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P Profice

Publications and source records attributed to P Profice.

At least 19 recordsLinked to original sources
PubMed2006

Origin of facilitation of motor-evoked potentials after paired magnetic stimulation: direct recording of epidural activity in conscious humans.

A magnetic transcranial conditioning stimulus given over the motor cortex at intensities below active threshold for obtaining motor-evoked potentials (MEPs) facilitates EMG responses evoked at rest in hand muscles by a suprathreshold magnetic stimulus given 10-25 ms later. This is known as intracortical facilitation (ICF). We recorded descending volleys produced by single and paired magnetic motor cortex stimulation through high cervical epidural electrodes implanted for pain relief in six conscious patients. At interstimulus intervals (ISIs) of 10 and 15 ms, although MEP was facilitated, there was no change in the amplitude or number of descending volleys. An additional I wave sometimes was observed at 25 ms ISI. In one subject, we also evaluated the effects of reversing the direction of the induced current in the brain. At 10 ms ISI, the facilitation of the MEPs disappeared and was replaced by slight suppression; at 2 ms ISI, there was a pronounced facilitation of epidural volleys. Subsequent experiments on healthy subjects showed that a conditioning stimulus capable of producing ICF of MEPs had no effect on the EMG response evoked by transmastoidal electrical stimulation of corticospinal tract. We conclude that ICF occurs because either 1) the conditioning stimulus has a (thus far undetected) effect on spinal cord excitability that increases its response to the same amplitude test volley or 2) that it can alter the composition (but not the amplitude) of the descending volleys set up by the test stimulus such that a larger proportion of the activity is destined for the target muscle.

Adult↗
PubMed2006

Effects of aging on motor cortex excitability.

To determine whether aging is associated with changes in excitability of the cerebral cortex, we evaluated the excitability of the motor cortex with transcranial magnetic stimulation (TMS). We compared TMS related measures obtained in a group of young people with those of a group of old people. Motor evoked potential (MEP) amplitude was significantly smaller in older than in younger controls (1.3+/-0.8 mV versus 2.7+/-1.1 mV; p<0.0071). Mean cortical silent period (CSP) duration was shorter in older than in younger controls (87+/-29 ms versus 147+/-39 ms; p<0.0071). SP duration/MEP amplitude ratios were similar in both groups. Our results are consistent with an impaired efficiency of some intracortical circuits in old age.

Adult↗
PubMed2003

Ketamine increases human motor cortex excitability to transcranial magnetic stimulation.

Subanaesthetic doses of the N-methyl-D-aspartate (NMDA) antagonist ketamine have been shown to determine a dual modulating effect on glutamatergic transmission in experimental animals, blocking NMDA receptor activity and enhancing non-NMDA transmission through an increase in the release of endogenous glutamate. Little is known about the effects of ketamine on the excitability of the human central nervous system. The effects of subanaesthetic, graded incremental doses of ketamine (0.01, 0.02 and 0.04 mg kg-1 min-1, I.V.) on the excitability of cortical networks of the human motor cortex were examined with a range of transcranial magnetic and electric stimulation protocols in seven normal subjects. Administration of ketamine at increasing doses produced a progressive reduction in the mean resting motor threshold (RMT) (F(3, 18) = 22.33, P < 0.001) and active motor threshold (AMT) (F(3, 18) = 12.17, P < 0.001). Before ketamine administration, mean RMT +/- S.D. was 49 +/- 3.3 % of maximum stimulator output and at the highest infusion level it was 42.6 +/- 2.6 % (P < 0.001). Before ketamine administration, AMT +/- S.D. was 38 +/- 3.3 % of maximum stimulator output and at the highest infusion level it was 33 +/- 4.4 % (P < 0.002). Ketamine also led to an increase in the amplitude of EMG responses evoked by magnetic stimulation at rest; this increase was a function of ketamine dosage (F(3, 18) = 5.29, P = 0.009). In contrast to responses evoked by magnetic stimulation, responses evoked by electric stimulation were not modified by ketamine. The differential effect of ketamine on responses evoked by magnetic and electric stimulation demonstrates that subanaesthetic doses of ketamine enhance the recruitment of excitatory cortical networks in motor cortex. Transcranial magnetic stimulation produces a high-frequency repetitive discharge of pyramidal neurones and for this reason probably depends mostly on short-lasting AMPA transmission. An increase in this transmission might facilitate the repetitive discharge of pyramidal cells after transcranial magnetic stimulation which, in turn, results in larger motor responses and lower thresholds. We suggest that the enhancement of human motor cortex excitability to transcranial magnetic stimulation is the effect of an increase in glutamatergic transmission at non-NMDA receptors similar to that described in experimental studies.

