Stimulation Of Ulnar Nerve Research Articles

Acceleromyography in neonates and small infants: baseline calibration and recovery of the responses after neuromuscular blockade with rocuronium

We have evaluated the use of the TOF-Guard (TOF, train-of-four) acceleromyographic thumb responses to ulnar nerve stimulation in neonates and infants and the return of the responses after neuromuscular blockade. Baseline acceleromyographic recording of thumb adduction to ulnar nerve stimulation during volatile anaesthesia was performed in 22 babies aged less than 30 weeks. At the start of stimulation the automatic set-up procedure of the TOF-Guard was used to see if a 100% control twitch height could be achieved. Irrespective of the ability to achieve a 100% control twitch height, TOF stimulation was used thereafter. When no automatic 100% control twitch could be reached, the transducer signal gain factor was set manually to obtain a 100% value. In 14 of the 22 children the recovery after neuromuscular blockade with rocuronium 0.3 mg kg(-1) was recorded. In nine of 22 patients a 100% baseline twitch height was obtained with the automatic set-up. In the other 13 babies the TOF-Guard display indicated that the transducer signal was too low. The mean time to recovery of control twitch to 75% of baseline after rocuronium 0.3 mg kg(-1) was 51 min (SD = 21) and the time to recovery of the TOF ratio to 70% was 49 min (SD = 19). The mean final twitch height and TOF after recovery from rocuronium blockade were 101% (SD = 15) and 92% (SD = 12), respectively. The recovery of the responses after neuromuscular blockade to near baseline values shows that acceleromyography can be used to measure neuromuscular block and recovery in neonates and infants.

Acceleromyography in neonates and small infants: baseline calibration and recovery of the responses after neuromuscular blockade with rocuronium

Background: We have evaluated the use of the TOF-Guard® (TOF, train-of-four) acceleromyographic thumb responses to ulnar nerve stimulation in neonates and infants and the return of the responses after neuromuscular blockade. Methods: Baseline acceleromyographic recording of thumb adduction to ulnar nerve stimulation during volatile anaesthesia was performed in 22 babies aged less than 30 weeks. At the start of stimulation the automatic set-up procedure of the TOF-Guard® was used to see if a 100% control twitch height could be achieved. Irrespective of the ability to achieve a 100% control twitch height, TOF stimulation was used thereafter. When no automatic 100% control twitch could be reached, the transducer signal gain factor was set manually to obtain a 100% value. In 14 of the 22 children the recovery after neuromuscular blockade with rocuronium 0.3 mg kg−1 was recorded. Results: In nine of 22 patients a 100% baseline twitch height was obtained with the automatic set-up. In the other 13 babies the TOF-Guard® display indicated that the transducer signal was too low. The mean time to recovery of control twitch to 75% of baseline after rocuronium 0.3 mg kg−1 was 51 min (SD = 21) and the time to recovery of the TOF ratio to 70% was 49 min (SD = 19). The mean final twitch height and TOF after recovery from rocuronium blockade were 101% (SD = 15) and 92% (SD = 12), respectively. Conclusion: The recovery of the responses after neuromuscular blockade to near baseline values shows that acceleromyography can be used to measure neuromuscular block and recovery in neonates and infants.

Suxamethonium administration prolongs the duration of action of subsequent rocuronium

