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PubMed2002

Gabapentin for neuropathic pain following spinal cord injury.

STUDY DESIGN: Retrospective review of patient data. OBJECTIVE: To present two years of experience in the use of gabapentin for the alleviation of neuropathic pain in spinal cord injury patients. SETTING: Supra-regional Spinal Cord Service, Melbourne, Australia. METHOD: Data were retrieved from the medical records of all spinal cord injury patients prescribed gabapentin for neuropathic pain. Pain was assessed prior to and during treatment at 1, 3 and 6 months with a 10 cm visual analogue scale which ranged from 0 ('no pain') to 10 ('worst pain imaginable'), or by the documentation of a verbal description of pain. RESULTS: Seventy-six per cent of patients receiving gabapentin reported a reduction in neuropathic pain. In those patients with data at all four measurement points, the mean pretreatment score was 8.86. Following treatment with gabapentin the score dropped to 5.23, 4.59 and 4.13 at 1, 3 and 6 months, respectively. Where only a verbal description of pain was documented, the trend was that the pretreatment report of 'unbearable' was replaced by 'liveable' during treatment. CONCLUSION: Our experience suggests that gabapentin offers an effective therapeutic alternative for the alleviation of neuropathic pain following spinal cord injury. Controlled clinical trials are now required to confirm these observations.

Acetates↗
PubMed1999

Gabapentin for the treatment of dysesthetic pain after reconstructive surgery.

BACKGROUND: Debilitating, postoperative dysesthetic pain after reconstructive surgery is a rare but problematic complication. Conventional therapy is either marginally effective or fraught with side effects. Gabapentin is a new, novel antiepileptic drug helpful in the management of other pain states. OBJECTIVE: A case of disturbing, postoperative dysesthetic pain after reconstructive surgery is presented. METHODS: A trial of gabapentin in escalating dose was initiated and the results and side effects were recorded. RESULTS: Treatment with gabapentin was associated with a substantial decrease in pain, which relapsed after tapering the medication. Relief was obtained with dose escalation, and a successful taper was eventually accomplished. Side effects were minimal. CONCLUSION: This is the first reported use of gabapentin in the treatment of postoperative dysesthetic pain. Although this type of neuropathic pain is difficult to manage, gabapentin produced substantial relief with few side effects. Further investigation is warranted.

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PubMed2003

Gabapentin-induced hypoglycemia in a long-term peritoneal dialysis patient.

An end-stage renal disease patient on long-term peritoneal dialysis was admitted with dizziness, fatigue, hypoglycemia, and hypotension. The hypotension resolved with intravenous normal saline, but the hypoglycemia persisted for 3 days despite an intravenous dextrose drip and discontinuation of gabapentin. The patient became normoglycemic on the fourth day of admission. None of the known causes for the hypoglycemia were identified except gabapentin, the dose of which was recently doubled 1 month before admission. Insulin and C-peptide levels were high during the hypoglycemic episode and returned to normal after discontinuation of gabapentin. The patient remains off gabapentin and has had no further episodes of hypoglycemia. To our knowledge, this is the first case of hypoglycemia induced by gabapentin.

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PubMed2006

Gabapentin attenuates the pressor response to direct laryngoscopy and tracheal intubation.

BACKGROUND: Laryngoscopy and tracheal intubation increase blood pressure and heart rate (HR). The aim of the present study was to investigate the effect of gabapentin when given before operation on the haemodynamic responses to laryngoscopy and intubation. METHODS: Forty-six patients undergoing abdominal hysterectomy for benign disease were randomly allocated to receive gabapentin 1,600 mg or placebo capsules at 6 hourly intervals starting the day (noon) before surgery. Anaesthesia was induced with propofol and cis-atracurium. Systolic, diastolic arterial blood pressures (SAP, DAP) and heart rate (HR) were recorded before and after the anaesthetic and 0, 1, 3, 5 and 10 min after tracheal intubation. RESULTS: SAP was significantly lower in the gabapentin vs the control group 0, 1, 3, 5 and 10 min after intubation [128 (27) vs 165 (41), P=0.001, 121 (14) vs 148 (29), P=0.0001, 115 (13) vs 134 (24), P=0.002, 111 (12) vs 126 (19), P=0.004 and 108 (12) vs 124 (17), P=0.001 respectively]. DAP also was lower in the gabapentin group 0, 1, 3, and 10 min after intubation [81 (18) vs 104 (19), P=0.0001, 77 (9) vs 91 (16), P=0.001, 71 (10) vs 84 (13), P=0.001 and 67 (10) vs 79 (12), P=0.004]. HR did not differ between the two groups at any time [82 (11) vs 83 (15), 79 (10) vs 80 (12), 86 (17) vs 92 (10), 82 (11) vs 88 (10), 81 (12) vs 81 (11), 77 (13) vs 79 (13), and 75 (15) vs 78 (12)]. CONCLUSION: Gabapentin, under the present study design attenuates the pressor response but not the tachycardia associated with laryngoscopy and tracheal intubation.

