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

Clinical, electrodiagnostic, and morphological studies were performed on three patients with localized hypertrophic neuropathy (LHN). LHN is characterized clinically by slowly progressive motor mononeuropathy without significant pain or numbness. Nerve conduction studies and needle electrode examination show severe focal motor and sensory axonal loss. Morphological findings in the localized areas of enlarged nerves are different from those of generalized hypertrophic neuropathy, entrapment neuropathy, and neurofibroma, and consist of primary perineurial cell hyperplasia. The tumor is thus a perineurioma. This rare tumor can occur both in generalized neurofibromatosis and in isolated form and appears to be the cause of localized hypertrophic neuropathy.
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PMID:Perineurioma as the cause of localized hypertrophic neuropathy. 677 21

Lumbosacral or primary buttock pain and cutaneous anesthesia in the distribution of the posterior femoral cutaneous nerve were the initial symptoms in 5 patients later proven to have extensions of previously resected colorectal malignancy. The initial electromyographic impression of an inferior gluteal nerve mononeuropathy associated with recurrent neoplasia was confirmed by a positive colon biopsy in 1 case and widespread pelvic metastasis demonstrated at laparotomy in the 4 remaining cases. Four of the 5 patients also had increased levels of carcinoembryonic antigen. Roentgenographs and other laboratory data were otherwise normal in all 5 cases. Entrapment of the inferior gluteal nerve and the accompanying posterior femoral cutaneous nerves is facilitated by its medial, intrapelvic fixation at its origin from the sciatic nerve and the crowding effect of the piriformis muscle above, the dorsal rim of the sciatic notch behind and the inferior gluteal vessels and nodes below. The demonstration of hypestesia over the inferior lateral buttock and a concomitant history of colorectal malignancy should alter the examiner to the possible presence of an inferior gluteal nerve neuropathy.
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PMID:Electromyographic evidence of inferior gluteal nerve compromise: an early representation of recurrent colorectal carcinoma. 705 17

We report a case of common peroneal mononeuropathy caused by an intraneural ganglion in a 9-year-old boy. The mass and the contiguous nerve fascicles were excised under the operating microscope. Histologically, the cyst wall was composed of layers of elongated cells merging with fascicles that exhibited changes suggestive of a pressure-ischemia effect. Electron microscopy showed that the cells forming cyst wall were myofibroblasts, similar to the cells found in ganglia arising from joints elsewhere in the body. A review of the English literature on intraneural ganglia discloses 44 additional cases, of which 86% involved the common peroneal nerve. The most common clinical feature was motor dysfunction (followed by pain, sensory loss, and the presence of a palpable mass), and a significant male predominance is noted. The pathogenesis of this nerve lesion is discussed in light of our findings.
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PMID:Intraneural ganglion: a case report with electron microscopic observations. 724 5

The antinociceptive action of the systemically administered alpha 2-adrenoceptor agonist clonidine was evaluated in a rat model of peripheral unilateral mononeuropathy produced by loose ligatures around the common sciatic nerve, using nociceptive tests based on mechanical (vocalization threshold to paw pressure) or thermal (struggle latency to paw immersion in a cold (10 degrees C) or hot (44 degrees C) water bath) stimuli. Experiments were performed 2-3 weeks after surgery when pain-related behavior was fully developed. We demonstrated a dissociative action depending on the test used: clonidine (30-100 micrograms/kg i.v.) had a moderate effect on the abnormal reactions to the mechanical stimulus. By contrast it dramatically increased the struggle latency to hot or cold stimuli. These latter effects were completely prevented by prior administration of the alpha 2-adrenoceptor antagonist idazoxan (0.5 mg/kg i.v.).
Pain 1995 Mar
PMID:Systemic clonidine differentially modulates the abnormal reactions to mechanical and thermal stimuli in rats with peripheral mononeuropathy. 759 23

In spite of the routine usage of spinal cord stimulation (SCS) as treatment of chronic pain, there is an insufficient understanding of the mechanisms underlying its effect. The method was originally developed as a spin-off from experiments demonstrating the inhibitory control of nociceptive signals by the activation of large afferent fibers, and on the basis of these findings the gate-control theory was advanced. Later experiments showed that stimulation of the dorsal columns can inhibit the relay of nociceptive impulses to second-order neurons in the dorsal horn. It should be emphasized that all these experiments were performed with acute noxious stimuli; it is now universally recognized that SCS in patients is preferentially, or exclusively, effective for chronic neuropathic types of pain. For these and other reasons the mode of action of SCS in clinical pain cannot be inferred from these early animal experiments. In ongoing studies we have used animal models of mononeuropathy (rat) in which we have applied SCS acutely or chronically with stimulation parameters similar to those used in patients. In these animals the first component of the flexor reflex appears with a lower stimulus threshold in the nerve lesioned than in the intact, sham-operated leg. SCS was applied at the approximate level of Th-XII during 10-20 min and produced a marked augmentation of the stimulus threshold. This abnormally high threshold was not normalized until 30-60 min after the end of SCS. In awake animals SCS was applied via an implanted spinal electrode and the effect on behavior changes associated with mononeuropathy was studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An experimental animal model of spinal cord stimulation for pain. 763 Oct 77

