Co-Planar Stereotaxic Atlas of the Human Brain—3-Dimensional Proportional System: An Approach to Cerebral Imaging, J. Talairach, P. Tournoux. Georg Thieme Verlag, New York (1988), 122 pp., 130 figs. DM 268

I have developed "tennis elbow" from lugging this book around the past four weeks, but it is worth the pain, the effort, and the aspirin. It is also worth the (relatively speaking) bargain price. Including appendixes, this book contains 894 pages of text. The entire panorama of the neural sciences is surveyed and examined, and it is comprehensive in its scope, from genomes to social behaviors. The editors explicitly state that the book is designed as "an introductory text for students of biology, behavior, and medicine," but it is hard to imagine any audience, interested in any fragment of neuroscience at any level of sophistication, that would not enjoy this book. The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or

Principles of Neural Science

Components of heart rate variability have attracted considerable attention in psychology and medicine and have become important dependent measures in psychophysiology and behavioral medicine. Quantification and interpretation of heart rate variability, however, remain complex issues and are fraught with pitfalls. The present report (a) examines the physiological origins and mechanisms of heart rate variability, (b) considers quantitative approaches to measurement, and (c) highlights important caveats in the interpretation of heart rate variability. Summary guidelines for research in this area are outlined, and suggestions and prospects for future developments are considered.

https://www.onlinelibrary.wiley.com/doi/epdf/10.1111/j.1469-8986.1997.tb02140.x

Heart rate variability: Origins, methods, and interpretive caveats

Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for “central” fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal cha...

Spinal and Supraspinal Factors in Human Muscle Fatigue

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

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1993.sp019912

Corticocortical inhibition in human motor cortex.

1. Multi-unit and single-unit recordings were made of muscle spindle afferent activity from the pretibial muscles of human subjects who were initially relaxed. The muscles were subjected to a stretching perturbation of 1 s duration, occurring irregularly, on average once every 5 s. In test sequences, an auditory or visual warning was provided 1 . 06 s before some of the perturbations. Subjects were required to oppose every perturbation by contracting the receptor-bearing muscle as rapidly as possible. 2. Following the warning all subjects sometimes tensed the receptor-bearing muscle unintentionally in preparation for the perturbation. In these contractions, the discharge of a spindle ending accelerated only if the contraction strength exceeded the ending's threshold for activation, established in control voluntary contractions performed under isometric conditions. 3. When the receptor-bearing muscle did not contract in the interval between warning and perturbation, there was no detectable change in the multi-unit recordings of spindle activity or in recordings from twelve of thirteen single spindle afferents. The thirteenth spindle afferent discharged prior to the perturbation in the absence of detectable e.m.g. in response to (only) three of twenty-three warning stimuli. However, this ending had been so responsive during isometric voluntary contractions that a contraction level at which it did not respond could not be established, and it is suggested that the findings with this ending resulted from its low threshold rather than from selective activation of the fusimotor system. 4. When subjects were warned of the perturbations, the dynamic response of spindle endings to the perturbations was not increased in size or altered in latency. 5. The motor response to perturbations without warning generally contained only long-latency (volitional) e.m.g. activity occurring 107--200 ms after the onset of the perturbation. When a warning was given, short-latency (reflex) e.m.g. activity was also recorded, beginning 46--76 ms after the onset of the perturbation. 6. It is concluded that anticipation of the need to contract a muscle does not result in selective activation of fusimotor neurones in preparation for the contraction. The change in stretch reflex gain that occurs as a result of ‘anticipation’ occurs through a central process which does not involve the fusimotor system.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1980.sp013400

Anticipation and fusimotor activity in preparation for a voluntary contraction.

This study was undertaken to compare the excitability changes of sensory and motor axons during hyperventilation and ischaemia, and to determine why ectopic impulse activity develops more readily during hyperventilation, and in sensory fibres. During hyperventilation for 20 min, all six subjects reported paraesthesiae in the hand and face, and four out of the six developed muscle twitching and cramps, associated with significant decreases of 20-30% in the threshold current required to produce sensory and motor potentials of constant size. During ischaemia four out of the six subjects reported paraesthesiae, but none reported muscle twitching. There were significant decreases of 15-20% in threshold for sensory and motor fibres. Ischaemia produced a marked decrease in supernormality, an increase in refractoriness and an increase in latency of the test compound sensory or motor potential, changes that were not seen with hyperventilation. The decrease in threshold during these manoeuvres was associated with a significant increase in strength--duration time constant (tau SD), indicating a relatively greater decrease in rheobase current. Using the technique of latent addition, we found that the changes in tau SD were consistent with a recently proposed model in which non-inactivating, voltage-dependent 'threshold channels' (presumably persistent Na+ channels) are active at resting potential. The failure of hyperventilation to alter conduction velocity, refractoriness or supernormality appreciably indicates that, unlike ischaemic depolarization, hyperventilation does not increase inactivation of conventional Na+ channels or activation of K+ channels, and this implies that the hyperventilation-induced increase in excitability is not the result of conventional depolarization, as seems to occur during ischaemia. These results suggest that hyperventilation has a rather selective action on the threshold channels, and they help to explain its greater effectiveness compared with ischaemia in provoking ectopic discharges. The greater expression of threshold channels in sensory than in motor fibres can explain why hyperventilation induces paraesthesiae before fasciculation and why only paraesthesiae occur during ischaemia.

/pdf/excitability-changes-in-human-sensory-and-motor-axons-during-5dei69ylfq.pdf

David Burke

Papers

Anticipation and fusimotor activity in preparation for a voluntary contraction.

Excitability changes in human sensory and motor axons during hyperventilation and ischaemia.

The response to muscle stretch and shortening in parkinsonian rigidity

Cutaneous and muscle afferent components of the cerebral potential evoked by electrical stimulation of human peripheral nerves.

Are spinal “presynaptic” inhibitory mechanisms suppressed in spasticity?☆