Adult↗
PubMed2002

Noninvasive in vivo assessment of cholinergic cortical circuits in AD using transcranial magnetic stimulation.

BACKGROUND: A recently devised test of motor cortex excitability (short latency afferent inhibition) was shown to be sensitive to the blockade of muscarinic acetylcholine receptors in healthy subjects. The authors used this test to assess cholinergic transmission in the motor cortex of patients with AD. METHODS: The authors evaluated short latency afferent inhibition in 15 patients with AD and compared the data with those of 12 age-matched healthy controls. RESULTS: Afferent inhibition was reduced in the patients (mean responses +/- SD reduced to 85.7% +/- 15.8% of the test size) compared with controls (mean responses +/- SD reduced to 45.3% +/- 16.2% of the test size; p < 0.001, unpaired t-test). Administration of a single oral dose of rivastigmine improved afferent inhibition in a subgroup of six patients. CONCLUSIONS: The findings suggest that this method can be used as a noninvasive test of cholinergic pathways in AD. Future studies are required to evaluate whether short latency afferent inhibition measurements have any consistent clinical correlates.

Aged↗
PubMed2001

Descending spinal cord volleys evoked by transcranial magnetic and electrical stimulation of the motor cortex leg area in conscious humans.

1. Descending corticospinal volleys evoked after transcranial magnetic or electrical stimulation of the leg area of the motor cortex were recorded from an electrode in the spinal epidural space of six conscious patients who had electrodes implanted for treatment of chronic pain, and from one anaesthetised patient undergoing surgery for a spinal tumour. 2. At threshold, the shortest-latency volley (L1 volley) was evoked by stimulation with an anode 2 cm lateral to the vertex. Anodal stimulation at the vertex also elicited a volley at this latency in two patients, but in the other patients the first volley evoked appeared 1-1.3 ms later (L2 volley), at the same latency as the initial volley evoked by magnetic stimulation. High-intensity stimulation of any type could evoke both the L1 and L2 waves as well as later ones (L3, L4, etc.) that had a periodicity of about 1.5 ms. 3. Voluntary contraction increased the amplitude of the L2 and later volleys, but had no effect on the L1 volley. 4. Intracortical inhibition between pairs of magnetic stimuli resulted in clear suppression of the L4 and later waves. The L2 and L3 waves were unaffected. 5. In the anaesthetised patient the L1 volley occurred 1.7 ms later than the volley produced by transmastoid stimulation of the corticospinal pathways in the brainstem. 6. The L1 volley is likely to be a D wave produced by the direct activation of pyramidal axons in the subcortical white matter; the L2 and later volleys are likely to be I waves produced by the trans-synaptic activation of corticospinal neurones. The implication is that electrical stimulation with an anode at the vertex is more likely to evoke I waves preferentially than stimulation over the hand area. A more secure way to ensure D wave activation of corticospinal fibres from the leg area is to place the anode 2 cm lateral to the vertex.

Adult↗
PubMed2001

The effect on corticospinal volleys of reversing the direction of current induced in the motor cortex by transcranial magnetic stimulation.

Descending corticospinal volleys were recorded from a bipolar electrode inserted into the cervical epidural space of four conscious human subjects after monophasic transcranial magnetic stimulation over the motor cortex with a figure-of-eight coil. We examined the effect of reversing the direction of the induced current in the brain from the usual posterior-anterior (PA) direction to an anterior-posterior (AP) direction. The volleys were compared with D waves evoked by anodal electrical stimulation (two subjects) or medio-lateral magnetic stimulation (two subjects). As reported previously, PA stimulation preferentially recruited I1 waves, with later I waves appearing at higher stimulus intensities. AP stimulation tended to recruit later I waves (I3 waves) in one of the subjects, but, in the other three, I1 or D waves were seen. Unexpectedly, the descending volleys evoked by AP stimulation often had slightly different peak latencies and/or longer duration than those seen after PA stimulation. In addition the relationship between the size of the descending volleys and the subsequent EMG response was often different for AP and PA stimulation. These findings suggest that AP stimulation does not simply activate a subset of the sites activated by PA stimulation. Some sites or neurones that are relatively inaccessible to PA stimulation may be the low-threshold targets of AP stimulation.

