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PubMed2004

Treatment of diabetic neuropathic pain with gabapentin alone or combined with vitamin B complex. preliminary results.

Neuropathic pain is a syndrome that affects around 1% of population. This condition can be severely disabling and traditional analgesics are useless against this type of pain. Several adjuvants such as the anticonvulsive agent gabapentin have been used to treat diabetic neuropathy with several degrees of effectiveness, but it is characterized of a high incidence of dizziness, somnolence and ataxia. Previously we have found a functional synergistic interaction after co-administration of gabapentin and B vitamins by using a neuropathic pain model in the rat. In order to evaluate the efficacy of gabapentin and B vitamins in the treatment of diabetic neuropathy in humans we carried out a comparative trial. In this study are presented preliminary results from 6 patients assigned to two groups: group A (n=3) received gabapentin, and group B (n=3) received gabapentin plus B vitamins. In both groups, the dose was increased at weekly intervals, and characteristics of pain and some parameters of quality of life were assessed. Both treatments significantly reduced pain and improved quality of life in the patients. Dizziness was the main adverse event observed in both groups. Data suggest that the combination of gabapentin and B vitamins could be an alternative treatment for diabetic neuropathic patients.

Activities of Daily Living↗
PubMedDate not supplied

Prophylactic gabapentin for prevention of postoperative nausea and vomiting in patients undergoing laparoscopic cholecystectomy: a randomized, double-blind, placebo-controlled study.

BACKGROUND: Gabapentin is an antiepileptic drug. Its antiemetic effect is demonstrated in chemotherapy-induced acute and delayed onset of nausea and vomiting in breast cancer patients. AIM: To evaluate the antiemetic effect of gabapentin on incidence and severity of postoperative nausea and vomiting in laparoscopic cholecystectomy. SETTINGS AND DESIGN: Double-blind, randomized, placebo-controlled study. MATERIALS AND METHODS: Two hundred and fifty patients of ASA physical status I and II, scheduled for laparoscopic cholecystectomy were randomly assigned into two equal groups to receive 600 mg gabapentin or matching placebo two hours before surgery. Standard anaesthesia technique was used. Fentanyl was used as rescue postoperative analgesic. Ondansetron 4 mg was used intravenously as rescue medication for emesis. The total number of patients who had nausea or vomiting, and its severity and total fentanyl consumption in the first 24 hours were recorded. STATISTICAL ANALYSIS: "Z test" was used to test the significance of severity of post-operative nausea and vomiting between groups. Fentanyl consumed in each group (Mean+/-SD) within 24 hrs was compared using student t test. P value < 0.05 was considered significant. RESULTS: There were no demographic difference between the two groups. Incidence of post-operative nausea and vomiting within 24 hrs after laparoscopic cholecystectomy was significantly lower in gabapentin group (46/125) than in the placebo group (75/125) (37.8% vs 60%; P =0.04). There was a significantly decreased fentanyl consumption in gabapentin group (221.2+/-92.4 microg) as compared to placebo group (505.9+/-82.0 microg; P =0.01). CONCLUSION: Gabapentin effectively suppresses nausea and vomiting in laparoscopic cholecystectomy and post-operative rescue analgesic requirement.

Adult↗
PubMed1985

Gabapentin decreases monoamine release without affecting acetylcholine release in the brain.

Superfused rat brain cortex slices preincubated with 3H-noradrenaline or 3H-serotonin and superfused rabbit caudate nucleus slices preincubated with 3H-choline were used to examine the effects of gabapentin (an amino acid chemically related to gamma-aminobutyric acid, GABA) on the electrically evoked 3H overflow. Gabapentin inhibited the electrically (3 Hz) evoked 3H overflow from slices preincubated with the 3H-monoamines in a concentration-dependent manner (at 1 mmol/l by 20-30%), but did not affect the evoked overflow from slices preincubated with 3H-choline. The following drugs did not modify the inhibitory effects of gabapentin: bicuculline, RS-baclofen, GABA, phentolamine, metitepin, cocaine, and the inhibitor of serotonin uptake, 6-nitroquipazine. Gabapentin did not modify the inhibitory effect of GABA on the evoked 3H overflow from slices preincubated with 3H-serotonin. In slices preincubated with 3H-noradrenaline the inhibitory effect of gabapentin was still observed when the stimulation frequency was 10 instead of 3 Hz. In conclusion, gabapentin mimics GABAB receptor activation, but it appears to act by a GABA receptor-independent, as yet unidentified mechanism.

