Biomedical subjects

J C Rothwell

Publications and source records attributed to J C Rothwell.

At least 145 records · Page 8Linked to original sources

PubMed1998

Central motor conduction time in progressive multiple sclerosis. Correlations with MRI and disease activity.

The purpose of this study was to relate abnormalities of motor conduction time to the presence of spinal cord MRI lesions in progressive multiple sclerosis and to investigate the relationship between changes in motor conduction over time and clinical and MRI changes. Central motor conduction time (CMCT), serial MRI of the brain and spinal cord, and clinical evaluations were carried out in 20 patients with primary and secondary progressive multiple sclerosis. CMCT was carried out at the beginning and end of the study whilst the clinical and MRI examinations occurred at monthly intervals for 12 months. Median CMCT to abductor pollicis brevis was 14.8 ms (range 8.8-27.4 ms). The response latency to tibialis anterior correlated with disability measured on the Expanded Disability Status Scale. Latencies to upper limb muscles correlated with cervical MRI lesion load and the presence of atrophy of the cervical cord. Over the 12-month study period, 15 of 19 patients deteriorated clinically. However, an increase in motor response latencies occurred only in the four patients who had developed new cord lesions. The results suggest that prolonged CMCT is related to spinal cord lesion load and that, over time, changes in the CMCT occur only when spinal cord lesion load increases. Clinical change in progressive multiple sclerosis may therefore occur without either the development of new lesions on MRI scans or an increase in motor conduction time. This suggests that clinical deterioration in these patients may occur by a mechanism other than increasing demyelination. This may be progressive axonal degeneration.

Adult↗

PubMed1998

The pathophysiology of primary dystonia.

Co-contraction and overflow of EMG activity of inappropriate muscles are typical features of all dystonic movements whether voluntary or involuntary. Voluntary movements are slow and more variable than normal, and there is particular difficulty switching between component movements of a complex task. Reduced spinal cord and brainstem inhibition is common to many reflex studies (long-latency reflexes, cranial reflexes and reciprocal inhibition). These reflex abnormalities may contribute to the difficulties in voluntary movements but cannot be causal as they can occur outside the clinically involved territory. Clinical and neurophysiological studies have emphasized the possible role of sensory feedback in the generation of dystonic movements. Abnormalities of cortical and basal ganglia function have been described in functional imaging and neurophysiological studies of patients with dystonia and in animal models of primary dystonia. Studies of cortical function have shown reduced preparatory activity in the EEG before the onset of voluntary movements, whilst magnetic brain stimulation has revealed changes in motor cortical excitability. Functional imaging of the brain in primary dystonia has suggested reduced pallidal inhibition of the thalamus with consequent overactivity of medial and prefrontal cortical areas and underactivity of the primary motor cortex during movements. These findings are supported by preliminary neuronal recordings from the globus pallidus and the thalamus at the time of stereotaxic surgery in patients with dystonia. All this evidence suggests that primary dystonia results from a functional disturbance of the basal ganglia, particularly in the striatal control of the globus pallidus (and substantia nigra pars reticulata). This causes altered thalamic control of cortical motor planning and executive areas, and abnormal regulation of brainstem and spinal cord inhibitory interneuronal mechanisms.

Animals↗

PubMed1998

The effects of transcranial magnetic stimulation over the dorsolateral prefrontal cortex on suppression of habitual counting during random number generation.

Random number generation is an attention-demanding task that engages working memory and executive processes. Random number generation requires holding information 'on line', suppression of habitual counting, internally driven response generation and monitoring of responses. Evidence from PET studies suggests that the dorsolateral prefrontal cortex (DLPFC) is involved in the generation of random responses. We examined the effects of short trains of transcranial magnetic stimulation (TMS) over the left or right DLPFC or medial frontal cortex on random number generation in healthy normal participants. As in previous evidence, in control trials without stimulation participants performed poorly on the random number generation task, showing repetition avoidance and a tendency to count. Brief disruption of processing with TMS over the left DLPFC changed the balance of the individuals' counting bias, increasing the most habitual counting in ones and reducing the lower probability response of counting in twos. This differential effect of TMS over the left DLPFC on the balance of the subject's counting bias was not obtained with TMS over the right DLPFC or the medial frontal cortex. The results suggest that, with disruption of the left DLPFC with TMS, habitual counting in ones that has previously been suppressed is released from inhibition. From these findings a network modulation model of random number generation is proposed, whereby suppression of habitual responses is achieved through the modulatory influence of the left DLPFC over a number-associative network in the superior temporal cortex. To allow emergence of appropriate random responses, the left DLPFC inhibits the superior temporal cortex to prevent spreading activation and habitual counting in ones.

