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Biomedical subjects

J C Rothwell

Publications and source records attributed to J C Rothwell.

At least 271 records · Page 15Linked to original sources
PubMed1989

Reciprocal inhibition between forearm muscles in patients with writer's cramp and other occupational cramps, symptomatic hemidystonia and hemiparesis due to stroke.

Reciprocal inhibition of H reflexes in the forearm flexor muscles was examined in a group of 16 patients with writer's and other occupational cramps. The early disynaptic phase of reciprocal inhibition was normal. However, there was a reduction in the amount of later, presynaptic inhibition, when compared with age-matched normal subjects. Similar findings were seen in 2 patients with symptomatic hemidystonia in whom structural brain lesions were present. However, this reduction in presynaptic inhibition was not specific to patients with dystonia. In a further group of 13 patients with hemiparesis or hemiplegia due to stroke, abnormalities of both early and later phases of reciprocal inhibition were found. The patients with spasticity exhibited less disynaptic inhibition than those with normal tone or flaccid limbs. The changes in the presynaptic phase of reciprocal inhibition did not correlate with the clinical signs of spasticity and increased muscle tone. These results provide objective evidence of a physiological basis for the action or task-specific focal dystonias such as writer's cramp.

Adolescent↗
PubMed1989

The treatment of severe action myoclonus.

Ten patients with severe disabling myoclonus were treated with clonazepam, sodium valproate, primidone and piracetam alone, or in different combinations. Electrophysiological assessment indicated a cortical origin for the myoclonus in every case. Considerable improvement of myoclonus was achieved with combinations of these drugs in all patients, but this was not possible with monotherapy. In one patient two drugs were necessary (clonazepam and piracetam); in the others more than two drugs were required. The combination of sodium valproate, clonazepam and primidone (3 patients), or piracetam, clonazepam and primidone (3 patients), or the four drugs together (3 patients) was necessary to provide substantial relief of myoclonus. Such polytherapy generally was tolerated well. The benefits of treatment continued for more than 1 year in all cases, although progressive underlying pathology often caused other increasing disability.

Adolescent↗
PubMed1989

Electric and magnetic stimulation of human motor cortex: surface EMG and single motor unit responses.

1. The effects of different forms of brain stimulation on the discharge pattern of single motor units were examined using the post-stimulus time histogram (PSTH) technique and by recording the compound surface electromyographic (EMG) responses in the first dorsal interosseous (FDI) muscle. Electrical and magnetic methods were used to stimulate the brain through the intact scalp of seven normal subjects. Electrical stimuli were applied either with the anode over the lateral central scalp and the cathode at the vertex (anodal stimulation) or with the anode at the vertex and the cathode lateral (cathodal stimulation). Magnetic stimulation used a 9 cm diameter coil centred at the vertex; current in the coil flowed either clockwise or anticlockwise when viewed from above. 2. Supramotor threshold stimuli produced one or more narrow (less than 2 ms) peaks of increased firing in the PSTH of all thirty-two units studied. Anodal stimulation always produced an early peak. The latencies of the peaks produced by other forms of stimulation, or by high intensities of anodal stimulation, were grouped into four time bands relative to this early peak, at intervals of -0.5 to 0.5, 1-2, 2.5-3.5 and 4-5.5 ms later. Peaks occurring within these intervals are referred to as P0 (the earliest anodal), P1, P2 and P3 respectively. 3. At threshold, anodal stimulation evoked only the P0 peak; at higher intensities, the P2 or more commonly the P3 peak also was recruited. The size of the P0 peak appeared to saturate at high intensities. 4. In five of six subjects, cathodal stimulation behaved like anodal stimulation, except that there was a lower threshold for recruitment of the P2 or P3 peak relative to that of the P0 peak. In the other subject, the P3 peak was recruited before the P0 peak. 5. Anticlockwise magnetic [corrected] stimulation, at threshold, often produced several peaks. These always included a P1 peak, and usually a P3 peak. A P0 peak in the PSTH was never produced by an anticlockwise stimulation [corrected] at intensities which we could explore with the technique. 6. Clockwise magnetic [corrected] stimulation never recruited a P1 peak; in most subjects a P3 peak was recruited first and at higher intensities was accompanied by P0 or P2 peaks. 7. On most occasions when more than one peak was observed in a PSTH, the unit fired in only one of the preferred intervals after each shock. However, double firing was seen in five units when high intensities of stimulation were used.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Magnetic stimulation over the spinal enlargements.

