Biomedical subjects

S J Fellows

Publications and source records attributed to S J Fellows.

17 recordsLinked to original sources

PubMed2001

Deficits in sensorimotor control during precise hand movements in Huntington's disease.

OBJECTIVES: To investigate the performance of patients with Huntington's disease (HD) while manipulating objects using a precision grip. METHODS: The grip forces developed by the fingers were studied while subjects lifted an object of unpredictable weight in the hand. The ability to stabilize grip force after externally imposed weight change was also studied. RESULTS: Patients used higher grip forces than the normal subjects in both the lifting and holding phases, particularly with a lighter weight. Lift timing was slowed in the patients, most markedly with a lighter weight. Increased levels of inter-trial variation were observed only with a light weight. This indicates that the slowing in HD differs from that in Parkinson's disease, which remains constant regardless of object load, and that the slowing in HD is not due to involuntary antagonist muscle activity resulting from an underlying chorea. The grip force response to sudden weight change was normal, but appeared after a delay which increased at lower rates of weight change. CONCLUSIONS: Disturbances in precision grip timing and magnitude in HD may result from a reduced ability to process relevant tactile afferent input. The delay in the adaptive response suggests an increased threshold for detection of weight change in HD. Alternatively, this delay may arise from mediation of the response over an additional cerebellar pathway to compensate for damage to the basal ganglia.

Adult↗

PubMed2001

Precision grip deficits in cerebellar disorders in man.

OBJECTIVE: To investigate the effect of a variety of cerebellar pathologies on a functional motor task (lifting an object in a precision grip). METHODS: The study involved 8 patients with unilateral damage in the region of the posterior inferior cerebellar artery (PICA), 6 with damage in the region of the superior cerebellar artery (SUPCA), 12 patients with familiar or idiopathic cortical cerebellar degeneration, and 45 age-matched normal subjects. Subjects lifted an object of unpredictable load (internally guided task) or responded to a sudden load increase while holding the object steadily (externally guided task). RESULTS: Damage to the dentate nucleus (SUPCA) or its afferent input (cerebellar atrophy) resulted in disruption of the close coordination normally seen between proximal muscles (lifting the object) and the fingers (gripping the object) during a self-paced lift. Both the SUPCA group and, more markedly, the atrophy group, showed exaggerated levels of grip force. All patients showed a normal rate of grip force development. Damage in the PICA region had no significant effect on any of the measured lifting parameters. All patient groups retained the ability to scale grip force to different object loads. The automatic grip force response to unexpected load increase of a hand held object showed normal latency and time course in all patient groups. The response was modulated by the rate of the load change. Response magnitude was exaggerated in the atrophy patients at all 3 rates tested. CONCLUSIONS: Disturbances associated with cerebellar disorders differed from those seen following damage to the basal ganglia, with no evidence of slowed rates of grip force development. Disruption of temporal coordination between the proximal muscles (lifting) and the fingers (gripping) in a lift was apparent, supporting the role of the cerebellum in coordinating the timing of multi-joint movement sequences. Exaggeration of grip force levels was found in association with damage to the dentate nucleus or, in particular, to its afferent input. This could support a role or the cerebellum in sensorimotor processing, but might also represent a failure to time correctly the duration of grip force generation.

Action Potentials↗

PubMed1998

Precision grip and Parkinson's disease.