Adult↗

PubMed1998

Vestibular hypersensitivity to clicks is characteristic of the Tullio phenomenon.

OBJECTIVES: The frequency of pathologically reduced click thresholds for vestibular activation was explored in patients with the Tullio phenomenon (sound induced vestibular activation). METHODS: Seven patients (eight affected ears) with symptoms of oscillopsia and unsteadiness in response to loud external sounds or to the patient's own voice were examined. In all but one patient, vestibular hypersensitivity to sound was confirmed by the fact that eye movements could be produced by pure tones of 110 dB intensity or less. Conventional diagnostic imaging was normal in all cases and three of the patients had normal middle ears at surgical exploration. Thresholds for click evoked vestibulocollic reflexes were compared with those of a group of normal subjects. Galvanic stimulation was used as a complementary method of examining the excitability of vestibular reflexes. RESULTS: All the patients showed a reduced threshold for click activation of vestibulocollic reflexes arising from the affected ear. Short latency EMG responses to clicks were also present in posterior neck and leg muscles, suggesting that these muscles receive vestibular projections. Galvanic stimulation produced a normal pattern of body sway in four of the five patients tested. CONCLUSIONS: A pathologically reduced threshold to click activation (< or = 70 dB NHL (average normal hearing level)) seems to be a consistent feature of the Tullio phenomenon and a useful diagnostic criterion. This in turn is most likely to be due to an increased effectiveness of the transmission of sound energy to saccular receptors. Activation of these receptors probably contributed to the vestibular symptoms experienced by the patients.

Acoustic Stimulation↗

PubMed1998

Spinal and pudendal nerve modulation of human corticoanal motor pathways.

We investigated the effects of lumbosacral and pudendal nerve stimulation on the corticofugal pathways to the human external anal sphincter. In 11 healthy subjects, anal sphincter electromyographic responses, evoked to transcranial magnetic stimulation of the motor cortex, were recorded 5-500 ms after lumbosacral root or pudendal nerve stimulation. Lumbosacral and pudendal nerve stimulation alone evoked responses with amplitudes of 293 +/- 73 and 401 +/- 153 microV and latencies of 3.2 +/- 0.2 and 2.2 +/- 0.2 ms, respectively. Cortical stimulation also evoked responses with amplitudes of 351 +/- 104 microV and latencies of 20.9 +/- 1.1 ms. When lumbosacral or pudendal nerve stimulation preceded cortical stimulation, the cortically evoked responses were facilitated (P < 0.01), with the effect appearing greatest at 5-20 ms after both lumbosacral and pudendal excitation and at 50-100 ms after lumbosacral excitation alone. Our results demonstrate that cortical pathways to the external anal sphincter are facilitated by prior lumbosacral and pudendal nerve stimulation, indicating that sensorimotor interactions are important in the central neural control of sphincter function.

Adult↗

PubMed1998

Intracortical inhibition and facilitation in different representations of the human motor cortex.

Intracortical inhibition and facilitation in different representations of the human motor cortex. J. Neurophysiol. 80: 2870-2881, 1998. Intracortical inhibition (ICI) and intracortical facilitation (ICF) of the human motor cortex can be studied with paired transcranial magnetic stimulation (TMS). Plastic changes and some neurological disorders in humans are associated with changes in ICI and ICF. Although well characterized in the hand representation, it is not known if ICI and ICF vary across different body part representations. Therefore we studied ICI and ICF in different motor representations of the human motor cortex. The target muscles were rectus abdominus (RA), biceps brachii (BB), abductor pollicis brevis (APB), quadriceps femoris (QF), and abductor hallucis (AH). For each muscle, we measured the rest and active motor thresholds (MTs), the motor-evoked potential (MEP) stimulus-response curve (MEP recruitment), ICI, and ICF. The effects of different interstimulus intervals (ISIs) were studied with a conditioning stimulus (CS) intensity of 80% active MT. The effects of different CS intensities were studied at ISI of 2 ms for ICI and ISI of 15 ms for ICF. MT was lowest for APB, followed by BB, AH, and QF, and was highest for RA. Except for BB, MEP recruitment was generally steeper for muscles with lower MT. ICI and ICF were present in all the motor representations tested. The stimulus intensity necessary to elicit ICI was consistently lower than that required to elicit ICF, suggesting that they are mediated by separate mechanisms. Despite wide differences in MT and MEP recruitment, the absolute CS intensities (expressed as percentage of the stimulator's output) required to elicit ICI and ICF appear unrelated to MT and MEP recruitment in the different muscles tested. These findings suggest that the intracortical mechanisms for inhibition and facilitation in different motor representations are not related to the strength of corticospinal projections.

