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

As humans, we perceive feelings from our bodies that relate our state of well-being, our energy and stress levels, our mood and disposition. How do we have these feelings? What neural processes do they represent? Recent functional anatomical work has detailed an afferent neural system in primates and in humans that represents all aspects of the physiological condition of the physical body. This system constitutes a representation of 'the material me', and might provide a foundation for subjective feelings, emotion and self-awareness.

How do you feel? Interoception: the sense of the physiological condition of the body.

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

The prevalence and cost of chronic pain is a major physical and mental health care problem in the United States today. As a result, there has been a recent explosion of research on chronic pain, with significant advances in better understanding its etiology, assessment, and treatment. The purpose of the present article is to provide a review of the most noteworthy developments in the field. The biopsychosocial model is now widely accepted as the most heuristic approach to chronic pain. With this model in mind, a review of the basic neuroscience processes of pain (the bio part of biopsychosocial), as well as the psychosocial factors, is presented. This spans research on how psychological and social factors can interact with brain processes to influence health and illness as well as on the development of new technologies, such as brain imaging, that provide new insights into brain-pain mechanisms.

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The Biopsychosocial Approach to Chronic Pain: Scientific Advances and Future Directions

http://www.back-in-business-physiotherapy.com/images/files/DescendingControl.pdf

Descending control of pain.

The present review examines the experimental evidence supporting the existence of central mechanisms able to modulate the synaptic effectiveness of sensory fibers ending in the spinal cord of vertebrates. The first section covers work on the mode of operation and the synaptic mechanisms of presynaptic inhibition, in particular of the presynaptic control involving axo-axonic synapses made by GABAergic interneurons with the terminal arborizations of the afferent fibers. This includes reviewing of the ionic mechanisms involved in the generation of primary afferent depolarization (PAD) by GABAergic synapses, the ultrastructural basis underlying the generation of PAD, the relationship between PAD and presynaptic inhibition, the conduction of action potentials in the terminal arborizations of the afferent fibers, and the modeling of the presynaptic inhibitory synapse. The second section of the review deals with the functional organization of presynaptic inhibition. This includes the segmental and descending presynaptic control of the synaptic effectiveness of group-I and group-II muscle afferents, the evidence dealing with the local character of PAD as well as the differential inhibition of PAD in selected collaterals of individual muscle-spindle afferents by cutaneous and descending inputs. This section also examines observations on the presynaptic modulation of large cutaneous afferents, including the modulation of the synaptic effectiveness of thin myelinated and unmyelinated cutaneous fibers and of visceral afferents, as well as the presynaptic control of the synaptic actions of interneurons and descending tract neurons. The third section deals with the changes in PAD occurring during sleep and fictive locomotion in higher vertebrates and with the changes of presynaptic inhibition in humans during the execution of a variety of voluntary movements. In the final section, we examine the non-synaptic presynaptic modulation of transmitter release, including the possibility that the intraspinal endings of primary afferents also release colocalized peptides in a similar way as in the periphery. The outcome of the studies presently reviewed is that intraspinal terminals of sensory fibers are not hard-wired conductors of the information generated in their peripheral sensory receptors, but dynamic systems that convey information that can be selectively addressed by central mechanisms to specific neuronal targets. This central control of information flow in peripheral afferents appears to play an important role in the generation of integrated movements and processing of sensory information, including nociceptive information.

Presynaptic inhibition in the vertebrate spinal cord revisited.

An acute experimental arthritis was induced in the right knee joint of adult cats anesthetized with chloralose, and the activity of single fine afferent units of the medial articular nerve was recorded from filaments of the saphenous nerve. All units included in this study were sensitive to local mechanical probing of the medial and anteromedial aspects of the knee joint. The units were identified by their conduction velocity as belonging either to group III (2.5-20 m/s, 48 U) or group IV (less than 2.5 m/s, 29 U). After the identification, the resting activity was measured, and the evoked activity was determined using local mechanical stimulation with glass rods and von Frey hairs, and passive movements of the knee joint. The results were compared with those obtained in a similar study of fine articular units from normal joints. Resting activity was observed in 75% of the group III and 83% of the group IV units. The discharges were irregular and often of high frequency. Both the percentages of units with resting activity and the frequencies of their discharges were more than twice as high as in the control sample. Nearly all units from inflamed joints had low threshold to movements (group III 89%, group IV 72%), and most units responded well to flexion and extension. In contrast, in units from normal joints only 33% of the group III and 10% of the group IV units responded well to passive movements in the normal working range of the joint. In inflamed as well as in normal joints the responses were mostly tonic in character and adapted slowly or not at all when the joint was held in a new position. In normal joints 24% of the group III and 36.5% of the group IV afferent units with local mechanosensitive receptive fields could not be excited by any physiological or noxious joint movements. Such units were only very occasionally seen in the present sample. The average number of receptive fields per unit found in inflamed joints exceeded considerably that in normal units, but no systematic drop in von Frey thresholds was seen when comparing the control sample with the inflamed one. From the above data we conclude that an acute inflammation sensitizes many fine articular units, making them active at rest and increasing the responsiveness more readily to normally innocuous joint movements. Both nociceptors and units with low threshold to movement seem to become sensitized by the inflammation.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of an experimental arthritis on the sensory properties of fine articular afferent units.

