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PubMed2006

Experience with gabapentin for neuropathic pain in adolescents: report of five cases.

Summary Gabapentin is an antiepileptic drug indicated for the treatment of partial seizures in children. Many studies have proved its analgesic action in the treatment of neuropathic pain in adults and we have noticed an analgesic action of gabapentin in neuropathic pain in children. Five patients treated in the Children's Hospital Pain Control Service for intractable neuropathic pain were included in gabapentin treatment. Four were cancer patients and one suffered from neuropathic pain in the neck (C3). The visual analog scale (VAS) scores of pain were compared before and during treatment with gabapentin. We noticed a rapid improvement, in 1 week, of our patients' VAS scores (from 9 or 10 to 4 or 3) with minimal adverse effects. In the follow-up period of 6 months we gradually reduced the dose of gabapentin. Our findings are that gabapentin should be included earlier in the treatment of neuropathic pain in adolescents, because it rapidly improves analgesia and has minimal side effects.

Adolescent↗
PubMed1999

Nonepileptic uses of gabapentin.

For decades, antiepileptic drugs (AEDs) have been used to treat a variety of nonepileptic conditions such as chronic pain, psychiatric disorders, and movement disorders. As indicated by recent published reports, gabapentin, a relatively new AED, is useful for treating a wide range of neurologic and psychiatric conditions. Although its exact mechanism of action has yet to be determined, gabapentin is likely to have multiple effects. Unlike conventional AEDs used to treat nonepileptic disorders (e.g., carbamazepine, phenytoin, valproate) gabapentin offers the advantages of low toxicity and a favorable side-effect profile. The largest area of nonepileptic use of gabapentin is neuropathic pain, in which it has demonstrated efficacy in treatment of postherpetic neuralgia, diabetic neuropathy, and trigeminal neuralgia. It has also been reported effective as therapy for several psychiatric disorders, most notably bipolar disorder. In addition, review of the published literature reveals the usefulness of gabapentin in movement disorders, migraine prophylaxis, and cocaine dependence. Future clinical studies will provide further insight into the range of conditions for which gabapentin is effective.

Acetates↗
PubMed2005

Novel role for gabapentin in neuroprotection of central nervous system in streptozotocine-induced diabetic rats.

AIM: To investigate the effect of gabapentin on neural [neuron-specific enolase (NSE)] and glial markers [glial fibrillary acidic protein (GFAP) and S100B] in different brain regions of diabetic rats. METHODS: Diabetes was induced by a single intraperitoneal injection of streptozotocine (50 mg/kg body weight). Rats in one diabetic group received gabapentin (50 mg.kg(-1).d(-1)) and rats in the other diabetic group received vehicle only for 6 weeks. The levels of GFAP, S100B, and NSE were determined by immunoblotting in the hippocampus, cortex, and cerebellum. Lipid peroxidation (LPO as malondialdehyde+ 4-hydroxyalkenals) and glutathione (GSH) levels were also determined in the same brain parts. RESULTS: Total and degraded GFAP content and S100B protein expression in different areas of brain tissues significantly increased in diabetic rats compared to control rats. Similarly, NSE levels were also significantly elevated in hyperglycemic rats. In addition, there was a significant increase in LPO levels in the diabetic rat brain compared to control rat brains. Pretreatment with gabapentin prevented the upregulation of GFAP, S100B, and NSE in all brain regions of diabetic rats. The level of LPO was reduced, but not completely halted, by treatment with gabapentin. CONCLUSION: These results suggest that diabetes causes glial and neuronal injury, possibly as a result of elevated oxidative stress, and that gabapentin protects neurons and glial cells. Thus, we predict that gabapentin treatment will attenuate the hippo-campal and cortical neurodegeneration observed during diabetes mellitus in rats.

Amines↗
PubMed2005

Synergic antinociceptive interaction between tramadol and gabapentin after local, spinal and systemic administration.

