic phase of movement as an index of sEMG amplitude. During elbow flexion, the antagonist activation of BB averaged 16.2% lower than TB, and this difference was statistically significant at all angular velocities. The normalized RMS values ranged from 26.0% +/- 19.0 at MVC to 37.8% +/- 13.9 at 240 degrees.s(-1) for antagonist TB activation, and from 5.7% +/- 5.2 at MVC to 18.9% +/- 8.6 at 240 degrees.s(-1) for antagonist BB activation. No influence of angular velocity on agonist and antagonist activity was found. Moreover, flexion and extension torques were both strongly affected by the amount of antagonist activation. The functional specialization of the two muscle groups could be responsible for the different levels of antagonist activation. The frequent use of BB, which is not assisted by gravity during daily activities, could lead to reduced coactivation due to a better functioning of the control system based upon reciprocal innervation. These findings may have significant implications in the design of rehabilitation programs directed to the elbow joint.     

Effect of shoulder angle on the activation pattern of the elbow extensors during a submaximal isometric fatiguing contraction

The aim of this study was to examine the effect of shoulder angle on the electromyographic (EMG) activation pattern of the elbow extensors during a fatiguing contraction. Ten young men (23.5 ± 1.7) were tested on two occasions with the elbow angle at 90° and the shoulder at either 0° or 90° of flexion. EMG was recorded by fine wire electrodes inserted into the lateral, medial, and long heads of the triceps brachii and the anconeus. An EMG‐torque relationship was determined prior to a sustained isometric contraction at 20% of maximum voluntary contraction (MVC) until target failure. Endurance time was shorter, and postfatigue MVC torque was lower at 90° (40.4 ± 12.7 Nm) versus 0° (47.9 ± 14.7 Nm) of flexion. EMG activity of the long head during the final 10% of the fatiguing contraction was significantly greater at 90° versus 0° with no effect of shoulder angle on any other muscle portions. The findings suggest that measures from one muscle portion of the elbow extensors are not representative of the whole group, and the relative activation of the two‐joint long head was changed depending on shoulder angle during a fatigue task. Muscle Nerve, 2010     

(S)-4C3HPG, a mixed group I mGlu receptor antagonist and a group II agonist, administered intrastriatally, counteracts parkinsonian-like muscle rigidity in rats

The aim of the present study was to determine whether S-4-carboxy-3-hydroxyphenylglycine (S)-4C3HPG, a mixed group I glutamate metabotropic receptor antagonist and a group II agonist, attenuated parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano and electromyographic method, which measured simultaneously the muscle resistance (MMG) of the rat's hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was induced by pretreatment with haloperidol (1 mg/kg i.p.). (S)-4C3HPG injected in doses of 5 and 15 microg/0.5 microl bilaterally, into the rostral region of the striatum, decreased both the haloperidol-induced muscle rigidity (MMG) and the enhanced electromyographic activity (EMG). The present results suggest that blockade of mGluR1 receptors and/or activation of mGluR2 ones, localized in the rostral part of the striatum, may be responsible for the anti-parkinsonian effect of (S)-4C3HPG.     

Nociceptive EMG suppression in triceps brachii muscle in humans.

OBJECTIVE: Inhibitory spinal reflexes in human hand muscles mediated by cutaneous afferents (=cutaneous silent periods, CSPs) serve to protect the hand from injury. Proximal muscles are included in a complex protective pattern implementing both excitatory and inhibitory reflexes. METHODS: We investigated the functional organization of CSPs in the triceps brachii muscle (TB) - the prime elbow extensor - assessing different stimulus intensities and elbow positions. Thirteen healthy subjects underwent recurrent electrical index finger tip stimulation with different intensities while volitionally activating TB against resistance. The rectified and averaged electromyogram (EMG) was recorded from TB with surface electrodes while the elbow joint was held in full flexion, full extension, and at an angle of 90 degrees. RESULTS: Digit II stimulation resulted in distinct CSPs in TB. Increasing stimulus intensities caused a more profound EMG suppression. Different elbow positions had a significant influence on CSP onset and end latency, and duration. CONCLUSIONS: The present findings are consistent with a functional organization of protective reflexes in the proximal human upper limb across several metameric segments. Spinal inhibitory neurons serving to rapidly suppress basic muscle synergies may compete with neural circuitry involved in postural control.     