In order to investigate sensorimotor processing and force development in Parkinson's disease, 16 patients, four patients with hemiparkinsonism and 12 age-matched normal subjects were assessed during lifting and holding of an object in a precision grip between thumb and forefinger, or holding the object in this grip at a fixed height above a table. In the former case, object loading could be changed between lifts without warning. In the latter case, unexpected step load changes to the object were applied to the object with a torque motor. All procedures could be applied with or without visual control of the hand and the object. Normal subjects lifted an unpredictable load employing the grip force parameters used in the preceding lift. If a load change was encountered, the parameters became adapted to the new conditions during the lift, modulating grip forces to match the loading. Parkinsonian patients retained this strategy and the ability to regulate grip forces according to load. Under all conditions, however, parkinsonian subjects developed abnormally high grip forces in both the lift and the hold phase, although the ratio of these forces remained normal. Lifting height was normal in parkinsonian subjects, but the duration of the lifting task was significantly prolonged, due to a marked slowing in the rate of grip force development in the lead-up to object lift-off and to prolongation of the movement phase. Forewarning of object loading, with or without visual control, did not reduce timing deficits or improve the rate of grip force development. However, it did allow parkinsonian subjects to reduce the safety margin significantly. Responses to step load changes imposed during holding without visual control showed minor abnormalities in the parkinsonian patients: onset latencies and EMG activity in the first dorsal interosseus and thenar muscles were normal up to 140 ms after displacement. Subsequent EMG activity in the first dorsal interosseus remained largely normal, but activity later in the slip response (140-210 ms), subject to voluntary influence, was reduced in the thenar muscle. Differences were less marked under visual conditions, but remained significant. We concluded that the internal parameter set for lifting an object in a precision grip and the automatic processes adapting precision grip to actual conditions are intact in Parkinson's disease. However, parkinsonian subjects generate abnormally high grip forces and require longer than normal subjects to complete a lift, particularly with lighter loads. This deterioration in performance reflects both reduced effectiveness of sensorimotor processing and impairment in the rate of force development in Parkinson's disease.

Activities of Daily Living↗

PubMed1997

The relevance of sensory input for the cerebellar control of movements.

The performance of a motor task not only requires subjects to plan, prepare, and initiate but also to monitor how a movement is performed. We used positron emission tomography to examine to what extent the human cerebellum is involved in controlling motor output or sensory input from movements in normal subjects. In the first study, we compared the active performance of a motor task (flexion and extension of the right elbow) to the passive execution of the same movements. Passive movements were driven by a motor with the arm fixed in a guide hinge. Active movements (compared to rest) elicited increases of rCBF mainly in the ipsilateral neocerebellar hemisphere and vermis of the posterior lobe. During passive movements, almost identical parts of the cerebellar hemispheres and vermis were activated (compared to the rest condition). The direct comparison of active and passive movement conditions revealed a small activation of the neocerebellar hemisphere of the posterior lobe and cerebellar nuclei ipsilateral to the movement. Approximately 90% of cerebellar neuronal activity was related to sensory input. In the second study, we compared the execution of a free selection joystick movement task to a condition in which subjects simply imagined the movements. The execution of movements (compared to rest) was associated with increases of rCBF in the ipsilateral neocerebellar hemisphere and vermis of the posterior lobe. During movement imagination, a small part of the ipsilateral cerebellar hemisphere and vermis of the posterior lobe was activated (compared to rest). The increase of rCBF during movement imagination accounted for only 20% of the signal seen during movement execution. Our results indicate that the neocerebellum may be much more concerned with sensory information processing than has been considered previously.

Adult↗

PubMed1996

Stretch reflexes of the proximal arm in a patient with mirror movements: absence of bilateral long-latency components.

The stretch reflex responses evoked by unilateral limb displacement in distal (first dorsal interosseus (FDI)) and in proximal (biceps brachii (Bb)) arm muscles were studied during matched bilateral contractions in a patient with congenital mirror movements. In this patient unilateral transcortical magnetic stimulation (TMS) elicited not only the normal contralateral EMG response but also a clear ipsilateral component in the EMG of both proximal and distal arm muscles. As expected from previous studies, the ipsilateral FDI muscle responded to stretch of the index finger with short- (M1) and long-latency (M2) reflex components. In addition, the FDI contralateral to displacement exhibited an abnormal mirrored response corresponding to the M2 interval. In contrast, whereas the ipsilateral Bb responded to imposed elbow extension with a marked M1/M2 reflex response, no mirroring of either reflex component was apparent in the contralateral Bb EMG. If the mirroring of the M2 in the FDI is accepted as evidence for the transcortical nature of the M2 reflex response, then it follows that the absence of such mirroring in the Bb indicates that a transcortical mechanism cannot play a major role in the generation of long-latency stretch reflex responses in proximal arm muscles.

