The field of neuroscience has, after a long period of looking the other way, again embraced emotion as an important research area. Much of the progress has come from studies of fear, and especially fear conditioning. This work has pin- pointed the amygdala as an important component of the system involved in the acqui- sition, storage, and expression of fear memory and has elucidated in detail how stimuli enter, travel through, and exit the amygdala. Some progress has also been made in understanding the cellular and molecular mechanisms that underlie fear conditioning, and recent studies have also shown that the findings from experimental animals apply to the human brain. It is important to remember why this work on emotion succeeded where past efforts failed. It focused on a psychologically well-defined aspect of emo- tion, avoided vague and poorly defined concepts such as "affect," "hedonic tone," or "emotional feelings," and used a simple and straightforward experimental approach. With so much research being done in this area today, it is important that the mistakes of the past not be made again. It is also time to expand from this foundation into broader aspects of mind and behavior

http://gruberpeplab.com/3131/LeDoux_2000_Emotioncircuitbrain.pdf

Emotion Circuits in the Brain

In an attempt to explain how and why some individuals with musculoskeletal pain develop a chronic pain syndrome, Lethem et al. (Lethem J, Slade PD, Troup JDG, Bentley G. Outline of fear-avoidance model of exaggerated pain perceptions. Behav Res Ther 1983; 21: 401-408).ntroduced a so-called 'fear-avoidance' model. The central concept of their model is fear of pain. 'Confrontation' and 'avoidance' are postulated as the two extreme responses to this fear, of which the former leads to the reduction of fear over time. The latter, however, leads to the maintenance or exacerbation of fear, possibly generating a phobic state. In the last decade, an increasing number of investigations have corroborated and refined the fear-avoidance model. The aim of this paper is to review the existing evidence for the mediating role of pain-related fear, and its immediate and long-term consequences in the initiation and maintenance of chronic pain disability. We first highlight possible precursors of pain-related fear including the role negative appraisal of internal and external stimuli, negative affectivity and anxiety sensitivity may play. Subsequently, a number of fear-related processes will be discussed including escape and avoidance behaviors resulting in poor behavioral performance, hypervigilance to internal and external illness information, muscular reactivity, and physical disuse in terms of deconditioning and guarded movement. We also review the available assessment methods for the quantification of pain-related fear and avoidance. Finally, we discuss the implications of the recent findings for the prevention and treatment of chronic musculoskeletal pain. Although there are still a number of unresolved issues which merit future research attention, pain-related fear and avoidance appear to be an essential feature of the development of a chronic problem for a substantial number of patients with musculoskeletal pain.

/pdf/fear-avoidance-and-its-consequences-in-chronic-25jwj42o35.pdf

Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art

&NA; In an attempt to explain how and why some individuals with musculoskeletal pain develop a chronic pain syndrome, Lethem et al.(Lethem J, Slade PD, Troup JDG, Bentley G. Outline of fear‐avoidance model of exaggerated pain perceptions. Behav Res Ther 1983; 21: 401‐408).ntroduced a so‐called ‘fear‐avoidance’ model. The central concept of their model is fear of pain. ‘Confrontation’ and ‘avoidance’ are postulated as the two extreme responses to this fear, of which the former leads to the reduction of fear over time. The latter, however, leads to the maintenance or exacerbation of fear, possibly generating a phobic state. In the last decade, an increasing number of investigations have corroborated and refined the fear‐avoidance model. The aim of this paper is to review the existing evidence for the mediating role of pain‐related fear, and its immediate and long‐term consequences in the initiation and maintenance of chronic pain disability. We first highlight possible precursors of pain‐related fear including the role negative appraisal of internal and external stimuli, negative affectivity and anxiety sensitivity may play. Subsequently, a number of fear‐related processes will be discussed including escape and avoidance behaviors resulting in poor behavioral performance, hypervigilance to internal and external illness information, muscular reactivity, and physical disuse in terms of deconditioning and guarded movement. We also review the available assessment methods for the quantification of pain‐related fear and avoidance. Finally, we discuss the implications of the recent findings for the prevention and treatment of chronic musculoskeletal pain. Although there are still a number of unresolved issues which merit future research attention, pain‐related fear and avoidance appear to be an essential feature of the development of a chronic problem for a substantial number of patients with musculoskeletal pain.

Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art.

Are the Dorsal and Ventral Hippocampus Functionally Distinct Structures

The field of neuroscience has, after a long period of looking the other way, again embraced emotion as an important research area. Much of the progress has come from studies of fear, and especially...

SUMMARYSixty-eight convergent dorsal horn neurones have been recorded at the lumbar level in anaesthetized intact rats. All cells received prominent Aα and C fibre afferents and correspondingly could be activated by high and low threshold stimuli applied to the peripheral excitatory receptive field.

Diffuse noxious inhibitory controls (DNIC). I. Effects on dorsal horn convergent neurones in the rat.

Peripheral and spinal mechanisms of nociception.

(1) Diffuse noxious inhibitory controls (DNIC) were tested for their effect on noxious only, non-noxious and proprioceptive cells in the dorsal horn of the intact anaesthetized rat. Unlike convergent neurones, as described in the previous paper, there was no effect of DNIC on these neurones. It is concluded that convergent neurones are specifically inhibited by DNIC. (2) The effect of DNIC could not be demonstrated for convergent neurones in the spinal animal. Thus the neuronal substrate for DNIC must involve supraspinal structures. (3) Because of the level of firing in convergent neurones induced by hair and touch receptors, presumably constantly and randomly activated in the freely moving animal, a noxious message arriving at higher centres may be partly masked by this background noise. On the basis of the known role of convergent neurones in nociception, we propose the following mechanism which may interpret this paradoxical convergence: two pools of convergent neurones are influenced by a painful peripheral stimulation, one segmental pool being activated whilst the remaining population of cells is inhibited; the "contrast" between the messages from these two pools may well produce a significant pain signalling output from the convergent dorsal horn cells. (4) These results and their theoretical implications are discussed with regard to the concept of the "analgesic system", certain clinical observations and the paradoxical pain relieving effects of counterirritation and some forms of acupuncture.