The possible interaction between tramadol and gabapentin on formalin-induced nociception in the rat was assessed. Tramadol, gabapentin or a fixed-dose ratio combination of gabapentin and tramadol were administered peripherally, spinally and orally to rats, and the antinociceptive effect was determined in the 1% formalin test. Isobolographic analyses were used to define the nature of the interactions between drugs. Tramadol, gabapentin and tramadol-gabapentin combinations produced a dose-dependent antinociceptive effect when administered locally, spinally or orally. ED30 values were estimated for the individual drugs and isobolograms were constructed. Theoretical ED30 values for the combination estimated from the isobolograms were 126.8 +/- 11.1 microg/paw, 23.1 +/- 2.6 microg/rat, and 2.23 +/- 0.32 mg/kg for the local, intrathecal and oral routes, respectively. These values were significantly higher than the actually observed ED30 values which were 13.3 +/- 2.1 microg/paw, 8.1 +/- 0.6 microg/rat and 0.71 +/- 0.10 mg/kg, indicating a synergistic interaction. Although efficacy was not improved, local peripheral administration resulted in the highest increase in potency, being about tenfold. Spinal and systemic administration increased potency threefold. Data indicate that low doses of the tramadol-gabapentin combination can interact synergistically to reverse formalin-induced nociception and may represent a therapeutic advantage for clinical treatment of inflammatory pain.

Administration, Oral↗
PubMed1996

Placebo-controlled trial of gabapentin in patients with amyotrophic lateral sclerosis. WALS Study Group. Western Amyotrophic Lateral Sclerosis Study Group.

We designed a phase II trial to evaluate the efficacy of gabapentin in slowing the rate of decline in muscle strength of patients with amyotrophic lateral sclerosis (ALS) and to assess safety and tolerability. Gabapentin (800 mg) or placebo was administered t.i.d. in a randomized, double-blinded, placebo-controlled, trial for 6 months. We enrolled 152 patients at eight sites in the United States. The primary outcome measure was the slope of the arm megascore, the average maximum voluntary isometric strength from eight arm muscles standardized against a reference ALS population. A secondary outcome measure was forced vital capacity. Slopes of arm megascores for patients on gabapentin were compared with slopes of those taking placebo using a two-way ANOVA. We observed a nonstatistically significant trend (p = 0.057-0.08) toward slower decline of arm strength in patients taking gabapentin compared with those taking placebo (mean difference 24%, median 37%). We observed no treatment effect on forced vital capacity. Gabapentin was well tolerated by patients with ALS. These results suggest that further studies of gabapentin in ALS are warranted.

Acetates↗
PubMed2004

The analgesic effects of gabapentin in monitored anesthesia care for ear-nose-throat surgery.

We investigated the efficacy and safety of gabapentin in rhinoplasty or endoscopic sinus surgery patients. Patients received either oral placebo or gabapentin 1200 mg 1 h before surgery. After standard premedication, 25 patients in each group received propofol, fentanyl, and local anesthesia at the operative site. Sedation was maintained by a continuous infusion of propofol adjusted according to the Ramsay scale. Sedation and pain scores were obtained at 5, 15, 30, 45, and 60 min during surgery and 30 min and 2, 4, 6, 8, 12, 16, 20, and 24 h after the procedure. Diclofenac 75 mg IM was administered as a rescue analgesic. Postoperative pain scores and intraoperative pain scores at 45 and 60 min were significantly lower in the gabapentin group. Fentanyl (122 +/- 40 microg versus 148 +/- 42 microg; P < 0.05) and diclofenac (33 +/- 53 mg versus 111 +/- 92 mg; P < 0.001) consumption was smaller and the time to first analgesic request (18 +/- 9 h versus 9 +/- 7 h; P < 0.001) was longer in the gabapentin group. A more frequent incidence of dizziness was found in the gabapentin (versus placebo) group (24% versus 4%, respectively). We conclude that gabapentin provided a significant analgesic benefit for intraoperative and postoperative pain relief in patients undergoing ambulatory rhinoplasty or endoscopic sinus surgery; however, dizziness may be a handicap for ambulatory use.

Acetates↗
PubMed2005

The comparative evaluation of gabapentin and carbamazepine for pain management in Guillain-Barré syndrome patients in the intensive care unit.

