Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Gabapentin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed2004

Analgesic effects of gabapentin after spinal surgery.

BACKGROUND: A combination of opioid and nonopioid analgesic drugs may improve the quality of postoperative analgesia as well as reduce opioid requirements and their associated side effects. Studies have shown synergism between gabapentin and morphine in animal and human experiments and in the treatment of incisional pain. Therefore, the authors investigated, in a randomized, placebo-controlled, double-blind study, the effects of gabapentin on acute postoperative pain and morphine consumption in patients undergoing spinal surgery. METHODS: After standard premedication, 25 patients in the control group received oral placebo, and 25 patients in the gabapentin group received 1,200 mg of gabapentin, 1 h before surgery in a randomized fashion. Anesthesia was induced with propofol and cisatracurium and was maintained with sevoflurane and remifentanil. The total intraoperative remifentanil consumption by each patient was noted. All patients postoperatively received patient-controlled analgesia with morphine (1 mg/ml) with an incremental dose of 2 mg, a lockout interval of 10 min, and a 4-h limit of 40 mg. The incremental dose was increased to 3 mg, and the 4-h limit to 50 mg, if analgesia was inadequate after 1 h. Patients were questioned for the first 1 h in the PACU and were later evaluated in the ward at 1, 2, 4, 6, 12, and 24 h. Pain scores, heart rate, oxygen saturation measured by pulse oximetry, mean blood pressure, respiratory rate, sedation, morphine use, and total dose of morphine were recorded. RESULTS: Overall, pain scores at 1, 2, and 4 h were significantly lower in the gabapentin group when compared with the placebo group. Total morphine consumption in the gabapentin group was 16.3 +/- 8.9 mg (mean +/- SD) versus 42.8 +/- 10.9 mg in the placebo patients. The incidence of vomiting and urinary retention was significantly (P < 0.05) higher in the placebo group, but there was no difference in incidence of other adverse effects between the groups. CONCLUSIONS: Preoperative oral gabapentin decreased pain scores in the early postoperative period and postoperative morphine consumption in spinal surgery patients while decreasing some morphine-associated side effects.

Acetates↗
PubMedDate not supplied

Effects of gabapentin on the motor response to levodopa: a double-blind, placebo-controlled, crossover study in patients with complicated Parkinson disease.

BACKGROUND: Motor fluctuations and dyskinesias affect many parkinsonian patients chronically treated with levodopa. Imbalance between gabaergic direct and indirect striatopallidal pathways may originate them. Manipulating GABA neurotransmission may be effective in the treatment of these patients. Gabapentin is an antiepileptic drug that increases the synthesis and release of GABA. Previous studies suggest that gabapentin may be useful in Parkinson disease (PD). OBJECTIVE: To know the effects of gabapentin on the motor response to levodopa in PD patients with motor complications. DESIGN: A randomized double-blind, placebo-controlled, cross-over trial with four weeks of treatment. SETTING: A tertiary referral center. PARTICIPANTS: Twenty subjects with PD and motor fluctuations and dyskinesias on stable antiparkinsonian treatment, took gabapentin up to a maximum dose of 2.400 mg/d in three doses and placebo. METHODS: Three levodopa challenges were performed: at the beginning of the study and at the end of each period of treatment (4 weeks). Basal (off) and best (on) motor status were assessed by the UPDRS III. Latency to peak effect, magnitude of motor response (difference between "on" and "off" scores in the UPDRS III), duration of motor response and severity and duration of dyskinesias after each levodopa challenge were assessed. Patients' diaries were administered. RESULTS: : Fifteen patients completed the study. A significant improvement in the basal UPDRS III resulting in a significant reduction in the magnitude of the motor response after gabapentin was obtained (P < 0.001). No other changes were observed, either on pharmacological parameters or in levodopa-induced dyskinesias. Number of daily hours spent in "on," "on with dyskinesias" and "off" also remained unchanged. Tolerance was good, dizziness being the most common side effect. CONCLUSION: Gabapentin improved parkinsonian symptoms (basal UPDRS III and magnitude of the motor response) following levodopa. This improvement was not reflected in the daily motor situation of patients. Dyskinesias remained unchanged. Gabapentin was well tolerated. Further studies are needed to know the impact of these results in the long-term.