1. In 37 cats anesthetized with alpha-chloralose recordings were made from single-afferent units of the medial articular nerve (MAN) of the right knee joint. First the mechanosensitivity of such units was characterized while the joint was in normal condition. Thereafter, keeping the afferents under continuous observation, an experimental arthritis was induced by injecting kaolin and carrageenan into the joint cavity. The effects of the developing arthritis including the time course of the changes were studied on low- and high-threshold units and on afferents that had no mechanosensitivity in the normal joint. 2. The arthritis increased the mechanosensitivity in the majority of the low-threshold units, i.e., in units that responded already in the normal joint to movements in the working range. Enhanced responses to movements were found for 12 of 16 thick myelinated group II, 10 of 10 fine myelinated group III, and 1 of 3 unmyelinated group IV afferents. The augmentation of reactions developed in most cases within the first hour after the injection of the inflammatory compounds, sometimes starting immediately after the injection. A further rise of the mechanosensitivity was observed within the following 2-4 h. In most group III units enhanced responses for movements were accompanied by an induction or increase of resting discharges. In 1 group II and 1 group IV unit spontaneous activity developed in the absence of any change of movement-sensitivity. 3. The inflammation led to enhanced mechanosensitivity in high-threshold afferents, i.e., in units that responded in the normal joint only to noxious movements exceeding the working range of the knee. One group II, 10 of 12 group III, and 5 of 10 group IV units of this type became responsive to movements in the working range during development of arthritis, in most cases within the second to third hour after induction of inflammation with a further increase later on. In a high proportion of these units resting activity was induced too. Few high-threshold units developed spontaneous discharges but no responses to movements in the working range. The time course for development of resting activity was similar to that for lowering of the mechanical threshold. 4. The experimental arthritis induced afferent activity in 1 of 2 group III and 10 of 14 group IV units that in the normal joint were unresponsive to local mechanical stimulation and to innocuous/noxious movements (but responsive to a bolus of a KCl-solution applied intraarterially close to the joint).(ABSTRACT TRUNCATED AT 400 WORDS)

Time course of mechanosensitivity changes in articular afferents during a developing experimental arthritis.

1. In cats anaesthetized with alpha-chloralose extracellular recordings were made from fine afferent units belonging to the medial articular nerve of the knee joint. The excitatory and sensitizing effects on articular afferents of prostaglandin E2 (PGE2) applied intra-arterially close to the joint were examined. 2. Bolus injections of PGE2 doses of 0.03-30 micrograms excited about 60% of both the group III (conduction velocity 2.5-20 m/s) and the group IV units (conduction velocity less than 2.5 m/s). The duration and size of the responses were dose dependent consisting in most cases of low-frequency discharges which lasted up to several minutes. Excitation was found among afferents with low and high mechanosensitivity. 3. Among the group III units PGE2 sensitized 64% for their responses to movements and 50% for their responses to bradykinin (applied intra-arterially close to the joint). Sensitization did not depend on the mechanical threshold previous to chemical stimulation. Among the group IV units PGE2 sensitized only 25% for their responses to movements but 75% for their reactions to bradykinin. In group IV fibres a low mechanical threshold predisposed for sensitization to movements and a higher threshold for sensitization to bradykinin. 4. Some units were sensitized and excited, others were either sensitized or excited and some units were not affected by PGE2. We conclude that PGE2 induces in a large proportion of fine articular afferents of normal joints discharges which are similar to those induced by an experimental inflammation. Thus PGE2 may be an inflammatory mediator which has a major role in the generation of the afferent activity developing in the course of an arthritis.

Excitation and sensitization of fine articular afferents from cat's knee joint by prostaglandin E2.

The sections in this article are:


1
Afferent Fibers from Skeletal Muscle and Their Receptors
1.1
Composition of Muscle Nerves

1.2
Muscle Spindles and Golgi Tendon Organs

1.3
Receptive Properties of Group III and Group IV Afferent Fibers




2
Central Pathways for Cardiovascular Reflexes from Skeletal Muscle Receptors
2.1
Spinal Termination of Primary Muscle Afferents

2.2
Central Pathways Arising From Myelinated Primary Muscle Afferents

2.3
Central Pathways Arising From Unmyelinated Primary Muscle Afferents

2.4
Ascending and Descending Spinal Pathways Involved in Cardiovascular Reflex Control From Skeletal Muscle




3
Organization of Efferent Outflow in Pre- and Postganglionic Neurons

4
Cardiovascular Responses from Skeletal Muscle Receptors
4.1
Effect of Activation of Afferent Fibers

4.2
Effect of Induced Muscular Contraction (Simulated Exercise)




5
Interaction of Muscle Afferents with Other Cardiovascular Reflexes
5.1
Arterial Baroreceptors

5.2
Cardiopulmonary Vagal Afferents




6
Role of Skeletal Muscle Afferents in Cardiovascular Response to Exercise in Humans
6.1
Dynamic and Static Exercise

6.2
Central Control (Central Command)

6.3
Peripheral Control

6.4
Integration of Neural Control Mechanisms During Exercise




7
Conclusion

Robert F. Schmidt

Papers

Presynaptic inhibition in the vertebrate spinal cord revisited.

Effects of an experimental arthritis on the sensory properties of fine articular afferent units.

Time course of mechanosensitivity changes in articular afferents during a developing experimental arthritis.

Excitation and sensitization of fine articular afferents from cat's knee joint by prostaglandin E2.

Cardiovascular Reflex Control by Afferent Fibers from Skeletal Muscle Receptors