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

The use of the recently released anticonvulsant, gabapentin (Neurontin), in the treatment of severe and refractory reflex sympathetic dystrophy (RSD) pain in six patients ranging in age from 42 to 68 years is reported. Satisfactory pain relief obtained in all six patients suggests that this medication is an effective treatment for RSD pain. In addition to pain control, early evidence of disease reversal in these patients is suggested. Patient 6 is the first documented case of successful treatment and cure of the RSD pain syndrome using gabapentin alone. Specifically, reduced hyperpathia, allodynia, hyperalgesia, and early reversal of skin and soft tissue manifestations were noted. Gabapentin was chosen because it has properties similar to other anticonvulsant drugs and because previous studies have shown that it is well tolerated and appears to have a benign efficacy-to-toxicity ratio. It was considered an acceptable and compassionate therapeutic choice because previous medical and surgical approaches had been ineffective for these patients, who represent the first case series documenting the use of gabapentin for pain management. Presently, the mechanism of pain relief in these patients is unknown. In this article, the pathophysiology of RSD is discussed, and a mechanism by which gabapentin provides pain relief is proposed. In view of encouraging results in these and other RSD patients, further scientific investigation is needed to delineate the role of gabapentin in the treatment of reflex sympathetic dystrophy.
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PMID:Reflex sympathetic dystrophy treated with gabapentin. 901 68

Gabapentin (Neurontin) is a novel anticonvulsant with an as yet unknown mechanism of action. This electrophysiological study investigated the potential antinociceptive actions of systemically administered gabapentin in normal animals and after inflammation induced by the injection of carrageenan. Gabapentin facilitated the noxious evoked responses of dorsal horn neurones recorded in normal animals. In complete contrast, gabapentin strongly and dose-dependently inhibited the C-fibre evoked response and post-discharge, but not the A beta-fibre evoked response, of neurones recorded in animals 3 h after the injection of carrageenan. This unique and selective profile of gabapentin may provide a novel treatment for clinical inflammatory pain states.
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PMID:Gabapentin, ineffective in normal rats, markedly reduces C-fibre evoked responses after inflammation. 910 28

Gabapentin is a novel anticonvulsant that may be of value for the relief of clinical pain. To determine whether gabapentin is antinociceptive after spinal administration, the drug was given via an intrathecal catheter in doses from 6 to 200 micrograms/rat 10 min prior to intraplantar formalin. Five percent formalin injected subcutaneously in the right hind paw produced a biphasic reaction consisting of flinching and licking behaviors (phase 1, 0-10 min; phase 2, 10-60 min). Gabapentin dose-dependently reduced the numbers of flinches and the duration of licking during phase 2 of the formalin test. The highest dose of gabapentin (200 micrograms/rat) did not affect the tail-flick response. These results demonstrate that spinal gabapentin is antinociceptive in the formalin test.
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PMID:Spinal gabapentin is antinociceptive in the rat formalin test. 912 25

Gabapentin, an anticonvulsant structurally related to gamma-aminobutyric acid (GABA) was recently reported to be effective in pain associated with reflex sympathetic dystrophy (RSD) and in pain associated with neuropathy. Yet, to our knowledge, the use of gabapentin for neuropathic pain in the presence of cognitive impairment has not been reported. In this report, we describe two patients (one with a traumatic brain injury, one with a putative acquired brain injury) who presented to a neurorehabilitation unit complaining of pain that was diagnosed as neurologically mediated. Within one week of receiving a daily 900 mg dose of gabapentin, both patients complained of heightened anxiety and restlessness. Correspondingly, each reported a diminution of psychological symptoms within 48 hours of gabapentin cessation. These two cases suggest that gabapentin may cause agitation in cognitive impaired patients. Physicians treating brain-injured patients and prescribing gabapentin for neuropathic pain may wish to closely monitor patients for similar signs of restlessness or anxiety.
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PMID:Psychomotor agitation following gabapentin use in brain injury. 921 Sep 89