We evaluated the effects of gabapentin and carbamazepine for pain relief in 36 Guillain-Barré syndrome patients. Patients were randomly assigned to receive gabapentin 300 mg, carbamazepine 100 mg, or matching placebo 3 times a day for 7 days. Fentanyl 2 microg/kg was used as a supplementary analgesic on patient demand. The pain score was recorded by using a numeric pain rating scale of 0-10, and sedation was recorded with a Ramsay sedation scale of 1-6 before medications were given and then at 6-h intervals throughout the study period. Total daily fentanyl consumption was recorded each day for each patient. The results of the study demonstrated that patients in the gabapentin group had significantly lower (P < 0.05) median numeric pain rating scale scores (3.5, 2.5, 2.0, 2.0, 2.0, 2.0, and 2.0) compared with patients in the placebo group (6.0, 6.0, 6.0, 6.0, 6.0, 6.0, and 6.0) and the carbamazepine group (6.0, 6.0, 5.0, 4.0, 4.0, 3.5, and 3.0). There was no significant difference in fentanyl consumption between the gabapentin and carbamazepine groups on Day 1 (340.1 +/- 34.3 microg and 347.5 +/- 38.0 microg, respectively), but consumption was significantly less in these 2 groups compared with the placebo group (590.4 +/- 35.0 microg) (P < 0.05). For the rest of the study period, there was a significant difference in fentanyl consumption among all treatment groups, and it was minimal in the gabapentin group (P < 0.05). We conclude that gabapentin is more effective than carbamazepine for decreasing pain and fentanyl consumption.

Adult↗
PubMed2006

The antiallodynic action target of intrathecal gabapentin: Ca2+ channels, KATP channels or N-methyl-d-aspartic acid receptors?

Gabapentin is a novel analgesic whose mechanism of action is not known. We investigated in a postoperative pain model whether adenosine triphosphate (ATP)-sensitive K+ (K(ATP)) channels, N-methyl-d-aspartic acid (NMDA) receptors, and Ca2+ channels are involved in the antiallodynic effect of intrathecal gabapentin. Mechanical allodynia was induced by a paw incision in isoflurane-anesthetized rats. Withdrawal thresholds to von Frey filament stimulation near the incision site were measured before and after incision and after intrathecal drug administration. The antiallodynic effect of gabapentin (100 mug) was not affected by intrathecal pretreatment with antagonists of K(ATP) channels, NMDA receptors or gamma-aminobutyric acid (GABA)(A) receptors. K(ATP) channel openers and GABA(A) receptor agonist, per se, had little effect on the postincision allodynic response. The Ca2+ channel blocker of N-type (omega-conotoxin GVIA, 0.1-3 microg), but not of P/Q-type (omega-agatoxin IVA), L-type (verapamil, diltiazem or nimodipine), or T-type (mibefradil), attenuated the incision-induced allodynia, as did gabapentin. Both the antiallodynic effects of gabapentin and omega-conotoxin GVIA were attenuated by Bay K 8644, an L-type Ca2+ channel activator. These results provide correlative evidence to support the contention that N-type Ca2+ channels, but not K(ATP) channels or NMDA or GABA(A) receptors, might be involved in the antiallodynic effect of intrathecal gabapentin.

Adenosine Triphosphate↗
PubMed2006

Mechanisms of the antinociceptive action of gabapentin.

Gabapentin, a gamma-aminobutyric acid (GABA) analogue anticonvulsant, is also an effective analgesic agent in neuropathic and inflammatory, but not acute, pain systemically and intrathecally. Other clinical indications such as anxiety, bipolar disorder, and hot flashes have also been proposed. Since gabapentin was developed, several hypotheses had been proposed for its action mechanisms. They include selectively activating the heterodimeric GABA(B) receptors consisting of GABA(B1a) and GABA(B2) subunits, selectively enhancing the NMDA current at GABAergic interneurons, or blocking AMPA-receptor-mediated transmission in the spinal cord, binding to the L-alpha-amino acid transporter, activating ATP-sensitive K(+) channels, activating hyperpolarization-activated cation channels, and modulating Ca(2+) current by selectively binding to the specific binding site of [(3)H]gabapentin, the alpha(2)delta subunit of voltage-dependent Ca(2+) channels. Different mechanisms might be involved in different therapeutic actions of gabapentin. In this review, we summarized the recent progress in the findings proposed for the antinociceptive action mechanisms of gabapentin and suggest that the alpha(2)delta subunit of spinal N-type Ca(2+) channels is very likely the analgesic action target of gabapentin.

Amines↗
PubMed1998

Gabapentin absorption: effect of mixing with foods of varying macronutrient composition.