Diffuse noxious inhibitory controls (DNIC). II. Lack of effect on non-convergent neurones, supraspinal involvement and theoretical implications.

1. Neurons were recorded in the parabrachial (PB) area, located in the dorsolateral region of the pons (with the use of extracellular micropipette), in the anesthetized rat. Parabrachioamygdaloid (PA) neurons (n = 67) were antidromically identified after stimulation in the centralis nucleus of the amygdala (Ce). The axons of these neurons exhibit a very slow conduction velocity, between 0.26 and 1.1 m/s, i.e., in the unmyelinated range. 2. These PA neurons were located in a restricted region of the PB area: the subnuclei external lateral (PBel) and external medial (PBem). A relative somatotopic organization was found in this region. 3. These units were separated into two groups: 1) a group of nociceptive-specific (NS) neurons (69%), which responded exclusively to noxious stimuli, and 2) a group of nonresponsive (NR) neurons (31%). 4. The NS neurons exhibited low or lacked spontaneous activity. They responded exclusively to mechanical (pinch or squeeze) and/or thermal (waterbath or waterjet greater than 44 degrees C) noxious stimuli with a marked and sustained activation with a rapid onset and generally without afterdischarge. Noxious thermal stimuli generally induced a stronger response than the noxious mechanical stimuli. These neurons exhibited a clear capacity to encode thermal stimuli in the noxious range: 1) the stimulus-response function was always positive and monotonic; 2) the slope of the curve progressively increased up to a maximum where it was very steep, then the steepness of the slope decreased close to the maximum response; and 3) the mean threshold was 44.1 +/- 2 degrees C, and the point of steepest slope of the mean curve was around 47 degrees C. 5. The excitatory receptive fields of the NS neurons were large in the majority (70%) of the cases and included several areas of the body. A more marked activation was often obtained from stimuli applied to one part of the body, denoted as the preferential receptive field (PRF). In the other cases (30%), the excitatory receptive field was relatively small (SRF) and restricted to one part of the body (the tail, a paw, a hemiface, or the tongue). Both the PRF and SRF were more often located on the contralateral side. In addition, noxious stimuli applied outside the excitatory receptive field were found to strongly inhibit the responses of NS neurons. 6. All the NS neurons responded to intense transcutaneous electrical stimulation applied to the PRF or SRF with two peaks of activation.(ABSTRACT TRUNCATED AT 400 WORDS)

The spino(trigemino)pontoamygdaloid pathway: electrophysiological evidence for an involvement in pain processes.

The organization of the efferent projections from the pontine parabrachial (pPB) area to the amygdala has been studied in the rat by using microinjections of Phaseolus vulgaris leucoagglutinin (PHA-L), a sensitive and selective anterograde axonal marker, into restricted subregions of the pPB area. The results confirmed that the pPB area primarily projected onto the ipsilateral nucleus centralis of the amygdala (Ce), and to a lesser extent onto the ipsilateral posterior basolateral (BLP), anterior basomedial (BMA), and amygdaloid cortical (ACo) nuclei of the amygdala. Substantial projections were also found in the substantia innominata dorsal/ventral portion of the globus pallidus (SId/GPv), substriatal (SStr), and fondus striatal (FStr) regions which continue the amygdala rostrally. The results demonstrated that the projections of the pPB area onto the Ce were topically organized: 1) The region of the pPB area mainly including the medial subnucleus (pPBm), the waist area (pPBwa), and a thin rostral lamina of the ventral lateral subnucleus (pPBvl) projects primarily to the medial portion of the Ce (CeM). Dense projections were also found in the BLP, BMA, and ACo nuclei of the amygdala, and in the SId/GPv, SStr, and FStr rostral areas. 2) The region of the pPB mainly including the rostral portion of the central lateral subnucleus (pPBcl) and the outer-rostral portion of the external lateral subnucleus (pPBel) projects primarily to the lateral portion of the Ce (CeL). 3) The region of the pPB mainly including the dorsolateral subnucleus (pPBdl), the remaining pPBel, and the external medial (pPBem) subnuclei projects primarily to the lateral capsular portion of the Ce (CeLC) and bilaterally to its rostral portion. Dense projections were also found in the regions which extend the CeLC rostrally and in the SId/GPv, SStr, and FStr rostral areas. The possible role of each of the three parabrachio-amygdaloid pathways described is discussed. It was suggested that the pPB-CeM pathway is mainly implicated in gustatory processes; the pPB-CeL pathway is mainly implicated in visceral and chemosensitive processes; and the pPB-CeLC pathway is mainly implicated in respiratory, cardiovascular, and nociceptive processes.

The organization of the efferent projections from the pontine parabrachial area to the amygdaloid complex: a Phaseolus vulgaris leucoagglutinin (PHA-L) study in the rat.

Jean-Marie Besson

Papers

Diffuse noxious inhibitory controls (DNIC). I. Effects on dorsal horn convergent neurones in the rat.

Peripheral and spinal mechanisms of nociception.

Diffuse noxious inhibitory controls (DNIC). II. Lack of effect on non-convergent neurones, supraspinal involvement and theoretical implications.

The spino(trigemino)pontoamygdaloid pathway: electrophysiological evidence for an involvement in pain processes.

The organization of the efferent projections from the pontine parabrachial area to the amygdaloid complex: a Phaseolus vulgaris leucoagglutinin (PHA-L) study in the rat.