Background and aim: Rocuronium may be given to patients for intubation and also after they have received suxamethonium for intubation. The neuromuscular profile of rocuronium given after recovery from suxamethonium may not be identical to that when rocuronium has been given alone. The neuromuscular effects of suxamethonium and rocuronium, and their effects on intraocular pressure (IOP), heart rate (HR) and arterial pressure were also recorded. Methods: Thirty patients were randomly allocated to receive either 0.6 mg kg−1 rocuronium (n = 15) or 1 mg kg−1 suxamethonium (n = 15) for intubation. Anaesthesia was first induced using propofol 2.5 mg kg−1 and fentanyl 2 μg kg−1 and maintained with propofol 6-12 mg kg−1 h−1. The response of the thumb to supramaximal train-of-four (TOF) ulnar nerve stimulation at the wrist was measured using a mechanomyograph. In the suxamethonium group, when the first twitch of the TOF had recovered to 90%, rocuronium 0.6 mg kg−1 was administered. Before administration of relaxant, baseline readings of HR, arterial pressure and IOP were measured until stable, then the appropriate relaxant administered. Thereafter, all readings were repeated at 30, 90, 150, 210 and 270 s. Tracheal intubation was performed 300 s after the intubating dose and all recordings repeated 30 s later. Mechanomyographic monitoring was continued until 70% TOF recovery. Results: Suxamethonium had a more rapid onset than rocuronium (49 s vs. 74 s, P < 0.0001). The onset time of rocuronium after suxamethonium was significantly reduced (56 s) and the time to recover to a TOF of 70% following rocuronium was increased by previous suxamethonium administration (47 vs. 58 min, P < 0.05). Suxamethonium caused a marked rise in IOP (>30%) and HR (>10%) while rocuronium had little effect on either. Conclusion: Previous suxamethonium administration decreases the onset time and increases the duration of action of rocuronium. Unlike suxamethonium, rocuronium has few cardiovascular effects and causes little change in IOP.

Suxamethonium administration prolongs the duration of action of subsequent rocuronium

Rocuronium may be given to patients for intubation and also after they have received suxamethonium for intubation. The neuromuscular profile of rocuronium given after recovery from suxamethonium may not be identical to that when rocuronium has been given alone. The neuromuscular effects of suxamethonium and rocuronium, and their effects on intraocular pressure (IOP), heart rate (HR) and arterial pressure were also recorded. Thirty patients were randomly allocated to receive either 0.6mg kg(-1) rocuronium (n = 15) or 1 mg kg(-1) suxamethonium (n = 15) for intubation. Anaesthesia was first induced using propofol 2.5 mg kg(-1) and fentanyl 2 microg kg(-1) and maintained with propofol 6-12 mg kg(-1) h(-1). The response of the thumb to supramaximal train-of-four (TOF) ulnar nerve stimulation at the wrist was measured using a mechanomyograph. In the suxamethonium group, when the first twitch of the TOF had recovered to 90%, rocuronium 0.6 mg kg(-1) was administered. Before administration of relaxant, baseline readings of HR, arterial pressure and IOP were measured until stable, then the appropriate relaxant administered. Thereafter, all readings were repeated at 30, 90, 150, 210 and 270 s. Tracheal intubation was performed 300 s after the intubating dose and all recordings repeated 30 s later. Mechanomyographic monitoring was continued until 70% TOF recovery. Suxamethonium had a more rapid onset than rocuronium (49s vs. 74s, P < 0.0001). The onset time of rocuronium after suxamethonium was significantly reduced (56 s) and the time to recover to a TOF of 70% following rocuronium was increased by previous suxamethonium administration (47 vs. 58 min, P < 0.05). Suxamethonium caused a marked rise in IOP (>30%) and HR (>10%) while rocuronium had little effect on either. Previous suxamethonium administration decreases the onset time and increases the duration of action of rocuronium. Unlike suxamethonium, rocuronium has few cardiovascular effects and causes little change in IOP.