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PubMed1997

Psychomotor agitation following gabapentin use in brain injury.

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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PubMed1998

[Gabapentin--a new antiepileptic agent].

Gabapentin is a new antiepileptic drug. Its mechanism of action is not clearly understood, but it seems to differ from that of other antiepileptic drugs. The favourable pharmacokinetic properties of gabapentin make it simple to use. Our preliminary clinical observations with gabapentin at the National Center for Epilepsy are presented. 58 adult patients (mean age 28.9 years), mainly with refractory partial seizures, had gabapentin added to their existing medication. The follow-up period was 6.9 months on average. Only one patient experienced a reduction in seizures of more than 50%, while 25 patients experienced a moderate reduction in seizures (10-50%). The clinical effect was most favourable in patients with secondary generalized tonic-clonic seizures. Gabapentin was well tolerated, and no clinically significant interactions were encountered. Recent observations show that the doses of gabapentin used in our study may have been too low.

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PubMed2000

Gabapentin-lactam (8-aza-spiro[5,4]decan-9-on; GBP-L) inhibits oxygen glucose deprivation-induced [3H]glutmate release and is a neuroprotective agent in amodel of acute retinal ischemia.

The modulation of the enhanced release of [3H]glutamate following ischemia-like conditions was studied in rat hippocampal slices using a superfusion system. Ischemia was simulated by a glucose-free medium equilibrated with 95% N2 and 5% CO2. In this model the potential neuroprotective effects of several substances on [3H]glutamate release induced by ischemia-like conditions were investigated. Gabapentin-lactam (8-aza-spiro-5,4-decan-9-on; GBP-L) was synthesised and patented in our laboratory. GBP-L (100 microM) reduced the oxygen glucose deprivation-induced [3H]glutamate release by 42.5%, CI95=[33.4%, 51.5%]. The KATP channel antagonist glibenclamide (1 microM) blocked this effect completely. The high antagonist potency was reflected by an apparent pA2-value of glibenclamide of 8.3, CI95=[6.8, 9.4]. Minoxidil sulfate (10 microM), a KATP channel opener, mimicked the effect of GBP-L (inhibition by 22.8%, CI95=[13.2%, 32.5%]). Similarly to its lactam, also gabapentin (100 microM) reduced the oxygen glucose deprivation-induced [3H]glutamate release by 30.6%, CI95=[15.5%, 45.7%], whereas the "antiglutamatergic" drug riluzole was ineffective. GBP-L and gabapentin were also tested in an in vivo model of acute retinal ischemia in rats. The intraocular pressure was elevated for 1 h above the systolic blood pressure. In the control group, 17.5%, CI95=[13%, 22%], of retinal ganglion cells had survived after 2 weeks. GBP-L doubled the number of surviving ganglion cells up to 35%, CI95=[27%, 43%], while gabapentin had no effect. This difference between gabapentin and its lactam may be due to different pharmacokinetic properties: In contrast to the gamma-amino acid gabapentin, GBP-L is uncharged and therefore might diffuse more easily through biological membranes, e.g. the plasma membrane, to get access to an intracellular locus of action. Thus, the neuroprotective properties in vivo and the diminished oxygen glucose deprivation-induced [3H]glutamate efflux in vitro of the presumed KATP channel agonist GBP-L suggest that this substance might be therapeutically applied in pathological situations induced by a rise in extracellular glutamate and/or neuronal cell death.

Algorithms↗
PubMed2006

Effect of Gabapentin on morphine demand and pain after laparoscopic sterilization using Filshie clips. A double blind randomized clinical trial.

