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Healthy aging limits the activities of daily living and personal independence. Furthermore, cognitive-motor interference in dual-task (e.g., walking while talking) appears to be more pronounced in the elderly. Transcranial direct current stimulation (tDCS), a form of the non-invasive brain stimulation technique, is known to modify cortical excitability and has been investigated as a tool for enhancing motor and cognitive performance in health and disease. The present study examined whether tDCS targeting the dorsolateral prefrontal cortex (DLPFC) could improve dual-task performance in healthy older adults. The effects of tDCS, among other factors, depend on stimulation polarity (anodal vs. cathodal), electrode setup (unilateral vs. bilateral) and the time of application (off-line vs. on-line). We therefore explored the effects of unilateral and simultaneous bilateral tDCS (anodal and cathodal) of left DLPFC while performing (on-line) the Grooved Pegboard Test (GPT) and Serial Seven Subtraction Test (SSST) alone or together (dual-tasking). The number of pegs and the number of correct subtractions were recorded before, during and 30 min after tDCS. The dual-task performance was measured as the percent change from single- to the dual-task condition (dual-task cost DTC). Only bilateral, anode left tDCS, induced a significant increase in subtracted numbers while dual-tasking, i.e., it reduced the DTC of manual dexterity (GPT) to a cognitive task. Significant changes 30 min after the stimulation were only present after bilateral anode right (BAR) tDCS on GPT dual-task costs. These findings suggest that anodal tDCS applied on-line interacts with a dual-task performance involving demanding cognitive and manual dexterity tasks. The results support the potential use of non-invasive brain stimulation for improvement of cognitive functioning in daily activities in older individuals.

© 2017 by the authors. We are glad to introduce the fourth Journal Club. This edition is focused on several relevant studies published in the last few years in the field of musculoskeletal disorders, chosen by our Editorial Board members. We hope to stimulate your curiosity in this field. The Editorial Board members wish you an inspiring lecture.

The complex interplay between hypernatremic osmotic disturbances and cerebral lesions is yet to be clarified. In this review, we discuss, on the basis of the reported data of hypernatremic CNS challenge in the adult population, the clinical and radiologic features of the condition. Our search captured 20 case studies and 1 case series with 30 patients in total who acquired acute hypernatremia due to different etiologies and developed CNS lesions. We explored the associations between premorbid conditions, clinical presentation, hypernatremic state, correction rate, and radiologic appearance, including the localization of brain lesions and the outcomes. The results revealed that altered mental status was the most commonly reported symptom and osmotic demyelination syndrome in the form of extrapontine myelinolysis was the prevailing radiologic pattern. Finally, we contrasted, when appropriate, clinical and experimental data related to hypernatremic and hyponatremic osmotic insults to aid the understanding of the pathophysiology of CNS osmotic brain injury.

Brain MRI and ¹⁸F-FDG PET/CT scans were performed in a patient who had survived a suicide attempt by fluoxetine overdose. The patient presented with the following clinical signs and symptoms, and neuroimaging findings: severe signs of serotonin toxicity, including comatose state, akinetic rigid syndrome and dysautonomia; bilateral globus pallidus changes consistent with extensive pallidal necrosis and subsequent reversible diffuse ischemic changes in white matter, with posterior predominance, involving the splenium of the corpus callosum on brain MRI; and marked hypometabolism in the frontal, parietal and temporal cortical regions as well as in both caudate nuclei on ¹⁸F-FDG PET/CT performed 37 days later. These findings suggest that acute severe serotonin toxicity can induce structural and long-standing functional changes in multiple cortical and subcortical brain regions that are associated with cognitive and extrapyramidal syndromes.