Action Potentials↗

PubMed1998

Cortical correlate of the Piper rhythm in humans.

Cortical correlate of the Piper rhythm in humans. J. Neurophysiol. 80: 2911-2917, 1998. The electromyogram (EMG) of healthy humans demonstrates a tendency to rhythmic oscillations at around 40 Hz (the Piper rhythm) during strong voluntary contraction. Why motor units should discharge synchronously locked to such a high-frequency is unclear. We recorded whole scalp magnetoencephalographic (MEG) signals simultaneously with surface EMG from 10 healthy subjects. In eight subjects, coherence and time domain analyses demonstrated correspondence between the MEG signal, originating near or in the hand region of the motor cortex, and the 35- to 60-Hz EMG recorded during repeated maximal isometric contractions of the contralateral forearm extensor muscles. Three of these subjects also showed similar coherence during isometric contractions of moderate strength and slow extension movements of the wrist. In addition, coherence and time domain analyses demonstrated correspondence between the MEG signals originating near or in the foot area of the motor cortex and EMG recorded during repeated maximal isometric contractions of the contralateral tibialis anterior muscle in the 30- to 60-Hz range. Most important, the frequency at the peak of the coherence spectrum differed between forearm and leg by as much as 10 Hz in the same subject. In contrast, the peak of the coherence spectrum occurred during sustained weak contraction in the 20- to 30-Hz range similarly for both forearm and foot. The lag between EMG and MEG activity in the leg was approximately 15 ms greater than that seen in the forearm, an interval appropriate for conduction in fast pyramidal pathways. It is concluded that the Piper rhythm in muscle may be driven by a comparable oscillatory activity in the contralateral motor cortex. This cortical rhythmicity can be picked up in several types of movement and seems distinct from the 20- to 30-Hz rhythmicity recorded during weak sustained contractions.

Adult↗

PubMed1998

Electrophysiological aids in distinguishing organic from psychogenic tremor.

The clinical differentiation of tremors of organic and psychogenic origin can be difficult. We describe a patient with unilateral upper limb tremor that was initially considered to have a psychogenic cause, but subsequent frequency analysis of EMG signals and accelerometer recordings indicated that the tremor was organic in nature. An ischemic lesion in the contralateral lentiform nucleus found on MRI supported this conclusion. Quantitative electrophysiologic studies may thus be useful in distinguishing organic from psychogenic tremor.

Aged↗

PubMed1997

Explaining oropharyngeal dysphagia after unilateral hemispheric stroke.

BACKGROUND: Oropharyngeal dysphagia occurs in up to a third of patients presenting with a unilateral hemiplegic stroke, yet its neurophysiological basis remains unknown. To explore the relation between cortical motor function of swallowing and oropharyngeal dysphagia, mylohyoid, pharyngeal, and thenar electromyographic responses to stimulation of affected and unaffected hemispheres were recorded in dysphagic and non-dysphagic patients. METHODS: The 20 patients studied had unilateral hemispheric stroke confirmed by computed tomography. Eight of them had associated swallowing difficulties. Electromyographic responses were recorded after suprathreshold transcranial magneto-electric stimulation of affected and unaffected hemispheres with a figure-of-eight coil. FINDINGS: Stimulation of the unaffected hemisphere evoked smaller pharyngeal responses in dysphagic patients than in non-dysphagic patients (mean 64 microV, median 48, interquartile range 44-86 vs 118 microV, 81, 73-150) (p < 0.02). With stimulation of the affected hemisphere, the pharyngeal responses were smaller than for the unaffected hemisphere but similar between the two patient groups (26 microV, 0, 0-48 vs 54 microV, 0, 0-80). Dysphagic and non-dysphagic patients showed similar mylohyoid and thenar responses to stimulation of the unaffected hemisphere as well as to stimulation of the affected hemisphere-unaffected mylohyoid (269 microV, 239, 89-372 vs 239 microV, 163, 133-307), thenar (572 microV, 463, 175-638 vs 638 microV, 485, 381-764); affected mylohyoid (60 microV, 41, 0-129 vs 96 microV, 0, 0-195); thenar (259 microV, 258, 0-538 vs 451 microV, 206, 8-717). INTERPRETATION: The findings indicate that dysphagia after unilateral hemispheric stroke is related to the magnitude of pharyngeal motor representation in the unaffected hemisphere.