Adult↗
PubMed2000

Gabapentin enhances the analgesic effect of morphine in healthy volunteers.

UNLABELLED: The most effective group of drugs for the treatment of severe pain is opioid analgesics. Their use, however, is limited by decreased effects in neuropathic and chronic pain as a result of increased pain and development of tolerance. Gabapentin (GBP) is effective in both experimental models of chronic pain and clinical studies of neuropathic pain. Therefore, we investigated, in a randomized, placebo-controlled, double-blinded study, the pharmacodynamic and pharmacokinetic interaction of GBP and morphine in 12 healthy male volunteers. Morphine (60 mg, controlled release) or placebo was administered at 8:00 AM, and GBP (600 mg) or placebo was administered at 10:00 AM, thus comparing the analgesic effect of placebo + GBP (600 mg) with placebo + placebo and morphine (60 mg) + GBP in comparison to morphine plus placebo by using the cold pressor test. The duration and intensity of the side effects were assessed by using visual analog scales. The analgesic effect was evaluated by the change in the area under the curve (h x %; 0% baseline before Medication 1) of pain tolerance. Placebo + GBP (18.9% x h, 95% confidence interval [CI]: -2.5 to 40.3) did not present any significant analgesic effect compared with placebo + placebo (4.7% x h, 95% CI: -16.7 to 26.1). A significant increase in pain tolerance was observed comparing the combination of morphine and GBP (75.5% x h, 95% CI: 54.0-96.9) with morphine + placebo (40.6% x h, 95% CI: 19. 2-62.0). The observed adverse events after placebo + GBP were not significantly different compared with placebo + placebo. Morphine + placebo led to the expected opioid-mediated side effects. They were significantly more pronounced compared with placebo + placebo but did not differ significantly compared with the combination of morphine + GBP. Concerning the pharmacokinetic variables of morphine and its glucuronides, no significant difference between morphine + placebo and morphine + GBP was observed, whereas the area under the curve of GBP (43.9 +/- 5.3 vs 63.4 +/- 16.2 microg. h(-1). mL(-1), P < 0.05) significantly increased, and apparent oral clearance (230.8 +/- 29.4 mL/min vs 178 +/- 97.9 mL/min, P = 0.06) and apparent renal clearance (86.9 +/- 20.6 vs 73.0 +/- 24.2 mL/min, P = 0.067) of GBP decreased when morphine was administered concomitantly. These results suggest two different sites for the pharmacokinetic interaction-one at the level of absorption and the other at the level of elimination. Our study reveals both a pharmacodynamic and pharmacokinetic interaction between morphine and GBP, leading to an increased analgesic effect of morphine + GBP. These results and the good tolerability of GBP should favor clinical trials investigating the clinical relevance of the combination of morphine and GBP for treating severe pain. IMPLICATIONS: In a randomized, placebo-controlled, double-blinded trial with 12 healthy volunteers, we studied the interaction of morphine and gabapentin using the cold pressor test. The anticonvulsant gabapentin enhanced the acute analgesic effect of morphine. Furthermore, the plasma concentration of gabapentin was increased when morphine was administered concomitantly. Therefore, the well tolerated combination of gabapentin and morphine may improve pain therapy, especially in pain states, like chronic and neuropathic pain, which respond poorly to opioids.

Acetates↗
PubMed1998

Characterization of the effects of gabapentin and 3-isobutyl-gamma-aminobutyric acid on substance P-induced thermal hyperalgesia.

