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Biomedical subjects

J C Rothwell

Publications and source records attributed to J C Rothwell.

At least 307 records · Page 17Linked to original sources
PubMed1986

A method of monitoring function in corticospinal pathways during scoliosis surgery with a note on motor conduction velocities.

Spinal cord potentials produced by high voltage electrical stimulation of the scalp over the motor cortex were recorded intraoperatively from bipolar electrodes inserted into the epidural space of eleven patients undergoing corrective surgery for scoliosis. Responses to single stimuli could be recorded from the cord at all levels from cervical to low thoracic regions. The potentials were larger in the cervical than in the thoracic region and sometimes were followed by later waves at high stimulation intensities. Conduction velocity in large corticomotoneuron fibres was estimated to be between 50-74 ms-1 in different patients. This technique for monitoring motor tract function may be a useful adjunct to conventional monitoring of the sensory pathways during surgery.

Adolescent↗
PubMed1986

Electrophysiological and positron emission studies in a patient with cortical myoclonus, epilepsia partialis continua and motor epilepsy.

A patient is described who had a combination of stimulus-sensitive cortical myoclonus, epilepsia partialis continua, and Jacksonian motor epilepsy. He eventually required surgery because of the severity of his seizures. Electrophysiological recordings made before and during surgery, and PET scans performed before surgery identified an abnormal area of cerebral cortex in the postcentral parietal region. It is suggested that the stimulus-sensitive myoclonus arose because input into this region from peripheral sensory afferents produced an abnormal discharge which was fed forwards via cortico-cortical connections to the precentral motor cortex, to produce a reflex muscle jerk. The epilepsia partialis continua may have been caused by spontaneous discharges arising in the same region of parietal cortex. Both forms of jerking disappeared after resection of this part of the cortex.

Adult↗
PubMed1986

Dystonia of the legs induced by walking or passive movement of the big toe in a patient with cerebellar ectopia and syringomyelia.

A 45-year-old man with dystonia of the legs was found to have cerebellar ectopia and syringomyelia. Both walking and passive movements of the big toes evoked dystonic postures of the legs. Electrophysiologic studies suggested that the dystonic movements were reflex in origin. We propose that the cervical spinal cord lesion, involving propriospinal pathways, resulted in an abnormal response of spinal interneurons to peripheral stimuli.

Cerebellar Diseases↗
PubMed1985

Increase of the Bereitschaftspotential in simultaneous and sequential movements.

The amplitude and duration of the Bereitschaftspotential were analysed in 9 normal subjects prior to four different motor tasks: (1) simple isotonic elbow flexion ('flex'), (2) simple isometric finger flexion ('squeeze'), (3) simultaneous performance of 'flex' and 'squeeze', and (4) sequential performance of 'flex' then 'squeeze'. The Bereitschaftspotential was much larger and slightly longer in the simultaneous and sequential movements than in the same movements performed separately. The amplitudes of the Bereitschaftspotential were measured 150 and 75 ms prior to electromyographic (EMG) onset of the prime mover, and at the time of EMG onset. Changes in size were seen in all leads (FCz, Cz, C3', C4') and at all time points. It is suggested that the increase of the Bereitschaftspotential prior to complex arm movements reflects a greater activation of the supplementary motor area before simultaneous and sequential movements.

Adult↗
PubMed1985

Cerebral potentials and electromyographic responses evoked by stretch of wrist muscles in man.

The cerebral evoked potential produced by rapid extension of the wrist was recorded from scalp electrodes in normal subjects while they exerted a small background flexor torque (0.24 Nm) against an electric motor. The initial part of the response consisted of a negative deflection (N1) with an average latency of 24.7 ms. This was followed by a biphasic P1/P2 (32 ms) response and a large later negative wave (N2) (76 ms). Passive wrist extension also evoked reflex EMG responses in the forearm flexor muscles which could be resolved into a short latency (25 ms) and long-latency (52 ms) component. The cerebral responses persisted almost unchanged during complete ischaemic anaesthesia of the hand produced by a pressure cuff around the wrist, and were reduced if the stretch was given during voluntary wrist flexion. The primary component (N1-P1/P2) of the cerebral response probably represents the arrival at the cortex of the muscle afferent volley. However, the significance of the secondary component (P1/P2-N2) is unknown. Under certain conditions, its size was related to the size of the long latency stretch reflex evoked by stretch of the flexor muscles. Thus, increasing the velocity of stretch or decreasing the repetition rate (from 1.0 to 0.15 Hz) at which stretches were applied, increased the size of both the muscle reflex and the cerebral response. The secondary component also could be changed by voluntary reaction to wrist stretch. Changes in the size of the secondary component of the evoked response may represent the earliest cortical sign of interaction between sensory input and motor output.

