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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Local injections of the sclerosing substance Polidocanol has been demonstrated to give good clinical results in a pilot study on patients with chronic Achilles tendinopathy. In this study, 20 consecutive patients (9 men and 11 women, mean age 50 years) with chronic painful mid-portion Achilles tendinopathy were randomised to injection treatment with either Polidocanol (5 mg/ml) (group A) or Lidocaine hydro-chloride (5 mg/ml) + Adrenaline (5 microg/ml) (group B). Both substances have a local anaesthetic effect, but Polidocanol also has a sclerosing effect. The patients and the treating physician were blinded to the substance injected. The short-term effects were evaluated after a maximum of two treatments, 3-6 weeks apart. Before treatment, all patients had structural tendon changes and neo-vascularisation demonstrated with US and colour doppler. Under US and colour doppler-guidance, the injections targeted the area of neo-vascularisation just outside the ventral part of the tendon. For evaluation, the patients recorded the severity of Achilles tendon pain during tendon loading activity, before and after treatment, on a VAS. Patient's satisfaction with treatment was also assessed. At follow-up (mean 3 months) after a maximum of two treatments, 5/10 patients in group A were satisfied with the treatment and had a significantly reduced level of tendon pain (p < 0.005). In group B, no patient was satisfied with treatment. In the pain-free tendons, but not in the painful tendons, neo-vascularisation was absent after treatment. After completion of the study, treatment with Polidocanol injections (Cross-over in group B and additional treatments in group A) resulted in 10/10 and 9/10 satisfied patients in group A and B, respectively. In summary, injections with the sclerosing substance Polidocanol have the potential to reduce tendon pain during activity in patients with chronic painful mid-portion Achilles tendinopathy.
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PMID:Sclerosing injections to areas of neo-vascularisation reduce pain in chronic Achilles tendinopathy: a double-blind randomised controlled trial. 1568 35

While it is well established that acute stress can produce antinociception, a phenomenon referred to as stress-induced analgesia, repeated exposure to stress can have the opposite effect. Since, chronic pain syndromes, such as fibromyalgia and rheumatoid arthritis, may be triggered and/or exacerbated by chronic stress, we have evaluated the effect of repeated stress on mechanical nociceptive threshold and inflammatory hyperalgesia. Using the Randall-Selitto paw pressure test to quantify nociceptive threshold in the rat, we found that repeated non-habituating sound stress enhanced the mechanical hyperalgesia induced by the potent inflammatory mediator, bradykinin, which, in normal rats, produces hyperalgesia indirectly by stimulating the release of prostaglandin E2 from sympathetic nerve terminals. Hyperalgesia induced by the direct-acting inflammatory mediator, prostaglandin E2 as well as the baseline nociceptive threshold, were not affected. Adrenal medullectomy or denervation, reversed the effect of sound stress. In sound stressed animals, bradykinin-hyperalgesia had a more rapid latency to onset and was no longer inhibited by sympathectomy, compatible with a direct effect of bradykinin on primary afferent nociceptors. In addition, implants of epinephrine restored bradykinin-hyperalgesia in sympathectomized non-stressed rats, lending further support to the suggestion that increased plasma levels of epinephrine can sensitize primary afferents to bradykinin. These results suggest that stress-induced enhancement of inflammatory hyperalgesia is associated with a change in mechanism by which bradykinin induces hyperalgesia, from being sympathetically mediated to being sympathetically independent. This sympathetic-independent enhancement of mechanical hyperalgesia is mediated by the stress-induced release of epinephrine from the adrenal medulla.
Pain 2005 Jul
PMID:Repeated sound stress enhances inflammatory pain in the rat. 1593 44