1. Gabapentin (neurontin) is a novel antiepileptic agent that binds to the alpha 2 delta subunit of voltage-dependent calcium channels. The only other compound known to possess affinity for this recognition site is the (S)-(+)-enantiomer of 3-isobutylgaba. However, the corresponding (R)-(-)-enantiomer is 10 fold weaker. The present study evaluates the activity of gabapentin and the two enantiomers of 3-isobutylgaba in formalin and carrageenan-induced inflammatory pain models. 2. In the rat formalin test, S-(+)-3-isobutylgaba (1-100 mg kg-1) and gabapentin (10-300 mg kg-1) dose-dependently inhibited the late phase of the nociceptive response with respective minimum effective doses (MED) of 10 and 30 mg kg-1, s.c. This antihyperalgesic action of gabapentin was insensitive to naloxone (0.1-10.0 mg kg-1, s.c.). In contrast, the R-(-)-enantiomer of 3-isobutylgaba (1-100 mg kg-1) produced a modest inhibition of the late phase at the highest dose of 100 mg kg-1. However, none of the compounds showed any effect during the early phase of the response. 3. The s.c. administration of either S-(+)-3-isobutylgaba (1-30 mg kg-1) or gabapentin (10-100 mg kg-1), after the development of peak carrageenan-induced thermal hyperalgesia, dose-dependently antagonized the maintenance of this response with MED of 3 and 30 mg kg-1, respectively. Similar administration of the two compounds also blocked maintenance of carrageenan-induced mechanical hyperalgesia with MED of 3 and 10 mg kg-1, respectively. In contrast, R-(-)-3-isobutylgaba failed to show any effect in the two hyperalgesia models. 4. The intrathecal administration of gabapentin dose-dependently (1-100 micrograms/animal) blocked carrageenan-induced mechanical hyperalgesia. In contrast, administration of similar doses of gabapentin into the inflamed paw was ineffective at blocking this response. 5. Unlike morphine, the repeated administration of gabapentin (100 mg kg-1 at start and culminating to 400 mg kg-1) over 6 days did not lead to the induction of tolerance to its antihyperalgesic action in the formalin test. Furthermore, the morphine tolerance did not cross generalize to gabapentin. The s.c. administration of gabapentin (10-300 mg kg-1), R-(-) (3-100 mg kg-1) or S-(+)-3-isobutylgaba (3-100 mg kg-1) failed to inhibit gastrointestinal motility, as measured by the charcoal meal test in the rat. Moreover, the three compounds (1-100 mg kg-1, s.c.) did not generalize to the morphine discriminative stimulus. Gabapentin (30-300 mg kg-1) and S-(+)-isobutylgaba (1-100 mg kg-1) showed sedative/ataxic properties only at the highest dose tested in the rota-rod apparatus. 6. Gabapentin (30-300 mg kg-1, s.c.) failed to show an antinociceptive action in transient pain models. It is concluded that gabapentin represents a novel class of antihyperalgesic agents.
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PMID:Gabapentin (neurontin) and S-(+)-3-isobutylgaba represent a novel class of selective antihyperalgesic agents. 928 83

There have been many proposed uses for gabapentin, including midscapular pain secondary to radiation myelopathy, RSD, neuropathic pain, postherpetic neuralgia, and migraine prophylaxis. However, the published reports consist of a small number of patients and limited data. Limited data provided in published case reports do not allow adequate evaluation of expected adverse effects or efficacy. It is unclear whether gabapentin is more effective for a specific type of pain and how gabapentin may compare with placebo or other therapeutic alternatives. Therefore, randomized, double-blind, placebo-controlled, prospective studies are warranted to further elucidate gabapentin uses beyond what is recommended by the Food and Drug Administration. Gabapentin should only be considered for pain management after well-established therapies have failed to produce desired outcomes.
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PMID:Use of gabapentin in pain management. 929 51

Gabapentin and S-(+)-3-isobutylgaba are anticonvulsant agents that selectively interact with the alpha2delta subunit of voltage-dependent calcium channels. This report describes the activities of these two compounds in a rat model of postoperative pain. An incision of the plantaris muscle of a hind paw induced thermal hyperalgesia and tactile allodynia lasting at least 3 days. Postoperative testing was carried out using the plantar test for thermal hyperalgesia and von Frey hairs for tactile allodynia. A single s.c. dose of gabapentin, 1 h before surgery, dose-dependently (3-30 mg/kg) blocked the development of allodynia and hyperalgesia with a minimum effective dose (MED) of 10 and 30 mg/kg, respectively. The highest dose of gabapentin prevented development of hyperalgesia and allodynia for 24 and 49 h, respectively. Similar administration of S-(+)-3-isobutylgaba also dose-dependently (3-30 mg/kg, s.c.) prevented development of hyperalgesia and allodynia with MED of 3 and 10 mg/kg, respectively. The highest dose of S-(+)-3-isobutylgaba completely blocked development of both nociceptive responses for 3 days. The administration of S-(+)-3-isobutylgaba (30 mg/kg s.c.) 1 h after surgery also completely blocked the maintenance of hyperalgesia and allodynia, but its duration of action was much shorter (3 h). The administration of morphine (1-6 mg/kg s.c.) 0.5 h before surgery prevented the development of thermal hyperalgesia with a MED of 1 mg/kg. However, unlike gabapentin and S-(+)-3-isobutylgaba, it had little effect on the development of tactile allodynia. It is suggested that gabapentin and S-(+)-3-isobutylgaba may be effective in the treatment of postoperative pain.
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PMID:Evaluation of gabapentin and S-(+)-3-isobutylgaba in a rat model of postoperative pain. 931 31