Acetates↗
PubMedDate not supplied

Tiagabine and gabapentin for the management of chronic pain.

OBJECTIVE: Agents that modulate gamma-aminobutyric acid transmission, such as gabapentin, are widely used for the management of chronic pain disorders/syndromes; however, the usefulness of the selective gamma-aminobutyric acid reuptake inhibitor tiagabine in this therapeutic area has yet to be investigated. This study evaluated the effectiveness and safety of tiagabine and gabapentin for the treatment of chronic pain. METHODS: This 3-month, open-label, comparative study randomized 91 patients with chronic pain to receive either tiagabine (maximum dose 24 mg/day) or gabapentin (2400 mg/day). Patients rated their pain intensity and sleep quality using 11-point (0-10) scales prior to treatment and after 3 months of continuous treatment. RESULTS: Of the 46 patients receiving tiagabine, 36 (78%) completed the study; 38 of 45 patients (84%) receiving gabapentin completed the study. Tiagabine and gabapentin significantly reduced pain intensity and improved sleep quality at 3 months, compared with baseline (P<0.01). Improvements in sleep quality were significantly greater in tiagabine versus gabapentin-treated patients (P=0.04). CONCLUSIONS: These results suggest that tiagabine and gabapentin are effective in the management of chronic pain, with tiagabine having a greater beneficial effect on sleep quality.

Adult↗
PubMed1991

Lack of a pharmacokinetic interaction between phenobarbitone and gabapentin.

Twelve subjects received a single oral dose (300 mg) of gabapentin and serial blood and urine samples were collected for drug measurements. Oral phenobarbitone (30-90 mg/day) was then administered to steady-state, and the gabapentin single dose study was repeated on day 42. Gabapentin was administered from days 49 to 52 to achieved steady-state, and further blood and urine samples were collected for drug measurements. Trough plasma phenobarbitone concentrations were monitored at frequent intervals. No statistically significant differences were observed in gabapentin Cmax, tmax, AUC, t1/2 or urinary drug recovery following single doses of gabapentin alone or combined with phenobarbitone. Phenobarbitone did not alter the disposition of gabapentin at steady state. Mean trough steady-state phenobarbitone concentrations were not significantly affected by concomitant gabapentin administration.

Acetates↗
PubMed2005

Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent.

OBJECTIVE: To assess whether there is a change in seizure activity in dogs with refractory epilepsy that are receiving appropriate doses of phenobarbitone and/or potassium bromide, when gabapentin is added to the therapeutic regimen. DESIGN: A prospective study of 17 dogs with a refractory seizure disorder, 16 of which have idiopathic epilepsy. PROCEDURE: Patients were stabilised using phenobarbitone and/or potassium bromide to produce tolerable therapeutic serum concentrations and dosed additionally with gabapentin at 35 to 50 mg/kg/d (divided twice or three times daily) for 4 months. Owners recorded seizure activity and side effects during this period in a standardised diary. Patients underwent monthly physical examinations and venepuncture to assess selected serum biochemical analytes, as well as phenobarbitone and bromide concentrations. Patients were further monitored for long-term response to adjunctive gabapentin therapy. RESULTS: There was no significant decrease in the number of seizures over the study period for the entire cohort, however three dogs stopped seizuring completely. There was a significant increase in the number of patients who showed an increase in the interictal period (P > 0.001). Serum alkaline phosphatase activity and triglyceride concentrations were elevated at baseline. There were no significant changes in biochemical analytes during the course of the study period. Side effects observed initially on addition of gabapentin included sedation and hind limb ataxia. The former resolved spontaneously after a few days; the latter after a slight reduction in bromide dose. Long-term, a further two patients became seizure free and ten patients remained on gabapentin indefinitely. No long-term side effects have become apparent. CONCLUSION: Addition of gabapentin to phenobarbitone and/or potassium bromide increased the interictal period and shortened the post-seizure recovery in some canine epileptics. In some dogs, seizures were prevented completely, while in others there was an increase in interictal period. The short-half life of gabapentin has advantages for seizure control, however its present high cost may prohibit therapy in large dogs.

Amines↗
PubMed2002

The anticonvulsant gabapentin (neurontin) does not act through gamma-aminobutyric acid-B receptors.