Stapedotomy for otosclerosis presents particular anaesthesiology demands as the surgeon has to assess functional results during the operation, work with some bleeding, be ensured the collaboration of the patient, and limit the occurrence of intra- and post-operative symptoms (dizziness, nausea, vomiting and pain). Remifentanyl, a micro-opioid selective agonist characterised by short latency and duration, has been used for about 2 years at the Otolaryngological Unit of the "Federico II" University of Naples for patients with otosclerosis undergoing stapedotomy. Aim of the study was, therefore, to assess: efficacy and tolerability of Remifentanyl in combination with a local anaesthetic in surgical procedures for otosclerosis; intra- and post-operative reduction in patient symptoms of dizziness, nausea, vomiting and pain; reduction of intra-operative bleeding; degree of patient collaboration and optimisation of anaesthesiological and vital parameters monitored during surgery. The study was carried out on 92 patients with otosclerosis, (17 M, 75 F), median age 41 years (range 25-56), undergoing stapedotomy. Patients were randomly assigned to one of two groups, which were homogeneous as far as concerns age, sex and pre-operative hearing: i. Group A (50 patients), received Remifentanyl infusion in combination with canal injection for local anaesthesia with Mepivacaine 2% and Adrenalin 1/100,000; ii. Group B (42 patients), received only local anaesthetic by infiltration of the external canal ear. Remifentanyl led to an improvement over the local anaesthetic technique previously used, with a clear decrease in intra- and post-operative neurovegetative symptoms such as dizziness, nausea, vomiting and pain, as well as reduced bleeding.
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PMID:Use of Remifentanil for sedo-analgesia in stapedotomy: personal experience. 1595 79

The new CPR guidelines are based on a scientific consensus which was reached by 281 international experts. Chest compressions (100/min, 4-5 cm deep) should be performed in a ratio of 30:2 with ventilation (tidal volume 500 ml, Ti 1 s, FIO2 if possible 1.0). After a single defibrillation attempt (initially biphasic 150-200 J, monophasic 360 J, subsequently with the respective highest energy), chest compressions are initiated again immediately for 2 min. Endotracheal intubation is the gold standard; other airway devices may be employed as well depending on individual skills. Drug administration routes for adults and children: first choice IV, second choice intraosseous, third choice endobronchial [epinephrine dose 2-3x (adults) or 10x (pediatric patients) higher than IV]. Vasopressors: 1 mg epinephrine every 3-5 min IV. After the third unsuccessful defibrillation attempt amiodarone IV (300 mg); repetition (150 mg) possible. Sodium bicarbonate (1 ml/kg 8.4%) only in excessive hyperkalemia, metabolic acidosis, or intoxication with tricyclic antidepressants. Consider atropine (3 mg) and aminophylline (5 mg/kg). Thrombolysis during spontaneous circulation only in myocardial infarction or massive pulmonary embolism; during CPR only during massive pulmonary embolism. Cardiopulmonary bypass only after cardiac surgery, hypothermia or intoxication. Pediatrics: best improvement in outcome by preventing cardiocirculatory collapse. Alternate chest thumps and chest compression (infants), or abdominal compressions (>1-year-old) in foreign body airway obstruction. Initially five breaths, followed by chest compressions (100/min; approximately 1/3 of chest diameter): ventilation ratio 15:2. Treatment of potentially reversible causes (4 "Hs", "HITS": hypoxia, hypovolemia, hypo- and hyperkaliemia, hypothermia, cardiac tamponade, intoxication, thrombo-embolism, tension pneumothorax). Epinephrine 10 microg/kg IV or intraosseously, or 100 microg (endobronchially) every 3-5 min. Defibrillation (4 J/kg; monophasic oder biphasic) followed by 2 min CPR, then ECG and pulse check. Newborns: inflate the lungs with bag-valve mask ventilation. If heart rate<60/min chest compressions:ventilation ratio 3:1 (120 chest compressions/min). Postresuscitation phase: initiate mild hypothermia [32-34 degrees C for 12-24 h; slow rewarming (<0.5 degrees C/h)]. Prediction of CPR outcome is not possible at the scene; determining neurological outcome within 72 h after cardiac arrest with evoked potentials, biochemical tests and physical examination. Even during low suspicion for an acute coronary syndrome, record a prehospital 12-lead ECG. In parallel to pain therapy, aspirin (160-325 mg PO or IV) and in addition clopidogrel (300 mg PO). As antithrombin, heparin (60 IU/kg, max. 4000 IU) or enoxaparine. In ST-segment elevation myocardial infarction, define reperfusion strategy depending on duration of symptoms until PCI (prevent delay>90 min until PCI). Stroke is an emergency and needs to be treated in a stroke unit. A CT scan is the most important evaluation, MRT may replace a CT scan. After hemorrhage exclusion, thrombolysis within 3 h of symptom onset (0.9 mg/kg rt-PA IV; max 90 mg within 60 min, 10% of the entire dosage as initial bolus, no aspirin, no heparin within the first 24 h). In severe hemorrhagic shock, definite control of bleeding is the most important goal. For successful CPR of trauma patients, a minimal intravascular volume status and management of hypoxia are essential. Aggressive fluid resuscitation, hyperventilation, and excessive ventilation pressure may impair outcome in severe hemorrhagic shock. Despite bad prognosis, CPR in trauma patients may be successful in select cases. Any CPR training is better than nothing; simplification of contents and processes remains important.
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PMID:[The new 2005 resuscitation guidelines of the European Resuscitation Council: comments and supplements]. 1691 4

