1,721,118 research outputs found

    Pain stress and headache

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    The association between pain and stress is an old one, but still it is not really clear who comes first. Pain induces stress, and stress induces pain. Pain is part of our homeostatic system and in this way is an emotion, i.e., it tells us that something is out-of-order (control), and emotion drives our behavior and one behavior is stress response. Stress comes from ourselves: the imagination we have or would like to have of us, from the image others give of us, from the goals we assume it is necessary to reach for our well-being or the goals others want us to fulfill. Stress comes from our social condition and the condition we would like, stress comes from dangerous situations we cannot control. Headache easily fits in the picture

    Is migraine a disorder of the central nervous system?

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    The chicken and the egg problem is how, in Italian or in English, some time ago one would have referred to a question as the one to be approached here: "Is migraine a disorder of the central nervous system?" or of the peripheral nervous system? Till some time ago, even an honest basic scientist or clinician could almost equally sustain one or the other origin and find data that substantiate her/his opinion. Nowadays, however, our improved knowledge is pushing in the direction of the central nervous system, although many mechanisms remain unclear. The confusion originates from the important role played by multiple and important bidirectional interactions between the peripheral and the central nervous systems, i.e., the trigeminovascular system and the cerebral cortex. The problems are: Who starts first? Who is not working properly? It appears now that the answer to the question has to be probably searched in the delicate balance present in the central nervous system between excitatory and inhibitory circuits, their adaptation to chronic stimuli and, within these circuits, the balance of neurotransmitters, neuromodulators, transporters and ion channels that keeps them well functioning

    Pain emotion and homeostasis

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    Pain has always been considered as part of a defensive strategy, whose specific role is to signal an immediate, active danger. This definition partially fits acute pain, but certainly not chronic pain, that is maintained also in the absence of an active noxa or danger and that nowadays is considered a disease by itself. Moreover, acute pain is not only an automatic alerting system, but its severity and characteristics can change depending on the surrounding environment. The affective, emotional components of pain have been and are the object of extensive attention and research by psychologists, philosophers, physiologists and also pharmacologists. Pain itself can be considered to share the same genesis as emotions and as a specific emotion in contributing to the maintenance of the homeostasis of each unique subject. Interestingly, this role of pain reaches its maximal development in the human; some even argue that it is specific for the human primate

    Le neuroscienze e la libertà del volere

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    In the last 30 years, neurosciences, with their mechanistic approach, have dealt with the study of freedom of the will, a field that is considered typical of philosophy or psychology. The studies in neurosciences have been paradoxically appreciated more by philosophers and psychologists than by the scientists themselves, who have straightened the methodological limits. From the considerations of those limits, coming precisely from the neurosciences themselves, rises an interpretation of the freedom of the will that throws a bridge towards positions that are considered typical of philosophical and psychological theories.   </p

    Pain, emotion, headache

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    Pain has been considered as part of a defensive strategy whose specific role is to signal an immediate active danger to the organism. This definition fits well for acute pain. It does not work well, however, for chronic pain that is maintained even in absence of an ongoing, active threat. Currently, acute and chronic pain are considered to be separate conditions. What follows is a review of the different theories about pain and its history. Different hypotheses regarding pain mechanisms are illustrated. New data emerging from scientific research on chronic pain (migraine in particular) involving innovative imaging techniques are reported and discussed

    Dissociation of tolerance and dependence to morphine: A possible role for cholecystokinin

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    Since cholecystokinin (CCK) has been suggested to be an endogenous opiate antagonist, we tried to evaluate if this peptide could be involved in the development of tolerance to morphine. Naive rats were chronically administered morphine, either alone or concomitantly with proglumide or benzotript, two putative CCK receptor antagonists. Chronic treatments with both CCK antagonists alone were also established. Drugs were administered by the oral route, dissolved in the drinking water. At the end of the chronic treatments, the development of tolerance to morphine was assessed by an evaluation of the analgesic responses evoked by graded doses of acutely injected morphine in the tail-flick and hot plate tests. Proglumide and benzotript were able to inhibit the shift to the right of the dose-response curve for morphine, i.e. they prevented the development of tolerance to morphine-induced analgesia. Chronically given alone, the two CCK antagonists never modified the responses to the acute challenge with morphine. We also determined the development of physical dependence by looking at the withdrawal syndrome precipitated by graded doses of acutely injected naloxone. In these experiments the concomitant treatment with morphine and proglumide or benzotript did not modify the occurrence of dependence. These observations are consistent with the hypothesis of CCK being an endogenous opiate antagonist, involved in the development of tolerance to morphine-induced analgesia but not of dependence. Moreover, tolerance to and dependence on morphine can be pharmacologically dissociated

    Human monocyte chemotactic activity of calcitonin and somatostatin related peptides: modulation by chronic peptide treatment

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    Neuropeptides are common mediators of the nervous and the immune systems. We investigated whether two families of peptides, calcitonin (CT) and somatostatin, possess human monocyte chemotactic activity. CT-related peptides induce a significant chemotactic response, and the potency order is: salmon CT > human CT > CT >> carbo-CT; CT gene-related peptide is completely inactive. This rank potency order differs from that in other systems (e.g. bone and nervous system). The chemotactic response of monocytes obtained from patients chronically treated with either salmon CT or carbo-CT is impaired, thus suggesting a phenomenon of down-regulation of a common receptor on monocytes. While somatostatin-(1-14) is completely inactive on monocyte chemotaxis, the synthetic analog SMS 201995 is extremely potent. Also, in this case the prolonged treatment of patients with SMS 201995 leads to an impaired chemotactic response

    Interleukin-1 and nociception in the rat

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    It has recently become accepted that several cytokines may affect peripheral and central nervous system functions. Consistently with these findings, accumulating evidence points toward an important role for interleukin-1 in the modulation of nociceptive information. Here we review the observations collected after the administration of this cytokine by intracerebroventricular, intrathecal or peripheral route in rats. Taken together, these data suggest that IL-1 can differently affect pain responsivity depending on the dose and the site of action, and clearly demonstrate that this immune factor is deeply involved in the modulation of neuronal functions

    Non-Analgesic Effects of Opioids: Mechanisms and Potential Clinical Relevance of Opioid-Induced Immunodepression

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    This review provides an overview of the immunological effects of commonly used analgesic opioid drugs, focusing mainly on two aspects: the mechanisms involved and the potential clinical relevance. The immunomodulatory effects of morphine have been characterized in animal and human studies. Morphine decreases the effectiveness of both natural and acquired immunity, interfering with intracellular pathways involved in immune regulation, both directly and indirectly via the activation of central receptors. The mechanisms and the targets at the basis of opioid-induced immunomodulation have started to be elucidated, demonstrating an interaction between opioid receptors and several molecules involved in the complex and well orchestrated immune response, such as transcription factors and receptors of both myeloid and lymphoid cells. Due to their widespread and expanding use, the immunological effects of opioid are receiving considerable attention because of concerns that opioid-induced changes in the immune system may affect the outcome of surgery or of variety of disease processes, including bacterial and viral infections and cancer. It is also emerging that not all opioids induce the same immunosuppressive effects and evaluating each opioid profile is important for appropriate analgesic selection. The impact of the opioid-mediated immune effects could be particularly dangerous in selective vulnerable populations, such as the elderly or immunocompromised patients. Indeed, it is evident that the possibility of reaching adequate and equivalent pain control by choosing either immunosuppressive drugs or drugs without an effect on immune responses may be an important consideration in opioid therapy
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