High-Frequency (600Hz) SEP Oscillations – Generators and Pathophysiological Aspects

Human median nerve somatosensory evoked potentials (SEP) contain a low-amplitude (<500 nV) high-frequency (˜600Hz) burst of repetitive wavelets (HFOs) which are superimposed onto the primary cortical response 'N20'. The following studies in human subjects are aimed to further clarify the cortical and subcortical structures involved in the generation of the HFOs and the (patho)physiological meaning of this somatosensory oscillatory activity. 1) 128-channel SEP recordings were obtained to right median nerve stimulation and ulnar nerve stimulation. Different source evaluation strategies provided converging evidence for a cortical HFO origin, with two different almost orthogonally oriented generators being active in parallel. The cortical HFO source constellation points to a „precortical“ source in terminals of thalamocortical fibers and a second intracortical HFO origin. Additionally, generation of the HFOs was localized in subcortical, near thalamic and subthalamic source sites. 2) We tested the hypothesis that HFOs might be more sensitive to temporal dispersion caused by demyelinating lesions in multiple sclerosis (MS) than the N20. HFOs in median nerve SEPs in 50 patients with definite MS and in 30 healthy controls were recorded. Three patterns of SEP alterations were found: (i) abolished HFOs with either normal (11% of stimulated limbs), or delayed N20 (16%); (ii) an attenuation of N20 amplitude with preserved HFOs (13%); and (iii) a mixture of both patterns (21%). The first pattern -normal N20 with abolished HFOs- indicates that the HFOs are a sensitive marker of slight demyelination. The second pattern is suggestive of a mainly axonal lesion type, while the third pattern points to a combined axonal/demyelinating process or a conduction block. Analysis of HFOs allows identification of slight demyelinating processes in MS patients in whom the N20 SEP component remains unaffected. 3) The behavior of HFOs in a cohort of schizophrenic patients in comparison to an age- and sex-matched group of controls was tested. HFOs in the group of patients showed a delayed latency. In the low frequency part of the SEPs an increase in amplitude was found. These results are interpreted as a lack of somatosensory inhibition in the somatosensory pathway, either on a thalamic or a cortical level. HFOs are an interesting tool to explore functionality and pathophysiology of the lemniscal system, especially of dysfunctions in thalamocortical impulse propagation.

Influence of a mutation of the calcium ATPase 2 (SERCA 2) gene in patients with Darier's disease on the central and peripheral nervous system

Objective: To investigate neurological manifestations in patients with Darier's disease Introduction: Darier's disease is an autosomal dominant skin disorder characterized by warty papules and plaques in the seborrheic area (central trunk, flexures, scalp, and forehead), palmoplantar pits, and nail abnormalities. ATP2A2, which encodes the sarcoplasmic reticulum calcium ATPase 2 (SERCA2) pump, has been identified as the defective gene in Darier's disease. SERCA2 belongs to a family of P-type membrane bound ATPase, which pumps calcium from the cytoplasm into reservoirs in the endoplasmic reticulum. Up to now neurological manifestations of the disease have not been described. Methods: 6 patients with Darier's disease were seen by a neurologist. AEP, nystagmography, EMG of the quadriceps muscle, and electroneurography of the lower limb were performed. Additionally isometric contractions of the adductor pollicis muscle were recorded after supramaximal ulnar nerve stimulation. The compound muscle action potential (CMAP) was recorded by surface electrodes. Results: In 5/6 patients the electrophysiological investigations including the electromyography were normal. One patient who was affected most heavily by Darier's disease showed a generalized muscular atrophy and myopathy in the EMG. The muscle contraction test was pathological in all patients. The contraction time and the half relaxation time (1/2 RT) were prolonged. In 5/6 patients the twitch potentiation after 2Hz stimulation was not detectable. Discussion: We could show for the first time that patients' with Darier's disease had a pathological muscle contraction. No pathological changes of the central nervous system were detectable. These muscle alterations correspond very well with the known mutation in the SERCA2 gene, coding for a calcium ATPase 2, and suggest a relevant physiological influence of the mutation for the muscle physiology.

Clinical pharmacology of GW280430A in humans.