BACKGROUND: The authors sought to characterize the pharmacologic characteristic and site of action of gabapentin (Neurontin) in a model of thermal hyperalgesia induced by intrathecal substance P administration. METHODS: Rats were prepared with long-term lumbar intrathecal catheters. Hind paw withdrawal latency was determined using a radiant heat stimulus focused through a glass surface onto the plantar surface of the paw. RESULTS: Within 5 min after intrathecal injection of substance P (30 nmol), hind paw withdrawal latency fell from 11 to 8 s. Gabapentin given intrathecally or intraperitoneally produced dose-dependent reversal of the thermal hyperalgesia, with complete reversal (ED100) occurring at 163 microg for intrathecal and 185 mg/kg for intraperitoneal administration. S(+)-3-isobutyl-gamma aminobutyric acid, but not R(-)-3-isobutyl-gamma aminobutyric acid, also produced dose-dependent reversal of the intrathecal substance P-induced thermal hyperalgesia (intrathecal ED100, 65 microg and intraperitonal ED100, 31 mg/kg). The effects of intraperitoneally administered gabapentin and 3-isobutyl-gamma aminobutyric acid were reversed by intrathecal pretreatment with D-serine (100 microg) but not by L-serine. All effects were observed at doses that had little effect on motor function or spontaneous activity. Intrathecal N-methyl-D-aspartate (2 nmol) induced thermal hyperalgesia, which was blocked by gabapentin (100 mg/kg intraperitoneally) and S(+)-3-isobutyl-gamma aminobutyric acid (30 mg/kg intraperitoneally). CONCLUSIONS: The structure-activity relationship and the stereospecificity noted after intrathecal delivery suggest that gabapentin and S(+)-3-isobutyl-gamma aminobutyric acid act at a common spinal locus to modulate selectively a facilitated state of nociceptive processing.

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PubMed2002

Gabapentin suppresses cutaneous hyperalgesia following heat-capsaicin sensitization.

BACKGROUND: The anticonvulsant gabapentin, proven effective for neuropathic pain in two large, placebo-controlled clinical trials, is widely used for treatment of chronic pain. Preclinical studies have demonstrated analgesic and antiallodynic effects in models involving neuronal sensitization and nerve injury, without affecting acute pain transmission. The aim of the present study was to link data from animal models and clinical trials for chronic pain by investigating the effect of gabapentin on acute nociception and experimentally induced cutaneous hyperalgesia in healthy volunteers. METHODS: The human experimental hyperalgesia model, the heat-capsaicin sensitization model, was induced in 25 healthy male volunteers. Subjects received oral gabapentin (1,200 mg) or placebo after heat-capsaicin sensitization was established on the forearm. The primary outcome measures were the sizes of the areas of secondary hyperalgesia to von Frey hair and brush stimulation on the forearm. Secondary outcome measures were as follows: (1) size of secondary hyperalgesia area in response to brief thermal sensitization procedure on the thigh; (2) heat pain detection thresholds in normal and sensitized skin; and (3) painfulness of 1 min of 45 degrees C stimulation in normal skin. RESULTS: Oral gabapentin profoundly suppressed established cutaneous sensitization on the forearm and prevented development of cutaneous sensitization on the thigh. Thermal nociception in normal skin was unchanged. Side effects were modest. CONCLUSION: The results link preclinical findings with results from clinical trials of neuropathic pain. The results further suggest that gabapentin may prove effective in acute pain disorders involving neuronal sensitization, such as postoperative pain and acute herpetic pain, and could prove effective in prevention of chronic pain.

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PubMed2005

Gabapentin normalizes spinal neuronal responses that correlate with behavior in a rat model of cancer-induced bone pain.

BACKGROUND: Cancer-induced bone pain is a major clinical problem for which current treatments lack full efficacy. Gabapentin is licensed for use in neuropathic pain yet is also effective against inflammatory stimuli in animals. METHODS: A rat model of cancer-induced bone pain using the MRMT-1 cell line injected into the tibia was established to investigate the efficacy of acute (10, 30, 100 mg/kg) and chronic (30 mg/kg) systemic gabapentin on electrophysiological superficial dorsal horn neuronal responses to natural and noxious electrical stimuli, as well as on pain-related behavior. RESULTS: In electrophysiological studies gabapentin worked both acutely (100 mg/kg) and chronically (30 mg/kg) to normalize the hyperexcitable superficial dorsal horn neuronal response, significantly reducing electrical-evoked and mechanical-evoked but not thermal-evoked responses. The behavioral study showed that chronic gabapentin (30 mg/kg) significantly attenuated pain behavior in MRMT-1 rats, restoring responses to preoperative baseline degrees, and that this attenuation was accompanied by a reversion to normal (non-MRMT-1) wide-dynamic-range: nociceptive specific superficial dorsal horn neuronal profiles. CONCLUSIONS: Pain-related behavior in this rat model of cancer-induced bone pain is strongly linked to hyperexcitability of a population of superficial dorsal horn neurones. Gabapentin normalizes the cancer-induced bone pain induced dorsal horn neuronal changes and attenuates pain behavior. It may therefore provide a novel clinical treatment for cancer-induced bone pain.