OBJECTIVE: To compare the oral absorption profile of gabapentin following administration of the contents of opened capsules that were mixed with food vehicles of varied macronutrient (protein) composition. DESIGN: An unblinded, randomized, single-dose, four-way crossover pharmacokinetic study in nine healthy adult men and women volunteers. METHODS: Following an overnight fast, a single 600-mg dose of gabapentin (2 x 300-mg Neurontin capsules) was given either as an intact capsule swallowed with 120 mL of tap water (control, phase I), or after capsule contents were opened and mixed with; 4 oz. of applesauce (phase II), 120 mL of orange juice (phase III), or 4 oz. of fat-free chocolate pudding (phase IV). Subjects fasted for 4 hours following drug ingestion. Serial venous blood samples were obtained over 24 hours to determine gabapentin serum concentrations. Pharmacokinetic variables including AUC, maximum serum concentration (Cmax), and time to maximum serum concentration (tmax) were calculated by using standard noncompartmental methods. Subjects served as their own controls, and were randomly crossed over following a minimum 7-day washout period. Statistical analysis was performed by using ANOVA and Student's t-test where appropriate. RESULTS: No statistically significant differences in any kinetic variable were found between any study arm. A trend was noted for a modest increase in both Cmax and AUC in phase IV (chocolate pudding) compared with control (+18.6% and +13.2%, respectively). In a comparison of protein (phase IV) versus nonprotein phases (phases I-III), gabapentin AUC was 26% greater (47.28+/-14.65 vs. 37.43+/-9.78 microg/mL x h; p = 0.03), and Cmax was 32% higher (4.72+/-1.04 vs. 3.56+/-0.92 microg/mL; p = 0.003). CONCLUSIONS: Opening and mixing the contents of gabapentin capsules does not significantly impair drug absorption. This may be a viable administration option for patients who are unable to swallow intact capsules. Dietary macronutrient composition (i.e., protein) may favorably influence gabapentin oral absorption.

Acetates↗
PubMed2003

Flumazenil and dialysis for gabapentin-induced coma.

OBJECTIVE: To describe a case of gabapentin-induced coma that was reversed with flumazenil and hemodialysis. CASE SUMMARY: We describe an 83-year-old dialysis-dependent white man who became comatose after a single dose of gabapentin for phantom limb pain. The patient was successfully revived from the coma with administration of flumazenil, which was then followed by hemodialysis. Serum concentration data before and 4 hours after dialysis document the effectiveness of hemodialysis for gabapentin toxicity. DISCUSSION: An objective causality assessment revealed that this adverse event was probably related to the gabapentin that the patient received. To our knowledge, this is the first documented case of not only gabapentin-induced coma, but also the effectiveness of flumazenil for treatment of this type of coma. Although therapeutic hemodialysis has been previously described, our case report is strengthened by the serum concentration monitoring accompanying it. CONCLUSIONS: This report underscores the importance of initiating gabapentin therapy at low doses in dialysis-dependent patients and introduces a novel treatment for those who experience toxicity.

Acetates↗
PubMed2003

Gabapentin: in postherpetic neuralgia.

Gabapentin is a structural analogue of the neurotransmitter gamma-aminobutyric acid (GABA) approved for use in adults with postherpetic neuralgia. Gabapentin does not bind to GABA(A) or GABA(B) receptors. Its mechanism of action in humans is unclear, but may involve binding to alpha2delta calcium channel subunits in animal models. Reductions in the mean daily pain score from baseline to week 7 or 8 of treatment (primary endpoint) were significantly greater with gabapentin 1800-3600 mg/day than placebo therapy in two well designed trials in patients with postherpetic neuralgia. The proportion of responders (patients showing a > or =50% reduction in mean daily pain score at endpoint versus baseline) was significantly greater with gabapentin than placebo. Daily sleep rating scores, the Short Form McGill Pain Questionnaire (total pain scores), Patient and Clinician Global Impression of Change and measures on the Short Form-36 Health Survey (including physical functioning, role-physical, bodily pain, vitality or mental health) improved to a significantly greater extent with gabapentin than placebo. Adverse events associated with gabapentin in patients with postherpetic neuralgia were usually mild to moderate in intensity, with dizziness, somnolence and peripheral oedema being commonly reported.

Acetates↗
PubMed2006

Addition of gabapentin to a modified FOLFOX regimen does not reduce oxaliplatin-induced neurotoxicity.