Adult↗
PubMed1985

The spectrum of cortical myoclonus. From focal reflex jerks to spontaneous motor epilepsy.

The purpose of this paper is to draw attention to the wide range of clinical motor phenomena which may be caused by abnormal sensorimotor cortical discharge. Eleven selected patients with cortical myoclonus are described. In all cases the brief muscle jerks appeared to involve cerebral cortical mechanisms, for there were enlarged cerebral evoked potentials to somatosensory or visual stimuli and (in 5 of the 6 cases investigated in this way) a time-locked cortical event preceded spontaneous or action-induced jerking. In some patients, cortical myoclonus occurred only in response to a variety of afferent inputs (cortical reflex myoclonus). In others, the myoclonus occurred only during movement, when cortical mechanisms were activated voluntarily (cortical action myoclonus), or the cortical discharge occurred spontaneously (spontaneous cortical myoclonus and epilepsia partialis continua), and even spread to cause focal motor epilepsy (Jacksonian seizures). Some patients showed combinations of stimulus sensitive and spontaneous myoclonus, epilepsia partialis continua, focal motor epilepsy and generalized grand mal seizures. Such variations probably represent subtle differences in the site of abnormality in sensorimotor cortical neuronal mechanisms.

Adolescent↗
PubMed1985

Pathophysiology of blepharospasm and oromandibular dystonia.

The pathophysiology of reflexes mediated by the fifth and seventh cranial nerves has been studied in 16 patients with blepharospasm and oromandibular dystonia compared with normal age-matched subjects. The EMG activity of the dystonic spasms in the periocular and jaw muscles was similar to that described in other muscles in patients with generalized torsion dystonia. The latency of the R1 and R2 components of the blink reflex and of the corneal reflex was normal. However, the amplitude and the duration of the R1 and R2 and the duration of the corneal reflex were increased. In some patients the R1 component was also present on the side contralateral to the stimulus, while in normal subjects it was present only on the ipsilateral side. The excitability cycle of recovery of the R2 component of the blink reflex after a prior conditioning shock was enhanced in the patients. There were no EEG potentials preceding blepharospasms in the patients, although a Bereitschaftspotential was seen beginning some 500 ms prior to voluntary blinks in the same individuals. Exteroceptive suppression in the contracting masseter and orbicularis oculi muscles was absent in 40 to 50 per cent of the patients. The jaw jerk was present in all the patients with normal latency. These results indicate that the neuronal arcs of the facial reflexes in blepharospasm and oromandibular dystonia are normal. However, there is an abnormal excitatory drive, perhaps from the basal ganglia, to the facial motoneurons and the interneurons which mediate the facial reflexes in the brainstem.

Adult↗
PubMed1985

Writing tremor: its relationship to benign essential tremor.

Nine patients with tremor on writing and one patient with tremor only on swinging a golf club were investigated. None of the patients had any other neurological symptoms or signs. The frequency of the tremor ranged from 5 to 6 Hz. Rapid passive supination or pronation of the forearm by a torque motor evoked a short burst of alternating tremor in seven patients. The tremor was improved by alcohol or propranolol in six patients. These characteristics of writing tremor (and of other isolated action tremors) suggest that it is a variant of benign essential tremor.

Adult↗
PubMed1985

The corneal reflex and the R2 component of the blink reflex.

A reflex contraction of the human orbicularis oculi muscles can be evoked by stimulation of either the supraorbital region ("blink reflex") or the cornea ("corneal reflex"). We found that the latency of the corneal reflex was longer, and the duration was longer than the R2 component of the blink reflex. The absolute refractory period of the R2 component of the blink reflex was longer after supraorbital than after corneal conditioning stimulation. When the R2 component of the blink reflex was habituated by repetitive stimuli, stimulation of the cornea still evoked a reflex, but supraorbital stimulation produced only a depressed R2 response. These findings suggest that the two reflexes do not have identical neural connections.

Adult↗
PubMed1984

Abnormalities in central motor pathway conduction in multiple sclerosis.

The technique of scalp stimulation of the motor cortex was used to demonstrate abnormalities in the corticomotoneuron pathway in multiple sclerosis. Unilateral or bilateral delays in corticomotoneuron conduction, dispersion of corticomotoneuron volleys, or both, were shown to occur in such patients. Changes may be seen even in patients with little clinical evidence of corticomotoneuron deficit.

