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PubMed2006

Evaluation of gabapentin and ethosuximide for treatment of acute nonconvulsive seizures following ischemic brain injury in rats.

Acute seizures following brain injury have been associated with a worsening of patient outcome, but they are often undiagnosed and untreated when they occur without motor convulsions. Here, we sought to compare the antiseizure profile of ethosuximide (EXM; 125-312.5 mg/kg i.v.) and gabapentin (GBP; 0.3-50 mg/kg. i.v.) in a rat model of nonconvulsive seizures (NCS) induced by brain ischemia. Seizures were detected by continuous electroencephalographic monitoring for 24 h following permanent middle cerebral artery occlusion (MCAo). Both "preseizure" and "postseizure" treatment effects were evaluated. Control rats experienced a 91% incidence of NCS (averaging 10-11 NCS/rat), which was significantly reduced following preseizure treatment (delivered 20 min post-MCAo) with either EXM (ED(50) = 161 mg/kg) or GBP (ED(50) = 10.5 mg/kg). In contrast to preseizure treatment effects, only GBP reduced NCS when given after the first seizure event. A further, albeit nonsignificant, 20% reduction in NCS incidence was measured when given in combination postseizure. Drug treatment also reduced infarct volume, which was positively correlated to the number of NCS events (r = 0.475; P < 0.001). EXM and GBP treatment of cultured neurons exposed to neurotoxic or ischemic insults showed no neuroprotective effects, suggesting that in vivo neuroprotection can be attributed to anti-seizure effects. We conclude that EXM and GBP significantly attenuate NCS in a dose-related manner and may help to improve patient outcome from brain ischemia-induced seizure activity.

Acute Disease↗
PubMed1987

Gabapentin as an antiepileptic drug in man.

Gabapentin, 1-(aminomethyl) cyclohexane acetic acid, is a GABA analogue whose antiepileptic properties were tested in a double blind cross-over trial design as add-on therapy in a dose ranging study which compared 300 mg, 600 mg, and 900 mg/day (each dose given for 2 months) in 25 patients with severe partial and generalised epilepsies. A dose related antiepileptic effect was observed. All three doses were well tolerated and no psychometric impairment was noted. No significant drug interactions were seen. The drug appears worthy of further assessment.

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PubMed1997

Gabapentin and cognition: a double blind, dose ranging, placebo controlled study in refractory epilepsy.

OBJECTIVE: To assess the effect of different doses of gabapentin (GBP) on cognitive function in treated epileptic patients. METHODS: Twenty seven patients with refractory partial seizures commenced a double blind, dose ranging, placebo controlled, crossover study of adjuvant GBP. Each treatment phase lasted three months, during which the dose of GBP or matched placebo was increased stepwise at intervals of four weeks (1200 mg/day, 1800 mg/day, and 2400 mg/day in three daily doses). Psychomotor and memory testing was carried out at the end of each four week period, at which time the patient also completed subjective measures of cognition, fatigue, worry, temper, and dysphoria. A visual analogue scale was used to assess drowsiness and a questionnaire was employed to gauge the severity of side effects. RESULTS: In the 21 patients completing the study, GBP produced a significant reduction in median monthly seizure frequency from 7 to 4.3 (P = 0.02), the decrease being most pronounced for secondarily generalised seizures (from 1.0 to 0.3, P = 0.01). Forty three per cent of patients reported a reduction in seizure frequency of at least 50% throughout all GBP doses. Mean (SD) plasma concentrations of GBP at 1200, 1800, and 2400 mg/day were 4.7 (2.6), 6.8 (3.8), and 8.6 (3.3) mg/l respectively. The drug had no effect on composite psychomotor and memory scores; nor was there alteration in any self assessment subscore. The mean drowsiness (P = 0.03) score was higher during treatment with 2400 mg GBP daily compared with matched placebo. Composite psychomotor (r = -0.47, P < 0.01), tiredness (r = 0.42, P < 0.01), and side effect (r = 0.61, P < 0.001) scores correlated significantly with seizure frequency but not with GBP dose. CONCLUSION: GBP is a well tolerated and effective antiepileptic drug which had no measurable effect on cognition but did produce sedation at the highest dose. This study also supports the suggestion that seizures can cause cognitive impairment.