An ultrashort-acting nondepolarizing neuromuscular blocking agent that could be an alternative to succinylcholine has been the focus of a concerted effort in the field of muscle relaxants. GW280430A showed a promising pharmacodynamic profile in preclinical work and a wide margin of safety and so was selected for study in humans. Thirty-one volunteers participated in this study, which determined the dose producing 95% block (ED95) and the safety and pharmacodynamics of increasing ED95 multiples. Anesthesia was induced and maintained with propofol, midazolam, and fentanyl. Neuromuscular transmission was measured at the adductor pollicis using ulnar nerve stimulation, and responses were recorded continuously by standard mechanomyographic monitoring. The ED95 for GW280430A is 0.19 mg/kg. The time to onset of 90% block ranged from 1.3 to 2.1 min, depending on the dose. Clinical durations ranged from 4.7 to 10.1 min and increased with increasing dose. Five to 95% and 25-75% recovery rates were approximately 7 and 3 min, respectively, and were independent of the dose administered. Transient cardiovascular side effects were observed at doses beginning at 3 x ED95 and above and were suggestive of histamine release. Most volunteers receiving 4 x ED95 exhibited plasma histamine concentrations indicative of significant histamine release. GW280430A has a rapid onset and ultrashort duration of action. The recovery rate is rapid, predictable, and independent of dose. Doses at least up to 2.5 x ED95 seem to be free of side effects and seem to be able to provide relaxation within 60-90 s.

Convergence of forelimb afferent actions on C7-Th1 propriospinal neurones bilaterally projecting to sacral segments of the cat spinal cord.

Propriospinal neurones located in the cervical enlargement and projecting bilaterally to sacral segments of the spinal cord were investigated electrophysiologically in eleven deeply anaesthetized cats. Excitatory or inhibitory postsynaptic potentials from forelimb afferents were recorded following stimulation of deep radial (DR), superficial radial (SR), median (Med) and ulnar (Uln) nerves. 26 cells were recorded from C7, 22 from C8 and 3 from Th1 segments. The majority of the cells were located in the Rexed's laminae VIII and the medial part of the lamina VII. In 10 cases no afferent input from the forelimb afferents was found. In the remaining neurones effects were evoked mostly from DR (88%) and Med (63%), less often from SR (46%) and Uln (46%). Inhibitory actions were more frequent than excitatory. The highest number of IPSPs was evoked from high threshold flexor reflex afferents (FRA)--all connections were polysynaptic. However, inhibitory actions were often evoked from group I or II muscle afferents (polysynaptic or disynaptic) and, less frequently, from cutaneous afferents (mostly polysynaptic). Di- or polysynaptic IPSPs often accompanied monosynaptic EPSPs from group I or II muscle afferents. Disynaptic or polysynaptic EPSPs from muscle and cutaneous afferents were also recorded in many neurones, while polysynaptic EPSPs from FRA were observed only exceptionally. Various patterns of convergence in individual neuronal subpopulations indicate that they integrate different types of the afferent input from various muscle and cutaneous receptors of the distal forelimb. They transmit this information to motor centers controlling hind limb muscles, forming a part of the system contributing to the process of coordination of movements of fore--and hind--limbs.

The natural history of central motor abnormalities in amyotrophic lateral sclerosis.