Experimental and clinical data suggest that high-frequency deep brain stimulation (DBS) of different subcortical structures can be used to control or modulate epileptic seizures. Recent studies showed that DBS of the substantia nigra reticulata (SNr) in rats has an anticonvulsant effect on forebrain clonic seizures. The aim of this study was to determine whether DBS of SNr could also suppress tonic epileptic seizures evoked in hindbrain structures. DBS with high frequency often mimics the effects of surgical ablation of a particular area of the brain. However, the optimal parameters of DBS stimulation to induce ablation-like effects on seizures are not well defined. Consequently, in the first experiment we examined the effects of different stimulation frequencies (80, 130, 260 and 390 Hz) on neuronal activation induced in SNr, using c-fos immunocytochemistry. The results showed that the stimulation of the SNr with 80 Hz has no inhibitory effect while stimulation with 130, 260 and 390 Hz produced a remarkable suppressive effect compared with the control unstimulated side. The aim of the second experiment was to determine whether bilateral inhibition of SNr with DBS could suppress tonic seizures induced by electric shock. Statistical analysis showed that the mean tonic seizure scores following SNr stimulation with either 130 or 260 Hz were not significantly different from scores following the application of the electrode without current. The data suggest that DBS of the SNr produces neuronal inhibition but fails to suppress tonic seizures. We conclude, therefore, that DBS of SNr with frequencies used in this study might not be effective for treatment of patients who suffer from tonic epileptic seizures.

Diabetic patients show a higher incidence of cardiac arrhythmias, including ventricular fibrillation and sudden death. Their electrocardiograms may show several alterations from normal patterns, many of them related to the QT. Various diastolic and systolic abnormalities are frequently reported in diabetic patients, and the severity of the abnormalities depend on the patients' age and the duration of diabetes. The aim of this experimental study has been to clarify the progressive effects on heart rhythm in neonatal alloxan (ALX) (induced at 5 days of age) diabetic male rats. Cardiac biopotential data were acquired in vivo with a biotelemetry system. After an overnight fast blood glucose in diabetic rats, compared to age-matched controls, was elevated before and at 60, 120 and 180min after a glucose challenge at 2 and 8 months of age. Heart rate and heart rate variability were modestly reduced and QT interval modestly prolonged in diabetic rats, compared to controls, at 2, 6 and 8 months of age. There was also an age-dependent decline in heart rate and prolongation in QT interval. At 8 months heart rate was 296±8bpm in diabetic compared to 311±10bpm in controls and heart rate variability was 27±3bpm in diabetic rats compared to 32±4bpm in controls. Physical activity was significantly reduced in diabetic rats, compared to controls, at 6 and 8 months of age. Body temperature was modestly reduced in diabetic rats, compared to controls, at 2, 6 and 8 months. In conclusion, the neonatal ALX-induced diabetes mellitus was associated with disturbances in heart rate, heart rate variability, QT interval which in turn may be associated with changes in physical activity and body temperature.

Recent evidence suggests that the dynamic-scaling behavior of the time-series of signals extracted from separate peaks of tremor spectra may reveal existence of multiple independent sources of tremor. Here, we have studied dynamic characteristics of the time-series of hand tremor movements in essential tremor (ET) patients using the detrended fluctuation analysis method. Hand accelerometry was recorded with (500 g) and without weight loading under postural conditions in 25 ET patients and 20 normal subjects. The time-series comprising peak-to-peak (PtP) intervals were extracted from regions around the first three main frequency components of power spectra (PwS) of the recorded tremors. The data were compared between the load and no-load condition on dominant (related to tremor severity) and non-dominant tremor side and with the normal (physiological) oscillations in healthy subjects. Our analysis shows that, in ET, the dynamic characteristics of the main frequency component of recorded tremors exhibit scaling behavior. Furthermore, they show that the two main components of ET tremor frequency spectra, otherwise indistinguishable without load, become significantly different after inertial loading and that they differ between the tremor sides (related to tremor severity). These results show that scaling, a time-domain analysis, helps revealing tremor features previously not revealed by frequency-domain analysis and suggest that distinct oscillatory central circuits may generate the tremor in ET patients.