Adult↗

PubMed1994

Voluntary movement at the elbow in spastic hemiparesis.

The relative importance of hyperreflexia and paresis in disturbances of voluntary arm movement was studied in a group of patients (n = 25) with spasticity arising from a unilateral ischemic cerebral lesion. Patient performance was evaluated against data obtained from normal subjects (n = 15). Spastic patients achieved lower maximum movement velocities during flexion or extension than did normal subjects. The more marked the paresis of the elbow flexor and extensor muscles of the patients, relative to the strength of the normal subjects, the greater was this reduction in maximum velocity. For a given velocity, however, the time taken to complete a movement and the time to reach the peak velocity were normal. No relationship was found between the degree of impairment of voluntary movement and the level of passive muscle hypertonia in the antagonist. Although overactivity of the antagonist muscle may play some role in disturbance of movements made at low velocities without an opposing load, antagonist activity during movements made against a load (i.e., under more natural conditions) was at or below normal levels, even in those patients with the most marked passive muscle hypertonia. It is concluded that agonist muscle paresis, rather than antagonist muscle hypertonia, plays the dominant role in the disturbance of voluntary elbow movement following stroke.

Adult↗

PubMed1994

Agonist and antagonist EMG activation during isometric torque development at the elbow in spastic hemiparesis.

Voluntary isometric step contractions of the elbow flexor and extensor muscles were studied in a group of patients with paresis arising as the result of unilateral cerebral lesion and in a control group of normal subjects. For each subject the maximum isometric torque in flexion and extension was obtained, along with a series of graduated torque steps up to this maximum, in order to perform a regression analysis between torque developed and the associated agonist and antagonist EMG. This relationship proved to be linear in all normal subjects and in all but the most paretic spastic patients. If the patients were grouped according to their ability to make discrete large angle flexion and extension movements at the elbow, a clear correspondence was seen between increasing movement disability and the degree of paresis. No significant differences were found in the torque/EMG relationship of spastic patients when either elbow extensors or flexors were acting as the agonist in a contraction. Similarly, no evidence of exaggerated antagonist co-activation was found. It is concluded that, in the upper arm muscles, hemiparesis following stroke cannot, under isometric conditions, be attributed to hyperactivity of antagonist muscles.

Adult↗

PubMed1993

Changes in the short- and long-latency stretch reflex components of the triceps surae muscle during ischaemia in man.

1. In order to establish the afferent source responsible for the M1 and M2 stretch reflex components of the voluntarily activated human triceps surae muscle, mechanical reflex testing was applied before and during ischaemic blockade of the lower limb. This procedure is known to affect large, fast conducting afferent fibres earliest, specifically Ia afferents arising from muscle spindle afferents. 2. It was found that both the M1 and M2 components were eliminated at the same time, at a point when the P40 peak in the somatosensory evoked potential, produced from stimulation of fast conducting peripheral afferents, was also abolished. This evidence indicates that both reflex components are mediated by information carried by muscle spindle Ia afferents. 3. The M1 component was selectively increased in the early stages of ischaemia. The M2 response did not increase during this period, but showed a tendency to reduce in amplitude. This effect may arise as the result of increased recruitment of motor units in the M1 component reducing the number of units available for activation in the M2 response. 4. These results do not support the view that the M2 reflex component of the triceps surae muscle is mediated by secondary afferent information, but indicate, rather, that both the M1 and M2 components are mediated by Ia afferent information acting on spinal pathways.

Adult↗

PubMed1993

The limitations of the tendon jerk as a marker of pathological stretch reflex activity in human spasticity.