The actions of the anticonvulsant gabapentin [1-(aminomethyl)cyclohexaneacetic acid, Neurontin] have been somewhat enigmatic until recently, when it was claimed to be a gamma-aminobutyric acid-B (GABA(B)) receptor agonist acting exclusively at a heterodimeric complex containing the GABA(B(1a)) splice variant (Mol Pharmacol 2001;59:144-152). In this study, we have investigated the effects of gabapentin on recombinant GABA(B(1a)) and GABA(B(1b)) receptors coexpressed with GABA(B(2)) in five different functional recombinant assays, its ability to inhibit [(3)H]GABA binding in a GABA(B) receptor-selective binding assay using rat synaptic membranes, and its ability to inhibit transient lower esophageal sphincter relaxations in Labrador retriever dogs. Up to a concentration of 1 mM, gabapentin displayed no agonistic effects on either the GABA(B(1a,2)) or the GABA(B(1b,2)) heterodimer, when these were expressed in Xenopus laevis oocytes or mammalian cells and assayed by means of electrophysiology, calcium mobilization, inositol phosphate, and fluorometry assays. Gabapentin did not displace [(3)H]GABA from GABA(B) receptor sites in rat synaptic membranes. Finally, in contrast to the classic GABA(B) receptor agonist baclofen, gabapentin was unable to inhibit transient lower esophageal sphincter relaxations in dogs. Because of high levels of GABA(B(1a)) in the canine nodose ganglion, this finding indirectly supports the inactivity of gabapentin on the GABA(B(1a,2)) heterodimer demonstrated in various in vitro assays. In light of these results, we find it highly questionable that gabapentin is a GABA(B) receptor agonist. Hence, the anticonvulsive effects of the compound have to arise from GABA(B) receptor-independent mechanisms. This also implies that the first GABA(B) receptor splice variant-selective ligand remains to be discovered.

Acetates↗
PubMed2004

The analgesic effects of gabapentin after total abdominal hysterectomy.

UNLABELLED: We investigated, in a randomized, placebo-controlled, double-blind study, the efficacy and safety of gabapentin on pain after abdominal hysterectomy and on tramadol consumption in patients. The 50 patients were randomized to receive either oral placebo or gabapentin 1200 mg 1 h before surgery. Anesthesia was induced with propofol and maintained with sevoflurane in 50% N(2)O/O(2) with a fresh gas flow of 2 L/min (50% N(2)O in O(2)) and fentanyl (2 microg/kg). All patients received patient-controlled analgesia with tramadol with a 50 mg initial loading dose, 20 mg incremental dose, 10-min lockout interval, and 4-h limit of 300 mg. The incremental dose was increased to 30 mg if analgesia was inadequate after 1 h. Patients were studied at 4, 8, 12, 16, 20, and 24 h for visual analog (VAS) pain scores, heart rate, peripheral oxygen saturation, mean arterial blood pressure, respiratory rate, sedation, and tramadol consumption. The VAS scores in the sitting and supine position at 1, 4, 8, 12, 16, and 20 h were significantly lower in the gabapentin group when compared with the placebo group up to 20 h after surgery. The tramadol consumption at 12, 16, 20, and 24 h and total tramadol consumption were significantly less in the gabapentin group when compared with placebo group. Sedation scores were similar at all the measured times. There were no differences between groups in adverse effects. Preoperative oral gabapentin decreased pain scores and postoperative tramadol consumption in patients after abdominal hysterectomy. IMPLICATIONS: This randomized, controlled trial examined the effects of preoperative oral gabapentin 1200 mg on postoperative pain and tramadol consumptions. We conclude that preoperative oral gabapentin is effective in reducing postoperative pain scores and tramadol consumption in patients after abdominal hysterectomy.

Acetates↗
PubMed2005

The neurological safety of epidural gabapentin in rats: a light microscopic examination.