Objective This study investigated whether exercise training, initiated at the onset of diabetes, could preserve the contractile properties of ventricular myocytes. Research Design and Methods The effects of a heavy exercise training program on shortening and intracellular Ca 2+ in unloaded ventricular myocytes from streptozotocin (STZ)-induced diabetic rats were examined. Animals were divided into four groups: control sedentary (CS), diabetic sedentary (DS), control heavy exercise (CHE), and diabetic heavy exercise (DHE). Exercise protocol: 5×60 min/week, 18 m/min, 5% gradient. Exercise training began 1 week after STZ treatment and continued for 12–23 (mean 17.5) weeks. Results Diabetes induced prolongation of time-to-peak (TPK) shortening (124±2 ms in DS compared to 97±2 ms in CS rats), which was further increased by exercise (133±3 ms in DHE and 112±2 ms in CHE myocytes). Diabetes had no significant effects on time-to-half (THALF) relaxation of shortening (61±2 ms in DS compared to 56±2 ms in CS myocytes). Exercise induced significant prolongation of THALF in control (66±3 ms) but not in diabetic (69±3 ms) myocytes. Diabetes, though not exercise, significantly prolonged TPK (76±3 ms in DS compared to 64±2 ms in CS) and THALF recovery (160±5 ms in DS compared to 118±4 ms in CS) of the Ca 2+ transient. Neither diabetes nor exercise had significant effects on the amplitude of myocyte shortening and the Ca 2+ transient. Conclusions Heavy long-term exercise alters the dynamics but not the amplitude of unloaded myocyte contraction in the STZ-induced diabetic rat.

Although repetitive Transcranial Magnetic Stimulation (rTMS) in treatment of stroke in humans has been explored over the past decade the data remain controversial in terms of optimal stimulation parameters and the mechanisms of rTMS long-term effects. This study aimed to explore the potential of different rTMS protocols to induce changes in gene expression in rat cortices after acute ischemic-reperfusion brain injury. The stroke was induced by middle cerebral artery occlusion (MCAO) with subsequent reperfusion. Changes in the expression of 96 genes were examined using low-density expression arrays after MCAO alone and after MCAO combined with 1Hz, 5Hz, continuous (cTBS) and intermittent (iTBS) theta-burst rTMS. rTMS over the lesioned hemisphere was given for two weeks (with a 2-day pause) in a single daily session and a total of 2400 pulses. MCAO alone induced significant upregulation in the expression of 44 genes and downregulation in 10. Two weeks of iTBS induced significant increase in the expression of 52 genes. There were no downregulated genes. 1Hz and 5Hz had no significant effects on gene expression, while cTBS effects were negligible. Upregulated genes included those involved in angiogenesis, inflammation, injury response and cellular repair, structural remodeling, neuroprotection, neurotransmission and neuronal plasticity. The results show that long-term rTMS in acute ischemic-reperfusion brain injury induces complex changes in gene expression that span multiple pathways, which generally promote the recovery. They also demonstrate that induced changes primarily depend on the rTMS frequency (1Hz and 5Hz vs. iTBS) and pattern (cTBS vs. iTBS). The results further underlines the premise that one of the benefits of rTMS application in stroke may be to prime the brain, enhancing its potential to cope with the injury and to rewire. This could further augment its potential to favorably respond to rehabilitation, and to restore some of the loss functions.

s / Brain Stimulation 8 (2015) 395e411 398 at 5Hz intervals). After this patient remitted following TBS-20Hz, this parameter was then successfully applied to other patients with treatment refractory MDD who had failed TBS-50Hz. We began to use TBS-20Hz as our initial treatment parameter after multiple patients failed TBS-50Hz but remitted after TBS-20Hz. Results: 9 of 10 MDD patients treated with TBS-20Hz remitted, with an average BDI-II score drop of 20 points (s.d.1⁄416.8), or 64.3%. Our only non-remitter had suffered a CVA several years prior, possibly altering the position of the LDLPFC target location. Discussion: The strong response seen after TBS-20Hz suggests this and perhaps other alternate pulse parameters could improve the efficacy and durability of TMS treatment for depression. Therefore, a larger controlled trial is warranted to confirm and expand upon these results.

The objective of this preliminary study was to quantify changes in complexity of EEG using fractal dimension (FD) alongside linear methods of spectral power, event-related spectral perturbations, coherence, and source localization of EEG generators for theta (4–7 Hz), alpha (8–12 Hz), and beta (13–23 Hz) frequency bands due to a memory load effect in an auditory–verbal short-term memory (AVSTM) task for words. We examined 20 healthy individuals using the Sternberg’s paradigm with increasing memory load (three, five, and seven words). The stimuli were four-letter words. Artifact-free 5-s EEG segments during retention period were analyzed. The most significant finding was the increase in FD with the increase in memory load in temporal regions T3 and T4, and in parietal region Pz, while decrease in FD with increase in memory load was registered in frontal midline region Fz. Results point to increase in frontal midline (Fz) theta spectral power, decrease in alpha spectral power in parietal region—Pz, and increase in beta spectral power in T3 and T4 region with increase in memory load. Decrease in theta coherence within right hemisphere due to memory load was obtained. Alpha coherence increased in posterior regions with anterior decrease. Beta coherence increased in fronto–temporal regions. Source localization delineated theta activity increase in frontal midline region, alpha decrease in superior parietal region, and beta increase in superior temporal gyrus with increase in memory load. In conclusion, FD as a nonlinear measure may serve as a sensitive index for quantifying dynamical changes in EEG signals during AVSTM tasks.

