Search PubMed⌕ Search

Biomedical subjects

B L Day

Publications and source records attributed to B L Day.

At least 37 records · Page 2Linked to original sources

Spatial differences in the sites of direct and indirect activation of corticospinal neurones by magnetic stimulation.

Transcranial magnetic stimulation (TMS) over the human motor cortex evokes multiple descending volleys possibly through activation of different elements within the brain. We have investigated whether such elements can be distinguished spatially. Using a figure of eight coil, TMS was delivered over multiple scalp sites during a low level voluntary contraction of the left first dorsal interosseous muscle. At near-threshold intensity, early or late surface electromyograph (EMG) components (relative to anodal response latency) could be preferentially evoked with the coil aligned in a medio-lateral (ML), antero-posterior (AP), or postero-anterior (PA) orientation. The optimal location of the earliest component with ML coil orientation was 8 mm medial and 5 mm anterior compared to a later component with AP orientation. The optimal location for the same latency EMG component mapped using two different coil orientations (AP and ML) was not significantly different. The optimal location of two different late components, one obtained with AP and the other with PA coil orientations, was similar. It is argued that the earliest TMS-evoked component results from direct activation of corticospinal cell axons while later components result from activation of these cells trans-synaptically (indirectly), and that consequently there is a substantial spatial separation between these activation sites.

Adult↗

Ipsilateral cortical stimulation inhibited the long-latency response to stretch in the long finger flexors in humans.

1. Transcranial magnetic stimulation over the motor cortex of one hemisphere is known to decrease the excitability of the motor cortex of the other hemisphere. We investigated the effect of this interhemispheric or transcallosal inhibition of the motor cortex on the reflex response to stretch in the long flexors of the fingers in human subjects. 2. Stretch of the long finger flexors, through extension of the proximal interphalangeal joints with a torque pulse, resulted in a reflex EMG response with short- and long-latency components. Magnetic stimulation was applied over the motor cortex ipsilateral to the muscles being stretched. When a magnetic shock but not stretch was given, a decrease in background EMG in the ipsilateral finger flexors occurred at a latency of 33 +/- 6.2 ms after the stimulus and with a duration of 25 +/- 8.5 ms. 3. If the magnetic shock and the stretch were given at appropriate interstimulus intervals, the long-latency stretch reflex (LLSR) showed inhibition in all subjects. LLSR was reduced to 49.2 +/- 19% (S.D.; n = 9) of the area of the control response. 4. The LLSR did not act as a single event in response to the magnetic shock. That is, part of the LLSR could be reduced in amplitude while the remainder was unaffected. The reduction in LLSR had an onset latency of 27 +/- 3.8 ms after the magnetic stimulus and a duration of 29-55 ms. Inhibition was only obvious when this interval after the magnetic stimulus coincided with the LLSR. 5. In most subjects the short-latency stretch reflex (SLSR) also showed some inhibition (83.4 +/- 11.2% of the control). However, this was less than the effect on the LLSR in all subjects. 6. The site of stimulation, over the ipsilateral motor cortex, was specific for inhibition of the LLSR. When the coil was moved anteriorly or to the midline, inhibition was significantly decreased. 7. We suggest that the inhibition of the LLSR of the long flexors of the fingers resulted from a reduction in excitability of the motor cortex produced by an inhibitory transcallosal pathway and conclude that the LLSR in this muscle has a transcortical component.

Electromyography↗

The movement-related cortical potential is abnormal in patients with idiopathic torsion dystonia.

Voluntary movements, such as the self-paced finger extension task used in the present experiments, are preceded by a slowly rising negative electroencephalographic potential [the movement-related cortical potential (MRCP)]. The early NS1 component of the potential was no different in patients with primary dystonia affecting the arm (n = 6) compared with matched controls. In contrast, the peak amplitude of the MRCP was smaller in the patients, despite the fact that the movements made by the two groups were very similar; it was of equal size over both left and right hemispheres, rather than being larger on the side contralateral to the movement. These results are similar to those observed by others in patients with symptomatic dystonia secondary to lesions of the basal ganglia or their output pathways and may reflect abnormal basal ganglia input to motor areas of cortex before the onset of a self-paced movement.