The motor disorders associated with human spasticity arise, partly from a pathological increase in the excitability of muscle stretch reflexes. In clinical practice, reflex excitability is commonly assessed by grading the reflex response to a blow delivered to the tendon of a muscle. This is a much simpler response than the complex patterns of activity which may be elicited following muscle stretch caused by active or passive movement. Changes in the biceps brachii tendon jerk response have been followed over the first year after stroke in a group of hemiparetic patients and compared with changes in short and medium latency reflex responses elicited by imposed elbow flexion of initially relaxed spastic muscle and with the development of the late reflex responses which contribute to spastic hypertonia. A progressive increase in tendon jerk responses occurred over the first year following stroke, whereas reflex responses to imposed displacement, in particular the late reflex responses contributing to muscle hypertonia, reached their peak excitability one to three months after stroke, with a subsequent reduction in activity. The tendon jerk reflex therefore provides an incomplete picture of the pathological changes in the reflex responses in spasticity.

Adult↗

PubMed1991

The time-course of bilateral changes in the reflex excitability of relaxed triceps surae muscle in human hemiparetic spasticity.

Short, rapid dorsiflexion of the normal human ankle induces a single, synchronised reflex EMG response in the initially relaxed triceps surae muscle (TS). In subjects in whom hemiparesis is present as a result of a unilateral ischaemic cerebral lesion, a reflex EMG response can be elicited on either side with timing identical to that of the normal response. The magnitude of the response in hemiparetic subjects, however, differs from the normal on both the side contralateral and that ipsilateral to the causative lesion. Furthermore, the magnitude of this response varies over the time-course of spasticity. Contralaterally to the lesion, a gradual increase in the magnitude of the response to imposed displacement occurs. One year after stroke, the response has reached a level significantly larger than normal. Changes in the magnitude of the contralateral Achilles tendon jerk reflex EMG are apparent earlier than changes in the response to imposed displacement, with exaggerated tendon jerks already being apparent between 1 and 3 months after stroke. On the side ipsilateral to the lesion, a profound depression of the response to imposed displacement is visible as early as a month after stroke. This depression diminishes over the 1st year, but the response has not even then returned to normal values. These changes are not reflected in the ipsilateral tendon jerk response, which remains normal throughout this period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Different mechanisms underlie the long-latency stretch reflex response of active human muscle at different joints.

1. Stretch of voluntarily activated human muscle results in a reflex response consisting of short-latency (M1) and delayed long-latency (M2) components. The mechanism of the M2 response remains the subject of controversy. The present study tested the universality of the hypothesis that the M2 response results from the transmission of low-threshold muscle afferent input travelling over a long-loop supraspinal pathway. Muscle reflex responses resulting from imposed stretch were obtained from the first dorsal interosseus (FDI), biceps brachii (BB), triceps brachii (TB) and triceps surae (TS) muscles. 2. Patients suffering from Huntington's disease (HD) show a selective loss of FDI-M2 responses, with sparing of the M1. This has been attributed to disruption of supraspinal pathways as a part of the disease pathology. Accordingly, HD has been used in the present study as a model to test the universality of the long-loop hypothesis: if this is so, then HD patients with an absent FDI M2 should also fail to show an M2 response in other muscles. 3. It is shown that a group of HD patients in whom the FDI-M2 response was absent or residual developed clear M2 responses in the TB, BB and TS muscles following stretch sufficient to invariably evoke this component in normal subjects. 4. It is thus concluded that longer-latency stretch reflex components are not invariably mediated over long-loop supraspinal pathways, but that this mode of control is dominant only in muscles, such as those of the hand, whose function depends largely on direct cortical control.

Adult↗

PubMed1991

Biomechanical changes at the ankle joint after stroke.