Degeneration of spinal motoneurons has been well documented in amyotrophic lateral sclerosis (ALS), but the evolution of central motor abnormalities is largely unknown. It has been suggested that glutamate-mediated neuroexcitotoxicity may be involved in the pathogenesis of ALS and that this may be manifest as an increase in corticomotor excitability early in the disease. Serial measurements of corticomotor threshold, central motor conduction time (CMCT), silent period duration and the amplitude of compound muscle action potentials (CMAPs) from ulnar nerve stimulation in the right and left first dorsal interosseous muscles were made in 76 patients with idiopathic ALS, 49 of whom were followed from presentation to death. Threshold to transcranial magnetic stimulation was determined by standard methods and CMCT was measured using the F-wave method. Silent period was estimated during a small background contraction of the muscle. Patients were classified according to the region of onset and the physical signs in the hands. The region of onset was bulbar in 17 patients, lower limb in 31 patients and upper limb in 28 patients. At presentation, 23 patients had no abnormal physical signs in the hands, 25 had lower motoneuron signs only, 14 had upper motoneuron signs only and the remainder (14) had mixed upper and lower motoneuron signs in the hands. Evolution of the central conduction parameters was determined in relation to time from onset of symptoms and also as a function of normalized total disease duration in the patients who had died. Corticomotor threshold and CMCT showed no change as the disease evolved except for patients with mixed signs, who had a terminal increase in threshold and prolongation of CMCT. Silent period duration was shorter than normal early in the disease and showed progressive lengthening throughout the illness, but nevertheless remained within the normal range regardless of the region of onset. CMAP amplitude showed a linear decline over the course of the disease. There was therefore no evidence of a phase of increased corticomotor hyperexcitability at any stage of disease progression. The early shortening of silent period, however, probably represents a shift in the balance of excitatory and inhibitory inputs to the cortical output cells responsible for voluntary action, and could be a reflection of degeneration of cortical interneurons. None of the measures of central motor function in ALS are likely to be useful for monitoring patients in a clinical trial setting.

Unilateral drop finger due to cervical spondylosis at the C6/7 intervertebral level

AbstractA 64-year-old man who presented right drop fingers without pyramidal signs due to cervical spondylosis is reported. Magnetic resonance imaging showed a high signal intensity change on T2-weighted scans of the spinal cord at the C6/7 intervertebral level. Evoked spinal cord potentials following ulnar nerve stimulation were attenuated at the C6/7 intervertebral level. Compound muscle action potentials (CMAPs) following right cervical nerve root stimulation were recorded from the extensor digitorum communis. CMAPs following right C8 nerve root stimulation were evoked with small amplitudes. Small polyphasic CMAPs with prolonged onset latency were recorded following right C7 nerve root stimulation. Simultaneous C7 radiculopathy and C8 segmental spinal cord lesion due to cervical spondylosis at the C6/7 intervertebral level were the causes of drop fingers in the present case. Unilateral drop finger is a clinical symptom commonly associated with posterior interosseus nerve palsy, but mention should be made about cervical lesions causing drop finger. Electromyographic abnormalities of the triceps and first dorsal interosseus muscle were the key findings for differentiating the cause from paralysis of the posterior interosseous nerve.

Increased cortical excitability induced by transcranial DC and peripheral nerve stimulation

This study investigated the effect of short periods of simultaneous weak anodal direct current (DC) stimulation and peripheral ulnar nerve (ES) stimulation on corticospinal excitability. The experiments involved repeated testing of ten normal subjects with four different protocols: (1) No Stimulation; (2) DC only; (3) ES only; (4) DC plus ES. Motor evoked potentials (MEP) were recorded from the First Dorsal Interosseous (FDI); Abductor Digiti Minimi (ADM) and Flexor Carpi Ulnaris (FCU). The baseline MEP amplitude was compared with that obtained immediately after the first set of stimulation, after the second set of stimulation, 15 min post stimulation and 30 min after stimulation. No significant change was seen with the No Stimulation and ES Only protocols. FDI showed a significant change in the DC protocol after the second set of stimulation but the changes were not present 15 or 30 min after. The DC plus ES protocol showed FDI changes that were significant after the second set of stimulation with the elevations persisting when tested 15 and 30 min post intervention. These observations show that a period of anodal DC stimulation preceding a period of ulnar nerve stimulation resulted in significant and persistent elevations in cortical excitability.

Criteria of adequate clinical recovery from neuromuscular block.