Pain is a frequent and distressing complaint in patients with multiple sclerosis (MS) and may present a difficult therapeutic problem. Conventional therapy is moderately effective and includes, among others, a variety of anticonvulsant medications. Gabapentin (Neurontin) is a new generation antiepileptic drug which appears to be advantageous in treatment of intractable pain of reflex sympathetic dystrophy. This study investigates the benefits of open-label treatment with gabapentin for pain control in 25 patients with MS. Excellent to moderate pain relief was obtained in a substantial number of patients. Throbbing pains and needles, and cramping pains responded best, and dull aching pains responded least to the medication. There was no significant change in distribution and type of pain as a result of this treatment. Mild to moderate side effects were observed. Cautious escalation of the dose of gabapentin is advisable in MS patients. Further clinical trials with larger patient groups are recommended.
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PMID:Open label gabapentin treatment for pain in multiple sclerosis. 937 9

Gabapentin is an effective option for the treatment of neuropathic pain syndromes because of its efficacy and favorable side-effect profile. A case is presented of a 58 year old man who developed a painful polyneuropathy while being treated with gabapentin.
Pain 1998 Feb
PMID:Gabapentin induced polyneuropathy. 987 May 79

There are few pharmacological studies of central neuronal measures in animal models of neuropathic pain. In the present study we have compared the effects of two anticonvulsants, carbamazepine and gabapentin, on spinal neuronal responses of nerve injured rats (selective ligation of spinal nerves L5 and L6, SNL) and sham-operated rats. The development and maintenance of cooling and mechanical allodynia of the lesioned hindlimb of SNL rats was followed with behavioural indices. The contralateral hindlimb of SNL rats and the ipsilateral hindlimb of sham-operated rats did not develop allodynia. Electrophysiological studies of SNL rats were then performed at two post-operative (PO) time points (PO days 7-10 and PO days 14-17). Spinal neurones of SNL rats, but not sham-operated rats, exhibited spontaneous activity at both PO days 7-10 and 14-17 (1 +/- 0.4 and 3 +/- 1 Hz, respectively). Paradoxically, the magnitude of electrical (C-fibre) and natural (mechanical and thermal) evoked neuronal responses of SNL rats at PO days 14-17 were smaller than the evoked neuronal responses of SNL rats at PO days 7-10 and sham-operated rats. The electrical evoked A-fibre responses of neurones were comparable for the three groups of rats. Both subcutaneous carbamazepine (0.5-22.5 mg/kg) and gabapentin (10-100 mg/kg) significantly reduced the spontaneous activity of spinal neurones of SNL rats at both PO time points. Carbamazepine had inhibitory effects on electrical C- and A-fibre and mechanical punctate (9 and 50 g) evoked neuronal responses of SNL rats which were significantly different to the lack of effect of carbamazepine on these measures in sham-operated rats. Gabapentin had comparable effects as carbamazepine on the electrical C-and A-fibre and mechanical punctate (9 and 50 g) evoked neuronal responses of SNL rats. In contrast to carbamazepine, gabapentin also reduced evoked neuronal responses of sham-operated rats and there was no difference between the effects of gabapentin in SNL and sham-operated rats. Robust behavioural changes in the SNL model of neuropathy are paralleled by a temporal increase in spontaneous activity and a paradoxical decrease in evoked spinal neuronal responses. The peripheral nerve dysfunction reveals an effect of carbamazepine which is maintained throughout the observation period, validating this experimental approach. Gabapentin, a novel treatment for neuropathic pain states, also reduced neuronal responses, but the actions of the drug were not dependent on nerve injury. Further studies at the spinal level may shed light on the physiology and pharmacology of the aberrant processes associated with neuropathic pain.
Pain 1998 Apr
PMID:Effects of systemic carbamazepine and gabapentin on spinal neuronal responses in spinal nerve ligated rats. 958 62


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