The effects of prior vibration of the antagonist triceps muscle on the performance of rapid discrete elbow flexion movements were studied in healthy volunteers. The subjects performed 520 movements over five experimental sessions. The application of prior vibration resulted in a shift of the initial position, an undershoot of the final position in untrained subjects, and also in trained subjects if not applied during practice. On the contrary, no undershoot occurred in trained subjects when prior vibration was applied during practice. Improvement in movement performance, as judged by a decrease in variability of the final position, was less successful when vibration was applied during practice. It is supposed that the undershoots were due to prior vibration-induced alterations in proprioceptive messages and a consequent erroneous sense of the arm position. These effects seem to be overcome by practice, but also seem to interfere with learning-based movement improvement.

Background/Aim. Transcranial magnetic stimulation (TMS) is a standard technique for noninvasive assessment of changes in central nervous system excitability. The aim of this study was to examine changes in responses to TMS in patients suffering from Parkinson's disease (PD) during sustained submaximal isometric voluntary contraction [60% of maximal voluntary contraction (MVC)] of the adductor pollicis muscle, as well as during a subsequent recovery period. Methods. Cortical excitability was tested by single TMS pulses of twice of the motor threshold intensity applied over the vertex. Testing was carried out during the sustained contraction phase every 10 s before and every 5 s after the endurance point, as well as at rest and during brief 60% MVC contractions before (control), immediately after the sustained contraction, and at 5 min intervals during the recovery period. Results. Although the PD patients could sustain the contraction at the required level for as long period of time as the healthy subjects (though contraction level subsided more rapidly after the endurance point), effects of muscle fatigue on the responses to TMS were different. In contrast to the findings observed in the healthy people where motor evoked potentials (MEP) and EMG silent period (SP) in fatigued muscle gradually diminished during contraction up to the endurance point, and increased thereafter, in the majority of patients no changes occurred in MEP size (peak and area) of the adductor pollicis muscle, either before or after the endurance point. On the other hand, changes in the SP of this muscle differed among the subjects, showing a gradual increase, a decrease or no changes in duration. The trends of changes in both MEP size and SP duration in the musculus brachioradialis varied among the tested PD patients, without any consistent pattern, which was in contrast with the findings in the healthy people where both measures showed a gradual increase from the beginning of the sustained contraction. A complete dissociation between changes in MEP and SP during fatigue was also of note, which differed sharply from the findings in the healthy people in who fatigue induced changes in these measures followed identical patterns. Conclusion. These results in the PD patients suggest the presence of impairment and/or compensatory changes in mechanisms responsible for adaptation of voluntary drive as well as for matching between cortical excitation and inhibition which become manifest in demanding motor tasks such as those imposed by muscle fatigue. Uvod/Cilj. Transkranijalna magnetna stimulacija (TMS) je standardna tehnika za neinvazivnu procenu promena ekscitabilnosti centralnog nervnog sistema. Cilj rada je bio da se prikažu promene odgovora na TMS kod obolelih od Parkinsonove bolesti (PB) za vreme trajanja submaksimalne voljne izometrijske kontrakcije [60% maksimalne voljne kontrakcije (MVK)] mišića adductor pollicis, kao i tokom perioda oporavka. Metode. Kortikalna ekscitabilnost testirana je TMS pulsevima dvostruko većeg intenziteta od motornog praga. Testiranje je vršeno za vreme održavanja kontrakcije na svakih 10 s do tačke izdržljivosti i na svakih 5 s posle toga, a, takođe, u miru kao i za vreme kratkotrajnih 60% MVK u periodu pre (kontrola), neposredno posle održavanja kontrakcije, i u intervalima od pet minuta za vreme perioda oporavka. Rezultati. Iako su bolesnici sa PB mogli da održavaju zahtevani nivo kontrakcije jednako dugo kao i zdravi ispitanici (mada je nivo opadao brže nakon tačke izdržljivosti), efekti mišićnog zamora na odgovor izazvan TMS-om bili su različiti. Za razliku od zdravih ispitanika kod kojih se motorni evocirani potencijali (MEP) i trajanje perioda EMG tišine (PT) u zamaranom mišiću postepeno smanjuju tokom kontrakcije do tačke izdržljivosti, a zatim rastu, kod većine bolesnika nije došlo do promena veličine (maksimalna amplituda i površina) MEP mišića adductor pollicis, bilo pre ili posle tačke izdržljivosti. S druge strane, promene PT ovog mišića su se razlikovale među ispitanicima, pokazujući bilo postepeno povećanje, smanjenje ili odsustvo promena. Promene kako amplitude MEP tako i trajanje PT u EMG mišića brahioradialisa varirale su među bolesnicima sa PB, bez nekog dominantnog obrasca, po čemu su se, takođe, razlikovale od promena nađenih kod zdravih ispitanika, kod kojih su se oba parametra postepeno povećavala od početka održavanja tonične kontrakcije. Upadljiva je, takođe, i potpuna disocijacija između promena MEP i PT tokom zamora, što je u oštroj suprotnosti sa nalazom kod zdravih ispitanika gde su promene ovih parametara pratile identičan obrazac. Zaključak. Rezultati kod bolesnika sa PB ukazuju na postojanje oštećenja i/ili kompenzatornih promena mehanizmima odgovornih za adaptaciju voljne pobude i usklađivanja kortikalne eksitacije i inhibicije, koji se manifestuju tokom mišićnog zamora i u drugim zahtevnim motornim zadacima.