This study was undertaken to compare the sensitivities of the train-of-four response (2 Hz for 2 s), the single twitch (0.15 Hz), and the tetanic response (50 Hz for 5 s) as indices of residual nondepolarizing block. Spontaneous or induced recovery of evoked thumb adduction in response to ulnar nerve stimulation was studied. One hundred and seven adult surgical patients were divided according to the relaxant used, into six groups. We found that when the single twitch recovered to control height, the train-of-four ratio was well below 1.0. This ratio was significantly lower during spontaneous recovery than following neostigmine antagonism of the block (P < 0.01). The tetanic response was fully sustained when the train-of-four ratio was above 0.7. When the ratio was less than 0.7, variable degrees of fade of tetanus were evident. Analysis of variance indicated similar train-of-four ratios among the six groups at complete recovery of the single twitch irrespective of the relaxant technique used (P < 0.1). It is concluded that a train-of-four ratio of 0.7 or higher reliably indicates the recovery of the single twitch to control height and a sustained response to tetanic stimulation at 50 Hz for 5 s. The clinical significance of this study is as follows: the train-of-four response provides the same indication of clinical recovery from nondepolarizing block as obtained from tetanic stimulation at a physiological frequency; and reliance on the recovery of the single twitch to control height as a criterion of spontaneous return to normal clinical neuromuscular function may be misleading.

Peripheral and segmental spinal abnormalities of median and ulnar somatosensory evoked potentials in Hirayama’s disease

Objectives: To investigate the origin of juvenile muscle atrophy of the upper limbs (Hirayama’s disease, a type of cervical myelopathy of unknown origin). Subjects: Eight male patients were studied; data...

RETRACTED: Monitoring of neuromuscular block after administration of vecuronium in patients with diabetes mellitus

We studied the supramaximal current for ulnar nerve stimulation during electromyographic monitoring of onset and recovery of neuromuscular block using a neuromuscular transmission module (M-NMT Module, Datex-Ohmeda) in patients with Type 2 diabetes undergoing anaesthesia with nitrous oxide, oxygen, isoflurane and fentanyl. Thirty-six diabetic patients were randomly assigned to a post-tetanic count (PTC) group (n=17) or train-of-four (TOF) group (n=19). In addition, 30 non-diabetic patients were divided into control PTC (n=15) and TOF groups (n=15). In the diabetic patients (diabetes PTC and diabetes TOF groups), the mean supramaximal stimulating current was significantly higher than in the non-diabetic patients (control PTC and TOF groups) (50.5 (SD 14.1) vs 33.4 (6.1) mA, P<0.01). Onset of neuromuscular block (time to disappearance of T1) after vecuronium 0.1 mg kg(-1) in the diabetic patients did not differ significantly from that in the non-diabetic patients (276 (77) vs 244 (44) s, P=0.055). Time to return of PTC1 did not differ significantly between the diabetes and control PTC groups (21.0 (12.1) vs 15.7 (5.0) min, P=0.126). Times to return of T1 and T4 in the diabetes TOF group were significantly longer than in the control TOF group (T1: 37.5 (15.2) vs 25.7 (7.6) min, P=0.01; T4: 61.4 (23.7) vs 43.5 (11.4) min, P=0.01). During recovery, PTC and T4/T1 in the diabetes PTC and TOF groups were similar to those in the control PTC and TOF groups, respectively. T1/T0 in the diabetes TOF group was significantly less than in the control TOF group, 80-120 min after vecuronium (P<0.05). In diabetic patients, supramaximal current is higher than in non-diabetic patients. After vecuronium, onset of neuromuscular block and recovery of PTC or T4/T1 are not altered, but time to return of T1 or T4, and recovery of T1/T0 are delayed in diabetic patients.

Verification of the median-to-ulnar and ulnar-to-median nerve motor fiber anastomosis in the forearm: an electrophysiological study.