Magnetic stimulation over the cervical and lumbar spinal enlargements was performed in 10 normal volunteers using a 9 cm diameter coil. Although the threshold and the amplitude of responses depended on the position of the coil and the direction of current flow within it, the latency was constant. The latencies obtained by magnetic stimulation were compatible with those obtained using high voltage electrical stimulation of the spinal nerve roots and always were shorter than the peripheral motor conduction time estimated by F-wave techniques. The site of activation by magnetic stimulation appears to be very similar to that stimulated by the high-voltage electrical method. Stimulation of descending motor tracts within the cord was not possible using the magnetic stimulator.

Action Potentials↗
PubMed1989

Rapid elbow movements in patients with torsion dystonia.

Rapid, self paced and self terminated elbow flexion movements were studied in a group of 10 patients with dystonia affecting the arms. The movements were slower and for small amplitude movements, more variable than those recorded in normal subjects. The duration of the first agonist burst was prolonged, even when compared with normal subjects deliberately moving slowly. Cocontraction of agonist and antagonist muscles during ballistic movements was common and may contribute to the bradykinesia. These findings are compared with similar studies of other diseases of the motor system. Unlike many other conditions which also reduce the speed of ballistic voluntary movements, the patients with dystonia in the present study showed a normal symmetry of acceleration and deceleration times. One interpretation of this finding is that aspects of the basic motor programmes are relatively preserved in this condition and account for the surprising retention of motor skills shown by some patients with dystonia.

Adolescent↗
PubMed1989

An exteroceptive reflex in the sternocleidomastoid muscle produced by electrical stimulation of the supraorbital nerve in normal subjects and patients with spasmodic torticollis.

We examined suppression of EMG activity in the contracting sternocleidomastoid muscles, produced by electrical stimulation of the supraorbital nerve in 10 normal subjects and 9 patients with spasmodic torticollis. This exteroceptive reflex in the sternocleidomastoid muscle consisted of 2 or 3 phases: (1) an early, small, and unstable phase of facilitation, followed by (2) a period of suppression beginning 35 msec after the stimulus, lasting for 35 msec with a reduction in EMG activity to approximately 40% of the prestimulus level, and (3) a further phase of facilitation at a latency of 70 msec, with duration 35 msec and an increase in EMG activity to approximately 35% above prestimulus levels. The latency and duration of the suppressive phase of this reflex were similar to the exteroceptive suppression of EMG activity in the masseter muscle after supraorbital nerve stimulation (masseter silent period). In patients with spasmodic torticollis, the depth of this exteroceptive suppression in the sternocleidomastoid muscles was less than that observed in an age-matched cohort of normal subjects, although the latency and duration were normal. In contrast, exteroceptive suppression in the masseter muscle was normal. These findings suggest abnormal function of inhibitory interneuronal networks between the 5th cranial nerve and the motor neurons of the spinal accessory and upper cervical nerves which mediate exteroceptive suppression in the sternocleidomastoid muscle in patients with spasmodic torticollis.

Adult↗
PubMed1989

[Percutaneous electric and magnetic stimulation of the motor cortex in man. Physiological aspects and clinical applications].

The new techniques of percutaneous electric and magnetic stimulation of the motor cortex in conscious man provide a unique opportunity of functional testing of the central motor pathways. These techniques seem to be safe and no immediate or delayed adverse reactions have been reported. The physiological studies so far performed suggest that the structures which are preferentially excited by these methods are the fast conducting pyramidal neurones. It has been shown that a single cortical stimulus is able to activate spinal motoneurones repeatedly. This phenomenon can easily be explained if the cortical stimulus generates multiple descending volleys in the central motor pathways. By comparison with experiments of stimulation of the exposed motor cortex in animals, it is likely that electric brain stimulation directly activates the axons of the pyramidal neurons at their origin and to a lesser extent also recruits these neurons transsynaptically, via some cortical interneurones. Magnetic stimulation of the brain at the vertex seems to act mostly by the latter mechanism. These different modes of action of the two methods of cortical stimulation explain the latency differences of the EMG responses obtained with either technique. Increased excitability of the spinal motoneurones and the existence of multiple descending volleys in response to a single cortical stimulus result in shortening of the latencies and greater amplitude of the responses recorded during voluntary contraction of the target muscle. Stimulation of the motor cortex has been used in pilot studies conducted on patients suffering from various disorders of the central motor pathways, such as multiple sclerosis, cervical spondylosis, motor neurone disease or stroke. The sensitivity of the technique looks promising. In M.S., the EMG responses usually show an increased central conduction latency, a reduced amplitude and a prolonged duration. The severity of the electrophysiological abnormalities is not very well correlated with clinical weakness, but the correlations seems to be better with hyperreflexia and the presence of brisk finger flexor jerks. The same abnormalities are observed in cervical spondylosis, although to a lesser extent. In motor neurone disease, the responses have a moderately increased latency and their size and duration are markedly reduced. Patients with acute hemispheric stroke usually show absent responses on the contralateral side. Finally, electric cortical stimulation can be very useful in monitoring the functional integrity of descending motor tracts during surgical operations performed on the spinal cord.