Adult↗

Effect of tonic voluntary activity on the excitability of human motor cortex.

1. The threshold for obtaining EMG responses after transcranial magnetic stimulation of the brain is reduced by voluntary contraction of the target muscle. The present experiments tested whether some of this effect is due to increased cortical, as opposed to spinal, excitability during the contraction. 2. Magnetic stimulation was delivered with a figure-of-eight coil oriented with the junction region along the interaural line and also (in 4 of 7 subjects) with a circular coil centred at the vertex. The intensity of the conditioning stimulus was subthreshold for evoking a motor response in the relaxed wrist flexor muscles of the forearm. The presence of a small descending corticospinal volley in both the relaxed and active conditions was detected by measuring the facilitation of test H reflexes elicited in the flexor muscles of the forearm. 3. In all subjects, magnetic stimulation with either coil facilitated the H reflex at conditioning-test intervals of -1 to -3 ms (median nerve stimulus before magnetic). This was followed by a long-lasting facilitation. In three of the seven subjects stimulation with the figure-of-eight coil elicited an additional, earlier peak of facilitation at a conditioning-test interval of -3 to -5 ms. 4. In all subjects, the threshold for obtaining facilitation of the H reflex using a conditioning-test interval of -1 to -3 ms was reduced, and the amount of facilitation was larger, if subjects performed a weak tonic voluntary contraction. In contrast, with a conditioning-test interval of -3 to -5 ms voluntary contraction had no effect on the threshold. 5. It is suggested that H reflex facilitation at the conditioning-test interval of -1 to -3 ms was produced by indirect activation of corticospinal neurones by the magnetic stimulus, whereas at -3 to -5 ms, the facilitation was produced by direct activation of corticospinal axons. It is concluded that tonic voluntary contraction of a target muscle decreases the threshold for indirect activation of corticospinal neurones but not for direct stimulation of their axons.

Conditioning, Psychological↗

The effect of magnetic coil orientation on the latency of surface EMG and single motor unit responses in the first dorsal interosseous muscle.

We examined the effect of the orientation of a figure-of-eight coil on the latency of surface electromyographic (EMG) responses and the firing pattern of single motor units evoked in the first dorsal interosseous muscle by transcranial magnetic brain stimulation. Two coil positions were used: the coil held on a parasagittal line either with the induced current in the brain flowing in a postero-anterior direction (PA) or with the current flowing latero-medially (LM). The results were compared with those observed after anodal electrical stimulation. LM stimulation produced surface and single unit responses which occurred 0-3 msec earlier than PA stimulation. In many cases responses to LM stimulation had the same latency as those produced by anodal electrical stimulation. Responses evoked by LM stimulation were less affected by changes in motor cortical excitability (cortico-cortical inhibition and transcallosal inhibition) than those to PA stimulation. We suggest that LM stimulation can sometimes stimulate corticospinal fibres directly, at or near the same site as anodal stimulation. In contrast, PA stimulation tends to activate corticospinal fibres trans-synaptically. The difference in stimulation sites may make a comparison of PA and LM stimulation a useful method of localising changes in corticospinal excitability to a cortical level.

Adult↗

Rapid wrist movements in patients with essential tremor. The critical role of the second agonist burst.

Ballistic wrist flexion movements towards 15, 30 and 60 degrees visual targets were studied in a group of 17 patients with hereditary essential tremor. Compared with age-matched normal subjects (n = 16), there were three main kinematic differences: patients overshot the target a little more; the kinematic profile of their movements was more 'asymmetric' due to higher peak decelerations; and their movements initiated tremor. Ballistic movements performed by patients with essential tremor were associated with a triphasic pattern of agonist-antagonist-agonist muscle activity similar to that of normal subjects. The duration and size of each EMG burst was normal. The onset latency of the antagonist EMG burst was also normal, but the onset of the second agonist EMG burst was delayed. The delay in the onset of the second agonist EMG activity resulted in unopposed action of the antagonist muscle in the second half of each movement. As a result, deceleration occurred too rapidly as the hand returned past the target leading to a series of damped oscillations around the point of aim. The onset latency of the second agonist EMG burst correlated significantly with the tremor period; the longer the period the later the burst. We speculate that the delay in the second agonist burst reflects an abnormality in the timing of anticipatory muscle activity in essential tremor and that this may involve cerebellar mechanisms.