BACKGROUND: A considerable number of patients require opioids during recovery after laparoscopic sterilization. This implies nausea, dizziness and sedation and increases the number of unplanned admissions. Gabapentin has shown excellent postoperative analgesic effect in a number of recent studies with few side effects. This study was designed to test whether gabapentin given preoperatively can reduce the number of patients needing morphine in the recovery period. METHODS: 80 females scheduled for laparoscopic sterilization using Filshie clips were randomized to two treatment groups (Gaba group and control group). All patients received lornoxicam 8 mg p.o. 30 min. before the procedure. Patients in the Gaba group received gabapentin 1200 mg p.o. and patients in the control group received placebo capsules prior to the procedure. All patients were anesthetized according to a protocol, using remifentanil and propofol. Postoperative analgesia was obtained with patient controlled infusion of morphine. Pain, nausea, dizziness and sedation were scored at 2 and 4 hours after end of anesthesia. The expenditure of morphine was the primary measure for the effect of analgesia and the number of patients demanding morphine was the primary endpoint. RESULTS: Three patients were excluded because of procedural errors and one because of conversion to open surgery. 38 patients completed the study in each group.32 (84%) patients in the gabapentin group and 37 (97%) patients in the control group did require morphine in the recovery period. (p = 0,049). There was no significant difference between mean morphine consumption, pain scores and frequency of adverse effects (nausea, dizziness, sedation and vomiting) CONCLUSION: The postoperative analgesic effect of gabapentin given preoperatively was confirmed in this study. For this procedure, with pain predominantly in the immediate recovery period, and of less intensity than after major surgical procedures, the effect demonstrated is much less pronounced than in similar studies of major surgery. General use of gabapentin as analgesic for laparoscopic sterilization is not supported by this study. TRIAL REGISTRATION: Current Controlled Trials ISCRTN39209275.

Journal Article↗
PubMed1994

Long-term study with gabapentin in patients with drug-resistant epileptic seizures.

OBJECTIVE: To study the efficacy and safety of gabapentin in long-term treatment. DESIGN: A 4-year follow-up study of 25 patients with visits at 3-month intervals. SETTING: The patients were followed up in the outpatient unit of the University Hospital of Kuopio (Finland). PATIENTS: We treated 25 patients with drug-resistant complex partial seizures and secondarily generalized seizures in an open-label long-term study, using gabapentin as an additional means of therapy after a 3-month double-blind, placebo-controlled phase. Thirteen patients showed no benefit from gabapentin; the study medication was discontinued after 4 to 6 months of treatment. Of the 12 patients who responded enough to continue treatment, five were withdrawn due to different reasons, one because of loss of response. MAIN OUTCOME MEASURES: The number of patients receiving the study drug in the follow-up and reduction of seizure frequency from baseline level as analyzed by the Wilcoxon test. RESULTS: Seven patients received gabapentin therapy for more than 4 years. The median follow-up time was 54 months. There was a significant reduction in seizure frequency throughout the follow-up period. Five of seven patients had a greater than 50% seizure frequency reduction at 4 years, representing 20% of the 25 patients who entered the study. CONCLUSIONS: Gabapentin possesses good efficacy in long-term treatment of patients with partial and secondarily generalized epileptic seizures. It is safe to use, and it is fairly well tolerated even in long-term treatment.

Acetates↗
PubMed1996

The effect of gabapentin on brain gamma-aminobutyric acid in patients with epilepsy.

Gabapentin has come into clinical use as adjunctive therapy in the treatment of epilepsy. Designed to mimic gamma-aminobutyric acid (GABA), its mechanism of action remains elusive. In vivo measurements of GABA in human brain were made using 1H magnetic resonance spectroscopy. We used a 2.1-T magnetic resonance imager-spectrometer and an 8-cm surface coil to measure a 13.5-cm3 volume in the occipital cortex. GABA levels were measured in 14 patients enrolled in an open-lbel trial of gabapentin. GABA was elevated in patients taking gabapentin compared with 14 complex partial epilepsy patients, matched for antiepileptic drug treatment. Brain GABA levels appeared to be higher in patients taking high-dose gabapentin (3,300-3,600 mg/day) than in those taking standard doses (1,200-2,400 mg/day). Gabapentin appears to increase human brain GABA levels.

Acetates↗
PubMed2005

Gabapentin can improve postural stability and quality of life in primary orthostatic tremor.