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PubMed1999

An audit of the perceived efficacy and tolerability of gabapentin therapy in an out-patient cohort with chronic epilepsy.

A retrospective audit of the perceived efficacy and tolerability of adjunctive gabapentin (GBT) therapy in patients with intractable epilepsy was carried out. The case-notes of 263 consecutive patients attending a tertiary referral centre in whom GBT had been added to concomitant anti-epileptic drugs were reviewed. There were 119 males (45%); the median age was 35 years (range 15-81 years) and the median duration of epilepsy was 20 years. The median dose of GBT administered was 1,600 mg (range 300-4,800 mg). Twenty-nine patients (11%) had a reduction in seizure frequency of greater than 50% and 7 (3%) achieved seizure freedom of 6 months' duration at least while taking GBT. Side-effects were reported by 169 patients (61%) and in 40 (15%) an increase in seizure frequency of 50% occurred, this being the commonest reason for GBT withdrawal. The median duration of treatment was 4 months (range 0.03-47 months). Ten patients, in whom GBT therapy had proven ineffective in doses of 900-1,800 mg, were rechallenged with doses of 300-4,800 mg. One individual experienced a 50% reduction in seizure frequency and 1 an increase in seizures of at least 50%. GBT was generally well tolerated at high doses and rechallenge of a small number with GBT in doses up to 4,800 mg did not result in further improvement in seizure frequency in the majority.

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PubMed2000

Low-dose gabapentin combined with either lamotrigine or carbamazepine can be useful therapies for trigeminal neuralgia in multiple sclerosis.

Paroxysmal symptoms occur frequently in multiple sclerosis (MS). Usually they are treated with carbamazepine (CBZ) and phenytoin, although these medications are often interrupted due to adverse effects. We report 11 MS patients with trigeminal neuralgia (TN): 6 intolerant to a therapeutic dosage of CBZ, showing serious adverse effects and subsequently treated with a combination of low-dose CBZ and gabapentin (GBP) (group 1); 5 treated with lamotrigine (LMT), showing adverse effects and subsequently treated with GBP (group 2). Subjective pain level and impairment in performing daily activities were rated utilizing a 3-point scale at time 0 and at optimal dosage time (T1). GBP was initiated at 300 mg daily and titrated, until pain control was achieved without new adverse effects, to a maximum dose of 1,200 mg daily. CBZ or LMT were reduced to a level which no longer produced adverse effects, although resulting in a lack of efficacy in relieving pain. Pain control was obtained in all patients but 1, with no side effects. The plasma level analysis, performed in 5 patients, resulted in normal values. The mean dosages at T1 were: group 1 CBZ 400 mg and GBP 850 mg daily; group 2 LMT 150 mg and GBP 780 mg daily. Combining drugs with complementary modes of action may provide a rational pharmacological approach to the management of TN in MS.

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PubMed1998

Lamotrigine and gabapentin. Alternative in the treatment of bipolar disorder.

The anticonvulsants carbamazepine and sodium valproate have efficacy in hypomania, bipolar depression and in the prophylaxis of bipolar disorder. This paper reviews published evidence on the effects of the new anticonvulsants gabapentin and lamotrigine in bipolar disorder. The conclusion is that there is good evidence from open studies to indicate that randomised double-blind trials of these compounds should be carried out. The pharmacology of these anticonvulsants is reviewed and putative predictors of good response identified.

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PubMed1994

New antiepileptic drugs for children: felbamate, gabapentin, lamotrigine, and vigabatrin.

After a 15-year hiatus, several new antiepileptic drugs have been approved or are under Food and Drug Administration investigation for use in the United States. This article reviews four of these new drugs--felbamate, gabapentin, lamotrigine, and vigabatrin. Although these drugs have been primarily developed for use in adults with partial seizures, they will also likely be used in children with partial epilepsy. Pediatric experience with several of these drugs has demonstrated safety and efficacy in other seizure types and epilepsy syndromes. These drugs will be an important addition to the therapeutic armamentarium for pediatric epilepsy. Additional studies are needed to fully explore the safety and efficacy of these drugs in a variety of pediatric epilepsies and to compare them to existing antiepileptic drugs.

