[Specifications of motivational interviewing within a cognitive-behavioral therapy of chronic pain]. / Spécificités de l'entretien motivationnel dans le cadre d'une prise en charge cognitivo-comportementale de la douleur chronique.

OBJECTIVES: Cognitive and behavioral approach of chronic pain presents encouraging results by improving physical, functional and psychological states of chronic pain patients. This specific treatment is partially based on the acquisition of new adaptive strategies to help the patients to manage more effectively chronic pain and to improve subsequently their subjective well-being. This requires in parallel to give up noxious emotional, cognitive and behavioral attitudes towards pain. Now, we have to admit that numerous therapeutic failures are directly imputable to difficulties introducing and making the indispensable changes continue in pursuit of the fixed therapeutic objectives. Readiness to change could play a considerable role in the success or not of chronic pain treatment. The main objective of this article is to present the data of the current literature concerning the specificities of the process of change in the field of the chronic pain. METHODS: We present a review of the literature describing at first, the psychological progress made by chronic pain patients longing to manage their suffering better via the trans-theoretical model of intentional change. Secondly, we develop the contributions of the technique of motivational interviewing in the improvement of chronic pain treatment. DISCUSSION: The identification of the motivational profile of chronic pain patients will determine how motivational interviewing can be conducted to improve their readiness for change. There are several strategies used with chronic pain patients in pre-contemplative and contemplative stages. Therapists may facilitate the problem recognition (help chronic pain patients to become aware of and identify the nature of the difficulties they face when trying to cope with their physical suffering); increase the personal concern (empowering chronic pain patients so that they feel fully involved in what they offer and invest in the therapy); develop the intention of change (ensure that the change becomes truly intentional); cultivate optimism (to help chronic pain patients to consider the present situation as being less desperate than it seems); ask open-ended questions (the direct questioning can be used to specify a request or reveal ambivalence about change); present personal feedback (the therapist provides the patient with a maximum of information that may help to appreciate the true value of the effectiveness of their current management of pain); review consequences of change versus non-change (to review the plausible positive (pros) and negative (cons) consequences of change); and summarizing (to summarize the key points discussed during the interview). In the active stage, therapists may use other strategies like: developing a plan for change (to suggest the adoption of certain coping strategies with pain); providing information advice (provide information advice in order to help chronic pain patients to determine how they will take concrete steps to initiate change); and using a change plan worksheet (help chronic pain patients to develop a synthetic view of the change process they will undertake). CONCLUSION: The various strategies discussed in this article are intended to accompany chronic pain patients to a process of change to help them consider a fundamental change in their ways of managing pain, when they are insufficient, ineffective and/or unintentionally aggravating their situation. It is important to help chronic pain patients to become aware of the nature of the adaptive problems they face, but also opportunities for change that are offered in order to encourage them to manage more efficiently and more autonomously their physical and mental suffering. In this context of openness to change, motivational interviewing can be an invaluable help to build a good therapeutic alliance in order to maximize the impact of supported global and multidimensional chronic pain by including a cognitive-behavioral approach for example.

Familial prion disease in a Hungarian family with a novel 144-base pair insertion in the prion protein gene.

About 15% of human prion diseases are inherited, and are associated with point or insertional mutations of the prion protein gene (PRNP). Four families with six octapeptide repeat insertions (OPRI) in the PRNP gene have been described in the literature so far. Here we report two cases in a Hungarian family with a new six OPRI (R1R2R2R3R2R3gR3R2R2R3R4) in the PRNP gene. The clinical features (progressive ataxia, dementia and anosmia), the age of onset and the duration of disease were almost identical. In addition to the cerebellar and parahippocampal pathological changes already described, we also found deposits of pathological prion protein in the olfactory system.

Noninvasive continuous arterial pressure measurements in the assessment of acute, severe central hypovolemia.

UNLABELLED: Acute, severe hypovolemia is a medical emergency. Traditional vital sign parameters allow no optimal triage. High predictive power of finger plethysmography-based stroke volume (SV) and pulse pressure (PP) was recently suggested. To assess the performance of the PP and SV parameters, lower body negative pressure of -40 mmHg, than -60 mmHg - corresponding to moderate and severe central hypovolemia - was applied in 22 healthy males (age 35 ± 7 years). Slow breathing induced fluctuations in the above indices, characterized by stroke volume variability (SVV), and pulse pressure variability (PPV), were assessed. Responses in heart rate (HR) and shock index (SI) were also studied. Discriminative capacity of these parameters was characterized by the area under the ROC (receiver operating characteristic) curves (AUC). RESULTS: In comparison of baseline to severe central hypovolemia SV, PP, HR, and SI showed good discriminating capacity (AUC 99%, 88%, 87%, and 93%, respectively). The discriminating capacity of SVV and PPV was poor (77% and 70%, respectively). In comparison of moderate and severe hypovolemia, the discriminating capacity of the studied parameters was uniformly limited. CONCLUSIONS: Plethysmography-based SV and PP parameters can be used to detect acute severe volume loss. Sensitive parameters discriminating moderate and severe central hypovolemia are still lacking.