The resistance of the relaxed ankle to slow displacement over the joint movement range was measured on both sides of a group of hemiparetic stroke patients, in whom spasticity had been established for at least one year and who showed no clinical signs of contractures. The ankle joints of the age-matched normal subjects were flexible over most of the movement range, showing dramatically increasing stiffness only when the foot was dorsiflexed beyond 70 degrees, with a neutral range between 90-100 degrees, and a less dramatic increase in stiffness during plantarflexion. Hemiparetic patients showed identical curves to the normal subjects on the "healthy" side, ipsilateral to the causative cerebral lesion, but were significantly stiffer in dorsiflexion on the contralateral side, without change in the minimum stiffness range or during plantarflexion. Therefore significant changes in passive biomechanical properties occur at the affected ankle of hemiparetic subjects, predominantly as the result of a loss of compliance in the Achilles tendon, although an increase in the passive stiffness of the triceps surae may also occur. The contribution of these changes to the locomotor disability of hemiparetic patients is discussed.

Ankle Joint↗

PubMed1991

The mechanism of spastic muscle hypertonus. Variation in reflex gain over the time course of spasticity.

The electromyographic (EMG) response of the initially passive biceps brachii muscle to imposed extension applied at the elbow was studied in 19 hemiparetic and 12 normal subjects. In relaxed normal subjects, the biceps muscle was found to respond only at displacement velocities above 175 deg/s, with a single early burst of activity in the biceps EMG. In contrast, the hemiparetic subjects, in addition to the early EMG activity, also showed considerable late activity, which persisted even with stretch velocities as low as 35 deg/s. This late activity is a stretch reflex, present in fully plegic arms. It was seen in all spastic subjects in whom the tone of the biceps had been clinically assessed to be raised, but was never observed in subjects with normal muscle tone. The mean level of this EMG response was highly correlated with displacement velocity and its duration to the duration of the applied displacement. It is suggested that this reflex EMG activity is the major factor in the genesis of spastic hypertonus in the arm and that it arises not from a reduction in the threshold of the stretch reflexes of the muscle, but from a pathological increase in stretch reflex gain. It is further shown that this activity is at a high level between the first and third months after the onset of spasticity and that the reflex gain is significantly reduced when spasticity is established for a year or more. It is concluded that, while changes in passive mechanical properties may play a role when spasticity has been established for more than a year, the major cause of spastic muscle hypertonus is a pathological increase in stretch reflex activity.

Adult↗

PubMed1990

Pathological stretch reflexes on the "good" side of hemiparetic patients.

The reflex EMG responses from a tendon tap or an imposed, medium amplitude (30 degrees), stretch at a range of stretch velocities have been recorded from the triceps and biceps muscles of normal human subjects and in both the affected and "unaffected" arms of hemiparetic patients under relaxed conditions. In the hemiparetic arm, exaggerated tendon jerks were, as expected, observed in both muscles. The response of the biceps to elbow extension was also exaggerated compared with normal values and displayed both an additional earlier component and a much reduced velocity threshold. The triceps, in contrast, showed depressed responses to elbow flexion, with a much higher velocity threshold than normal subjects. Furthermore, on the supposedly "unaffected" side of the hemiparetic subjects, the reciprocal pattern was seen, with depression of the biceps response and a raising of its threshold, along with considerably exaggerated responses in the triceps including earlier components not seen in the normal subjects. The increased excitability of the flexor musculature on the spastic side may be paralleled by increases in activity in the segmental pathways responsible for modulation of agonist/antagonist activity in the ipsi and contralateral limb, leading to an inhibition of the ipsilateral extensors and contralateral flexors and excitatory input to the contralateral extensors. Thus the "good" side of hemiparetic patients also receives pathological changes, and studies of the mechanisms of spasticity should avoid the use of the "unaffected" side of hemiparetic subjects as a control for monitoring pathological reflexes.

Adult↗

PubMed1989

The role of joint biomechanics in determining stretch reflex latency at the normal human ankle.