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PubMed1995

Potential use of gabapentin and lamotrigine.

Based on the proposed neurotoxic etiology of ALS and possible actions of gabapentin and lamotrigine, there is some reason to hope for a beneficial response when using these agents in patients with ALS. However, because of the lack of evidence supporting this use, the cost of treatment, and the risk of adverse effects, there is no rationale for this use before larger, controlled clinical trials are completed.

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PubMed1997

Gabapentin for familial paroxysmal dystonic choreoathetosis.

We present a 4-year-old girl with stereotyped episodes of inability to speak and dystonic posturing of the face and extremities lasting 20 minutes. An older brother and mother had similar spells in childhood. Routine and video-EEG during events were normal. The diagnosis was non-kinesigenic paroxysmal dystonic choreoathetosis since the episodes were not exacerbated by movement. Gabapentin 10 mg/kg/d eliminated most attacks.

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PubMed1998

An open-label trial of gabapentin treatment of paroxysmal symptoms in multiple sclerosis patients.

We conducted an open-label trial of gabapentin (GBP) as therapy for paroxysmal symptoms (PS) in 21 MS patients, including trigeminal neuralgia (6 patients), painful tonic spasms (11), dysesthetic or paresthetic symptoms (3) and ocular ataxia (1). Complete resolution of symptoms or partial improvement was obtained, respectively, in 14 and 4 of 18 patients who ended the study. Sustained improvement with minor side effects was obtained at dosages ranging from 600 to 1200 mg/d. Our findings suggest that GBP may be effective for PS in MS and warrant a further study in a double-blind placebo-controlled trial.

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PubMed2004

The effects of intrathecal gabapentin on spinal morphine tolerance in the rat tail-flick and paw pressure tests.

Analgesic tolerance to opioids has been described in both experimental and clinical conditions and may limit the clinical utility of these drugs. We have previously shown that systemic gabapentin (GBP), a non-opioid drug, prevents and reverses tolerance to systemic morphine in the rat. In this study, we investigated the effect of intrathecal GBP on spinal morphine tolerance. Studied rats were given 7 days of intrathecal injections with saline (10 microL), GBP (300 microg), morphine (15 microg), or a GBP-morphine combination, and analgesic testing using tail-flick and paw-pressure tests was conducted before and 30 min after the drug injection. On Day 8, an antinociceptive dose-response curve was constructed and the 50% effective dose (ED(50)) values for morphine (given alone) were calculated for each study group. Coinjection of GBP with morphine blocked the development of tolerance, as shown by the preservation of morphine analgesia over 7 days as well as by a concomitant decrease in ED(50) values on Day 8, as compared with the morphine-alone group. Although additive analgesia over Days 1-7 cannot be ruled out, ED(50) reductions in the GBP-morphine combination group indeed suggest some suppression of tolerance. These data support previous evidence that GBP prevents opioid tolerance and, more specifically, indicate that intrathecal GBP prevents the development of spinal opioid tolerance. Future studies are required to examine the respective roles of supraspinal and peripheral sites of GBP-morphine interaction and to investigate the mechanisms underlying the action of GBP on opioid tolerance.

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PubMed2005

Multimodal analgesia with gabapentin and local anesthetics prevents acute and chronic pain after breast surgery for cancer.

We evaluated the effect of multimodal analgesia on acute and chronic pain after breast surgery for cancer. Fifty patients scheduled for breast cancer surgery were blindly randomized to receive gabapentin, eutectic mixture of local anesthetics cream, and ropivacaine in the wound or three placebos. Pain (visual analog scale) and analgesics were recorded in the postanesthesia care unit (PACU) 3, 6, and 9 h and 8 days after surgery. Three and 6 mo later, patients were assessed for chronic pain. The treatment group consumed less paracetamol in the PACU (469 versus 991 mg; P < 0.002) and less Lonalgal (1.0 versus 4.4 tablets; P = 0.003) than the controls, exhibited lower visual analog scale scores at rest in the PACU (P = 0.001) and on postoperative Days 1, 3, and 5 (P = 0.040, P = 0.015, and P = 0.045, respectively), and after movement in the PACU (P = 0.001) and on postoperative Days 2, 4, and 8 (P = 0.028, P = 0.007, and P = 0.032, respectively). Three and 6 mo after surgery, 18 of 22 (82%) and 12 of 21 (57%) of the controls reported chronic pain versus 10 of 22 (45%) and 6 of 20 (30%) in the treatment group (P = 0.028 and P = 0.424, respectively); 5 of 22 and 4 of 21 of the controls required analgesics versus 0 of 22 and 0 of 20 of those treated (P = 0.048 and P = 0.107, respectively). Multimodal analgesia reduced acute and chronic pain after breast surgery for cancer.

