Biomedical subjects

B L Day

Publications and source records attributed to B L Day.

At least 73 records · Page 4Linked to original sources

PubMed1991

Modulation of motor cortical excitability by electrical stimulation over the cerebellum in man.

1. We have stimulated over the cerebellum of intact human subjects by applying single electrical stimuli through electrodes placed on the back of the head, approximately at the level of the inion. The intensity of stimulation used was below that required to produce direct EMG responses in pre-activated muscles of the hand. 2. In ten subjects the effect of the stimulus over the cerebellum was to reduce the size of the EMG response in first dorsal interosseous muscle evoked by a magnetic stimulus to the cerebral cortex. In all subjects the onset of the period of suppression occurred when the test magnetic cortical shock followed the conditioning cerebellar shock by 5 ms. The duration of the suppression lasted from 3 to 7 ms. 3. The amount of suppression was related to the intensity of stimulation over the cerebellum. At 15% below the threshold for direct motor activation there was no effect; increasing suppression was evident at 10, 5 and 0% below motor threshold. 4. With a conditioning-test interval of 5-6 ms the suppression was the same whether the target muscle was relaxed or active. With longer conditioning-test intervals (12 and 15 ms) the amount of suppression was greater in active than relaxed muscles. 5. The short-latency suppression was greatest when the stimulating anode was ipsilateral to the target muscle and contralateral to the stimulated sensorimotor cortex. The later period of suppression was insensitive to the polarity of stimulation. When the stimulating electrodes were moved 2 cm caudally or cranially the short latency suppression disappeared whereas the longer latency suppression was still observed with the electrodes in the lower position. 6. Different results were obtained when the test EMG response was produced by an electrical (rather than magnetic) stimulus over the sensorimotor cortex. The short latency effect was no longer visible whereas the longer latency effect was the same as when testing with a magnetic cortical stimulus. 7. We suggest that a single electrical stimulus across the base of the skull (particularly with the anode over one cerebellar hemisphere) produces a short latency (5-6 ms) disfacilitation of the contralateral motor cortex through activation of cerebellar structures. A later (12 and 15 ms), less specific suppression which is present when testing in active muscles is thought to be mediated by a different mechanism and probably produces its effect at the level of the spinal cord.

Action Potentials↗

PubMed1991

The effect of posture on the normal and pathological auditory startle reflex.

The effect of posture on the EMG pattern of the normal auditory startle reflex was investigated. The startle response to an unexpected auditory tone was studied in eleven normal subjects when standing, and in six normal subjects when sitting relaxed or tonically plantar flexing both feet. Reflex EMG activity was recorded in the tibialis anterior and soleus about twice as frequently when standing, than when sitting relaxed. In addition, the median latencies to onset of reflex EMG activity in the tibialis anterior and soleus were about 40 and 60 ms shorter during standing, than when sitting relaxed. No short latency EMG activity was recorded in the calf muscles during tonic plantar flexion of the feet, while sitting. The effect of posture on the EMG pattern of the pathological auditory startle reflex was studied in five patients with hyperekplexia. In three patients the latency to onset of reflex EMG activity in the tibialis anterior was shorter when standing, than when sitting relaxed. The EMG pattern of the reflex response to sound was studied in detail in two of these patients and consisted of up to three successive components. The expression of each EMG component depended on the postural set of the limbs. In particular, a distinct short latency component was found in posturally important muscles following auditory stimulation. This short latency component was not recorded when sitting relaxed. It is concluded that the EMG pattern of the physiological and pathological auditory startle response is not fixed, but may change with the postural stance of the body. This finding supports the theory that the normal startle reflex and the abnormal startle reflex in hyperekplexia have a common brainstem origin.

Adolescent↗

PubMed1991

Intra-operative recording of motor tract potentials at the cervico-medullary junction following scalp electrical and magnetic stimulation of the motor cortex.

Activity in descending motor pathways after scalp electrical and magnetic brain stimulation of the motor cortex was recorded from the exposed cervico-medullary junction in six patients having trans-oral surgery of the upper cervical spine. Recordings during deep anaesthesia without muscle paralysis revealed an initial negative potential (D wave) at about 2 ms with electrical stimulation in five of the six patients. This was followed by a muscle potential which obscured any later waveforms. Magnetic stimulation produced clear potentials in only one patient. The earliest wave to magnetic stimulation during deep anaesthesia was 1-2 ms later than the earliest potential to electrical stimulation. Following lightening of the anaesthetic and the administration of muscle relaxants a series of later negative potentials (I waves) were more clearly seen to both electrical and magnetic stimulation. More I waves were recorded to magnetic stimulation during light anaesthesia than during deep anaesthesia. Increasing the intensity of electrical stimulation also produced an extra late I wave. At the highest intensity of magnetic stimulation the latency of the earliest potential was comparable to the D wave to electrical stimulation. The intervals between these various D and I waves corresponded to those previously described for the timing of single motor unit discharge after cortical stimulation.

Adult↗

PubMed1991

Axial myoclonus of propriospinal origin.