SCH 58261, an A(2A) adenosine receptor antagonist, counteracts parkinsonian-like muscle rigidity in rats

The aim of the present study was to find out whether blockade of adenosine A(2A) receptors by a selective antagonist, SCH 58261, influenced parkinsonian-like muscle rigidity. Muscle tone was examined using a combined mechano- and electromyographic method which simultaneously measured muscle resistance (MMG) of a rat hindfoot to passive extension and flexion in the ankle joint and electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity produced by reserpine (5 mg/kg + alpha-methyl-p-tyrosine, 250 mg/kg) was antagonized by SCH 58261 (0.1-5 mg/kg). SCH 58261 (5 mg/kg) also reduced reserpine-enhanced tonic and reflex EMG activities in both the gastrocnemius and the tibialis muscles. Moreover, SCH 58261 in doses of 1 and 5 mg/kg abolished muscle resistance induced by haloperidol (0.5 mg/kg). However, only the highest dose of SCH 58261 (5 mg/kg) decreased tonic EMG activity enhanced by haloperidol. Administration of L-DOPA (75 and 100 mg/kg) dose-dependently decreased the muscle resistance as well as tonic EMG activity evoked by haloperidol. Combined administration of SCH 58261 (0.1 mg/kg) and L-DOPA (50 mg/kg) in doses which did not affect the haloperidol-induced muscle rigidity produced a pronounced synergistic effect. The ability of SCH 58261 to diminish the parkinsonian-like muscle rigidity and to potentiate the effect of L-DOPA in this model seems to indicate a therapeutic value of this compound in the treatment of Parkinson's disease.     

Functional corticomuscular connection during reaching is weakened following stroke

ObjectiveTo investigate the functional connection between motor cortex and muscles, we measured electroencephalogram–electromyogram (EEG–EMG) coherence of stroke patients and controls.MethodsEight healthy controls and 21 patients with shoulder and elbow coordination deficits were enrolled. All subjects performed a reaching task involving shoulder flexion and elbow extension. EMG of the anterior deltoid (AD) and brachii muscles (BB, TB) and 64-channel scalp EEG were recorded during the task. Time-frequency coherence was calculated using the bivariate autoregressive model.ResultsStroke patients had significantly lower corticomuscular coherence compared with healthy controls for the AD and BB muscles at both the beta (20–30 Hz) and lower gamma (30–40 Hz) bands during the movement. BH procedure (FDR) identified a reduced corticomuscular coherence for stroke patients in 11 of 15 scalp area–muscle combinations. There was no statistically significant difference between stroke patients and control subjects according to coherence in other frequency bands.ConclusionPoorly recovered stroke survivors with persistent upper-limb motor deficits exhibited significantly lower gamma-band corticomuscular coherence in performing a reaching task.SignificanceThe study suggests poor brain-muscle communication or poor integration of the EEG and EMG signals in higher frequency band during reaching task may reflect an underlying mechanism producing movement deficits post-stroke.     

Amplitude- and velocity-dependency of rigidity measured at the wrist in Parkinson's disease

ObjectiveQuantify the effects of increased amplitude and rate of muscle stretch on parkinsonian rigidity.MethodsEighteen subjects with Parkinson’s disease participated in this study. Subjects’ tested hand was passively displaced through 60° and 90° ranges of wrist flexion and extension at velocities of 50°/s and 280°/s in both treated and untreated conditions. Joint angular position, resistance torque, and surface electromyography (EMG) of the wrist flexors and extensors were recorded. Rigidity was quantified by normalized work scores and normalized angular impulses for flexion and extension, separately. Reflex responses of stretched and shortened muscles were quantified by mean EMG and EMG ratio. A series of ANOVAs was performed to determine the effect of amplitude, velocity and medication on selected variables.ResultsBoth work scores and angular impulses revealed that the larger displacement amplitude and the higher velocity were associated with significantly greater rigidity, increased EMG ratio and mean EMG of stretched muscles. Dopaminergic medication was not associated with a reduction in rigidity.ConclusionsParkinsonian rigidity is modulated by the amplitude and rate of muscle stretch.SignificanceThese findings shed light on the biomechanical underpinnings and physiological characteristics of rigidity and may inform clinical rigidity assessment in Parkinson’s disease.     

A comparison of the effects of imposed extension and flexion movements on Parkinsonian rigidity.