Changes in discharge rate of fusimotor neurones to pretibial flexor muscles were recorded during and after long-lasting fatiguing isometric and/or isotonic contractions of triceps surae in decerebrate cats. The contractions were elicited by electrical stimulation of the nerves to triceps. Fusimotor spikes were recorded from nerve filaments dissected free from the peroneal nerve. Responses of the fusimotor neurones were diverse. In isometric regime, 22 out of 40 units recorded exhibited an initial increase at the onset of muscle contraction, different in amplitude and duration among the units. In seven of these units an additional brisk burst of spike discharges, of different duration, occurred at the end of the contraction. In 15 fusimotor neurones (14 units with the initial response and an additional unit without it) a slow increase in discharge rate developed, starting during the contraction and outlasting it. In another eleven units the initial response was a decrease in discharge rate, lasting in six of them throughout the contraction. Another six units exhibited a sustained increase in discharge rate throughout the contraction, as well as, at a lower level, but still above the spontaneous one, thereafter. Similar patterns of changes in discharge rate, recorded in 31 of the units, were encountered during isotonic triceps contractions. It should be mentioned that many (about 20) additional silent neurones, responding to manipulating the skin and paw and/or stroking the fur, but not to triceps contractions were encountered. The majority of changes in discharge rate of fusimotor neurones to pretibial flexors differed markedly from those found previously in fusimotor neurones to triceps and hamstring muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Extrapontine myelinolysis (EPM) and cortical laminar necrosis (CLN) have rarely been reported in association with severe hypernatremia. We describe a patient with EPM associated with CLN following severe hypernatremia due to hypertonic peritoneal lavage after a ruptured hydatid cyst of the liver. Clinical and neuroimaging findings in acute stage and serial brain MRI at two and five month follow-up are discussed in detail.