Three patients are described with nonrhythmic repetitive axial myoclonic jerks causing symmetric flexion of the neck, trunk, hips and knees. No electrophysiological evidence of a cortical or brainstem reticular origin for the myoclonus was found. In the first patient the axial jerks only occurred spontaneously. The latencies of recruitment of spinal segments during a jerk indicated that the discharge arose in the mid thoracic cord and then slowly spread at about 5 ms-1 up and down the cord to involve rostral and caudal segments. No structural lesion was identified in this patient. In the second patient spontaneous and reflex axial jerks developed following the excision of a cervical haemangioblastoma. In the stimulus-induced jerks the relative latencies of muscles innervated by rostral and caudal spinal segments suggested that the myoclonus originated between the upper cervical and midthoracic cord. In the final patient, EMG activity during spontaneous and stimulus-induced jerks commenced in the rectus abdominis, and was followed by later activity in muscles innervated by rostral spinal segments, suggesting that the myoclonus originated in the midthoracic cord. No structural lesion was identified in this patient. Electrophysiological evidence is used to argue a spinal origin for these axial jerks in all 3 cases. There are striking features common both to this form of human myoclonus and to long propriospinal pathways identified in animals. The new concept of propriospinal myoclonus is suggested.

Adult↗

PubMed1990

The blink reflex in patients with idiopathic torsion dystonia.

The blink reflex and its recovery cycle were examined in 57 patients with idiopathic dystonia affecting different parts of the body. The group comprised 9 patients with generalized and 15 with segmental forms, 19 with torticollis, and 14 with focal arm dystonia. None had blepharospasm. The duration and amplitude of the R2 component of the blink reflex showed only minor changes. However, its recovery cycle to paired supraorbital nerve stimuli was abnormal in all groups of patients, except those with focal arm dystonia. These findings may be interpreted as showing abnormal control of the interneuronal networks mediating the blink reflex in patients with dystonia affecting sites other than the facial muscles. The fact that the principal changes were seen in patients with torticollis, and generalized or segmental dystonia, suggests that the extent of dystonia (rather than the severity) and, therefore, the close proximity to the cranial muscles was important in determining the extent of the abnormal interneuron function.

Arm↗

PubMed1990

Diaphragmatic flutter, the moving umbilicus syndrome, and "belly dancer's" dyskinesia.

Five patients presenting with focal abnormal involuntary movements of the abdominal wall are described. One was shown to have diaphragmatic flutter, which may represent a variant of the palatal myoclonus syndrome. The other four had writhing movements and contractions of the abdominal wall at frequencies of approximately 30 per minute. In two of the latter cases, these abdominal movements were profoundly influenced by respiratory manoeuvres. They were quite unlike the movements of spinal myoclonus or axial torsion dystonia. None of the patients were taking drugs that might have provoked their abnormal movements, or had any other evidence of neurological deficit. No cause was established in any of the cases.

Abdominal Muscles↗

PubMed1990

Cortical outflow to proximal arm muscles in man.

Corticospinal influences on two antagonistic muscles of the shoulder were studied in 6 normal volunteers. Recordings were made of the discharges of single motor units from the deltoid and pectoralis major muscles and poststimulus time histograms constructed following either anodal electrical or magnetic cortical stimulation via the scalp. Contralateral anodal stimulation caused narrow short-latency peaks of excitation in motor units from both muscles, probably indicative of the arrival of the D or direct corticospinal volley. The size of the peaks led to estimates of the underlying excitatory postsynaptic potentials (EPSP) amplitude of 5.5 mV for the deltoid and 2.2 mV for the pectoralis motor units. Magnetic stimulation over the vertex caused multiple early peaks of excitation in motor units from both muscles but these peaks began at a greater latency than those produced by anodal stimulation. Additionally, magnetic cortical stimulation (and, occasionally, contralateral anodal stimulation) caused a previously undescribed period of medium latency excitation in both muscles. These medium latency periods of excitation differed from the earlier events in that they occurred independently of the direction of current flow in the magnetic coil. This raises the possibility that they are the consequence of stimulation of bilaterally distributed cortical motor outflow pathways. The short-latency excitation strongly suggests that, in man, corticomotoneuronal projections exist to proximal as well as distal muscles of the contralateral arm. The strength of the projection to deltoid assessed by this method is similar to that to an intrinsic muscle of the hand and significantly larger than that to its antagonist, pectoralis. The possible bilateral organization of the additional medium-latency projection to these proximal arm muscles may contribute to two characteristic clinical features after a unilateral cerebral lesion, such as stroke: the relative sparing of proximal arm strength compared with distal and, secondly, ipsilateral weakness.

Adult↗

PubMed1990

Cutaneous effects on presynaptic inhibition of flexor Ia afferents in the human forearm.