The effect of lidocaine pretreatment on thermal hyperalgesia and thermal skin asymmetries provoked by experimental mononeuropathy was investigated in rats. Forty anesthetized rats were given sciatic nerve ligatures according to the technique of Bennett and Xie. Rats were divided into 3 groups: 16 were ligated without lidocaine, 16 were ligated after lidocaine bathing of the nerve, and 8 were ligated after systemic lidocaine (6-8 mg/kg). Six sham-operated rats for each group were also prepared. From the first postoperative day the responses to the hot-plate test were assessed daily for 4 weeks by tracking the paw-licking latency (PLL) for both hindpaws. Shorter or longer latencies on the operated side were respectively considered sign of hyperalgesia and hypoalgesia. Infrared thermographic images of plantar hindpaws were taken in 22 operated rats in the 2nd postoperative week. Thermographic images of 8 non-operated rats were used as control. Animals operated without lidocaine exhibited shorter PLL (P < 0.001) and a decreased skin temperature on the operated side (P < 0.001). In the lidocaine-pretreated rats, no paw-licking reflex was present for a variable postoperative period (1 week or more) and afterwards there was a trend toward recovery of normal PLL values at the 4th week; the hindpaw skin temperature was symmetrical and normal. Sham-operated rats had normal tests. It is postulated here that lidocaine prevents behavioral and thermal manifestation of mononeuropathy by blocking early afferent injury barrage.
Pain 1995 Apr
PMID:Pre-injury lidocaine treatment prevents thermal hyperalgesia and cutaneous thermal abnormalities in a rat model of peripheral neuropathy. 764 45

Spinal cord stimulation (SCS) is efficacious for pain due to injury of peripheral nerves, and therefore models of mononeuropathy appear to be particularly suitable for an experimental approach to the study of mechanisms underlying the clinical effect of this mode of treatment in chronic neuropathic pain. Virtually all previous experimental studies on SCS have utilized acute and nociceptive types of peripheral pain stimuli to explore the attenuating effects of SCS. In the present study we made use of the two models of supposedly painful neuropathy developed by Bennett and Xie (1988) and Seltzer et al. (1990) to explore the effect of SCS applied with stimulus parameters similar to those used in clinical practice. In rats subjected to ligatures of the sciatic nerve according to these two methods, SCS was applied via chronically implanted electrodes, or acutely via a laminectomy in the lower thoracic region. In awake, freely moving animals SCS produced a marked increase of the withdrawal thresholds to innocuous mechanical stimuli in the form of von Frey filaments. This threshold elevation lasted for up to 40 min after 10 min of SCS. In about one-half of the animals there was also a moderate, but short-lasting increase in the intact leg. The degree and duration of the withdrawal threshold elevation was clearly related to the intensity of SCS which was kept below the level of which a response in the thoracic or leg musculature was produced. In a second series of experiments the effect of SCS, applied acutely via a laminectomy, on the early component (latency: 8-12 msec) of the flexor reflex was studied. As a result of nerve ligation with either of the methods used, the thresholds for evoking the early as well as the late component in the nerve-ligated leg were significantly lower than in the intact one. SCS resulted in a marked and long-lasting increase of the threshold of the early component in the nerve-ligated leg. On the intact side only a slight and short-lasting increase was observed. The late, C fibre-mediated component was not influenced by SCS. The first component of the flexor reflex is conceivably mediated by A beta-fibre activation and it presumably corresponds to the withdrawal response induced by innocuous mechanical stimuli. The lack of effect of SCS on the late reflex component indicates that it selectively influences transmission of A-fibre activity. (ABSTRACT TRUNCATED AT 400 WORDS)
Pain 1995 May
PMID:Spinal cord stimulation in animal models of mononeuropathy: effects on the withdrawal response and the flexor reflex. 765 33