Central Nervous System Diseases↗
PubMed1988

The coexistence of bradykinesia and chorea in Huntington's disease and its implications for theories of basal ganglia control of movement.

Investigation of motor function in a group of 17 patients with Huntington's disease reveals that, in addition to the chorea that many patients exhibit, defects in voluntary motor performance also are evident. Fast simple wrist flexion movements to 15 degrees or 60 degrees were slower, and individual movements showed greater variability than seen in normal subjects. This bradykinesia was most pronounced in those patients who were akinetic and rigid, but also was seen in those with chorea alone; bradykinesia was independent of the drug treatment that the patients were receiving (and was therefore not due to drug-induced parkinsonism). The electromyographic activity of the agonist muscles during such simple but slow movement differed from that seen in Parkinson's disease. The performance of complex movements revealed further deficits. Some patients were unable to combine two movements in a simultaneous or sequential movement task of squeezing the hand and flexing the elbow. Those who could perform these complex movements exhibited slowing of the velocity of the movement and prolongation of the interval between movements. These abnormalities were present in patients with chorea who were not taking neuroleptic drugs. It is argued that they represent an abnormality of motor programming of complex movements, over and above the defect in executing simple movements. The long latency stretch reflexes in wrist flexor muscles and flexor pollicis longus were reduced or absent, but this did not correlate with changes in motor performance, or with the reduced size of the early components of cortical sensory evoked potentials. Bradykinesia is thus shown to be an integral component of the motor disorder of Huntington's disease, in addition to the chorea. The coexistence of bradykinesia and chorea in this illness is compatible with current theories of the role of the basal ganglia in the control of movement.

Adult↗
PubMed1988

Piracetam in the treatment of different types of myoclonus.

Forty patients with different clinical and electrophysiological types of myoclonus were treated with piracetam (18-24 g per day, p.o.) alone, or with other drugs (clonazepam, sodium valproate, and primidone) in different combinations. Piracetam in monotherapy improved the electrophysiological abnormalities in patients with cortical reflex myoclonus, but had no useful clinical effect. Sixteen patients obtained benefit from piracetam when given in combination with other antimyoclonic drugs; improvement was dramatic in two patients, moderate in seven and mild in seven. All patients showing some response to piracetam had myoclonus of cortical origin; however, five other patients with similar cortical myoclonus failed to improve when piracetam was added. Tolerance was excellent and side effects were minimal and transient. It is concluded that piracetam probably has an antimyoclonic action, but its potential value as a therapeutic tool for disabling myoclonus requires further study.

Adolescent↗
PubMed1988

Percutaneous electrical stimulation of lumbosacral roots in man.

High voltage percutaneous electrical stimulation over the lumbosacral spinal column was used to assess conduction in the cauda equina of 13 normal subjects. Electromyographic activity elicited by such stimulation was recorded from various muscles of the lower limbs. The stimulating cathode was placed over the spinous process of each vertebral body and the anode kept on the iliac crest contralateral to the studied limb. Shifting the cathode in a rostro-caudal direction shortened the response latency in quadriceps, tibialis anterior and extensor digitorum brevis muscles. At moderate intensities (60% maximum), this occurred abruptly when the cathode was placed at levels corresponding to the exit sites from the spinal canal of the roots innervating these muscles. At these intensities, the size of the response in each muscle was largest when the cathode was placed over the conus medullaris or at or below the exit of the motor roots from the spine. Latencies were always equal to or shorter than those obtained with F-wave measurements, suggesting that peripheral motor axons, rather than intraspinal structures were activated by the stimulus. Collision experiments demonstrated that activation occurred at two sites: near the spinal cord and at the root exit site in the vertebral foramina. Recordings made from soleus indicated that larger diameter proprioceptive afferent fibres also could be activated. This technique might have useful clinical applications in the study of both proximal and distal lesions of the cauda equina and provide a non-invasive method of localising such lesions electrophysiologically.