Recently, it has been shown that the subthalamic nucleus (STN) has anticonvulsant effects on epileptic seizures originating from the forebrain. The aim of the present study was to determine whether the anticonvulsant properties of the STN extend to the suppression of tonic seizures originating from the brainstem elicited by electroshock in rats. Three different procedures were used to manipulate activity in the STN and in each case the duration of tonic hindlimb extension elicited by electroshock was used as a measure of seizure-severity. Under general anesthesia, two groups of rats received chronic implants of either bilateral stainless steel guide cannulae or bilateral bipolar stimulating electrodes stereotaxically implanted and aimed at the STN. After 3 days of recovery, each rat in the first group was tested with electroshock on three consecutive days after having received 220 nl bilateral microinjections into the STN of either 200 or 400 pmol of muscimol (a GABA agonist) dissolved in saline or the same volume of normal saline. In the second group the electroshock test was conducted, again on three consecutive days, immediately following high frequency electrical stimulation (HFS) of the STN at 130 or 260 Hz or a no current control condition. In the third group, rats were tested with electroshock before and after bilateral excitotoxic lesions of the STN with either kainic or ibotenic acids. None of these manipulations produced significant suppression of the tonic hind limb extension elicited by electroshock compared with the relevant control conditions. This suggests that, within the limitations of the current procedures, the anticonvulsant properties of the STN appear to be ineffective against tonic seizures originating in the brainstem.

Most of the previous studies on the effects of pain on Regional Cerebral Blood Flow (rCBF) had been done with brief cutaneous or intramuscular painful stimuli. The aim of the present study was to investigate the effect on rCBF of long lasting tonic experimental muscle pain. To this end we performed PET investigations of rCBF following tonic experimental low back pain induced by continuous intramuscular infusion of hypertonic (5%) saline (HS) with computer controlled infusion pump into the right erector spinae on L(3) level in 19 healthy volunteers. Changes in rCBF were measured with the use of (15)O labelled water during four conditions: Baseline (before start of infusion), Early Pain (4 min after start of infusion), Late Pain (20 min after start of infusion) and Post-Pain (15 min after stop of infusion) conditions. Results of SPM analysis showed relative rCBF increase in the right insula and bilateral decrease in the temporo-parieto-occipital cortex during initial phase of painful stimulation (Early Pain) followed by activation of the medial prefrontal region and bilateral inhibition of insula, anterior cingulate and dorso-lateral prefrontal cortex mainly in ipsilateral hemisphere during Late Pain conditions. The results show that longer lasting tonic experimental muscle pain elicited by i.m infusion of HS results in decreases rather than increases in rCBF. Possible explanations for differences found in rCBF during tonic hypertonic saline-induced experimental muscle pain as compared with previous findings are discussed.

A positron emission tomography imaging study was performed on 16 healthy volunteers to reveal changes in cortical activation during acute muscle pain induced by intra-muscular injection of hypertonic saline into the left triceps brachii muscle. Changes in regional cerebral blood flow (rCBF) were measured with the use of [(15)O] labelled water during 'Rest1', 'Needle' (insertion of a needle without injection), 'Rest2' and 'Pain' conditions. Differences in rCBF were found in the comparison of Pain and Needle, and Pain and Rest2 conditions, revealing activation of the contralateral insula and putamen. The results are discussed with respect to possible differences in brain processing of muscle and cutaneous noxious inputs.

We have tested the hypothesis that agonist and antagonist muscle fatigue could affect the final position of rapid, discrete movements. Six subjects performed consecutive elbow flexion and extension movements between two targets, with their eyes closed prior to, and after fatiguing the elbow extensor muscles. The results demonstrate that elbow extension movements performed in the post-test period systematically undershot the final position as compared to pre-test movements. However, attainment of the aimed final position in elbow flexion movements was unaffected by fatiguing of the extensor muscles. Undershoot of the final position obtained in extension movements was associated with agonist muscle fatigue, a result that was expected from the point of view of current motor control theories, and that could be explained by a reduced ability of the shortening muscle to exert force. On the other hand, the absence of the expected overshoot of the final position when the antagonist is fatigued, indicates the involvement of various reflex and/or central mechanisms operating around the stretched muscle that could contribute to returning the limb to the standard final position after a brief prominent overshoot.