Gabapentin acts primarily on the central nervous system. Therefore, we hypothesized that the direct epidural administration of gabapentin could have various advantages over its oral administration with respect to required dose, side effects, and efficacy. However, before administering gabapentin into the epidural space in a clinical setting, its neurotoxicity must be examined in animals. Thus, we evaluated neurotoxicity of epidural gabapentin by observing behavioral and sensory-motor changes, and by histopathological examinations of spinal cords and dorsal root ganglia in the rat. Twenty-seven rats were randomly divided into 3 groups, which were administered 0.3 mL (30 mg) of epidural gabapentin (group G, n = 9) and the same volume of epidural alcohol (group A, n = 9) or normal saline (group N, n = 9). No rats in groups G and N showed sensory-motor dysfunction, behavioral change, or histopathological abnormalities over a 3-wk observation period, whereas all rats in group A showed abnormalities. We conclude that the direct epidural injection of gabapentin in rats did not show any neurotoxic evidence in terms of sensory-motor functions and behavior, or by a microscopic histopathological evaluation. This study represents a first promising step toward the trial of epidural gabapentin in a clinical setting.

Amines↗
PubMed2004

Endogenous GABA does not mediate the inhibitory effects of gabapentin on spinal reflexes in rats.

The novel antiepileptic drug gabapentin was designed as a structural analog of gamma-aminobutyric acid (GABA). However, its mechanism of action remains unclear. In the present study, we investigated the effect of gabapentin on spinal reflexes in anesthetized rats. The mono- and polysynaptic reflex potentials were recorded from the ipsilateral L5 ventral root after stimulation of the L5 dorsal root. The dorsal root reflex potential, an index of presynaptic inhibition, was recorded from the ipsilateral L4 dorsal root. In non-spinalized (intact) and spinalized rats, intravenously administered gabapentin reduced the mono- and polysynaptic reflex potentials in a dose-dependent manner. These inhibitory effects of gabapentin were not suppressed by the GABA(A) antagonist picrotoxin. Moreover, gabapentin also decreased spinal reflexes in spinalized rats depleted of spinal GABA with semicarbazide, an inhibitor of the GABA-synthesizing enzyme. The dorsal root reflex potentials were not affected by gabapentin. These results suggest that endogenous GABA does not mediate the inhibitory effects of gabapentin on spinal reflexes.

Acetates↗
PubMed2004

GABAB receptors do not mediate the inhibitory actions of gabapentin on the spinal reflex in rats.

The clinical effectiveness of gabapentin for the treatment of epilepsy, spasticity, and neuropathic pain has been established. The mechanisms responsible for those actions, however, are still not clearly understood. We have recently demonstrated that gabapentin reduces the spinal reflex in rats via mechanisms that do not involve gamma-aminobutyric acid (GABA)A receptors. In the study, we attempted to explore the involvement of GABAB receptors in gabapentin-induced inhibition of the spinal reflexes in spinalized rats. Stimulation of the dorsal root at L5 elicited the segmental mono-(MSR) and polysynaptic reflex (PSR) in the ipsilateral ventral root. The microinjection of gabapentin (1.5 and 5 nmol) into the ventral horn reduced both MSR and PSR, whereas the injection into the dorsal horn only inhibited the PSR, indicating that systemic gabapentin inhibits the MSR at the ventral horn and it inhibits the PSR at both the ventral and dorsal horns. The GABAB-receptor antagonist CGP35348 (0.5 nmol) injected into the ventral horn antagonized the inhibition of the spinal reflexes by the GABAB-receptor agonist baclofen (i.v.) but not by gabapentin (i.v.). Thus, GABAB receptors do not appear to contribute to the gabapentin-induced inhibition of the spinal reflex.

Amines↗
PubMed2001

Gabapentin for treatment of behavioral and psychological symptoms of dementia.

OBJECTIVE: To report the use of gabapentin in the treatment of behavioral and psychological symptoms of dementia (BPSD) and to review the available literature relating to the use of gabapentin in this population. CASE SUMMARY: A 62-year-old white man was admitted to the hospital due to a worsening state of confusion, anxiety, depressed mood, insomnia, and verbal and physical aggressiveness toward his wife. He had a past medical history significant for vascular dementia. He had been intolerant of or had failed to respond to numerous antidepressants, benzodiazepines, and neuroleptics. The addition of gabapentin to the patient's medication regimen resulted in reduced agitation, sexual inappropriateness, and lability. He was discharged to his home on a dose of gabapentin 300 mg three times daily. DATA SOURCES: A MEDLINE search (1966-August 2000) was performed to identify case reports and clinical trials discussing the efficacy of gabapentin in the treatment of BPSD. DISCUSSION: Gabapentin, like other anticonvulsants, has been used with success in several psychiatric illnesses. Available literature indicates that the drug may have some efficacy in the treatment of BPSD. It has a favorable adverse effect profile in the elderly, which makes it an attractive altemative to standard therapies, including benzodiazepines and neuroleptics. Optimal dosing remains unclear. CONCLUSIONS: This case suggests that gabapentin is a reasonable alternative therapy for patients whose behavioral symptoms do not respond to conventional agents.