Adult↗

PubMed1997

Techniques and mechanisms of action of transcranial stimulation of the human motor cortex.

Electrical and magnetic methods are available to stimulate the human brain through the intact scalp. Although both are successful, magnetic stimulation is now used almost exclusively because the discomfort is minimal compared with that caused by electrical stimulation. Nevertheless, electrical stimulation is still used occasionally since comparison of results from both techniques can often yield useful clinical and scientific information not available from either method in isolation.

Action Potentials↗

PubMed1997

Latent addition in motor and sensory fibres of human peripheral nerve.

1. The time constants of motor and sensory nerve fibres were studied in normal human ulnar nerves by the method of latent addition, using threshold tracking to follow the recovery of excitability after brief conditioning current pulses. The 60 microseconds test and conditioning stimuli were applied at the wrist, and the conditioning stimuli were set to 90, 60, 30, -30, -60 and -90% of the control threshold current. Compound muscle action potentials were recorded from abductor digiti minimi, and sensory nerve action potentials from the little finger. 2. Recovery from depolarizing conditioning pulses was slower than recovery from hyperpolarizing pulses and strongly dependent on conditioning pulse amplitude. The voltage dependence of latent addition was attributed to subthreshold activation of sodium channels (local response). 3. Motor and sensory nerve excitability generally recovered from -90% hyperpolarizing pulses as the sum of two exponential components, although the slow component was negligible in some motor nerves. The fast component (time constant 43.3 +/- 2.0 microseconds, mean +/- S.E.M., n = 9) was similar between motor and sensory fibres in the same subject. It showed no consistent voltage dependence, and was attributed to a passive input time constant of the fibres. The slow component of recovery from hyperpolarizing pulses was greater in sensory than in motor fibres and was voltage dependent: it could be greatly increased in motor and sensory fibres by steady depolarization. It was attributed to a regenerative membrane current, active at the resting potential in sensory and at least some motor nerves. 4. The latent addition responses were compared with the computed responses of four theoretical models. Both motor and sensory responses were well fitted by a model in which a fraction of the sodium channels (less in motor than in sensory fibres) were activated at potentials 20 mV more negative than normal and at half the normal rate, and did not inactivate. 5. It is concluded that the differences in latent addition between motor and sensory fibres are primarily due to differences in non-classical, voltage-dependent ion channels, active close to the resting potential. These "threshold channels' may help to account for the longer strength-duration time constant of sensory fibres, for their lower rheobase, and for their greater tendency to fire repetitively.

Adult↗

PubMed1997

Short- and long-term survival and function of unilateral intrastriatal dopaminergic grafts in Parkinson's disease.

Six patients with Parkinson's disease were followed for 10 to 72 months after human embryonic mesencephalic tissue from four to seven donors was grafted unilaterally into the putamen (4 patients) or putamen plus caudate (2 patients). After 8 to 12 months, positron emission tomography showed a 68% increase of 6-L-[18F]-fluorodopa uptake in the grafted putamen, no change in the grafted caudate, and minor decreases in nongrafted striatal regions. There was therapeutically valuable improvement in 4 patients, but only modest changes in the other 2, both of whom developed atypical features. Patient 4 was without L-dopa from 32 months and had normal fluorodopa uptake in the grafted putamen at 72 months. Overall, the L-dopa dose was reduced by a mean of 10 and 20%, "off" time was reduced by 34 and 44%, and the "off" phase Unified Parkinson's Disease Rating Scale motor score by 18 and 26%, and the duration of the response to a single L-dopa dose increased by 45 and 58% during the first and second years after surgery, respectively. Rigidity and hypokinesia improved bilaterally, but mainly contralateral to the implant. No consistent changes in dyskinesias were observed. We conclude that transplantation of embryonic mesencephalic tissue leads to highly reproducible survival of dopaminergic neurons, inducing clinically valuable improvements in most recipients.