Adult↗
PubMed1988

Writer's cramp.

Explore the source record for details and available documents.

Adult↗
PubMed1987

Modulation of the long-latency reflex to stretch by the supplementary motor area in humans.

Surface-recorded, electromyographic responses to 200-ms ramp stretches were studied in the wrist flexor muscles from both arms of a patient with clinical and radiographic evidence of infarction in the right supplementary motor area (SMA). They were compared with those from 8 age-matched control subjects. The latencies of the spinal component of the stretch reflex were slightly longer than normal in both arms of the patient (normal subjects: 28.5 +/- 2.6 ms; patient: 35 ms, right arm and 32 ms left arm). However, the amplitude and duration of the short-latency response were identical in both arms. The onset of the long-latency response to stretch was symmetrical in both the patient's arms and was slightly later than normal (normal subjects 55.5 +/- 4.0 ms, patient: 72 ms right arm and 70 ms left arm); however, its duration was considerably prolonged in the arm contralateral to the SMA lesion (normal subjects: 44.8 +/- 6.0 ms; patient: 48 ms right arm. 105 ms left arm). These results are consistent with the hypothesis that the long-latency stretch reflex is mediated via a transcortical loop.

Adult↗
PubMed1987

Examination of motor function in lesions of the spinal cord by stimulation of the motor cortex.

Electrical stimulation of the motor cortex was performed in 3 patients with cervical cord trauma and in 3 with cervical myelopathy caused by cervical spondylosis. Abnormal conduction in central motor tracts was demonstrated in 5 of the 6 patients; yet in 4 of these, cortical somatosensory evoked potentials from the same limb were of normal latency. In the remaining patient who had normal motor latencies, the somatosensory evoked potentials were delayed on one side. Electrophysiological examination of the motor pathways by cortical stimulation may therefore be of considerable value in the assessment and management of patients with traumatic and compressive disease of the spinal cord.

Adult↗
PubMed1987

The Bereitschaftspotential, L-DOPA and Parkinson's disease.

Bereitschaftspotentials (BPs) prior to extension movements of the index finger were studied in normal subjects and in patients with Parkinson's disease. In both, BPs were studied before and after L-DOPA therapy; in addition, the normal subjects were studied after dopamine antagonists. In both patients and normal subjects, L-DOPA caused an increase in the amplitude of the early part of the BP and of the point of peak negativity, just prior to EMG onset (N1) but it did not cause an increase of the late lateralized part of the BP (NS' of Shibasaki); in normal subjects dopaminergic antagonists caused a decrease in the amplitude of the N1. Control experiments suggested that the change caused by L-DOPA was not the result of slower movement or poorer triggering when OFF drugs. For patients with Parkinson's disease there was no correlation between the change in their peak BP negativity (N1) after L-DOPA and their change in clinical mobility; in addition, there was no difference in the peak BP negativity of patients OFF therapy and that of age-matched normals, though there was a slight decrease in the amplitude of the early part of the BP for the patients with Parkinson's disease; this was the same part that had been enlarged by L-DOPA therapy. These findings suggest that the N1 is not affected by Parkinson's disease and that the effect of dopaminergic drugs on the N1 is mediated by actions on dopaminergic mechanisms elsewhere than in the striatum, perhaps in the cerebral cortex itself. The effect of L-DOPA will need to be taken into account in subsequent studies of the BP in Parkinson's disease.

Adult↗
PubMed1987

The interpretation of electromyographic responses to electrical stimulation of the motor cortex in diseases of the upper motor neurone.

The complexities of interpreting results of electrical stimulation of the motor cortex in pathological states are discussed and illustrated by reference to results from a variety of patients with diseases affecting the upper motor neurone (multiple sclerosis, cervical spondylosis and myelopathy, motor neurone disease, hemiparesis due to cerebral infarction, and hereditary spastic paraplegia). The abnormalities of the electromyographic (EMG) responses after anodal cortical stimulation consisted of delay in the latency to onset, dispersion or reduction in response size or even absence of EMG responses. These changes were not confined to any specific condition or pathology. Previous work has suggested that the sequence of events that follow anodal cortical stimulation involves repetitive excitatory inputs to spinal motoneurones and transmission across at least one central synapse. Accordingly, delayed latencies may not exclusively indicate slowing of motor conduction, while the absence of any response may not indicate complete failure of conduction in corticomotoneurone pathways.

Adult↗