OBJECTIVE: To test a hypothesis that Parkinsonian rigidity is more pronounced in imposed extension than flexion movement. METHODS: Twelve Parkinsonian subjects (both "Off" and "On" medication states) and seven control subjects participated in the protocol, in which a servomotor imposed wrist flexion and extension. Rigidity was quantitatively evaluated by the rectified torque integral with time, i.e., temporal score, and by the torque integral with joint angle, i.e., work score, for extension and flexion, respectively. RESULTS: In the "Off" state, the imposed extension induced a significantly higher resistance than did flexion. Dopaminergic medication significantly reduced the temporal score associated with imposed extension, and significantly decreased the work score of both movements. Compared with controls, the scores were higher for patients in the "On" state. CONCLUSIONS: Rigidity is more readily elicited in extension movement. The distinction is not evident in clinical practice, whereas it can be clearly revealed with the application of biomechanical analyses. SIGNIFICANCE: This distinction may prove to be a standard feature of rigidity. The procedures may be helpful in diagnosis and useful in evaluating new treatments and developing rehabilitation programs.     

Quantitative measurement of trunk rigidity in parkinsonian patients

We aimed to develop an objective measurement to quantify trunk rigidity in patients with Parkinson's disease (PD), and to examine its reliability, validity and sensitivity in differentiating PD patients from control subjects. In Study 1, an isokinetic dynamometer was employed to assess trunk rigidity in 6 PD patients and 6 healthy controls. Passive trunk flexion and extension at 4 angular velocities were applied and resistive torques were recorded. Both work done and resistive peak torques to passive trunk flexion (Torque(PF)) and extension (Torque(PE)) were found to be highly reliable within a 2-day interval in PD patients and control subjects. In Study 2, trunk muscle tone was compared between 15 PD and 15 control subjects. Significantly higher muscle tone, as shown by increases in work done, and in Torque(PF) and Torque(PE )at higher movement speeds, was found in PD patients. Within each subject group, resistive trunk muscle tone was found to increase with increasing velocity of passive movement, but the extent of increase was greater in PD patients. Our results thus suggest that the objective method developed by us was reliable and could differentiate trunk rigidity in PD patients from that of healthy subjects.     

Muscle relaxation is impaired in dystonia: a reaction time study.

A simple visual reaction time (RT) paradigm was used to investigate whether the velocity of relaxation is impaired in dystonia. In 16 subjects with a clinical diagnosis of adult-onset focal, segmental or multifocal dystonia and in 15 age-matched normal controls, the relaxation reaction time (R-RT) and the contraction reaction time (C-RT) were compared across different tasks involving the flexor carpi radialis (FCR), biceps brachii (BB) and triceps brachii (TR) arm muscles. In normal controls, the latency of EMG termination (R-RT) was significantly shorter than the latency of electromyographic (EMG) onset (C-RT) in the BB and TR muscles, but not in the FCR muscle. In dystonic patients, the latency of EMG termination (R-RT) was significantly longer than the latency of EMG onset (C-RT) in the FCR and BB muscles. No significant difference of the C-RT was observed between patients and controls whereas the R-RT was prolonged significantly in the BB and TR muscles of patients with dystonia and almost significantly in the FCR muscle. This study indicates that muscle relaxation is abnormal in patients with focal (multifocal or segmental) dystonia. The impaired muscle relaxation may contribute to the longer overlap of agonist-antagonist activities (co-contraction) typically observed in dystonia and to the slowness of voluntary movement sequencing.     

Sensitivity of motor unit potential analysis in facioscapulohumeral muscular dystrophy

Template-operated motor unit potential (MUP) analysis has made quantitative electromyography (EMG) feasible, even in busy laboratories, but validation of this approach is still necessary. In the present study, the utility of multi-MUP analysis was assessed in patients with a molecular genetic diagnosis of facioscapulohumeral muscular dystrophy (FSHD). Manual assessment of muscle strength and concentric-needle EMG of the biceps brachii and vastus lateralis muscles were performed. The sensitivity for diagnosing myopathy (mean values and outliers) was tested for eight MUP parameters and four of their combinations. The group comprised 31 patients. Elbow flexion and knee extension strength was normal in 45% and 52% of patients, respectively. The most sensitive MUP parameter was thickness, followed by duration. A combination of three MUP parameters (thickness, amplitude, and duration/area) was needed for maximal sensitivity. The study demonstrated a high sensitivity of multi-MUP analysis in FSHD. Myopathic abnormalities were demonstrated in all weak biceps brachii muscles, and in 77% of biceps brachii muscles with normal strength.     

