Articles describing motor function in five chronic musculoskeletal pain conditions (temporomandibular disorders, muscle tension headache, fibromyalgia, chronic lower back pain, and postexercise muscle soreness) were reviewed. It was concluded that the data do not support the commonly held view that the pain of these conditions is maintained by some form of tonic muscular hyperactivity. Instead, it seems clear that in these conditions the activity of agonist muscles is often reduced by pain, even when this does not arise from the muscle itself. On the other hand, pain causes small increases in the level of activity of the antagonist. As a consequence of these changes, force production and the range and velocity of movement of the affected body part are often reduced. To explain how such changes in the behaviour come about, we propose a neurophysiological model based on the phasic modulation of excitatory and inhibitory interneurons supplied by high-threshold sensory afferents. We suggest that the "dysfunction" that is characteristic of several types of chronic musculoskeletal pain is a normal protective adaptation and is not a cause of pain.

The Golgi silver impregnation technique gives detailed information on neuronal morphology of the few neurons it labels, whereas the majority remain unstained. In contrast, the Nissl staining technique allows for consistent labeling of the whole neuronal population but gives very limited information on neuronal morphology. Most studies characterizing neuronal cell types in the context of their distribution within the tissue slice tend to use the Golgi silver impregnation technique for neuronal morphology followed by deimpregnation as a prerequisite for showing that neuron's histological location by subsequent Nissl staining. Here, we describe a rapid method combining Golgi silver impregnation with cresyl violet staining that provides a useful and simple approach to combining cellular morphology with cytoarchitecture without the need for deimpregnating the tissue. Our method allowed us to identify neurons of the facial nucleus and the supratrigeminal nucleus, as well as assessing cellular distribution within layers of the dorsal cochlear nucleus. With this method, we also have been able to directly compare morphological characteristics of neuronal somata at the dorsal cochlear nucleus when labeled with cresyl violet with those obtained with the Golgi method, and we found that cresyl violet-labeled cell bodies appear smaller at high cellular densities. Our observation suggests that cresyl violet staining is inadequate to quantify differences in soma sizes.

1. The aim of these experiments was to examine the physiological properties and patterns of firing of trigeminal interneurons during fictive mastication in anesthetized and paralyzed rabbits. Antidromic stimulation was used to show that the 82 interneurons projected to the area of the contralateral fifth nerve motor nucleus (NVmot). 2. Straight-line conduction velocities calculated from stereotaxic coordinates of the stimulating and recording electrodes for 63 interneurons were found to range between 3.7 and 16.3 m/s (mean, 9.5 m/s). 3. Histological reconstructions of recording electrode tracks showed that the interneurons observed in this study were located in the lateral brain stem in or just medial to the rostral trigeminal sensory nuclei, including the intertrigeminal (NVint) and supratrigeminal (NVs) areas, the main sensory nucleus of the fifth nerve (NVsnpr), the rostral subdivision of the oral nucleus of the spinal trigeminal tract (NVor tau), and the rostral part of the parvocellular reticular nucleus (NRpc alpha). 4. Forty-six interneurons were shown to have low-threshold (LT) peripheral receptive fields, and 41 of these (88%) were in the oral cavity. Most of the responses were rapidly adapting. 5. Twenty-eight interneurons changed their pattern of firing during cortically induced fictive mastication. The discharge frequency of 20 neurons varied in phase with the fictive masticatory motor output, which was recorded from central ends of cut hypoglossal nerves (XII) and/or from the NVmot. Others were briefly excited and then inhibited (n = 2), only inhibited (n = 4), or tonically excited during fictive mastication (n = 2). Fifteen others were unaffected by this test. 6. It was found that the rhythmically active neurons could be further subdivided into two categories: those receiving short-latency excitatory input from the masticatory area of the cortex (n = 11) and those that did not (n = 9). No obvious differences in peripheral receptive fields for neurons in these categories were found. 7. We suggest that these phasically active premotor neurons are part of the circuitry generating the rhythmic masticatory pattern, specifically those that directly control the bursts of firing of the trigeminal motoneurons (burst generators, BGs). Their properties allow them to integrate sensory information and descending commands with the masticatory rhythm that is probably generated in midline brainstem reticular nuclei.