Haemodynamic parameters and cognitive function during modeled acute volume loss.

PURPOSE: The purpose of the present study was to find a noninvasive way of detecting even smaller volume loss which is easier to carry out and possibly more precise than the currently used (mostly sphygmomanometer-based) methods. Haemodynamic and EEG measurements were carried out in simulated volume loss, involving blood donation and orthostatic challenges to assess adaptive responses and cognitive performance. Cognitive performance was assessed in an oddball task and changes of the evoked potential P300 were analyzed. Both haemodynamic and cognitive parameters were recorded in 'pre-donation' and 'post-donation' conditions for purposes of comparison. RESULTS: Cognitive performance (as reflected by P300 changes) was found to be a poor marker of volume loss. Difference between the two conditions in none of the parameters reached the level of statistical significance (defined as p < 0.05) RR mean, baroreceptor sensitivity and pulse pressure were rather sensitive to the relatively mild volume loss (p < 0.01 between pre- and post-conditions). CONCLUSION: Our study indicates that traditional sphygmomanometer based values can safely be replaced by values yielded by finger plethysmography, combined with brief orthostatic challenges and that P300 as a cognitive marker cannot be used to assess volume loss.

Effects of eletriptan on the peptidergic innervation of the cerebral dura mater and trigeminal ganglion, and on the expression of c-fos and c-jun in the trigeminal complex of the rat in an experimental migraine model.

Nociceptive axons and terminals in the supratentorial cerebral dura mater display an intense calcitonin gene-related peptide (CGRP) immunoreactivity. In an experimental migraine model, it has been shown that electrical stimulation of the rat trigeminal ganglion induced an increase in the lengths of CGRP-immunoreactive axons, increased size and number of pleomorphic axonal varicosities in the dura mater, and an increased number of c-jun and c-fos protein-expressing nerve cells in the trigeminal complex. We demonstrate the effect of the highly specific and moderately lipophilic serotonin agonist eletriptan (Pfizer) which prevents the effects of electrical stimulation in the dura mater. Eletriptan also affected the caudal trigeminal complex; it markedly reduced the numbers of the oncoprotein-expressing cells, mainly after stimulation and to some extent also in nonstimulated animals. Eletriptan also affected expression of CGRP in perikarya of trigeminal ganglion cells, insofar as the number of small nerve cells exhibiting a compact CGRP immunoreaction was decreased to one quarter of the original value. In all these respects, eletriptan acted in a similar way to sumatriptan, with the notable exception that eletriptan also blocked the stimulation-induced effects in the nucleus caudalis trigemini and the upper cervical spinal cord (trigeminal complex), whereas sumatriptan did not. It is concluded that eletriptan, acting on perikarya and both the peripheral and the central axon terminals of primary sensory neurons, exerts its antimigraine effect by an agonist action on 5-HT1B/1D receptors throughout the entire trigeminal system, probably by passing the blood-brain-barrier because of its lipophilic character.

Infraterminal spreading and extrajunctional expression of nicotinic acetylcholine receptors in denervated rat skeletal muscle.

Through the use of biotinylated-bungarotoxin and monoclonal antibodies, the nicotinic acetylcholine receptor (nAChR) was localized in the subneural apparatus of mammalian motor end plates of the flexor digitorum brevis muscle of the adult rat at the light and electron microscopic levels. Under normal conditions, nAChR was located in the primary post-synaptic membrane of the neuromuscular junction, and the depths of the junctional folds constituting the secondary post-synaptic membrane did not contain any nAChR. Up to 75 days after repeated transection of the related motor nerve (sciatic), there was no major alteration in the light-microscopic localization of junctional nAChR in the subneural apparatus, except for a moderate shrinkage and increased immunocytochemical reactivity of the subneural apparatus. At the electron microscopic level, however, immunocytochemical reactivity gradually occupied the entire extent of the secondary post-synaptic membrane, including the depths of the junctional folds, which exhibited extensive branching. In non-innervated portions of the muscle fibers, nAChR receptor appeared in a linear localization on the surfaces of denervated muscle fibers. This linear reaction was not continuous with the nAChR reaction of the motor end plates. It is concluded that denervation supersensitivity might not be due to spreading of junctional nAChR from the end-plate area, but rather to expression of nAChR in non-innervated portions of the muscle fiber and to the infraterminal (subsynaptic) spreading of nAChR into the depths of junctional folds.