Acetates↗
PubMed2000

Use of gabapentin in the treatment of neuropathic pain.

OBJECTIVE: To evaluate the role of gabapentin for the treatment of neuropathic pain. DATA SOURCES: Clinical literature was identified through MEDLINE (from 1990 to October 1999). Key search terms were gabapentin and pain. DATA SYNTHESIS: Neuropathic pain can be a problematic, chronic syndrome that is frequently refractory to current drug treatments. Gabapentin is a newer generation antiepileptic drug that is commonly used in treatment of neuropathic pain. An evaluation of clinical trials using gabapentin to treat neuropathic pain was performed. CONCLUSIONS: Gabapentin appears to be effective in treating various neuropathic pain disorders. Gabapentin may have advantages over current therapies, such as a favorable safety profile and lack of drug interactions; however, cost issues and limited experience may limit the use of gabapentin as a first-line option.

Acetates↗
PubMed2005

Dystonia induced by gabapentin.

OBJECTIVE: To report a case of dystonia as an adverse effect of gabapentin. CASE SUMMARY: A 72-year-old woman was diagnosed with essential tremor and treated with propranolol 120 mg daily. The drug was withdrawn because of bradycardia, and gabapentin was prescribed 3 times a day at escalating doses to reach 2100 mg daily. The woman developed a dystonic reaction involving muscles of the neck and both arms that resolved rapidly after drug withdrawal. She was restarted on gabapentin with slow titration to 1800 mg daily, but the same dystonic reaction appeared, which led to definitive withdrawal of the drug. An objective causality assessment revealed that this adverse effect was highly probable. DISCUSSION: There have been only a few previous reports of gabapentin-induced dystonia. Other movement disorders reported with gabapentin include myoclonus, ataxia, and choreoathetosis. Gabapentin has been used to treat dystonias with variable results. CONCLUSIONS: Although gabapentin is widely used and well tolerated, it can cause dystonic reactions, which are reversible after drug withdrawal.

Aged↗
PubMed2003

Hemodynamic effects of gabapentin in rats.

Gabapentin has been known to elicit the antinociceptive effect. However, little has been known about the effect of gabapentin on the cardiovascular system. The author's aim of this experiment was to examine the hemodynamic effects of gabapentin. Male Sprague-Dawley rats were used. Intrathecal or intracerebroventricular catheters were implanted and gabapentin was delivered through each catheter or directly into the peritoneal cavity. For hemodynamic measurements, catheters were inserted into the tail artery. Blood pressure and heart rate were measured over 60 min following administration of gabapentin. Intrathecal and intraperitoneal gabapentin did not induce significant changes of hemodynamics over the 60 min compared to the baseline value. Intracerebroventricular gabapentin increased systolic and diastolic blood pressure, but there is no statistically difference in blood pressure change according to the dose.

Acetates↗
PubMed2004

Interaction between intrathecal gabapentin and adenosine in the formalin test of rats.

Spinal gabapentin and adenosine have been known to display an antinociceptive effect. We evaluated the nature of the interaction between gabapentin and adenosine in formalin-induced nociception at the spinal level. Male Sprague-Dawley rats were prepared for intrathecal catheterization. Pain was evoked by injection of formalin solution (5%, 50 microL) into the hindpaw. After examination of the effects of gabapentin and adenosine, the resulting interaction was investigated with isobolographic and fractional analyses. Neither gabapentin nor adenosine affected motor function. Gabapentin or adenosine decreased the sum of the number of flinches during phase 2, but not during phase 1 in the formalin test. Isobolographic analysis, in phase 2, revealed an additive interaction between gabapentin and adenosine. Taken together, intrathecal gabapentin and adenosine attenuated the facilitated state and interacted additively with each other.

Adenosine↗
PubMed2006

A double-blind, randomized, placebo-controlled, prophylaxis study of adjunctive gabapentin for bipolar disorder.