In some clinical settings it is necessary to inject large volumes of local anesthetic--and consequently very high doses--in order to provide an adequate level of block. Subsequent absorption of these high doses, or inadvertent intravenous administration of even small doses, has led to systemic toxicity. Thus, it is desirable to develop adjuvants that are inert alone, but would enhance the potency and/or efficacy of local anesthetics to improve their safety. Adelta/C fibers possess K(+) channels identified as sustained delayed rectifier type K(DR) currents and transient A-type K(A) currents. In the heart, the class III antiarrhythmic drug ibutilide blocks the cardiac component of the rapid delayed rectifying K(+) current (IKr). Experiments were conducted to determine whether co-administration of the K(+) channel blocker ibutilide would enhance the local anesthetic bupivacaine in mice. After injecting bupivacaine mixed with vehicle or ibutilide in the popliteal region of mice, paw withdrawal latencies were determined by applying the plantar aspect of a single hind-paw to the surface a 55 degrees C hot-plate device. 0.5% Bupivacaine+ibutilide (7.8x10(-5) M) elicited significantly longer hot-plate latencies than 0.5% bupivacaine+vehicle. In addition, bupivacaine was 2.6-fold more potent when co-administered with ibutilide rather than vehicle. Epinephrine extends the tissue concentrations of local anesthetics by inducing localized vasoconstriction. Epinephrine augmented the enhancement by ibutilide of bupivacaine's potency by 6.8-fold. In summary, ibutilide may enhance the effects of bupivacaine by blocking K(+) channels on sensory nociceptive nerves.
Eur J Pain 2007 Jul
PMID:Enhancement of bupivacaine local anesthesia with the potassium channel blocker ibutilide. 1691 81

Adrenal medullary chromaffin cells secrete several neuroactive substances including catecholamines and opioid peptides that produce analgesic effects in the central nervous system. This study was designed to investigate whether intrathecal microencapsulated chromaffin cells could release analgesic materials producing antiallodynic effects on the chronic neuropathic pain in rats induced by chronic constriction injury (CCI) of the sciatic nerve. Prior to intrathecal implantation, chromaffin cells were encapsulated with alginate and poly-L-lysine to protect them from the host immune system. Behavior tests were performed before CCI, 1 week later, and at 4, 7, 14, 21, 28 days postimplantation. At the end of study, we performed cerebrospinal fluid (CSF) collection and implant retrieval. We observed that intrathecal implantation of encapsulated xenogenic chromaffin cells reduced the mechanical and cold allodynia in a model of neuropathic pain. CSF levels of catecholamines and metenkephalin in the rats that received implants were higher than the controls. In addition, we observed chronic survival of implants. These results suggested that intrathecal microencapsulated chromaffin cells may represent a new approach to chronic neuropathic pain management.
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PMID:Intrathecal implants of microencapsulated xenogenic chromaffin cells provide a long-term source of analgesic substances. 1711

Vasovagal syncope refers to a reflex cardiovascular depression that gives rise to loss of consciousness with bradycardia and profound vasodilatation. This response commonly occurs during regional anesthesia, hemorrhage or supine inferior vena cava compression in pregnancy. The changes in circulatory response from the normal maintenance of arterial pressure to parasympathetic activation and sympathetic inhibition may cause severe hypotension. This change is triggered by reduced cardiac venous return as well as episodes of emotional stress, excitement or pain. Occasionally, these vasovagal responses may be unpredictable and may dramatically proceed to asystole with circulatory collapse, and may even result in death. In these circumstances, hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilatation. Regional anesthesia, decreased venous return, hemorrhage and abnormal fetal presentation cumulatively increase the risk of vasovagal syncope in cesarean section patients. When a vasovagal response occurs, ephedrine is the drug of first choice because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anesthesia.
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PMID:Perioperative vasovagal syncope with focus on obstetric anesthesia. 1717 65