Adult↗
PubMed1984

Duration of the first agonist EMG burst in ballistic arm movements.

In normal subjects, fast arm movements are accomplished by a diphasic or triphasic EMG activation of the agonist and antagonist muscles. The duration of the first agonist burst (Ag1) has been said to be constant for movements of different size, whilst its amplitude is variable. Previous studies focused on relatively small movements (10-40 degrees). We have studied the behaviour of the Ag1 duration over the full physiological range of wrist and elbow flexion movements in normal subjects. The results showed that the principle of invariance of Ag1 duration was true when small movements of about 15-30 degrees were studied, but when larger movements were made burst length increased. A similar increase in Ag1 burst duration also was seen during movements performed against a load and in contractions made with fatigued muscles. Changes in duration of the Ag1 burst appear to be part of the normal mechanism for increasing the impulsive force provided in rapid contractions.

Adult↗
PubMed1984

Movements not involved in posture are abnormal in Parkinson's disease.

We have studied movements of the top joint of the thumb in a group of patients with Parkinson's disease. Even when movements were performed with the proximal phalanx of the thumb clamped, and with the forearm fully supported, movement time was prolonged and multiple bursts of EMG activity were present in the flexor pollicis longus. An abnormality of such movements performed with complete external postural support suggests that disease of the basal ganglia affect all movements, not just those involved in posture.

Aged↗
PubMed1984

Muscle spasms associated with Sudeck's atrophy after injury.

Four patients developed abnormal involuntary movements of a limb after injury. All subsequently developed sympathetic algodystrophy with Sudeck's atrophy and then abnormal muscle spasms or jerks of the affected limb, lasting years. Sympathetic block in three patients did not relieve the abnormal movements. Two patients obtained partial recovery spontaneously, but the other two required surgery for relief. The pathophysiology of this condition remains to be determined but the evidence suggests that it is a distinct, disabling clinical syndrome.

Adult↗
PubMed1984

Effects of motor cortex stimulation on spinal interneurones in intact man.

The effect of a descending corticospinal volley on a spinal inhibitory pathway, has been studied in five intact human subjects. Approximately 63% inhibition of the H-reflex evoked in wrist and finger flexor muscles, was produced by motor threshold stimulation of the radial nerve. When a submotor threshold cortical shock was given 2 to 4 ms before the H-reflex, this inhibition was reduced to approximately 38%. The timing of this effect is compatible with either a monosynaptic or disynaptic corticospinal tract projection onto the spinal inhibitory interneurone.

Electric Stimulation↗
PubMed1984

Reciprocal inhibition between the muscles of the human forearm.

Peripheral and central mechanisms of reciprocal inhibition between antagonist muscles in the forearm have been studied in ten human subjects. H reflexes were evoked in flexor muscles by stimulating the median nerve with single shocks at around motor threshold intensity. Peripheral inhibition of the flexor H reflex was produced by motor threshold stimulation with a single shock of the radial nerve supplying the extensor muscles. The conditioning radial nerve stimulus produced inhibition of the flexor H reflex consisting of three phases. In some individuals, an H reflex could be evoked in extensor muscles of the forearm. Stimulation of the median nerve produced inhibition of the extensor H reflex with a similar time course to that from extensors to flexors. The first phase of inhibition was apparent when the test median nerve shock was given from 1 ms before to 3 ms after the conditioning radial nerve shock. It was abrupt in onset and short in duration and could be evoked with a conditioning stimulus intensity as low as 0.75 X motor threshold. The second and third phases of inhibition were evident when the conditioning radial nerve stimulus preceded the median nerve test shock by 5 to 50, and 50 to 500 ms respectively. The characteristics of these later phases of inhibition are to be the subject of a separate report. The difference in timing of the peak initial short-latency inhibition from extensor to flexor and from flexor to extensor muscles enabled an estimate to be made of the central synaptic delay of the inhibitory process. This method yielded a central delay of 0.95 ms in excess of that of the H reflex. We conclude that the first phase of inhibition is mediated via large group I afferents acting through a single inhibitory interneurone . Central inhibition of the flexor H reflex was demonstrated with the radial nerve anaesthetized by injection of local anaesthetic at the elbow. Subjects were asked to try to contract the paralysed extensor muscles. Under this condition, attempted voluntary wrist extension inhibited the flexor H reflex even though no movement occurred. A shock was delivered to the radial nerve at a site proximal to the anaesthetic block. When the shock was applied in conjunction with an attempted voluntary contraction of the paralysed extensor muscles, the depth of inhibition was greater than that predicted from the effect of either a shock or a willed contraction acting independently.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