Adult↗

The myoclonus in corticobasal degeneration. Evidence for two forms of cortical reflex myoclonus.

The clinical and physiological characteristics of myoclonus in 14 patients with corticobasal degeneration are described. The myoclonus was focal, confined to one limb (usually the arm) and was most prominent on voluntary action or in response to sensory stimulation. On clinical inspection, the myoclonus appeared to occur at rest but EMG recordings revealed that apparently spontaneous myoclonus occurred only on a background of more or less continuous muscle activity (responsible for the rigidity and dystonia). The jerks consisted of hypersynchronous short duration bursts of EMG activity coincident in agonists and antagonists. Reflex myoclonus in hand muscles, to stimulation of the median nerve at the wrist, had a latency of approximately 40 ms. In 13 of the 14 patients reflex myoclonus was not associated with enlargement of the cortical sensory evoked potentials (SEPs); the later components of the parietal SEP were poorly formed and dominated by a broad positive wave with a peak latency approximately 45 ms. Prefrontal components of the SEP were relatively preserved, but there were no significant differences between the SEPs evoked from myoclonic and non-myoclonic limbs. Action myoclonus was not preceded by an identifiable cortical wave in the electroencephalogram back-averaged before each jerk. Magnetic, but not electric, brain stimulation evoked repetitive bursts of myoclonus suggesting enhanced cortical excitability. The combination of focal, predominantly distal, hypersynchronous jerks, evidence of enhanced cortical excitability, together with the known cortical pathology in corticobasal degeneration suggests that the myoclonus in these patients may be cortical in origin. Since the latency of reflex myoclonus in corticobasal degeneration is only 1-2 ms longer than the sum of the afferent and efferent times to and from the cortex, we propose the reflex myoclonus is mediated by direct sensory input to motor cortical areas that activate corticospinal tract output. Such myoclonus differs from the typical form of cortical reflex myoclonus in which reflex jerks have a longer latency (50 ms in hand muscles), cortical SEPs are enlarged and action myoclonus is preceded by a cortical discharge. It is proposed that these various forms of cortical myoclonus can be explained by the presence of different cortical relays of sensory information to cortical motor areas. The myoclonus of corticobasal degeneration may represent enhancement of a direct sensory input to the motor cortex. In contrast, the more widely recognized variety of cortical reflex myoclonus may involve abnormal relays through sensory cortex to motor cortex, either directly or via cerebellar-thalamo-cortical projections.

Adult↗

Modulation of postural wrist tremors by magnetic stimulation of the motor cortex in patients with Parkinson's disease or essential tremor and in normal subjects mimicking tremor.

The effect of magnetic brain stimulation on postural wrist tremor was studied in 10 patients with Parkinson's disease, 12 with hereditary essential tremor, and 10 normal subjects who mimicked tremor by making rapid alternating wrist movements. In all patients and normal subjects, magnetic brain stimulation over the contralateral motor cortex at an intensity approximately 10% above threshold produced the following sequence of events: (1) a small direct electromyographic (EMG) response, followed by (2) suppression of the rhythmic EMG activity responsible for the tremor, before (3) reappearance of the tremor time-locked to the stimulus. It is concluded that magnetic brain stimulation over the motor cortex can modulate the oscillatory mechanisms responsible for the generation of postural tremors. Group analysis revealed that the time to reappearance of rhythmic EMG activity varied significantly with the period of parkinsonian postural tremors, but not with the period of essential or mimicked tremors. Magnetic stimulation also significantly shortened the period of parkinsonian postural tremors, but did not influence the period of essential or mimicked tremors. These behavioral differences indicate differences in the pathophysiological mechanisms underlying parkinsonian postural tremor and essential tremor.

Adult↗

Effectiveness of piracetam in cortical myoclonus.