Amines↗
PubMed1997

Gabapentin, ineffective in normal rats, markedly reduces C-fibre evoked responses after inflammation.

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

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PubMedDate not supplied

Long-term use of gabapentin for treatment of pain after traumatic spinal cord injury.

OBJECTIVE: To determine the long-term efficacy of gabapentin as a treatment of pain after spinal cord injury. DESIGN: All patients with traumatic-onset spinal cord injury treated with gabapentin were identified and followed up using a longitudinal observational design with two contact points (6 and 36 months after the trial) using a semi-structured interview. The first follow-up interview attempted to capture all 31 patients placed on therapeutic trial. The second follow-up interview attempted to capture those reporting a favorable response (n = 14) to the therapeutic trial at the first follow-up. RESULTS: Of the 27 patients contacted at the first follow-up (87% response rate), 6 (22%) discontinued the trial secondary to intolerable side effects; therefore, the pain analgesic effects of gabapentin in these patients could not be determined. Of the remaining 21 patients, 14 (67%) reported a favorable response (i.e., a 2 or greater point reduction on a 0-10 pain-rating scale). The second follow-up interview captured 11 (79% response rate) of the 14 patients reporting a favorable response at the first interview, and 91% (10 of 11 patients) continued to report that gabapentin was an effective analgesic. There was no evidence to suggest dosing difficulties due to tolerance over the 3-year period. Sedation, dizziness, and forgetfulness were the most common side effects. CONCLUSIONS: Gabapentin may be an effective treatment of pain after spinal cord injury among those able to tolerate initial and long-term side effects.

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PubMedDate not supplied

Amenorrhea in a patient after treatment with gabapentin for complex regional pain syndrome type II.

A 35-year-old woman suffered a traumatic injury to her right sciatic nerve requiring nerve exploration and external neurolysis. Following the surgery, the patient developed complex regional pain syndrome (CRPS) type II and was treated with gabapentin for pain control. Three months after the initiation of gabapentin therapy (1800 mg/day), the patient reported complete cessation of her menses. Based on hormonal tests, her gynecologist concluded that her amenorrhea was secondary to gabapentin therapy. The patient was weaned off the gabapentin over 6 days with return of her menses 2 weeks later. I conclude that gabapentin has the potential to cause amenorrhea with return of menses occurring after discontinuation of the drug.

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PubMedDate not supplied

Gabapentin treatment for muscle cramps: an open-label trial.

To evaluate the efficacy and safety of gabapentin in the treatment of muscle cramps, we engaged an open-label trial with a group of 30 patients with frequent (> 5 cramps/week), stable, long-lasting cramps, associated with different diseases. Gabapentin was effective in reducing the frequency and severity of muscle cramps and associated sleep disturbances (clinical outcome measures) within the first 2 weeks of medication at 600 mg/d. At the 1 month control (mean dosage, 825 +/- 35 mg), almost every patient had responded to treatment and two thirds experienced a total remission of symptoms. After 3 months of therapy (mean dosage, 892 +/- 180 mg), cramps disappeared in 100% of patients and this benefit persisted as long as 6 months. Additionally, we evaluated in 10 patients the Cramps Threshold Frequency (CTF) (neurophysiological outcome measure) before and during gabapentin treatment. Gabapentin significantly increased the CTF, returning it to normal values. With the limitation of an open-label methodology, our clinical and neurophysiologic experience suggests that a gabapentin dose of 600-1200 mg/d would be helpful in the treatment of muscular cramps.

Acetates↗
PubMed2000

Placebo-controlled study of gabapentin treatment of panic disorder.