Primary orthostatic tremor (OT) is characterized by leg tremor and instability on standing. High frequency (13-18 Hz) tremor bursting is present in leg muscles during stance, and posturography has shown greater than normal sway. We report on an open-label add-on study of gabapentin in 6 patients with OT. Six patients were studied with surface electromyography, force platform posturography, and a modified Parkinson's disease questionnaire (PDQ-39) quality of life (QOL) scale before and during treatment with gabapentin 300 mg t.d.s. If on other medications for OT, these were continued unchanged. Of the 6 patients, 4 reported a subjective benefit of 50 to 75% with gabapentin, 3 of whom showed reduced tremor amplitude and postural sway of up to 70%. Dynamic balance improved in all 3 patients who completed the protocol. QOL data from 5 patients showed improvement in all cases. No adverse effects were noted. Gabapentin may improve tremor, stability, and QOL in patients with OT, and symptomatic response correlated with a reduction in tremor amplitude and postural sway. The findings confirm previous reports of symptomatic benefit with gabapentin and provide justification for larger controlled clinical trials. Further work is required to establish the optimal dosage and to validate the methods used to quantify the response to treatment.

Aged↗
PubMed1998

Effective treatment of orthostatic tremor with gabapentin.

We report seven patients with orthostatic tremor (OT) who were successfully treated with the anticonvulsant gabapentin. Five of the patients had been previously tried on clonazepam, the most commonly used drug for OT, four without any benefit. The degree of improvement perceived by the patients with gabapentin varied from 60-80% (mean 73%). The effective dose of gabapentin ranged from 300-1800 mg/day (mean 1030 mg/day). The side effects were generally mild, transient, and dose-related. Duration of response has so far ranged from 2-22 months (mean 11 months) with all patients still currently benefiting from gabapentin. We conclude that gabapentin may be an effective treatment for OT. Further trials are indicated.

Acetates↗
PubMed2004

Preemptive gabapentin decreases postoperative pain after lumbar discoidectomy.

PURPOSE: We investigated whether the preemptive use of gabapentin, a structural analogue of gamma amino butyric acid could reduce postoperative pain and fentanyl consumption in patients after single-level lumbar discoidectomy. METHODS: Fifty-six ASA I and II patients were randomly allocated into two equal groups to receive either gabapentin 300 mg or placebo two hours before surgery. After surgery, the pain was assessed on a visual analogue scale (VAS) at intervals of 0-6, 6-12, 12-18, and 18-24 hr at rest. Total fentanyl consumption in the first 24 hr after surgery was also recorded. Fentanyl 2 mug.kg(-1) intravenously was used to treat postoperative pain on patients' demand. RESULTS: Patients in the gabapentin group had significantly lower VAS scores at all time intervals of 0-6, 6-12, 12-18, and 18-24 hr than those in the placebo group (3.5 +/- 2.3, 3.2 +/- 2.1, 1.8 +/- 1.7, 1.2 +/- 1.3 vs 6.1 +/- 1.7, 4.4 +/- 1.2, 3.3 +/- 1.1, 2.1 +/- 1.2; P < 0.05). The total fentanyl consumed after surgery in the first 24 hr in the gabapentin group (233.5 +/- 141.9, mean + SD) was significantly less than in the placebo group (359.6 +/- 104.1; P < 0.05). CONCLUSION: Preemptive gabapentin 300 mg po significantly decreases the severity of pain postoperatively in patients who undergo single-level lumbar discoidectomy.

Adult↗
PubMed2003

Cellular and molecular action of the putative GABA-mimetic, gabapentin.

Gabapentin was originally designed as an anti-convulsant gamma-aminobutyric acid (GABA) mimetic capable of crossing the blood-brain barrier. In the present review we show that although gabapentin is not a GABA mimetic, it has great utility as an add-on therapy for epilepsy and as a first-line treatment for neuropathic pain. We summarise the studies that have been performed which demonstrate that gabapentin appears to interact with a novel binding site expressed at high density within the central nervous system (CNS), namely the alpha2delta voltage-dependent calcium channel subunit. The review continues by examining the effects of gabapentin on calcium channel function and neurotransmitter release before, in the latter part of the review, summarising the more recently discovered actions of gabapentin in relation to intracellular signalling.

Acetates↗
PubMed2001

[Gabapentin therapy for pain].