Twenty-one patients with disabling spontaneous, reflex, or action myoclonus due to various causes, who had shown apparent clinical improvement on introduction of piracetam, entered a placebo-controlled double-blind crossover trial of piracetam (2.4-16.8 g daily). All but one patient had electrophysiological evidence of cortical myoclonus. Patients were randomly allocated to a 14-day course of piracetam followed by identical placebo, or placebo followed by piracetam. Nineteen patients received piracetam/placebo in addition to their routine antimyoclonic treatment (carbamazepine, clonazepam, phenytoin, primidone, sodium valproate, or tryptophan plus isocarboxazid, alone or in combination) and two received piracetam/placebo as monotherapy. All patients were rated at the end of each treatment phase using stimulus sensitivity, motor, writing, functional disability, global assessment, and visual analogue scales. Ten of the 21 patients had to be rescued from the placebo phase of the trial because of a severe and intolerable exacerbation of their myoclonus. No patients required rescue from the piracetam phase of the double-blind trial. When the 21 patients were considered together, there was a significant improvement in motor, writing, functional disability, global assessment, and visual analogue scores during treatment with piracetam compared with placebo. The total rating score also improved significantly with piracetam, by a median of 22%. Piracetam, usually in combination with other antimyoclonic drugs, is a useful treatment for myoclonus of cortical origin.

Adult↗

Postural electromyographic responses in the arm and leg following galvanic vestibular stimulation in man.

Application of a small (around 1 mA), constant electric current between the mastoid processes (galvanic stimulation) of a standing subject produces enhanced body sway in the approximate direction of the ear behind which the anode is placed. We examined the electromyographic (EMG) responses evoked by such stimulation in the soleus and in the triceps brachii muscles. For soleus, subjects stood erect, with their eyes closed, leaning slightly forward. The head was turned approximately 90 degrees to the right or left relative to the feet. In averaged records (n = 40), current pulses of 25 ms or longer modulated the EMG in a biphasic manner: a small early component (latency 62 +/- 2.4 ms, mean +/- SEM) was followed by a larger late component (latency 115 +/- 5.2 ms) of opposite sign, which was appropriate to produce the observed body sway. The early component produced no measurable body movement. Lengthening the duration of the stimulus pulse from 25 to 400 ms prolonged the late component of the response but had little effect on the early component. Short- and long-latency EMG responses were also evoked in the triceps brachii muscle if subjects stood on a transversely pivoted platform and had to use the muscle to maintain their balance in the anteroposterior plane by holding a fixed handle placed by the side of their hip. The latency of the early component was 41 +/- 2.6 ms; the latency of the late component was 138 +/- 4.3 ms and was again of appropriate sign for producing the observed body sway. Galvanic stimulation evoked no comparable responses in either triceps brachii or soleus muscles if these muscles were not being used posturally.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Transcranial electric and magnetic stimulation of the leg area of the human motor cortex: single motor unit and surface EMG responses in the tibialis anterior muscle.

We compared single motor unit and surface EMG responses in the active right tibialis anterior following anodal electrical or magnetic stimulation of the motor cortex over the vertex. Magnetic stimulation used a monophasic current pulse through a circular coil centred 3 cm anterior to the vertex. Lowest threshold magnetic stimulation occurred when the current in the coil flowed from the left to the right side at the posterior rim of the coil. Such stimulation produced single unit and surface EMG responses which had the same latency as those produced by anodal electric stimulation. If the direction of the magnetic stimulating current was reversed, response latencies became more variable from unit to unit, and on average they occurred 1.0 +/- 0.5 msec later. In single motor units anodal and magnetic post-stimulus time histogram (PSTH) peaks had the same duration. This was similar to the duration of the PSTH peaks produced by a single low intensity stimulus given to the common peroneal nerve. We conclude that magnetic stimulation can produce direct activation of corticospinal neurones to the tibialis anterior if the direction of induced current flow is optimal. This projection is likely to be either monosynaptic or oligosynaptic.

Adult↗

Some saccadic eye movements can be delayed by transcranial magnetic stimulation of the cerebral cortex in man.