A randomized, double-blind, placebo-controlled, parallel-group study was conducted to evaluate the efficacy and safety of gabapentin in relieving the symptoms of panic disorder. One hundred three patients were randomly assigned to receive double-blind treatment with either gabapentin (dosed flexibly between 600 and 3,600 mg/day) or placebo for 8 weeks. No overall drug/placebo difference was observed in scores on the Panic and Agoraphobia Scale (PAS) (p = 0.606). A post hoc analysis was used to evaluate the more severely ill patients as defined by the primary outcome measure (PAS score > or = 20). In this population, the gabapentin-treated patients showed significant improvement in the PAS change score (p = 0.04). In patients with a PAS score of 20 or greater, women showed a greater response than men regardless of treatment. Adverse events were consistent with the known side effect profile of gabapentin and included somnolence, headache, and dizziness. One patient experienced a serious adverse event during the study. No deaths were reported. The results of this study suggest that gabapentin may have anxiolytic effects in more severely ill patients with panic disorder.

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PubMedDate not supplied

Gabapentin for the management of hot flushes: a case series.

OBJECTIVE: To audit the effectiveness of the anticonvulsant gabapentin on hot flushes in postmenopausal women. DESIGN: This was an open case series involving 11 postmenopausal women who were willing to take gabapentin for the relief of their hot flushes and were willing to keep a diary recording the number and intensity of their hot flushes, both before and during treatment. Gabapentin was started at a dose of 300 mg, to be taken at night, and the women were instructed to increase the dose up to 1,200 mg, according to symptom behavior. RESULTS: Eleven women agreed to participate for on average 53.22 days (range, 2-79 days), but two discontinued participation-one before starting treatment and one after 2 days-so there are complete data sets for nine women. Gabapentin was found to be extremely effective in reducing hot flush activity (P < 0.001; Fig. 1). A significant reduction in symptoms was observed with a dose of 300 mg/day (P < 0.001). Scores on the Green Climacteric Scale were significantly improved from a mean of 25.72 (range, 12-42) to 19.25 (range, 13-31; P < 0.001). Palpitations (P = 0.001), panic attacks (P = 0.0001), mood (P = 0.023), muscle and joint pains (P = 0.021), and paresthesias and loss of sensation in the extremities (P = 0.001) were also shown to improve with treatment. CONCLUSIONS: In the present case series, gabapentin was well tolerated and could be a valuable alternative for the treatment of hot flushes in women with contraindications to hormonal replacement therapy. It would be particularly beneficial for women in whom aches and pains and paresthesias are also a significant feature of the climacteric syndrome.

Acetates↗
PubMed2004

Gabapentin is a first line drug for the treatment of neuropathic pain in spinal cord injury.

STUDY DESIGN: Prospective, randomized, double blind, placebo-controlled, crossover clinical trial. OBJECTIVES: To determine the efficacy of gabapentin in the treatment of neuropathic pain related to spinal cord injury. SUMMARY OF BACKGROUND DATA: Neuropathic pain is initiated or caused by a primary lesion or dysfunction in the nervous system. Neuropathic pain associated with spinal cord injury is quite refractory, and current treatments are not effective. Gabapentin, an anticonvulsant, has become the first choice in the treatment of neuropathic pain. The place of gabapentin in the treatment of spinal cord injury-related neuropathic pain was questioned in only a few recent reports; however, they are retrospectively designed, nonstandardized, and uncontrolled studies, or involve a very small series of patients using less than optimum doses. METHODS: A total of 18-week study period included a 4-week medication/placebo titration period. This was followed by a 4-week stable dosing period when the patients continued to receive maximum tolerated doses, a 2-week washout period, then a crossover of 4 weeks of medication/placebo titration, and another 4 weeks of stable dosing period. Twenty paraplegic patients (female/male: 7/13) with complete spinal cord injury at the thoracic and lumbar level, aged between 20 and 65 years, with neuropathic pain for more than 6 months were recruited for the study. RESULTS: All patients completed the study. Gabapentin reduced the intensity as well as the frequency of pain, relieved all neuropathic pain descriptors except the itchy, sensitive, dull, and cold types, and improved the quality of life (P < 0.05). CONCLUSIONS: Gabapentin can be added to the list of first-line medications for the treatment of chronic neuropathic pain in spinal cord injury patients. It is a promising new agent and offers advantages over currently available treatments.

Acetates↗
PubMed2002

Gabapentin and the neurokinin(1) receptor antagonist CI-1021 act synergistically in two rat models of neuropathic pain.