Acute Disease↗
PubMed2000

[Current data on gabapentin].

OBJECTIVE: To review the current data on gabapentin (GBP) with regard to its mechanism of action, pharmacokinetic characteristics, clinical efficacy, tolerance and mode of administration. DEVELOPMENT: GBP has a multiple mechanism of action which justifies its use in many clinical conditions besides epilepsy. These include neuropathic pain, psychiatric disorders, disorders of movement, and migraine. Its pharmacokinetic characteristics are nearly those of an ideal drug, with no interactions. Regarding clinical efficacy, there is much evidence of this in polytherapy and in monotherapy in adults and children with partial crises, with rare adverse effects and the exceptional possibility to establish the total dose of GBP in only a few days. CONCLUSIONS: GBP is an effective drug in patients of all ages with partial crises. Because of its excellent tolerance and decreasing dose-dependent kinetics, conditioned by less absorption of the drug, we recommend the administration of GBP at doses higher than those normally used. Thus we suggest a dose of 900 to 2,400 mg/day in patients with a new diagnosis, of 1,800 to 3,600 mg/day as a second therapeutic alternative and even 2,400 to 4,800 mg/day when other antiepileptic drugs have failed to be of use.

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PubMed2000

A retrospective chart review of gabapentin for the treatment of aggressive and agitated behavior in patients with dementias.

In a 24-patient case series from retrospective chart review, the authors examined the use of gabapentin for the treatment of aggressive and agitated behaviors in nursing home patients with a DSM-IV diagnosis of dementia. On Clinical Global Rating Scale scores, 17 of 22 patients were much or greatly improved; 4 were minimally improved; and only 1 remained unchanged. Two of the 24 patients discontinued use of the medication because of excessive sedation. No other significant side effects were noted in treatment lasting up to 2 years.

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PubMed2000

Stimulus-dependent modulation of [(3)H]norepinephrine release from rat neocortical slices by gabapentin and pregabalin.

Gabapentin (GBP; Neurontin) has proven efficacy in several neurological and psychiatric disorders yet its mechanism of action remains elusive. This drug, and the related compounds pregabalin [PGB; CI-1008, S-(+)-3-isobutylgaba] and its enantiomer R-(-)-3-isobutylgaba, were tested in an in vitro superfusion model of stimulation-evoked neurotransmitter release using rat neocortical slices prelabeled with [(3)H]norepinephrine ([(3)H]NE). The variables addressed were stimulus type (i.e., electrical, K(+), veratridine) and intensity, concentration dependence, onset and reversibility of action, and commonality of mechanism. Both GBP and PGB inhibited electrically and K(+)-evoked [(3)H]NE release, but not that induced by veratridine. Inhibition by these drugs was most pronounced with the K(+) stimulus, allowing determination of concentration-effect relationships (viz., 25 mM K(+) stimulus: GBP IC(50) = 8.9 microM, PGB IC(50) = 11.8 microM). R-(-)-3-Isobutylgaba was less effective than PGB to decrease stimulation-evoked [(3)H]NE release. Other experiments with GBP demonstrated the dependence of [(3)H]NE release inhibition on optimal stimulus intensity. The inhibitory effect of GBP increased with longer slice exposure time before stimulation, and reversed upon washout. Combination experiments with GBP and PGB indicated a similar mechanism of action to inhibit K(+)-evoked [(3)H]NE release. GBP and PGB are concluded to act in a comparable, if not identical, manner to preferentially attenuate [(3)H]NE release evoked by stimuli effecting mild and prolonged depolarizations. This type of modulation of neurotransmitter release may be integral to the clinical pharmacology of these drugs.

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PubMedDate not supplied

R3 nociceptive reflex in multiple sclerosis patients with paroxysmal symptoms treated with gabapentin.