BACKGROUND: Sensory neurotoxicity is dose limiting for oxaliplatin, an effective drug in the treatment of colorectal cancer (CRC) and other malignancies. This study assessed the impact of gabapentin on oxaliplatin dose intensity and neurotoxicity. PATIENTS AND METHODS: Patients with previously untreated metastatic CRC were recruited sequentially to 2 cohorts: the first used a modified FOLFOX6 (fluorouracil/leucovorin/oxaliplatin) regimen alone with oxaliplatin 100 mg/m(2) every 2 weeks (mFOLFOX; n = 40), and the second included the addition of gabapentin (mFOLFOX+G; n = 41). Gabapentin commenced at 300 mg daily, increasing to a maximum of 600 mg 3 times daily to decrease neurotoxicity. RESULTS: Doses of gabapentin were increased in 31 of 41 patients, with 39% of patients receiving >or= 900 mg daily. The median relative dose intensity of oxaliplatin and requirement for dose reductions or delays because of neurotoxicity were similar in the 2 cohorts. There was no grade 4 neurotoxicity. Whereas grade 3 neurotoxicity was observed in 10% of patients treated with gabapentin versus 21% of patients treated with mFOLFOX alone, there was no statistically significant difference in the severity of neurotoxicity between the 2 cohorts (P = 0.89) or the time to recover from grade 2/3 neurotoxicity (P = 0.97). There were also no significant differences in nonneurologic toxicity or antitumor efficacy between the 2 cohorts. CONCLUSION: This study does not support a role for gabapentin in reducing the incidence or severity of oxaliplatin-induced sensory neurotoxicity.

Amines↗
PubMed2006

Gabapentin versus nortriptyline in post-herpetic neuralgia patients: a randomized, double-blind clinical trial--the GONIP Trial.

BACKGROUND: Gabapentin and nortriptyline have not been compared in a randomized trial in post-herpetic neuralgia (PHN). The present study was, therefore, undertaken to determine their comparative efficacy and tolerability in the treatment of post-herpetic neuralgia. PATIENTS AND METHODS: The study was a randomized, double-blind, parallel-group trial of 9 weeks duration. Adult PHN patients with history of > 8 weeks of PHN pain after healing of rash, a pain intensity of at least 40 mm on a 100 mm visual analog scale at screening and at randomization, and average pain score of at least 4 on the Likert scale during the baseline week were included in the study. Gabapentin and nortriptyline were given in incremental doses at 2-weekly intervals till a maximum tolerated dose was obtained. The primary efficacy parameter was change in pain score (11-point Likert scale) from baseline to the end of the study period. RESULTS: 70 patients were available for intention-to-treat analysis. The average pain scores on the Likert scale were significantly reduced at the end of study in both the treatment groups with 47.6% and 42.8% reduction in pain scores in nortriptyline and gabapentin groups, respectively. Patients showed significant improvement in sleep scores in both the treatment groups nortriptyline (46.0%) and gabapentin (52.0%). The VAS and the SF-MPQ scores for pain were significantly reduced in both the groups. Gabapentin was, however, better tolerated as compared to nortriptyline. CONCLUSION: Gabapentin was shown to be equally efficacious but was better tolerated compared to nortriptyline and can be considered a suitable alternative for the treatment of PHN.

Aged↗
PubMed2006

Narrative review: the promotion of gabapentin: an analysis of internal industry documents.

BACKGROUND: Internal documents from the pharmaceutical industry provide a unique window for understanding the structure and methods of pharmaceutical promotion. Such documents have become available through litigation concerning the promotion of gabapentin (Neurontin, Pfizer, Inc., New York, New York) for off-label uses. PURPOSE: To describe how gabapentin was promoted, focusing on the use of medical education, research, and publication. DATA SOURCES: Court documents available to the public from United States ex. rel David Franklin vs. Pfizer, Inc., and Parke-Davis, Division of Warner-Lambert Company, mostly from 1994-1998. DATA EXTRACTION: All documents were reviewed by 1 author, with selected review by coauthors. Marketing strategies and tactics were identified by using an iterative process of review, discussion, and re-review of selected documents. DATA SYNTHESIS: The promotion of gabapentin was a comprehensive and multifaceted process. Advisory boards, consultants meetings, and accredited continuing medical education events organized by third-party vendors were used to deliver promotional messages. These tactics were augmented by the recruitment of local champions and engagement of thought leaders, who could be used to communicate favorable messages about gabapentin to their physician colleagues. Research and scholarship were also used for marketing by encouraging "key customers" to participate in research, using a large study to advance promotional themes and build market share, paying medical communication companies to develop and publish articles about gabapentin for the medical literature, and planning to suppress unfavorable study results. LIMITATIONS: Most available documents were submitted by the plaintiff and may not represent a complete picture of marketing practices. CONCLUSION: Activities traditionally considered independent of promotional intent, including continuing medical education and research, were extensively used to promote gabapentin. New strategies are needed to ensure a clear separation between scientific and commercial activity.

