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

A prospective study of pain after brachial plexus injury was carried out on 246 patients with at least 2 years follow-up. All of them had closed traction injury from motorcycle accidents. There were 16 females and 230 males aged from 16 to 44 years old. The patients' biodata, onset of pain, characteristics of pain and treatment were recorded. Changes in pain after conservative and operative treatment and the outcome of treatment were analysed. Two hundred and nineteen patients (89%) had significant pain and 182 patients (74%) had severe pain. Most of them had continuous pain with 2 to 20 peaks of severe pain per day. Crushing type of pain was the most common but mixed type of pain caused the most distress. Conservative treatment before surgery could relieve the pain in 39 patients (15.8%). Surgical reconstruction could further relieve the pain in 176 patients (80.36%). However, 21 patients (8.5%) still had severe pain. Improvement in sensory function had more effect on pain reduction than motor function.
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PMID:Brachial plexus injury and pain: incidence and the effects of surgical reconstruction. 1093 3

Crushing injury of the hand usually causes "explosive" damage. Subsequent swelling of the palmar structures further impairs venous outflow, and hemorrhage into structural spaces increases the pressure. The arterial system and the large dorsal veins, however, are seldom obstructed and provide adequate circulation unless hampered by improper bandaging. A bandage that compresses the dorsal veins causes back-pressure, which increases the swelling further and brings about ischemia. Swelling and pain cause the patient to restrict exercise of the injured hand, which permits contractures to develop. The author has averted this sequence in more than 100 cases by preserving integrity of veins during debridement, arresting hemorrhage, bandaging the hand with compression dressings in functional flexion, and reducing swelling with hyaluronidase. In these cases, on removal of bandages in 24 hours, swelling was reduced and continued to diminish. All patients exercised the hand at this time without discomfort and only a few required aspirin for pain.
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PMID:Crushing injury of the hand; prevention of ischemic contracture. 1363 24

Visceral pain, which originates from organ tissues of the thorax, abdomen or pelvis, is generally perceived as a deep, dull and vague sensation; in most cases it cannot even be clearly described, being a sense of discomfort, malaise or oppression rather than real pain. Crushing, cutting and burning generally have no algogenic effect in the viscera whereas mechanical stimulation, ischemia and chemical stimulation, separately or in combinations, may cause pain. With these characteristics, visceral pain differs from somatic pain. The characteristics of visceral pain, perception and transmission of painful visceral stimuli are explained, some common visceral pain syndromes are presented and sympathetic neurodestructive approaches as a treatment option are described in this review.
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PMID:Visceral pain. 1515 83

Nerve injury produces a long lasting neuropathic pain, manifested as allodynia, a decrease in pain threshold and hyperalgesia, an increase in response to noxious stimuli. The mechanism underlying the lasting abnormal pain is not well understood. Our previous works have shown that electrical tetanic stimulation of the sciatic nerve induces long-term potentiation (LTP) of C-fiber evoked field potentials in the spinal dorsal horn, which is considered as a synaptic model of pathological pain. In the present study we tested if nerve injury, which is proved to produce neuropathic pain, induced the spinal LTP in intact rats. C-fiber evoked field potentials in spinal dorsal horn produced by electrical stimulation (10-20 V, 0.5 ms, 1/min) of the sciatic nerve were recorded. For induction of LTP of C-fiber evoked field potentials, three types of noxious stimuli were applied. (1) Electrical tetanic stimulation (40 V, 0.5 ms pulses at 100 Hz for 1 s repeated four times at 10 s intervals). (2) Transection of the sciatic nerve at 4-5 mm distal to the stimulation electrode. (3) Crushing the sciatic nerve with a forceps four times at 4-5 mm distal to stimulation electrode (from distal to proximal with 1 mm spacing at 10 s intervals), which simulated electrical tetanic stimulation. Acute nerve injury was made by either transection of the sciatic nerve at the distal to the stimulating electrode or crushing the sciatic nerve. We found that nerve injury by cutting or crushing the sciatic nerve produced LTP of C-fiber evoked field potentials lasting until the end of the experiments (3-9 h), and that pretreatment of the sciatic nerve with lidocaine 10 min prior to the nerve transectoin completely blocked LTP induced by nerve transection. The nerve transection-induced LTP was blocked by NMDA receptor antagonist AP5. LTP produced by nerve transection could not be further potentiated by electrical tetanic stimulation, while LTP induced by single electrical tetanic stimulation could be further potentiated by transection of the sciatic nerve. However, when LTP was saturated by several times of electrical tetanic stimulation, nerve transection did not affect the spinal LTP. We conclude that acute nerve injury induces LTP of C-fiber evoked field potentials in intact animals and that nerve transection is more powerful than electrical tetanic stimulation for induction of the spinal LTP. The results further support the notion that LTP of C-fiber evoked field potentials may underlie neuropathic pain.
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PMID:Acute nerve injury induces long-term potentiation of C-fiber evoked field potentials in spinal dorsal horn of intact rat. 1549 39

Nerve injury elicits both universal and limited responses. Among the former is regenerative growth, which occurs in most peripheral neurons, and among the latter is the long-term hyperexcitability that appears selectively in nociceptive sensory neurons. Since positive injury signals communicate information from the site of an injury to the cell body, we hypothesize that a nerve injury activates both universal and limited positive injury signals. Studies in Aplysia indicate that protein kinase G is a limited signal that is responsible for the induction of long-term hyperexcitability. Given that long-term hyperexcitability contributes to chronic pain after axotomy in rodent neuropathic pain models, we investigated its underlying basis in the rat peripheral nervous system. Using biochemical assays, Western blots, and immunocytochemistry we found that the Type 1alpha protein kinase G is the predominant isoform in the rat periphery. It is present primarily in axons and cell bodies of nociceptive neurons, including populations that are isolectin B4-positive, isolectin B4-negative, and those that express transient receptor potential vanilloid receptor-1. Surprisingly, protein kinase G is not present in the facial nerve, which overwhelmingly contains axons of motor neurons. Crushing the sciatic nerve or a cutaneous sensory nerve activates protein kinase G in axons and results in its retrograde transport to the neuronal somata in the DRG. Preventing the activation of protein kinase G by injecting Rp-8-pCPT-cGMPS into the crush site abolished the transport. The protein kinase A inhibitor Rp-8-pCPT-cAMPS had no effect. Extracellular signal-related kinases 42/44 are also activated and transported after nerve crush, but in both motor and sensory axons. Chronic pain has been linked to long-term hyperexcitability following a nerve inflammation in several rodent models. We therefore injected complete Freund's adjuvant into the hindpaw to induce an inflammation and found that protein kinase G was activated in the sural nerve and transported to the DRG. In contrast, the extracellular signal-related kinases in the sensory axons were not activated by the complete Freund's adjuvant. These studies support the idea that the extracellular signal-related kinases are universal positive axonal signals and that protein kinase G is a limited positive axonal signal. They also establish the association between protein kinase G, the induction of long-term hyperexcitability, and chronic pain in rodents.
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PMID:Activation and retrograde transport of protein kinase G in rat nociceptive neurons after nerve injury and inflammation. 1673 Sep 16