Adult↗

PubMed1997

Cerebellar axial postural tremor.

Three cases are presented with a predominantly axial postural tremor, without visible palatal tremor. Tremor varied in frequency between 3 and 10 Hz, often jumping from one frequency to another in this band. All three patients had evidence of cerebellar pathology. Cases 1 and 2 developed tremor in the setting of a late-onset cerebellar degeneration and after excision of a right cerebellar haemangioblastoma, respectively. Etiology was unclear in Case 3. Nevertheless, this patient had a cerebellar dysarthria. The tremor was similar to that sometimes seen in conjunction with palatal tremor, and EMG studies in Case 3 demonstrated a subclinical modulation of palatal muscle activity simultaneous with the truncal tremor. It is suggested that an axial postural tremor may be due to pathology of the cerebellum and its outflow pathways, despite the absence of clinically apparent palatal tremor.

Adult↗

PubMed1997

Frequency peaks of tremor, muscle vibration and electromyographic activity at 10 Hz, 20 Hz and 40 Hz during human finger muscle contraction may reflect rhythmicities of central neural firing.

The output from the central nervous system to muscles may be rhythmic in nature. Previous recordings investigating peripheral manifestations of such rhythmic activity are conflicting. This study attempts to resolve these conflicts by employing a novel arrangement to measure and correlate rhythms in tremor, electromyographic (EMG) activity and muscle vibration sounds during steady index finger abduction. An elastic attachment of the index finger to a strain gauge allowed a strong but relatively unfixed abducting contraction of the first dorsal interosseous (1DI). An accelerometer attached to the end of the finger recorded tremor, surface electrodes over 1DI recorded EMG signals and a heart-sounds monitor placed over 1DI recorded vibration. This arrangement enabled maintenance of a constant overall muscle contraction strength while still allowing measurement of the occurrence of tremulous movements of the finger. Ten normal subjects were studied with the index finger first extended at rest and then contracting 1DI to abduct the index finger against three different steady forces up to 50% of maximal voluntary contraction (MVC). Power spectral analysis of tremor, EMG activity and muscle vibration signals each revealed three frequency peaks occurring together at around 10 Hz, 20 Hz and 40 Hz. Coherence analysis showed that the same three peaks were present in the three signals. Phase analysis indicated a fixed time lag of tremor behind EMG of around 6.5 ms. This is compared with previous measurements of electromechanical delay. Other experiments indicated that the three peaks were of central nervous origin. Introducing mechanical perturbations or extra loading to the finger and making recordings under partial anaesthesia of the hand and forearm demonstrated preservation of all the peaks, suggesting that they did not originate from mechanical resonances or peripheral feedback loop resonances. It is concluded that, at least for a small hand muscle, there exist not one but a number of separate peak frequencies of oscillation during active contraction, and that these oscillations reflect synchronization of motor units at frequencies determined within the central nervous system. It is proposed that the multiple oscillations may be a means of frequency coding of motor commands.

Adult↗

PubMed1997

Stimulus/response curves as a method of measuring motor cortical excitability in man.

We investigated whether input/output curves of human motor cortex could provide similar information to cortical mapping under two conditions where the motor maps are known to change dramatically: ischaemic anaesthesia and amputation. Stimulus/response curves were constructed by recording the size of EMG responses evoked in arm muscles with transcranial magnetic stimulation at a single site using a range of intensities. Changes in the slope of this relationship during ischaemic anaesthesia (6 normal subjects) or amputation (two patients) were compared to changes in cortical motor maps produced by stimulating different sites at the same intensity. At rest both interventions increased map areas, as well as the slope of the stimulus/response curves. During voluntary activity they had no effect. We conclude that stimulus/response curves can detect changes in cortical motor maps, and discuss potential mechanisms for this effect.

Adult↗

PubMed1997

Rapid rate transcranial magnetic stimulation--a safety study.