In 15 normal subjects we investigated the effect on visually guided saccadic eye movements of giving a single transcranial magnetic stimulus through a circular coil centered at the vertex. In the normal paradigm, subjects fixated a target which moved randomly to the left or right by 11 degrees. The mean saccadic reaction time of 189 ms was increased by 40-50 ms if a magnetic stimulus was given in random trials some 60 ms prior to the expected onset time of control saccades. The duration and amplitude of the saccades was unchanged. The delay was smaller if the stimulus was given earlier in the reaction period, or if the coil was moved anterior or posterior to the vertex. Larger stimulus intensities produced longer delays. Three subjects were trained to produce express saccades (mean saccadic reaction times of 107-141 ms) in a 'gap' paradigm. The latency of these saccades, which are thought to be mediated by collicular mechanisms without involvement of the cortex, was not affected by magnetic stimulation. This suggests that magnetic stimulation delays normal visually guided saccades by an action on the cerebral cortex, rather than on the oculomotor centres of the brainstem. Five subjects made non-targeted saccades in darkness in response to an auditory stimulus. These saccades, like visually guided saccades, could be delayed by magnetic brain stimulation. We conclude that saccadic delay is produced by interference with cortical areas involved in the execution of saccades rather than by interfering with the perception of the visual or auditory 'go' stimulus. These probably include supplementary and frontal eye field and posterior parietal cortex. The fact that visually guided saccades emerged intact after the delay indicates that the instructions for amplitude and direction were stored separately from those involved in timing when the movement was to occur.

Acoustic Stimulation↗

Vestibular induced postural responses in Parkinson's disease.

We have tested the hypothesis that dysfunction of the vestibular control of posture is a principal cause of parkinsonian instability by measuring the body sway response induced by galvanic vestibular stimulation (0.5 mA for 2 s) in a group of patients with Parkinson's disease (n = 15). Responses were compared with those obtained from a group of age-matched control subjects (n = 10). Subjects were stimulated (randomized polarity) whilst standing with feet together, eyes closed and maintaining one of five head yaw angles. The motion of the body and the ground reaction forces were measured in three dimensions. There was no significant difference between patients and controls in the speed or direction of the induced body sway response. When the patients were subdivided into two groups according to a clinical assessment of postural deficit, the more disabled group was found to respond with significantly greater body speed than either the control group or the mildly affected patient group. However, the baseline speed of spontaneous body sway was also greater in these patients and it was found that response speed was linearly related to baseline body sway even for the control group. There were no significant differences between any of these groups in the latency to onset, latency to peak or peak amplitude of the initial horizontal ground reaction force response to the stimulus. We conclude that vestibular dysfunction does not explain the postural deficits of patients who are mildly or moderately affected by Parkinson's disease.

Biomechanical Phenomena↗

Effect of vision and stance width on human body motion when standing: implications for afferent control of lateral sway.

1. Measurements of human upright body movements in three dimensions have been made on thirty-five male subjects attempting to stand still with various stance widths and with eyes closed or open. Body motion was inferred from movements of eight markers fixed to specific sites on the body from the shoulders to the ankles. Motion of these markers was recorded together with motion of the point of application of the resultant of the ground reaction forces (centre of pressure). 2. The speed of the body (average from eight sites) was increased by closing the eyes or narrowing the stance width and there was an interaction between these two factors such that vision reduced body speed more effectively when the feet were closer together. Similar relationships were found for components of velocity both in the frontal and sagittal planes although stance width exerted a much greater influence on the lateral velocity component. 3. Fluctuations in position of the body were also increased by eye closure or narrowing of stance width. Again, the effect of stance width was more potent for lateral than for anteroposterior movements. In contrast to the velocity measurements, there was no interaction between vision and stance width. 4. There was a progressive increase in the amplitude of position and velocity fluctuations from markers placed higher on the body. The fluctuations in the position of the centre of pressure were similar in magnitude to those of the markers placed near the hip. The fluctuations in velocity of centre of pressure, however, were greater than of any site on the body. 5. Analysis of the amplitude of angular motion between adjacent straight line segments joining the markers suggests that the inverted pendulum model of body sway is incomplete. Motion about the ankle joint was dominant only for lateral movement in the frontal plane with narrow stance widths (< 8 cm). For all other conditions most angular motion occurred between the trunk and leg. 6. The large reduction in lateral body motion with increasing stance width was mainly due to a disproportionate reduction in the angular motion about the ankles and feet. A mathematical model of the skeletal structure has been constructed which offers some explanation for this specific reduction in joint motion.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Corticocortical inhibition in human motor cortex.