SUMMARY1. The fluorescent compound Lucifer Yellow was injected into the somata of nine identified jaw-elevator muscle spindle afferents, located in the V mesencephalic nucleus. Reconstructions of the central course of their axons were subsequently made from serial, transverse, sections to identify sites of projection.2. Three sites of termination were identified on the basis of collaterals that ended in varicosities and/or boutons. All afferents projected to the V nucleus oralis and, all but one, also to the V motor nucleus. Two out of nine afferents had terminations in the supra-trigeminal nucleus, though a further four appeared to send collaterals to this area.3. The relative density of projection, judged by the number of collaterals supplied to each area, decreased in the order: V nucleus oralis, V motor nucleus and supra-trigeminal nucleus. The central course of the afferent axons was such that impulses from the periphery would arrive first at the V motor nucleus, then the V nucleus oralis, the supra-trigeminal nucleus, and finally the afferent somata in the V mesencephalic nucleus. 4. In animals in which the masseter nerve was exposed in-continuity for electrical stimulation, electrophysiological recordings were made in the three areas described above to identify units that received a monoysnaptic input from spindles in the masseter muscle.5. Criteria were formulated on the basis of the pattern of responses on stimulation of the masseter nerve, and the morphology of labelled neurones, for differentiating between afferents, interneurones, and motoneurones.6. In the V motor nucleus, monosynaptic excitatory post-synaptic potentials (e.p.s.p.s) were obtained in both synergist and masseter motoneurones. These were assumed to arise from a masseter muscle spindle input as the thresholds for exciting such afferents and eliciting e.p.s.p.s were similar. Some interneurones, chiefly in the V nucleus oralis, were activated at thresholds close to that of muscle spindle afferents and could also fire in response to muscle stretch. As their latencies (measured Present addresses:

Single jaw-muscle spindle afferent axons were characterized physiologically and intracellularly stained to determine whether particular physiological types of spindle afferent show distinctive morphologies. Microelectrodes filled with either horseradish peroxidase (HRP) or biotinamide (Neurobiotin) were advanced into the mesencephalic trigeminal nucleus (Vme) in anesthetized rats. Intracellular recordings then were characterized by their response: to palpation of the jaw muscles; when pressure was applied to the teeth and during passive ramp and hold and sinusoidal jaw movement. Seventy-one afferents were characterized physiologically and injected with HRP; an additional 61 afferents were typed and injected with biotinamide. The response of 43 stained neurons was recorded in the presence of suxamethonium. The major projection areas of these afferents were the: trigeminal motor nucleus (Vmo); region dorsal to Vmo; reticular formation, spinal trigeminal nucleus, superior cerebellar peduncle and Vme. One afferent type was modulated strongly during stretching of the jaw-elevator muscles. Based on their high sensitivity during stretching of the jaw muscles and/or their silencing during the release phase of muscle stretch, these afferents were classified as primary-like spindle afferents. These afferents projected most strongly to Vmo. A second type of afferent was modulated only modestly during stretching of the jaw-elevator muscles. These tonic afferents were classified as secondary-like spindle afferents because of their low dynamic sensitivity during ramp muscle stretch and their continued discharge during the release phase of muscle stretch. Secondary-like afferents projected most strongly to the region dorsal to Vmo. Boutons (n = 3,834) from 11 afferents were studied in detail. Secondary-like afferents had statistically larger boutons within Vmo. In both secondary- and primary-like spindle afferents, only a small number of boutons were associated closely with the somata and proximal dendrites of trigeminal motoneurons. In these cases, however, two to five boutons appeared to contact individual motoneurons, implying multiple monosynaptic inputs to a selective subset of jaw-elevator motoneurons. Some "giant" boutons were present dorsal to Vmo and in Vme. These results demonstrate that dynamically sensitive and nondynamically sensitive jaw-elevator muscle spindle afferents project preferentially to different regions. Primary-like spindle afferents are capable of providing feedback related to the dynamic phases of muscle stretch and project most heavily to Vmo. Secondary-like spindle afferents can transmit a feedback signal associated with muscle length and project most strongly to the supratrigeminal region. Both types of afferent have projections caudal to Vmo that may serve longer latency jaw-muscle stretch reflexes and/or the projection of proprioceptive information to the thalamus and cerebellum.