Quantification of spasticity and assessment of drug action in multiple sclerosis patients by a scoring system based on an optical mark reader documentation system. Preliminary results

To evaluate “spasticity” and “rigidity” several clinical parameters were set up in a scoring system on a one-page documentation sheet. This system is based on an optical mark reader documentation system. In this way muscle strength, tone in flexion and extension, clonus, rigidity superficial cutaneous and muscle stretch reflexes as well as synergisms and automatisms from various muscle groups of the upper and lower extremities were recorded. In addition, the general state of performance as well as the subjective statements and the possible factors of disturbance were taken into consideration. Preliminary results of more than 200 examinations are presented.     

(S)-4C3HPG, a mixed group I mGlu receptor antagonist and a group II agonist, administered intrastriatally, counteracts parkinsonian-like muscle rigidity in rats

The aim of the present study was to determine whether S-4-carboxy-3-hydroxyphenylglycine (S)-4C3HPG, a mixed group I glutamate metabotropic receptor antagonist and a group II agonist, attenuated parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano and electromyographic method, which measured simultaneously the muscle resistance (MMG) of the rat’s hind foot to passive extension and flexion in the ankle joint and the electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was induced by pretreatment with haloperidol (1 mg/kg i.p.). (S)-4C3HPG injected in doses of 5 and 15 μg/0.5 μl bilaterally, into the rostral region of the striatum, decreased both the haloperidol-induced muscle rigidity (MMG) and the enhanced electromyographic activity (EMG). The present results suggest that blockade of mGluR1 receptors and/or activation of mGluR2 ones, localized in the rostral part of the striatum, may be responsible for the anti-parkinsonian effect of (S)-4C3HPG.     

EMG activity and kinematics of human cycling movements at different constant velocities

Surface electromyographic (EMG) activity was recorded from the rectus femoris, vastus medialis, biceps femoris, gastrocnemius and tibialis anterior in the human lower extremity while subjects performed bicycling movements over a range of constant pedalling velocities. Kinematics of knee and hip cyclical movements were analyzed from 16 mm film. The reciprocal pattern of activation in agonist and antagonist muscles and timing of EMG initiation relative to knee joint were studied.

Reciprocal activation of rectus femoris and biceps femoris muscles was generally observed to occur during the mid-extension or mid-flexion phase of knee movements. This timing of activation pattern coincided well the period of peak angular velocity and zero angular acceleration.

As pedalling speeds approached maximum, activation times of the bifunctional, biarticular rectus femoris, biceps and gastrocnemius muscles were considerably advanced in phase relative to knee joint angles, whereas, EMG initiation of monofunctional, single joint, tibalis anterior and vastus medialis muscles maintained a relatively stable knee position-activation time relationship. At higher velocities, biceps femoris EMG activity was characterized as having a double burst pattern of activation. A less distinctive double burst pattern was seen in the rectus femoris EMG at higher cycling speeds.

EMG pattern analysis of the rectus femoris and biceps femoris muscles revealed an earlier onset of activity for both muscles during maximum cycling velocities, relative to cyclical phases of the knee joint angle. Considerable overlapping of the EMG bursts was seen beyond pedalling rates of 1 Hz. Co-contraction between rectus femoris and biceps femoris muscles could be observed during the acceleration period involving an abrupt switch to maximum pedalling performance. When co-contraction was observed, the joint angular acceleration curves observed during the knee flexion period accounted for a larger portion of a single cycle, and were more irregular than the angular accelerations observed during knee extension.     

Strength and activation of the knee musculature in Parkinson's disease: effect of medication

The specific neuromuscular mechanisms for compromised muscle strength with PD, and the improvement that occurs with medication, have not been clearly delineated. This study assessed knee extension and flexion strength of PD patients whilst on and off medication and examined the neural mechanisms responsible for any changes. Ten idiopathic PD patients were assessed whilst on and off medication (≥ 12-h after drug withdrawal), ～ 7 days apart. Isometric strength of the knee extensors and flexors was assessed, and the interpolated twitch technique used to measure activation of the knee extensors. Surface EMG was also used to measure neural drive to the agonists and antagonists. Without medication isometric strength of the knee extensors (7%) and flexors (11%) was impaired and the interpolated twitch technique revealed activation of the knee extensors was reduced (8%, P=0.005). Maximum agonist amplitudes for nkee extension and flexion were unchanged off-medication (0.59 P< 0.77). The agonist and antagonist EMG-force relationships, and the maximum antagonist EMG, were unaffected by medication withdrawal. The decrease in knee extension strength when PD patients were off medication was due to reduced activation of the agonist muscle, rather than any change in antagonist co-activation, and these changes were associated with reduced locomotory performance.