Advisory Committees↗
PubMed1999

Gabapentin attenuates nociceptive behaviors in an acute arthritis model in rats.

In this study, we investigated the effectiveness of gabapentin (Neurontin), administered spinally with a microdialysis fiber, in reducing nociceptive behavioral responses induced by a knee joint inflammation model. This model is produced by injection of the knee joint with kaolin and carrageenan in rats. The resultant knee joint inflammation produces a secondary hyperalgesia to radiant heat applied to the hindpaw. Both pretreatment and post-treatment protocols were examined. Spinal administration of gabapentin (10 mg/ml) infused 1.5 h before induction of knee joint inflammation, although having no effect on the baseline, prevented the development of heat hyperalgesia. Gabapentin also prevented the development of other pain-related behaviors scored subjectively. Gabapentin had no effect, however, on the joint circumference increase typical in this model. In animals with fully developed knee joint inflammation, gabapentin produced a reversal of heat hyperalgesia. The paw withdrawal latency responses and subjective pain scores were no longer significantly different from baseline, but joint circumference increases remained. These data suggest that gabapentin is an effective antinociceptive agent when administered either before or after induction of knee joint inflammation acting through a central neurogenic mechanism.

Acetates↗
PubMedDate not supplied

[Possible gabapentin phenytoin interaction].

INTRODUCTION: We report a possible case of gabapentin induced phenytoin toxicity. CASE REPORT: White man, 26 years old, chronically treated with phenytoin (for the past 4 years) and gabapentin (for the past 17 months). He was seen after complaining of dysarthria, ataxia and vertigo for the past 3 months, although having noted slight dizziness and a general, though undefined, indisposition from the start of taking gabapentin. The total and free serum levels of phenytoin found were clearly toxic. Gabapentin was discontinued definitively, and phenytoin for the next 7 days. The clinical symptoms had disappeared completely and phenytoin returned to within therapeutic levels. According to the criteria of causation it can be considered a possible adverse reaction caused by phenytoin related to incorporation of gabapentin. The mechanisms of this possible drug interaction are discussed, with emphasis on cytochrome P450 metabolism. CONCLUSION: The present case is a warning of the possible interaction of a drug (gabapentin) not contemplated when starting or when monitoring an antiepileptic treatment.

Acetates↗
PubMed2003

Inflammation unmasks gabapentin's effect on A delta-fiber evoked excitatory postsynaptic currents in substantia gelatinosa neurons of rat spinal cord.

OBJECTIVE: To study the analgesic mechanism of gabapentin, an anticonvulsant, during antinociceptive clinical treatment. METHODS: Whole-cell voltage-clamp recordings were taken from adult rat spinal cord slices to investigate the effect of gabapentin on primary afferent A delta-fiber evoked excitatory postsynaptic currents (EPSCs) to substantia gelatinosa (SG) neurons in normal and inflamed (established by plantar injection of carrageenan) rats. RESULTS: Gabapentin (5 - 20 micro mol/L for 5 min) depressed dorsal root A delta fiber evoked polysynaptic, but not monosynaptic EPSCs to SG experiencing inflammation by about 25% (n = 10, P < 0.01). However, gabapentin did not depress the evoked polysynaptic or monosynaptic EPSCs in normal rats. Gabapentin failed to block a glutamate receptor subtype, N-methyl-D-aspartate (NMDA), -induced slow excitatory currents on SG neurons. CONCLUSIONS: Inflammation, at least in part, unmasks the gabapentin depression on nociception transmission in the dorsal horn, and this depression is not due to the blockade of postsynaptic NMDA receptor.

Acetates↗