1. In ten normal volunteers, a transcranial magnetic or electric stimulus that was subthreshold for evoking an EMG response in relaxed muscles was used to condition responses evoked by a later, suprathreshold magnetic or electric test shock. In most experiments the test stimulus was given to the lateral part of the motor strip in order to evoke EMG responses in the first dorsal interosseous muscle (FDI). 2. A magnetic conditioning stimulus over the hand area of cortex could suppress responses produced in the relaxed FDI by a suprathreshold magnetic test stimulus at interstimulus intervals of 1-6 ms. At interstimulus intervals of 10 and 15 ms, the test response was facilitated. 3. Using a focal magnetic stimulus we explored the effects of moving the conditioning stimulus to different scalp locations while maintaining the magnetic test coil at one site. If the conditioning coil was moved anterior or posterior to the motor strip there was less suppression of test responses in the FDI. In contrast, stimulation at the vertex could suppress FDI responses by an amount comparable to that seen with stimulation over the hand area. With the positions of the two coils reversed, conditioning stimuli over the hand area suppressed responses evoked in leg muscles by vertex test shocks. 4. The intensity of both conditioning and test shocks influenced the amount of suppression. Small test responses were more readily suppressed than large responses. The best suppression was seen with small conditioning stimuli (0.7-0.9 times motor threshold in relaxed muscle); increasing the intensity to motor threshold or above resulted in less suppression or even facilitation. 5. Two experiments suggested that the suppression was produced by an action on cortical, rather than spinal excitability. First, a magnetic conditioning stimulus over the hand area failed to produce any suppression of responses evoked in active hand muscles by a small (approximately 200 V, 50 microsecond time constant) anodal electric test shock. Second, a vertex conditioning shock had no effect on forearm flexor H reflexes even though responses in the same muscles produced by magnetic cortical test shocks were readily suppressed at appropriate interstimulus intervals. 6. Small anodal electric conditioning stimuli were much less effective in suppressing magnetic test responses than either magnetic or cathodal electric conditioning shocks.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Modulation of postural tremors at the wrist by supramaximal electrical median nerve shocks in essential tremor, Parkinson's disease and normal subjects mimicking tremor.

The response of postural wrist tremors to supramaximal median nerve stimulation was examined in patients with hereditary essential tremor (n = 10) and Parkinson's disease (n = 9), and in normal subjects mimicking wrist tremor (n = 8). The average frequency of on-going tremor was the same in all three groups. Supramaximal peripheral nerve shocks inhibited and then synchronised the rhythmic electromyographic (EMG) activity of all types of tremor. The duration of inhibition ranged from 90 to 210ms, varying inversely with the frequency of on-going tremor. There was no significant difference in mean duration of inhibition or in the timing of the first peak after stimulation on the average rectified EMG records between the three groups. The degree to which supramaximal peripheral nerve shocks could modulate the timing of rhythmic EMG bursts in the forearm flexor muscles was also quantified by deriving a resetting index. No significant difference in mean resetting index of the three groups was found. These results suggest that such studies cannot be used to differentiate between the common causes of postural wrist tremors.

Adult↗

The Bereitschaftspotential preceding simple foot movement and initiation of gait in Parkinson's disease.

We compared the Bereitschaftspotential preceding a simple foot movement while sitting and a stepping movement while standing in a group of normal subjects and seven patients with mild to moderate Parkinson's disease (PD) while off medication. None had major difficulties stepping to initiate gait. Electromyographic signals from tibialis anterior triggered the averaging of electroencephalographic signals from the scalp. Bereitschaftspotential preceding a standing stepping movement were larger than those before a foot movement while sitting in normal subjects, but no difference was observed in patients with PD. The absence of an increase in the Bereitschaftspotential when stepping in PD may reflect an impairment of the preparation and assembly of the complex sequences of movement necessary to initiate walking, even in the early stages of the illness.

Adult↗