In order to study the influence of biomechanical factors on the timing of stretch reflex activity in the ankle extensor musculature, well defined, small amplitude and relatively rapid dorsiflexing stretch was applied to the ankle of seated normal human subjects at a series of angles within the range of physiological movement. If the ankle musculature was relaxed, a single reflex component appeared in the Triceps surae (TS) EMG with a latency compatible with a predominantly monosynaptic pathway. The latency of this response could be prolonged by applying stretch from an initially plantarflexed position and, similarly, decreased by applying stretch from a dorsiflexed position. A decrease in latency of 5-30 ms could be achieved by altering the pre-displacement ankle angle from 105 to 75 degrees. Intermediate changes in the start angle led to intermediate changes in latency. This trend was highly linear. If stretch was applied while the subject maintained a low level contraction in the TS, however, this shift in latency was abolished, with the earliest reflex components appearing with a latency obtained in the relaxed state at or close to maximum dorsiflexion. It is suggested that this shift in latency results from the properties of the long, compliant tendon through which joint movements are transmitted to the TS muscle. This shift in latency caused by passive alteration in the ankle angle at which a reflex was evoked should be taken into account when classifying reflexes arising from a mechanical input, or when using latency determinations as evidence for the involvement of particular pathways in their genesis.

Adult↗

PubMed1987

Changes in the length of the human biceps brachii muscle during elbow movements.

1. Needles inserted into the biceps move with the muscle as the elbow flexes or extends. Pairs of needles were used to indicate changes in length of the muscle fibres. 2. During low-frequency flexion-extension movements the biceps lengthened as the joint extended. 3. When, however, joint movements at greater than 2.2 Hz were maintained by external electrical stimulation of triceps and the long head of biceps, or of biceps alone, the biceps lengthened and shortened in antiphase to the joint movement. The elastic properties of the biceps tendons then combined with the mass of the forearm as a spring-mass system whose natural frequency was about 2.2 Hz. 4. No such phase reversal appeared during voluntary elbow movements at frequencies up to 5 Hz. It was concluded that the combined tendons of biceps, brachialis and brachioradialis made a much less compliant muscle-to-bone coupling. 5. The results are discussed in relation to possible tremor mechanisms.

Arm↗

PubMed1983

Response of the normal human ankle joint to imposed sinusoidal movements.

Ankle joints were subjected to sinusoidal movements at a range of amplitudes and frequencies. Records were made of electromyograms (e.m.g.s) in calf muscles, and of the forces at the joints. When the leg is relaxed, the ankle joint resists an imposed sinusoidal movement with a small approximately sinusoidal force. It is stiffer in its resistance to small movements than to large ones, and this resistance is greater when the joint is dorsiflexed than when it is plantarflexed. If the subject exerts a steady mean flexing force, the imposed sinusoidal movement generates reflex activity which may be recorded as a modulation of the gastrocnemius and soleus e.m.g.s. The e.m.g. response to the sinusoidal movement occurs later in cycles of movement at high than at low frequencies, as one could expect of a reflex pathway that involves a delay. The results suggest that this delay is between 50 and 60 ms, and we conclude that under these circumstances spinal stretch reflexes are playing the important part. The relation of the resisting force to the movement has been displayed as a vector. As the frequency changes, this vector describes the circular path that is characteristic of a system which includes delays or lags; this path enables one to draw conclusions about the amplitude and timing of the reflex resistance to the movement. When a subject exerts a moderate flexing force against the sinusoidal movement for some minutes, the reflex response becomes progressively potentiated. A subject whose reflex responses are normally slight may then exhibit a vigorous reflex response to the movement of that ankle. This enhancement of spinal reflex activity was accompanied by an increase in the myotatic reflex response at the ankle. Reflex responses to sinusoidal movement were most clearly seen when the subject exerted a mean flexing force that amounted to about one-fifth of his maximum. Very small movements (+/- 0.5 degrees) generated little or no reflex response. With large amplitudes of movement there was more reflex activity, but at some amplitude (which varied from subject to subject and from time to time) the reflex mechanism appeared to 'saturate', and further increases in amplitude were not accompanied by comparable increases in the reflex response. With movements at 10-15 Hz the e.m.g. response often became large in alternate cycles, with less activity in the intervening cycles.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