In 1985 Barker and his colleagues (Barker et al., 1985a) produced the first practical magnetic stimulator which, when placed over the skull, was capable of exciting neurons within the human brain. The advance for the study of neural function in intact man was enormous in practical terms because the technique was non-invasive, painless and well tolerated by subjects, even children. In contrast, electrical stimulation via an electrode placed on the skull is quite painful and not well tolerated even by highly motivated subjects such as members of a research team. The application of electrical current to the scalp for stimulation of brain cells is limited by the fact that current flow is attenuated by skin and bone. The intensity of surface current needed to achieve excitation of nerve cells at a depth within the brain needs to be so high that it excites small myelinated axons and unmyelinated axons of free nerve endings in the skin of the scalp and the meninges - hence the pain. The rapidly changing magnetic field produced by a brief current pulse in a wire coil placed over the head is not attenuated by tissues of the head. Although there is a rapid decrease in intensity of the magnetic field with distance from the coil, the magnetic stimulators currently available commercially are able to stimulate neurons within the grey matter of the cerebral cortex but do not appear capable of exciting axons deep within the white matter or nuclei below the cortex.

The aim of this study was to investigate the effects of agonist and antagonist muscle fatigue on the performance of rapid, self-terminating movements. Six subjects performed rapid, consecutive elbow flexion and extension movements between two targets prior to and after fatiguing either the elbow flexor or elbow extensor muscles. The experiments demonstrated consistent results. Agonist muscle fatigue was associated with a decrease in peak velocity and peak deceleration, while a decrease in peak acceleration was particularly prominent. Antagonist muscle fatigue, however, was associated with a decrease in peak deceleration, while a decrease in both the peak velocity and peak acceleration was modest and, in some tests, non-significant. The relative acceleration time (i.e. acceleration time as a proportion of the total movement time) increased when agonists were fatigued, but decreased when antagonists were fatigued. Taken together, these results emphasize the mechanical roles of the agonist and antagonist muscles; namely, the fatigue of each muscle group particularly affected the movement phase in which that group accelerated a limb, while changes of the movement kinematics pattern provided more time for action of the fatigued muscles. In addition, the results presented suggest that agonist muscle fatigue affects movement velocity more than antagonist muscle fatigue, even in movements that demonstrate prominently both mechanical and myoelectric activity of the antagonist muscles, such as rapid, self-terminating movements.

Changes in responses to transcranial magnetic stimulation (TMS) during submaximal isometric voluntary contraction (60% of maximal voluntary contraction (MVC) of the adductor pollicis muscle and the subsequent recovery period have been studied in healthy volunteers. TMS at twice the motor threshold was applied during the sustained contraction, as well as at rest and during short-lasting (2 s) 60% MVCs before and immediately after the sustained contraction, and at 5 min intervals during the recovery period. Both motor evoked potential (MEP) magnitude (peak and area) and silent period (SP) duration in electromyographic activity (EMG) of the adductor pollicis muscle showed a gradual decrease up to the endurance point and an increase thereafter. MEPs elicited at rest immediately after the fatiguing contraction were larger, whereas those elicited later on during the recovery period did not differ significantly from the controls. It is suggested that the changes in responses to TMS, divergent from those in ongoing voluntary EMG during the sustained 60% MVC, indicate complex processes at levels preceding the motor cortex output cells in an attempt to maintain a submaximal contraction of the fatigued muscle. The increase in MEP magnitude after the sustained 60% MVC may indicate residual changes in cortical activity after fatiguing contraction.

Diabetes mellitus is associated with a variety of cardiovascular complications including impaired cardiac muscle function. The effects of insulin treatment on heart rate, body temperature and physical activity in the alloxan (ALX)-induced diabetic rat were investigated using in vivo biotelemetry techniques. The electrocardiogram, physical activity and body temperature were recorded in vivo with a biotelemetry system for 10 days before ALX treatment, for 20 days following administration of ALX (120 mg/kg) and thereafter, for 15 days whilst rats received daily insulin. Heart rate declined rapidly after administration of ALX. Pre-ALX heart rate was 321±9 beats per minute, falling to 285±12 beats per minute 15-20 days after ALX and recovering to 331±10 beats per minute 5-10 days after commencement of insulin. Heart rate variability declined and PQ, QRS and QT intervals were prolonged after administration of ALX. Physical activity and body temperature declined after administration of ALX. Pre-ALX body temperature was 37.6±0.1 °C, falling to 37.3±0.1 °C 15-20 days after ALX and recovering to 37.8±0.1 °C 5-10 days after commencement insulin. ALX-induced diabetes is associated with disturbances in heart rhythm, physical activity and body temperature that are variously affected during insulin treatment.