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.

Tracking small sensory nerve action potentials in human axonal excitability studies.

The supraspinal control of the tonic vibration reflex.

Case report DR J. D. MACKIE: A 37-year-old white man was admitted for a renal transplant on August 21, 1984. He had developedinsulin-dependentdiabetes mellitus at the age of 14 years. In 1980, renal impairment was first documented and a renal biopsy at that time showeddiffuse nodular diabetic glomerulosclerosis. He also had retinopathy, smallvessel peripheral vascular disease and peripheral neuropathy. Haemodialysis was commenced on July 15, 1983 by means of an arteriovenous fistula in the left arm. In the month before transplantation his diabetic control had been poor in spite of the monitoring of blood-glucose levels at home and regular readjustment of his insulin dosage. Two weeks before admission to hospital he developedan upper respiratory tract infection that was followed by vomiting and diarrhoea. All symptoms had settled at the time of his admission to hospital. Examination revealed a healthy looking man with a pulse rate of 70 beats/min and a blood pressure of 105/80 mmHg; his temperature was 36.7 °C and his weight was 88 kg. A soft systolic ejection murmur was present at the cardiac apex and the apical impulse was palpable in the anterior axillary line; these abnormalities had been observed previously. There were no signs of fluid overload. The patient was blind in the right eye and tunnel vision was present in the left eye. A sensory peripheral neuropathy, in a glove-and-stocking distribution, was present in the lower limbs. Initial investigations showed: normal serum sodium level, 130 mmollL; normal serum potassium level, 4.0 mmollL; normal serum chloride level, 95 mmollL; normal serum bicarbonate level, 23 mmollL; blood urea level, 28 mmollL (normal, 2.8-7.8 mmoIlL); serum creatinine level, 930 IlmollL (normal, 65-115 IlmoIlL); and a normal serum albumin level, 37 giL. Total haemoglobin concentration was 68 gil (normochromic, normocytic picture; normal,

David Burke

Papers

Tracking small sensory nerve action potentials in human axonal excitability studies.

The supraspinal control of the tonic vibration reflex.

An unusual infection after renal transplantation.

Excitability of sensory axons in amyotrophic lateral sclerosis.

The Circuitry of the Human Spinal Cord: Recurrent inhibition