1. In six subjects, H reflexes obtained in the flexor muscles in the forearm were inhibited by single motor threshold shocks to the radial nerve in the spiral groove. The first two phases of the inhibitory time course were studied: with intervals between the radial and median nerve shocks of -1 to +1 ms, and +5 to +30 ms. These two phases are thought to be due respectively to disynaptic inhibition between radial Ia afferents and flexor alpha-motoneurones, and to presynaptic inhibition of flexor Ia afferents. 2. Single or short trains (10 ms, 400 Hz) of cutaneous stimuli to the dorsal or palmar aspect of the proximal phalanx of the index finger or to the superficial radial nerve at the wrist, reduced the amount of presynaptic inhibition by 10-20%, but had no effect on the earlier disynaptic inhibition. Single stimuli to either side of the index finger or trains of stimuli to the ventral side, had no effect on the size of control H reflexes elicited alone. 3. Effects of cutaneous nerve shocks on presynaptic inhibition could be seen with stimuli as small as 1.5 x perceptual threshold. 4. Anaesthesia of the hand in one subject reversibly increased the amount of presynaptic inhibition and decreased the amount of disynaptic inhibition. 5. We conclude that, as in the cat, cutaneous input can modulate transmission in presynaptic inhibitory pathways in man.

Adult↗

PubMed1989

Interruption of motor programmes by electrical or magnetic brain stimulation in man.

These experiments describe the effect on voluntary movement of an electrical or magnetic stimulus delivered to the brain through the scalp. Subjects were trained to flex or extend their wrists as rapidly as possible in response to an auditory tone. A single brain stimulus delivered after the tone, and before the usual time of onset of the voluntary reaction, could delay the movement for up to 150 ms, without affecting the pattern of agonist and antagonist EMG bursts. Movement was not delayed when similar experiments were performed with supramaximal stimulation of the median nerve instead of the brain stimulus. The delay following a cortical shock was not due to spinal motoneurones being inaccessible to input during the delay, since H-reflexes given in the middle of the delay period were capable of activating the muscle. Neither could the delay be explained by the brain stimulus altering the time of the subject's intention to respond, since a stimulus delivered to one hemisphere prior to an attempted simultaneous bilateral wrist movement produced a far greater delay on the contralateral than the ipsilateral side. We suggest that the brain stimulus delayed movement by inhibiting a group of strategically placed neurones in the brain (probably in the motor cortex) which made them unresponsive for a brief period to the command signals which initiate agonist and antagonist muscle activity.

Cerebral Cortex↗

PubMed1989

The Bereitschaftspotential is abnormal in Parkinson's disease.

The average Bereitschaftspotential (BP) preceding a rapid, self-paced voluntary extension movement of the index finger was recorded from 6 scalp locations in 14 patients with Parkinson's disease who had been withdrawn from their normal drug therapy for at least 12 h before testing. The amplitude of the potential was measured at the peak negativity (N1) and 650 ms prior to this (NS1), and compared with that recorded in a group of 12 age-matched control subjects. The N1 amplitude was the same as in the normals, but the NS1 component was smaller in the patients, especially in midline leads. As a result, the rise in the BP between the peak NS1 and N1 component (termed NS2) was larger in the patient group. The NS1 component of the BP is thought to reflect preparatory activity in the supplementary motor area (SMA) of cortex. Since the basal ganglia provide a major source of afferent input to SMA, the reduction in NS1 in the patients probably results from inadequate basal ganglia activation of SMA. The larger NS2 component may reflect extra activity in other brain areas to compensate for the reduced SMA activity.

Aged↗

PubMed1989

Delay in the execution of voluntary movement by electrical or magnetic brain stimulation in intact man. Evidence for the storage of motor programs in the brain.

Experiments were undertaken to study the effect on voluntary movement of an electrical or magnetic stimulus delivered to the brain through the scalp. Subjects were trained to flex or extend their wrist rapidly in response to an auditory tone. A single brain stimulus (electrical or magnetic) delivered after the tone and before the usual time of onset of the voluntary reaction could delay the execution of the movement for up to 150 ms, without affecting the pattern of the agonist and antagonist EMG bursts. The delay increased with increasing stimulus intensity and with stimuli which were applied nearer to the usual time of onset of the voluntary reaction. A stimulus given after the onset of the first voluntary agonist EMG burst only delayed the onset of the first antagonist and later EMG bursts. Movement was not delayed when similar experiments were performed with supramaximal stimulation of the median nerve instead of the brain stimulus. The delay following a cortical shock was not due to spinal motoneurons being inaccessible to descending input during the delay period since a second brain stimulus, given in the middle of the delay period, was capable of producing a direct muscle response. Neither could the delay be explained by the brain stimulus altering the time of the subject's intention to respond since a stimulus delivered to one hemisphere before an attempted simultaneous bilateral wrist movement produced a far greater delay of the contralateral than the ipsilateral movement. We suggest that the brain stimulus delayed movement by inhibiting a group of strategically placed neurons in the brain (probably in the motor cortex) which made them unresponsive for a brief period to the command signals they receive which initiate the motor program of agonist and antagonist muscle activity. The results have implications for the issues of the storage of motor programs, internal monitoring of central movement commands and the site of organization of the antagonist EMG burst.

Adult↗

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

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↗