To estimate the real occurrence of the motor median-to-ulnar nerve anastomosis in the proximal forearm (Martin-Gruber anastomosis, MGA), as its frequency varies between 6 and 44% in the literature and to investigate the incidence of the ulnar-to-median nerve anastomosis in the distal forearm. Compound muscle action potentials (CMAP) recorded over thenar, hypothenar, and first dorsal interosseus muscle on median or ulnar nerve stimulation at wrist and elbow and collision blocks of the median and ulnar nerve were compared in a group of 50 healthy volunteers. Particular precautions were undertaken in order to avoid false positive results due to stimulus spread to the neighboring nerve. Cases of uncertain MGA were classified as either MGA or non-MGA on the basis of posterior probabilities estimated by discriminant analysis. The estimated frequency of MGA was 54% using the potential comparison method and 46% using the collision technique. An ulnar-to-median nerve anastomosis was not found in any subject. While the MGA is very common, the ulnar-to-median nerve anastomosis is a rarity. Standard nerve conduction studies of the median nerve with CMAP recordings solely over thenar will detect less than 14% of MGA cases.

Remote effects of self-paced teeth clenching on the excitability of hand motor area.

We studied remote effects of teeth clenching on motor cortical and spinal cord excitability using transcranial magnetic stimulation (TMS), brainstem electrical stimulation (BES), and ulnar nerve stimulation (F-wave) in eight normal volunteers. The TMS, BES, and ulnar nerve stimulation at the wrist were given at different intervals (0-200 ms) after the onset of masseter contraction. Surface electromyographic responses were recorded from the first dorsal interosseous muscle. Responses at different intervals were compared with the response elicited when the subject made no teeth clenching (control response). In TMS, conditioned responses (during teeth clenching) were significantly larger than the control at all intervals. In contrast, in BES and F-waves, conditioned responses were not larger than the control at an early phase (intervals shorter than 50 ms), whereas they were larger than the control at later intervals (longer than 50 ms). These results suggest that facilitation occurs in the hand motor area at the early phase of teeth clenching, and spinal facilitation dominates at its late phase. This time course of facilitation may indicate that the motor cortex must regulate hand muscles finely at the early phase of teeth clenching, and spinal cord may stabilize them firmly at the late phase. The excitability changes of the hand motor area may be in parallel with that of the masseter motor area which reflects the pattern of masseter contraction when the subject activates the masseter muscle phasically at the early phase and sustains that contraction at the late phase.

Time course of induction of increased human motor cortex excitability by nerve stimulation.

Manipulation of afferent input induces changes in the excitability and organisation of human corticomotor representations. These changes are generally short lived, although can be prolonged by repetition. Here, we charted the time-course of the change of motor cortex excitability induced by electrical stimulation of radial and ulnar nerves. Corticomotor excitability was evaluated by measuring the amplitude of the motor evoked potentials in the first dorsal interosseous muscle by transcranial magnetic stimulation of the optimal cortical area. Measurements were carried out before the start of peripheral nerve stimulation, and then during the peripheral nerve stimulation at 15 min intervals over a period of 2 h. The amplitudes of the motor evoked potentials significantly increased during the 2 h period of peripheral nerve stimulation. Cortical excitability peaked after about 45-60 min stimulation. These clear-cut changes in cortical excitability following peripheral nerve stimulation may reveal some of the mechanisms underlying motor learning and cortical plasticity.

Time-course of action of rocuronium 0.3 mg.kg-1 in children with and without endstage renal failure.

The time-course of the neuromuscular effects of rocuronium 0.3 mg.kg-1 during nitrous oxide-halothane anaesthesia in children with and without renal failure is unknown. This study compared the neuromuscular blocking effects in these groups. The study was approved by the Hospital Ethical Committee. In the control group, 14 healthy children without renal disease were scheduled for various elective surgical procedures. Sixteen children with endstage renal failure, 14 of whom were already on renal dialysis, were scheduled for (re)placement of dialysis catheters (n=14) or for renal transplantation (n=2). Anaesthesia was induced and maintained with halothane and nitrous oxide in oxygen. Acceleromyographic thumb adduction after supramaximal ulnar nerve stimulation was recorded using train-of-four stimulation every 15 s. The onset time, the time to recovery of the first twitch to 25% or 75% and to recovery of a train-of-four ratio of 0.7 after rocuronium 0.3 mg.kg-1 were measured. Statistical analysis was performed with Student's t-test. P < 0.05 was considered statistically significant. The onset time was longer in children with renal failure (139 s, SD=71) than in control children (87 s, SD=43) (P=0.02). There were no significant differences in the duration of action of rocuronium between children without renal failure and in 15 out of 16 children with renal failure. In children with renal failure, aged over 1 year, a single bolus dose of rocuronium 0.3 mg.kg-1 does not cause a prolonged block, but has a slower onset than in healthy children.