The present study examines the effect of combinations of gabapentin (Neurontin) and a selective neurokinin (NK)(1) receptor antagonist, 1-(1H-indol-3-ylmethyl)-1-methyl-2-oxo-2-[(1-phenylethyl)amino]ethyl]-2-benzofuranylmethyl ester (CI-1021), in two models of neuropathic pain. Dose responses to both gabapentin and CI-1021 were performed against static allodynia induced in the streptozocin and chronic constriction injury (CCI) models. Theoretical additive lines were calculated from these data. Dose responses to various fixed dose ratios of a gabapentin/CI-1021 combination were then examined in both models. In the streptozocin model, administration of gabapentin/CI-1021 combinations at fixed dose ratios of 1:1 and 60:1 resulted in an additive effect with dose response similar to the theoretical additive line. However, a synergistic interaction was seen after fixed dose ratios of 10:1, 20:1, and 40:1 with static allodynia completely blocked and the dose responses shifted approximately 8-, 30-, and 10-fold leftward, respectively, from the theoretical additive values. In the CCI model, after fixed dose ratios of 5:1 and 20:1, combinations of gabapentin and CI-1021 produced an additive response. At the fixed dose ratio of 10:1 static allodynia was completely blocked with an approximate 10-fold leftward shift of the dose response from the theoretical additive value, indicating synergy. The combination of gabapentin with a structurally unrelated NK(1) receptor antagonist, (2S,3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine (CP-99,994), also produced synergy, at a fixed dose ratio of 20:1. This ratio completely blocked streptozocin-induced static allodynia and was approximately shifted leftward 5-fold from the theoretical additive value. These data suggest a synergistic interaction between gabapentin and NK(1) receptor antagonists in animal models of neuropathic pain.

Acetates↗
PubMed2006

The effects of gabapentin and memantine in acquired and congenital nystagmus: a retrospective study.

BACKGROUND: Pharmacological treatment has been successful in some forms of acquired neurological nystagmus. However, drugs are not known to be effective in idiopathic infantile nystagmus or nystagmus associated with ocular diseases. METHODS: The authors retrospectively analysed Snellen visual acuity (VA), subjective visual function, and eye movement recordings of 23 patients with nystagmus (13 secondary to multiple sclerosis, three associated with other neurological diseases, two idiopathic infantile, and five with associated ocular diseases) treated with gabapentin or memantine. RESULTS: With gabapentin, 10 of 13 patients with nystagmus secondary to multiple sclerosis (MS) showed some improvement. Memantine improved the VA in all three patients with MS who did not improve on gabapentin. There was no change of nystagmus in other neurological disorders. Patients with congenital nystagmus showed reduction of nystagmus and their VA changes depended on the ocular pathology. CONCLUSION: Gabapentin and memantine may be effective in acquired nystagmus secondary to MS. To the authors' knowledge this is the first series of patients showing that gabapentin is effective in improving nystagmus in congenital nystagmus/nystagmus associated with ocular pathology. Memantine may be useful as an alternative drug in treating patients with nystagmus.

Adolescent↗
PubMed2003

Gabapentin versus ropinirole in the treatment of idiopathic restless legs syndrome.

Dopaminergic agents such as ropinirole are the drugs of first choice in treating restless legs syndrome (RLS). Recently, gabapentin, a structural analogue of gamma-aminobutyric acid, has also been shown to improve sensorimotor symptoms in RLS. Therefore, the tolerability and efficacy of randomized treatment with either gabapentin or ropinirole in patients with idiopathic RLS was evaluated in this 4-week open clinical trial. Patients with idiopathic RLS were treated with either 300 mg of gabapentin (n = 8) or 0.5 mg of ropinirole (n = 8) as the initial dose, and the dose was up-titrated until relief of symptoms was achieved (gabapentin mean dosage 800 +/- 397 mg, range 300-1,200 mg; ropinirole mean dosage 0.78 +/- 0.47 mg, range 0.25-1.50 mg). In both groups, International Restless Legs Syndrome Study Group questionnaire scores improved significantly (p < or = 0.018), whereas the scores of the Epworth sleepiness scale remained unchanged within normal limits. Polysomnographic data showed a reduction of periodic leg movements during sleep (PLMS; p < 0.03) and PLMS index (p < 0.02) in both groups. Side effects were only mild and mostly transient. After 6-10 months of follow-up, in most patients, RLS symptoms were still improved. We conclude that gabapentin and ropinirole provide a similarly well-tolerated and effective treatment of PLMS and sensorimotor symptoms in patients with idiopathic RLS.

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