Adult↗
PubMed2001

Inhibition of biceps brachii muscle motor area by painful heat stimulation of the skin.

ract This study aimed to evaluate whether painful cutaneous stimuli can affect specifically the excitability of the arm proximal muscle motor area. The motor evoked potentials (MEPs), recorded from the right biceps brachii muscle after either transcranial magnetic or electrical anodal stimulation of the left primary motor (MI) cortex, were conditioned by painful CO2 laser stimuli delivered either on the right hand dorsum or on the lateral surface of the right arm. Painful CO2 laser stimuli delivered on the hand skin reduced significantly the amplitude of MEPs evoked by the transcranial magnetic stimulation of the contralateral MI area, while the MEP amplitude was not significantly modified by CO2 laser pulses delivered on the arm skin. The inhibitory effect followed the arrival of the nociceptive inputs to the cerebral cortex. The amplitude of MEPs evoked by anodal electrical stimulation of the motor cortex was not decreased by conditioning painful stimuli delivered on the hand dorsum. Since the magnetic stimulation led to transynaptic activation of pyramidal neurons, while the anodal stimulation activated directly corticospinal axons, our findings suggest that CO2 laser pulses delivered on the hand are able to inhibit the arm proximal muscle motor area.

Adult↗
PubMed2000

Concomitant post-traumatic craniocervical junction epidural hematoma and pontomedullary junction infarction: clinical, neurophysiologic, and neuroradiologic features.

STUDY DESIGN: A case report. OBJECTIVES: To report and discuss a case of post-traumatic epidural hematoma of the craniocervical junction with concomitant brain stem infarction. SUMMARY OF BACKGROUND DATA: Post-traumatic epidural hematoma of the cervical spine and brain stem post-traumatic infarction are very rare disorders. Post-traumatic epidural hematoma is usually located dorsally in the epidural space. METHODS: The clinical, neuroradiologic, and neurophysiologic findings in one patient with post-traumatic epidural hematoma located ventrally at the cervicomedullary junction and associated with medial infarction at the pontomedullary junction are reported. RESULTS: The main clinical finding in this patient was bilateral corticospinal and corticobulbar tract involvement. A magnetic resonance image showed displacement and flattening of the medulla oblongata and of the most cranial portion of cervical cord, which were caused by the epidural hematoma associated with an ischemic lesion of the pontomedullary junction. Results of central motor conduction studies indicated that the abnormality of the central motor pathways was localized at brain stem level, and that there was normal conduction from the cervicomedullary junction to spinal cord. CONCLUSION: This is the first reported case of spinal epidural hematoma located ventrally in the cervical spine at the cervicomedullary junction level and concomitant infarction at the pontomedullary junction resulting from whiplash injury.

Aged↗
PubMed2000

Short latency inhibition of human hand motor cortex by somatosensory input from the hand.

1. EMG responses evoked in hand muscles by transcranial stimulation over the motor cortex were conditioned by a single motor threshold electrical stimulus to the median nerve at the wrist in a total of ten healthy subjects and in five patients who had electrodes implanted chronically into the cervical epidural space. 2. The median nerve stimulus suppressed responses evoked by transcranial magnetic stimulation (TMS) in relaxed or active muscle. The minimum interval between the stimuli at which this occurred was 19 ms. A similar effect was seen if electrical stimulation was applied to the digital nerves of the first two fingers. 3. Median or digital nerve stimulation could suppress the responses evoked in active muscle by transcranial electrical stimulation over the motor cortex, but the effect was much less than with magnetic stimulation. 4. During contraction without TMS, both types of conditioning stimuli evoked a cutaneomuscular reflex that began with a short period of inhibition. This started about 5 ms after the inhibition of responses evoked by TMS. 5. Recordings in the patients showed that median nerve stimulation reduced the size and number of descending corticospinal volleys evoked by magnetic stimulation. 6. We conclude that mixed or cutaneous input from the hand can suppress the excitability of the motor cortex at short latency. This suppression may contribute to the initial inhibition of the cutaneomuscular reflex. Reduced spinal excitability in this period could account for the mild inhibition of responses to electrical brain stimulation.