OBJECTIVE: To conduct the first randomized, controlled trial assessing the prophylactic efficacy of gabapentin in bipolar disorder. METHOD: We conducted a 1-year, double-blind, randomized, comparative, placebo-controlled, parallel-group, multicenter study. As this was a pure prophylactic trial, only euthymic bipolar I and II patients (DSM-IV) were randomly assigned in a 1:1 ratio to gabapentin (N = 13) or placebo (N = 12) added to the current treatment (lithium, valproate, carbamazepine, or any combination but not antipsychotics or antidepressants). Subjects participated in the study for 12 months. The primary efficacy parameter was the Clinical Global Impressions scale for Bipolar Illness, Modified (CGI-BP-M), which was assessed at all visits. Other assessments were the Young Mania Rating Scale (YMRS), Hamilton Rating Scale for Depression (HAM-D), Hamilton Rating Scale for Anxiety (HAM-A), Pittsburgh Sleep Quality Index (PSQI), and the systematic collection of reported adverse events. Data were collected from May 1999 to February 2004. RESULTS: The change from baseline to month 12 in mean CGI-BP-M scores between groups was statistically significant (p = .0046). Mean score change from baseline to endpoint in the gabapentin group was -2.1, and the mean score change in the placebo group was -0.6. No emerging manic or depressive symptoms were seen in either group as measured with the YMRS, HAM-D, HAM-A, and PSQI. In the PSQI-6 subscale (use of sleeping medication), the mean score change at month 12 in the gabapentin group was 0.9, and the mean score change in the placebo group was 0.05 (p = .0267). Overall, gabapentin was well tolerated. CONCLUSION: This small, randomized clinical trial comparing the prophylactic efficacy of adjunctive gabapentin to placebo suggests that, despite lack of acute efficacy, treatment with gabapentin might provide some benefit on the long-term outcome of bipolar disorder.

Amines↗
PubMed1999

Gabapentin suppresses ectopic nerve discharges and reverses allodynia in neuropathic rats.

Repetitive ectopic discharges from injured afferent nerves play an important role in initiation and maintenance of neuropathic pain. Gabapentin is effective for treatment of neuropathic pain but the sites and mechanisms of its antinociceptive actions remain uncertain. In the present study, we tested a hypothesis that therapeutic doses of gabapentin suppress ectopic afferent discharge activity generated from injured peripheral nerves. Mechanical allodynia, induced by partial ligation of the sciatic nerve in rats, was determined by application of von Frey filaments to the hindpaw. Single-unit afferent nerve activity was recorded proximal to the ligated sciatic nerve site. Intravenous gabapentin, in a range of 30 to 90 mg/kg, significantly attenuated allodynia in nerve-injured rats. Furthermore, gabapentin, in the same therapeutic dose range, dose-dependently inhibited the ectopic discharge activity of 15 injured sciatic afferent nerve fibers through an action on impulse generation. However, the conduction velocity and responses of 12 normal afferent fibers to mechanical stimulation were not affected by gabapentin. Therefore, this study provides electrophysiological evidence that gabapentin is capable of suppressing the ectopic discharge activity from injured peripheral nerves. This action may contribute, at least in part, to the antiallodynic effect of gabapentin on neuropathic pain.

Acetates↗
PubMed1999

Using gabapentin to treat neuropathic pain.

OBJECTIVE: To review use of gabapentin as an adjuvant agent to treat neuropathic pain. QUALITY OF EVIDENCE: MEDLINE was searched from 1995 to October 1998 for reports. There were approximately 20 citations. Additional articles from Pain and other medical journals were reviewed. No double-blind studies have examined gabapentin and its use as an analgesic adjuvant agent. MAIN MESSAGE: Gabapentin is an anticonvulsant medication used recently as an effective adjuvant agent for treating neuropathic pain. It is a structural analogue of gamma-aminobutyric acid (GABA), but its receptor and biochemical function remain unknown. Gabapentin has desirable pharmacokinetic properties and acceptable side effects, which simplify its use. There are very few interactions between gabapentin and other medications, and gabapentin is well tolerated. CONCLUSION: Gabapentin could be an effective adjuvant agent for many neuropathic pain states.

Acetates↗