Voltage-dependent Na+ channels consist of the principal alpha-subunit (approximately 260 kDa), without or with auxiliary beta-subunit (approximately 38 kDa). Nine alpha-subunit isoforms (Na(v)1.1-Na(v)1.9) are encoded in nine different genes (SCN1A-SCN5A and SCN8A-SCN11A). Besides initiating and propagating action potentials in established neuronal circuit, Na+ channels engrave, maintain and repair neuronal network in the brain throughout the life. Adrenal chromaffin cells express Na(v)1.7 encoded in SCN9A, which is widely distributed among peripheral autonomic and sensory ganglia, neuroendocrine cells, as well as prostate cancer cell lines. In chromaffin cells, Na(v)1.7-specific biophysical properties have been characterized; physiological stimulation by acetylcholine produces muscarinic receptor-mediated hyperpolarization followed by nicotinic receptor-mediated depolarization. In human patients with Na(v)1.7 channelopathies, gain-of-pathological function mutants (i.e. erythermalgia and paroxysmal extreme pain disorder) or loss-of-physiological function mutant (channelopathy-associated insensitivity to pain) proved the causal involvement of mutant Na(v)1.7 in generating intolerable pain syndrome, Na(v)1.7 being the first molecular target convincingly identified for pain treatment. Importantly, aberrant upregulation/hyperactivity of even the native Na(v)1.7 produces pain associated with inflammation, nerve injury and diabetic neuropathy in rodents. Various extra- and intracellular signals, as well as therapeutic drugs modulate the activity of Na(v)1.7, and also cause up- and downregulation of Na(v)1.7. Na(v)1.7 seems to play an increasing number of crucial roles in health, disease and therapeutics.
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PMID:Voltage-dependent Na(v)1.7 sodium channels: multiple roles in adrenal chromaffin cells and peripheral nervous system. 1802 27

Sexual assault occurs with alarming frequency in Canada. The prevalence of Posttraumatic Stress Disorder (PTSD) in assault survivors is drastically higher than the national prevalence of the disorder, which is a strong indication that the current therapies for sexual-assault-related PTSD are in need of improvement. Increasing knowledge and understanding of the pathologies associated with rape trauma in biological, psychological and sociological domains will help to develop more effective treatments for survivors. A dysregulation of the Hypothalamic-Pituitary-Adrenal (HPA) axis is observed in survivors of sexual assault and this may be a fundamental cause of the structural and functional abnormalities contributing to PTSD symptoms. Pharmacotherapies are available to treat PTSD; however, they are often inadequate or unwanted by the survivor. Psychological health is compromised following interpersonal trauma and many psychological therapies are available, but with varying efficacy. A person's cognitions have a dramatic effect on the onset, severity, and progress of PTSD following sexual assault. Sociological impacts of assault influence the development of PTSD through victim-blaming attitudes and the perpetuation of rape myths. Perceived positive regard and early social support is shown to be important to successful recovery. Education is vital in rape prevention and to foster a supportive environment for survivors. The biological, psychological and sociological impacts and treatments should not remain mutually exclusive. A better appreciation of the biopsychosocial repercussions of sexual assault will aid in developing a more holistic and individualized therapy to help alleviate the physical and emotional pain following the trauma of rape.
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PMID:Sexual assault and posttraumatic stress disorder: a review of the biological, psychological and sociological factors and treatments. 1852 13

Many problems may arise when defining whether adrenal lesions are primary to the adrenal glands or represent other tissue, whether they are benign or malignant and whether they are functioning or nonfunctioning. Adrenal imaging complements the clinical and hormonal evaluation of these patients. We present a patient with lumbar pain and bilateral adrenal masses.
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PMID:[Lumbar pain and bilateral adrenal masses]. 1962 47


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