Adult↗
PubMed2000

Muscarinic receptor blockade has differential effects on the excitability of intracortical circuits in the human motor cortex.

The aim of the present study was to investigate whether muscarinic receptor blockade with scopolamine modifies the excitability of specific cortical networks of the human motor cortex as tested with transcranial magnetic stimulation. The effects of scopolamine on the excitability of human motor cortex were investigated in four healthy subjects using transcranial magnetic stimulation before and after an intravenous dose of scopolamine (0.006 mg/kg). We measured the threshold for motor responses, amplitude of motor responses, the duration of the cortical silent period, intracortical inhibition and facilitation, and short-latency inhibition produced by somatosensory input from the hand. In addition, we evaluated the amplitude of motor responses evoked by electrical anodal stimulation, since these responses originate from direct activation of corticospinal axons in the white matter and are not sensitive to changes in cortical excitability. Scopolamine decreased the threshold to magnetic stimuli and increased the amplitude of motor responses evoked by magnetic stimulation. In contrast, motor responses evoked by electrical stimulation were unaffected by administration of scopolamine. Scopolamine also led to a highly significant reduction in the amount of short-latency inhibition produced by somatosensory input from the hand. In contrast, short-latency intracortical inhibition and facilitation were not modified by scopolamine. The differential effect of scopolamine on motor responses evoked by magnetic and electrical stimulation of the motor cortex and the selective effect on somatosensory inhibition demonstrate that muscarinic blockade modifies the excitability of specific cortical networks in the human motor cortex.

Acetylcholine↗
PubMed2000

Visual disorders after traumatic brain injury in developmental age.

Visual disorders secondary to TBI are common, often multiple, associated with complex clinical pictures; in developmental age they may particularly interfere with the development process, and compromise the rehabilitation and outcome processes. The aim of this study is to identify visual disorders in 56 post-traumatic children admitted to the Traumatic Brain Injury Unit. All patients underwent a complete clinical, neurological and neuroophthalmological assessment. Correlations were studied between visual disorders and clinical parameters of acute phase, age at trauma, neuroimaging data and outcome, in order to identify possible risk factors for their occurrence. A high incidence was found of complex visual disorders following head trauma: decreased visual acuity, together with a convergence oculo-motor deficit, is the most frequently detected deficit. Trauma severity, indicated by duration of coma, is associated with most of the visual disorders and appears to be the main risk factor conducive to their appearance.

Acute Disease↗
PubMed1999

Direct demonstration of interhemispheric inhibition of the human motor cortex produced by transcranial magnetic stimulation.

Electromyographic (EMG) responses evoked in hand muscles by a magnetic test stimulus over the motor cortex can be suppressed if a conditioning stimulus is applied to the opposite hemisphere 6-30 ms earlier. In order to define the mechanism and the site of action of this inhibitory phenomenon, we recorded descending volleys produced by the test stimulus through high cervical, epidural electrodes implanted for pain relief in three conscious subjects. These could be compared with simultaneously recorded EMG responses in hand muscles. When the test stimulus was given on its own it evoked three waves of activity (I-waves) in the spinal cord, and a small EMG response in the hand. A prior conditioning stimulus to the other hemisphere suppressed the size of both the descending spinal cord volleys and the EMG responses evoked by the test stimulus when the interstimulus interval was greater than 6 ms. In the spinal recordings, the effect was most marked for the last I-wave (I3), whereas the second I2-wave was only slightly inhibited, and the first I-wave (I1) was not inhibited at all. We conclude that transcranial stimulation over the lateral part of the motor cortex of one hemisphere can suppress the excitability of the contralateral motor cortex.

Adult↗
PubMed1999

Effects of voluntary contraction on descending volleys evoked by transcranial electrical stimulation over the motor cortex hand area in conscious humans.