Gabapentin (GBP) is a new, well-tolerated antiepileptic drug found to be effective for painful paroxysmal symptoms (PS) in multiple sclerosis (MS). The aim of this study was to obtain a neurophysiological evaluation of the effects of GBP on the nociceptive system of MS patients suffering PS. We studied 10 MS patients, 6 males, 4 females (mean age 47.3 years), suffering PS (3 had trigeminal neuralgia, 1 painful tonic spasms and 6 dysesthetic or paresthetic symptoms). Three patients were, at the same time, also being treated with carbamazepine. Pain was evaluated by means of the Visual Faces Scale. R3 nociceptive reflex was recorded after 2 weeks' treatment. R3 thresholds and latencies were evaluated and a statistical analysis was performed. A significant variation was found in R3 thresholds between the values recorded before and during GBP treatment; no significant variation was observed in R3 latencies.

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PubMed2001

Differential effect of gabapentin on neuronal and muscle calcium currents.

Calcium channels modulate cell function by controlling Ca(2+) influx. A main component of these proteins is the alpha 2/delta subunit. Nevertheless, how this subunit regulates channel activity in situ is unclear. Gabapentin (GBP), an analgesic and anti-epileptic agent with an unknown mechanism of action, specifically binds to the alpha 2/delta subunit. Using the patch clamp technique, we tested the effects of GBP on Ca(2+) currents from dorsal root ganglion (DRG) cells, the mediators of pain perception, to determine how GBP binding modifies channel activity. In DRGs, GBP significantly reduced whole cell Ca(2+) current amplitude at positive membrane potentials when a pulse preceded the test pulses or when cells were stimulated with a train of pulses. In control cells, neither prepulse depolarization nor pulse trains reduced Ca(2+) currents at positive potentials. GBP did not reduce the low-voltage activated Ca(2+) current under any experimental condition. Similar to DRG cells, GBP attenuated Ca(2+) current in skeletal myotubes at positive membrane potentials in the presence of a depolarizing prepulse. However, GBP did not significantly alter Ca(2+) currents in cardiac myocytes. Reverse transcription-polymerase chain reaction was used to confirm expression of the alpha 2/delta subunit in these cells. Each cell type expressed multiple isoforms of alpha 2/delta. Muscle cells showed a more variable expression of alpha 2/delta subunits than did DRG cells. Our results suggest a possible participation of the alpha 2/delta subunit in the action of GBP. Our data also indicate that GBP inhibits Ca(2+) channels in a use- and voltage-dependent manner at a therapeutically relevant concentration.

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PubMedDate not supplied

Spectrofluorimetric determination of vigabatrin and gabapentin in dosage forms and spiked plasma samples through derivatization with 4-chloro-7-nitrobenzo-2-oxa-1,3-diazole.

A highly sensitive and specific method is proposed for the determination of vigabatrin (I) and gabapentin (II) in their dosage forms and spiked human plasma. The method is based on coupling the drugs with 4-chloro-7-nitrobenzo-2-oxa-1,3-diazole in borate buffer at pH 7.1 and measuring the resulting fluorescence at 532 nm after excitation at 465 nm. The fluorescence intensity was a linear function of the concentration of the drugs over the ranges of 1.3-6.5 and 1.7-8.5 microg/mL for I and II, respectively. Minimum detectability values were 0.54 microg/mL (4.2 x 10(-6)M) and 0.97 microg/mL (5.7 x 10(-6)M) for I and II, respectively, under the described conditions. The proposed method was successfully applied to the determination of the 2 drugs in their dosage forms, and the percent recoveries +/- standard deviation (SD) were 104.53 +/- 1.2 and 100.00 +/- 1.32 of the label claim for I and II, respectively. The method was further applied to the determination of vigabatrin in spiked plasma samples. The percent recovery +/- SD was 101.58 +/- 2.68. Interference from endogenous alpha-amino acids was overcome through selective complexation with freshly prepared Cu(OH)2. The interference likely to be encountered from co-administered drugs, such as carbamazepine, cimetidine, clonazepam, clopazam, phenobarbital, valproic acid, and lamotrigine, was also studied. A reaction pathway is suggested.

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