Gabapentin, which has been approved for add-on therapy of focal seizures, is increasingly used for treatment of neuropathic pain. Its analgesic effect is supposed to be due to reduction of glutamatergic transmission, improvement of GABAergic transmission and to binding to voltage-dependent calcium channels. Experimental studies demonstrated an ameliorating effect of gabapentin on neuropathic pain. Placebo-controlled studies revealed an efficacy of gabapentin against pain in diabetic neuropathy and postherpetic neuralgia and in prophylaxis of migraine. Case reports show an analgesic effect of gabapentin in trigeminus neuralgia and in reflex sympathetic dystrophy. The main adverse events are dizziness, ataxia and somnolence. Controlled studies, which compare the efficacy of gabapentin with that of the respective reference drug, are needed to evaluate its importance in treatment of pain.

Acetates↗
PubMed2001

[Gabapentin for therapy of neuropathic pain].

Gabapentin, which has been approved for add-on therapy of focal seizures, is increasingly used for treatment of neuropathic pain. Its analgesic effect is supposed to be due to reduction of glutamatergic transmission, improvement of GABAergic transmission and to binding to voltage-dependent calcium channels. Experimental studies demonstrated an ameliorating effect of gabapentin on neuropathic pain. Placebo-controlled studies revealed an efficacy of gabapentin against pain in diabetic neuropathy and postherpetic neuralgia and in prophylaxis of migraine. Case reports show an analgesic effect of gabapentin in trigeminus neuralgia and in reflex sympathetic dystrophy. The main adverse events are dizziness, ataxia and somnolence. Controlled studies, which compare the efficacy of gabapentin with that of the respective reference drug, are needed to evaluate its importance in treatment of pain.

Acetates↗
PubMed1996

Effect of gabapentin (Neurontin) [corrected] on mood and well-being in patients with epilepsy.

1. Global improvement data from five double-blind clinical trials of gabapentin as add-on therapy in patients with epilepsy were reviewed to assess the effects of gabapentin on mood. 2. One hundred and ninety-four (46%) of 423 gabapentin-treated patients reported improvements in general well-being as compared with 79 (29%) of the 271 placebo-treated patients. 3. Findings support anecdotal reports of improved affective status among patients taking gabapentin and suggest that the study of gabapentin in psychiatric populations may be warranted.

Acetates↗
PubMed1995

Pancreatic acinar cell neoplasia in male Wistar rats following 2 years of gabapentin exposure.

Gabapentin, an anticonvulsant agent designated chemically as 1-(aminomethyl)-cyclohexaneacetic acid, was evaluated in a 2-year tumor bioassay in male Wistar rats. Three groups of 50 rats were fed gabapentin at 250, 1000 and 2000 mg/kg in the diet for 104 weeks. A fourth group was fed diet without drug. All rats were subjected to full histopathological evaluation. Body weight gain suppression occurred at 1000 and 2000 mg/kg. Survival was comparable across all groups. There was a treatment-related increase in the number of pancreatic acinar cell carcinomas; 0, 4, 3 and 8 of these carcinomas were observed in the control, 250, 1000 and 2000 mg/kg groups, respectively. There were no other increases in other tumor types, and there were no tumor increases in female rats. The frequency of pancreatic acinar cell hyperplasia was similar in treated and control groups. Biologically, the pancreatic carcinomas were not invasive, did not metastasize, were of late onset and did not compromise survival. Thus, gabapentin was a carcinogen in male Wistar rats. However, the tumorigenic response was of low-grade because it constituted a late tumor response which required very high doses. We reported recently that mice treated with gabapentin had no increase in pancreatic tumors. Therefore, neoplastic development was confined to the pancreas in a single sex and species of rodent. Consequently, gabapentin at therapeutic doses poses a low carcinogenic risk to humans.

Acetates↗
PubMed1994

Gabapentin increases GABA-induced depolarization in rat neonatal optic nerve.

Membrane potential changes of rat neonatal optic nerves were studied in a sucrose-gap chamber. Nipecotic acid (NPA), which blocks uptake and promotes release of GABA, resulted in a bicuculline-sensitive depolarization (3.08 +/- 0.3 mV, n = 5). Pretreatment of the nerves with the anticonvulsant gabapentin (100 microM for 1 h) resulted in a near doubling of the NPA-induced depolarization (6.64 +/- 0.54 mV, n = 5). Gabapentin itself did not alter membrane potential, nor did brief applications of gabapentin enhance the NPA- or GABA-induced depolarization. Thus, gabapentin appears to enhance the releasable pool of GABA in this CNS neural system. These results have implications for the mechanism of the anticonvulsant properties of gabapentin.

Acetates↗