The spinal volleys evoked by electric anodal and cathodal stimulation over the cerebral motor cortex hand area were recorded from a bipolar electrode inserted into the cervical epidural space of two conscious human subjects. We measured the size of volleys elicited by electric stimulation at active motor threshold and at 3% of maximum stimulator output above this value with subjects at rest and during maximum voluntary contraction of the contralateral first dorsal interosseous muscle. Surface EMG activity was recorded at the same time. Electrical anodal stimulation evoked a single negative wave that we termed D-wave in analogy with data in experimental animals. Cathodal stimulation evoked a single negative wave with a latency of 0.2 ms longer than the D-wave recruited by anodal stimulation. At both intensities tested, voluntary contraction did not modify the amplitude of the descending waves. We conclude that changes in cortical excitability induced by voluntary activity do not modify the corticospinal volley evoked by electric stimulation and that the D-waves evoked by both anodal and cathodal electric stimulation are probably initiated several nodes distant to the cell body.

Adult↗
PubMed1999

Intracortical origin of the short latency facilitation produced by pairs of threshold magnetic stimuli applied to human motor cortex.

Under certain conditions, EMG responses evoked by pairs of transcranial magnetic stimuli over the motor cortex are larger than the sum of the responses to each stimulus given alone. This occurs with interstimulus intervals of around 1.3, 2.5 and 4.3 ms and could be due to interaction between the responses to each stimulus at either the cortex or spinal cord. We recorded the descending volleys set up by such pairs of stimuli from the cervical epidural space of five patients implanted with chronic stimulators for pain control. Interstimulus intervals of 1, 1.2, 1.4 and 2 ms were used to investigate the first peak of facilitation. Enhanced EMG responses occurred after pairs of stimuli at 1, 1.2 and 1.4 ms, and these were accompanied by larger and more numerous descending volleys than expected from the sum of each stimulus alone. We conclude that facilitatory interaction between the stimuli can occur within the cerebral cortex. This may involve elements that produce repetitive I-wave activity in response to a single stimulus.

Adult↗
PubMed1999

Cerebral blood flow and metabolic changes produced by repetitive magnetic brain stimulation.

We evaluated cerebral variation in oxyhemoglobin, deoxyhemoglobin, and cytochrome oxidase before and after transcranial magnetic and electrical stimulation in ten healthy volunteers using near-infrared spectroscopy. Immediately after magnetic but not after electric stimulation a significant increase in oxyhemoglobin and a decrease in cytochrome oxidase were observed (P < 0.05). Our data suggest that repetitive transcranial magnetic stimulation induces metabolic activation of the cerebral cortex together with an increase in cerebral blood flow.

Adult↗
PubMed1999

The diagnostic value of motor evoked potentials.

OBJECTIVE: To assess the diagnostic usefulness of motor evoked potentials (MEPs) and to identify the optimal method for calculating the central conduction time. The test results were evaluated in a prospective study of 1023 neurological patients. METHODS: We evaluated the correlation between clinical and electrophysiological findings, the accuracy, the sensitivity, the percentage of subclinical abnormalities and the false negative rates of MEPs in different neurological disorders. In patients with lower motor neuron involvement, we compared the central conduction time calculated as the difference between the latency of the cortical and magnetic root stimulation responses with that calculated using the F-wave method. RESULTS: The agreement index between electrophysiological and clinical findings was 87%. The overall accuracy of the test was 0.97. The higher sensitivity values were demonstrated in spinal cord disorders (0.85), hereditary spastic paraplegia (0.80) and motor neuron diseases (0.74). The higher percentages of subclinical abnormalities were found in motor neuron disorders (26%) muscular diseases (24%), multiple sclerosis (13.5%) and spinal cord diseases (12.5%). The higher false negative rates were found in sylvian stroke (0.36) and hereditary spastic paraplegia (0.16). Central conduction study using magnetic paravertebral stimulation but not using the F-wave method, resulted in 12% and 10% of false positive values in lower limb multiradiculopathies and in neuropathies, respectively. CONCLUSIONS: MEPs represent a highly accurate diagnostic test. MEP clinical value is maximum in motor neuron, muscle and spinal cord diseases. In patients with lower motor neuron involvement, the gold standard for central conduction determination is the F-wave method.

Adult↗