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Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pain related to fibromyalgia may consist of a complex interaction of nociceptive, neuropathic, dysregulatory central nervous system and psychosomatic mechanisms. Nociceptor pain is based on the excitation of nervous sensors specialized to signal potentially harmful stimuli, i.e., the nociceptors. Metabolic deficiencies in muscle and neurogenic inflammation induced by the release of substance P and other neuropeptides from the peripheral nerve endings may result in chemical sensitization of nociceptors and an ensuing hyperalgesia particularly present in tender points. Neuropathic pain is due to pathological mechanisms within nerve cells and fibers in the peripheral and central nervous system. Pathophysiology may be related to compression (such as in the carpal tunnel syndrome or a vertebral disk herniation) or regeneration of nerves, resulting in ectopic impulse discharges and disturbances of axonal transport. The ensuing neuronal hyperexcitability and trophic changes induced by a disturbed axonal transport system may be major factors of pain in fibromyalgia. Dysregulatory pain denotes pain maintained by dysfunction of efferent control loops. Thus, if spinal motoneuron output results in excessive tension of postural muscle, nociceptors in muscles, tendons and joints might become more excited. Persistent abnormal spinal reflex transmission due to, e.g., peripheral trauma or inappropriate postural habits may result in a vicious circle between muscle hypertension and pain. Similarly, a defective sympathetic control may result in disturbed microcirculation and nociceptor excitation (e.g., in sympathetic algodystrophy). Many symptoms of pain in fibromyalgia (trigger points, pain referral, pain associated with muscle spasm or neurogenic joint immobilization) can be attributed to abnormal control mechanisms in a complex cybernetic system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiological mechanisms of fibromyalgia. 181 May 27

Oral medication is the simplest way in treatment of chronic pain. For cancer pain oral analgesics are efficacious in more than 90% of the patients. When a causal therapy of pain (e.g. chemotherapy, operation) fails an analgesic ladder with oral analgesics is instituted. This ladder starts with a non-narcotic analgesic in a sufficient dose. The regular dose of acetylsalicylic acid or paracetamol is 4 g daily. When this dose does not work sufficiently, a weak opioid (e.g. dihydrocodeine) is given concomitantly at an individual dose. When the weak opioid fails, strong opioids are given (e.g. morphine). The drugs should be given by mouth whenever possible. The most important point is the regular application according to a time-schedule. This time-schedule is related to the action time of the drug. Patients with severe vomiting or dysphagia can receive a continuous subcutaneous infusion. These measures are based on recommendations of the WHO.The same medications can be employed in patients with chronic non-malignant pain, provided that all other conventional measures in pain treatment fail. However, many states of pain are not opioid-responsive. Pain related to the sympathetic nervous system is more responsive to antidepressants than to opioids or NSAID. Neuropathic pain as in trigeminal neuralgia responds to anticonvulsants. Pain from muscle spasm is better controlled by muscle relaxants than by analgesics. Bone pain is more sensitive to NSAID than to any other drug.In any state of pain the response to the different groups of drugs should be evaluated first. Then a stepwise pharmacological approach should be performed. In most cases pain can be treated effectively by oral drugs.
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PMID:[Not Available]. 1841 67