Long lasting effects of rTMS and associated peripheral sensory input on MEPs, SEPs and transcortical reflex excitability in humans.

We tested the effect of repetitive transcranial magnetic stimulation (rTMS) over the motor cortex on the size of transcortical stretch and mixed nerve reflexes. Fourteen healthy subjects were investigated using either 25 min of 1 Hz rTMS or 30 min of 0.1 Hz rTMS paired with electrical stimulation of the motor point of the first dorsal interosseous muscle (FDI). Following treatment, we measured the effect on the size of: (1) EMG responses evoked in FDI by transcranial magnetic stimulation (MEPs), (2) somatosensory evoked potentials (SEPs) evoked by ulnar nerve stimulation, and (3) transcortical stretch or electrically elicited reflexes. rTMS at 1 Hz reduced the amplitude of both MEPs and long latency reflexes by 20-30 % for about 10 min after the end of stimulation. Short latency reflexes were unaffected. SEPs were not studied, as it has been shown previously that they are also suppressed. rTMS at 0.1 Hz paired with motor point stimulation (interstimulus interval of 25 ms) increased the amplitude of the MEP and the cortical components of the SEP (N20/P25 and later peaks) for up to 10 min. Long latency reflexes were facilitated with the same time course. We conclude that rTMS over the motor cortex either alone or in conjunction with peripheral inputs can decrease or increase the excitability of the sensory and motor cortex for short periods after the end of stimulation. These changes affect not only MEPs and SEPs but also EMG responses to more 'natural' inputs involved in transcortical stretch reflexes.

Influence of proprioceptive input on parkinsonian tremor.

Previous studies have shown a modification of parkinsonian tremor (PT) by proprioceptive input induced by passive joint movements. The authors investigated the impact of electrically evoked proprioceptive input on PT. In eight patients with PT they recorded surface EMG from the opponens pollicis muscle, and forearm extensors and flexors. Rhythmic electrical stimulation was applied to the ipsilateral median nerve at the wrist using a submaximal stimulus intensity and stimulus frequencies between two stimuli per second and five stimuli per second. The tremor frequency did not adapt to the stimulus frequency. Tremor frequency of parkinsonian resting tremor increased significantly in the directly stimulated opponens pollicis muscle (mean +/- standard deviation, 4.35 +/- 0.64 Hz without stimulation versus 4.53 +/- 0.68 Hz with stimulation; P < 0.05, paired t-test), the not directly stimulated forearm muscles (4.90 +/- 0.72 Hz versus 5.18 +/- 0.73 Hz, P < 0.001), and the upper arm muscles (5.13 +/- 0.61 Hz versus 5.36 +/- 0.68 Hz, P < 0.01). Furthermore, the parkinsonian postural tremor accelerated significantly during ipsilateral median nerve stimulation (5.31 +/- 0.99 Hz versus 5.44 +/- 1.03 Hz, P < 0.05). Parkinsonian resting tremor in the forearm muscles also accelerated significantly during ipsilateral ulnar nerve stimulation (4.85 +/- 0.57 Hz versus 5.05 +/- 0.65 Hz, P < 0.05). Contralateral median nerve stimulation had no significant effect. These results suggest a close interaction between proprioceptive input and PT generation.