We assessed the safety of repeated short trains (4 stimuli) of rapid-rate transcranial magnetic stimulation (rrTMS) over the left motor cortex in 6 healthy normal subjects. rrTMS involved two separate blocks of 50 consecutive trains of 4 stimuli at a frequency of 20 Hz and an intensity of 5-10% above active motor threshold. We monitored EEG, and assessed aspects of neurological (balance, gait, two-point discrimination, blood pressure, pulse rate), cognitive (attention, memory, executive function) and motor function (speed of movement initiation and execution and manual dexterity) before and after the two blocks of rrTMS. EMG was also recorded from a number of hand, forearm and arm muscles contralateral to the site of stimulation. Two blocks of repeated rrTMS at 20 Hz and 5-10% above active motor threshold did not produce any adverse effects. Measures of neurological, cognitive and motor function showed no change following rrTMS. From the EMG recording there was evidence of increase in the amplitude of the motor evoked potentials (MEPs) recorded from the biceps in one subject during the first block of rrTMS, but this did not occur in the second block. A similar magnification of MEPs was also observed in another subject only during the second block of stimulation. When applied using parameters falling within published guidelines (Pascual-Leone et al., 1993; Pascual-Leone et al., 1994), repeated rrTMS is a relatively safe technique in healthy normal subjects. As rrTMS allows disruption of cortical function for a longer period, it has the potential of becoming a particularly useful tool for the study of cognitive function as well as sensory or motor function.

Adult↗

PubMed1997

An electrophysiological study of the mechanism of fatigue in multiple sclerosis.

Fatigue is a common and disabling symptom in multiple sclerosis but is poorly understood. We investigated 'physiological' fatigue in 21 patients with multiple sclerosis who complained of disabling fatigue by measuring the decline in strength during a 45 s maximal contraction of the adductor pollicis muscle. The results were compared with those from a control group of 19 healthy subjects. The strength of control subjects declined by approximately 20% during the contraction; twitch interpolation showed central drive remained almost maximal throughout, and therefore that the fatigue was peripheral in origin. Patients had normal baseline strength, but developed greater fatigue (approximately 45%), which was central in origin. In both cases, the decline in strength followed a roughly linear time course suggesting that the patients, like the normals, were trying to maintain a maximum voluntary effort. Evidence for frequency-dependent conduction block (FDCB) in the patients' central motor pathways was sought by measuring the EMG responses to single and paired transcranial magnetic stimuli. Fatigue had no effect on the latency or size of EMG responses to transcranial magnetic stimulation, suggesting that FDCB was unlikely to have occurred. This was supported by measurements of the maximum speed of voluntary muscle contraction; although the patients showed relatively slow speeds before exercise, the decline in speed after fatigue was no greater than in normal subjects. We conclude that excessive 'physiological' fatigue contributes to the symptom of fatigue in multiple sclerosis and is central in origin. However, since the degree of exercise-induced fatigue did not correlate with the baseline complaint of fatigue, other factors must also be operating to produce the full range of clinical symptoms. We found no conclusive evidence that central fatigue is related to increased dysfunction in the primary central motor pathways and no evidence that FDCB is the pathophysiological mechanism. We postulate that central fatigue in multiple sclerosis is due to impaired drive to the primary motor cortex and several lines of evidence strongly suggest that this is not due to a lack of motivation.

Adult↗

PubMed1997

Does parkinsonian action tremor contribute to muscle weakness in Parkinson's disease?

The aim of this study was to see whether action tremor contributes to the weakness which can be measured in some muscles in patients with Parkinson's disease, by preventing fully fused contraction of motor units. Strength and action tremor were recorded during maximal wrist extension in patients when they were on and off antiparkinsonian medication, and in age- and sex-matched healthy subjects. Peak torque and mean rectified EMG levels were reduced by 25% and 30% (n = 7), respectively, when patients were off medication (compared with when they were on medication). In parkinsonian patients off treatment, action tremor was visible in torque and EMG records, and had a frequency of approximately 10 Hz. The absolute amplitude of this tremor was considerably smaller in patients on medication and in control subjects. In patients, medication reduced action tremor in torque and EMG by 37% and 57%, respectively, so that tremor amplitude approached that in normals. Similar changes were seen when action tremor was expressed as % peak torque of % mean rectified EMG. In parkinsonian patients off medication, a 10-Hz synchronizing influence dominates muscle activity at the wrist. The results is an incompletely fused muscle contraction, which is an important factor contributing to the weakness present in the off-medication state. Antiparkinsonian medication releases motor units from the 10-Hz synchronizing influence, enabling higher discharge rates, fused contraction and improved force generation.

Aged↗