This study evaluated the effect of surgical sympathectomy on pain-related behaviours in a well established model of peripheral mononeuropathy produced by loose ligatures around the common sciatic nerve in the rat. Behavioural abnormalities include spontaneous abnormal position of the hindpaw after the nerve constriction, indicative of "spontaneous pain", and changes in responses to mechanical or thermal stimuli applied to this paw. These changes are usually maximal at week 2 after the surgery, stable until weeks 3-4, and disappear between weeks 8 and 12. To assess the role of the sympathetic nervous system in the development and persistence of these abnormalities, four groups of rats were behaviourally tested: (i) rats receiving a complete sham surgery, (ii) rats with a sciatic nerve constriction produced by loose ligatures around the common nerve trunk plus a sham sympathectomy, (iii) rats receiving a lumbar sympathectomy with a sham nerve ligature, and (iv) rats receiving a simultaneous surgical lumbar sympathectomy and a sciatic nerve constriction. The efficacy of the sympathectomy was assessed by the measure of the noradrenaline level in the sciatic nerve. Sympathectomy reduced selectively or even prevented the abnormal reaction to cold temperature and to heat (45 degrees C) in rats with a peripheral mononeuropathy. In contrast, the abnormal reaction to mechanical pressure was not influenced, and the behavioural abnormalities indicating spontaneous pain were still present. Sympathectomy alone resulted in a reduction of the vocalization threshold to pressure on both hindpaws, but also a short-lasting increased tolerance to cold immersion. This study confirms the selective role of the sympathetic nervous system in affecting the development and maintenance of some abnormal pain-related behaviours to thermal stimuli in rats with a moderate, but persistent, constriction of one sciatic nerve.
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PMID:Influence of the sympathetic nervous system in the development of abnormal pain-related behaviours in a rat model of neuropathic pain. 767 15

The effect of the ganglioside GM1 on autotomy, a nociceptive behavioral marker for neuropathic pain, and substance P depletion was determined in a rat model of peripheral mononeuropathy, sciatic cryoneurolysis (SCN). SCN is produced by the application of a cryoprobe to the common sciatic nerve using a freeze-thaw-freeze cycle. Due to structural sparing of the nerve, regenerative processes are not precluded. After this peripheral nerve insult, behavioral and neurochemical changes occur that support the use of SCN as a neuropathic pain model. These changes include: autotomy with coincident transient weight loss and paling of eye color suggestive of increased sympathetic activity, spontaneous nociceptive behaviors, touch-evoked allodynia, prolonged mechanical allodynia, ipsilateral decrease of immunoreactive substance P, and increases in spinal cord dynorphin expression. Incidence and severity of autotomy were assessed after the intraperitoneal administration of GM1 (1, 10, and 20 mg/kg) or saline injected daily for 2 days before SCN, the day of surgery, and for 14 days after surgery. In a subset of two rats from each treatment group, transcardiac perfusion was performed and spinal cords were processed for substance P immunoreactivity. GM1 at 10 and 20 mg/kg doses significantly attenuated autotomy as compared with saline-treated rats (P = 0.007 and 0.0001, respectively). However, GM1, at the doses studied, failed to alter the spinal substance P depletion 21 days after SCN. These results indicate that the ganglioside GM1 may have a role in the clinical management of neuropathic pain after peripheral nerve injury.
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PMID:The ganglioside GM1 decreases autotomy but not substance P depletion in a peripheral mononeuropathy rat model. 769 Jan 98

In a rat model of peripheral mononeuropathy produced by moderate constriction of the sciatic nerve, we have shown that various i.v. doses of morphine and selective opioid agonists produce potent and long-lasting antinociceptive effects on the vocalization threshold to paw pressure. For all the opioids, the antinociceptive effects were more marked for the paw on the nerve-injured side (nerve-injured paw) than for the sham-operated paw. One contributory mechanism could be a peripheral action of the opioid agonists in the nerve-injured paw. This hypothesis was tested in the present study, using systemic morphine and low doses of local naloxone or its quaternary salt naloxone methiodide, exhibiting peripherally acting antagonist properties. The effects of escalating doses of naloxone (0.5-2 microgram injected i.v. or intraplantar into the nerve-injured paw) or naloxone methiodide (5-30 micrograms into the nerve-injured paw) on the antinociceptive effect of morphine (1 mg/kg i.v.) were evaluated using the vocalization threshold to paw pressure in neuropathic rats at two weeks after placing ligatures, a time when the behavioural pain-related disorders have reached a maximum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for a peripheral component in the enhanced antinociceptive effect of a low dose of systemic morphine in rats with peripheral mononeuropathy. 770 May 37


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