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Thread: neurontin and spasticity

  1. #1

    neurontin and spasticity

    I take 600mg of neurontin 4x a day, and recently ran out. I had to go about 6 days before getting my refill and my spasms and tone were very bad. When I received my refill and started the neurontin again my spasms and tone decreased significantly.
    I was taking the neurontin for pain but didn't notice any increase in pain sensation after running out of the drug for those days, and when I started taking it again I had no difference in pain, either. At this point I guess I'll continue taking it for the effects on my spasticity (I already take 90mgs of baclofen per day, and 2mg valium morning and night for my bad spasticity).
    My question is whether others have had this experience (it is an anti-seizure med so it wouldn't surprise me if others benefit from it when it comes to spasms). I did try to extend my supply when I realized I was running out by stepping down from 2 capsules 4x day to 1 capsule 4x day, that lasted for 2 or 3 days before I completely ran out.
    If anyone has had this experience w/ neurontin please let me know. Thanks!

  2. #2
    ScottS,

    Good observation! Many studies indicate that gabapentin (Neurontin) significantly reduces spasticity in multiple sclerosis (Cutter, et al., 2000; Dunevsky & Perel, 1998; Metz, 1998; Mueller, et al. 1997; Paisley, et al. 2002) but also in amyotrophic lateral sclerosis (de Carvalho, et al. 2001), general spastic hypertonia (Francisco, et al. 2001), focal spasticity (Hesse & Mauritz,1997), upper motor neuronal spasticity (Kita & Goodkin, 2000), Parkinsonian rigidity and tremor (Jagustyn & Romaniak, 2002), cerebral palsy (Krach, 2001), cerebellar ataxia (Perlman, 2000) and spinal cord injury (Gruenthal, et al. 1997; Priebe, et al. 1997; Rosche, 2002).

    Wise.

    References

    • Cutter NC, Scott DD, Johnson JC and Whiteneck G (2000). Gabapentin effect on spasticity in multiple sclerosis: a placebo-controlled, randomized trial. Arch Phys Med Rehabil. 81: 164-9. University of Colorado Health Sciences Center, Denver, USA. OBJECTIVE: To investigate the effect of gabapentin on subject self-report and physician-administered spasticity scales in individuals with multiple sclerosis. DESIGN: Prospective, double-masked, placebo-controlled, crossover design. SETTING: The Multiple Sclerosis Center at the Denver Veterans Affairs Medical Center. INTERVENTION: Subjects were titrated to either 900 mg gabapentin orally three times a day or placebo over a 6-day period. Subjects underwent a 14-day washout and then were crossed over. No other changes were made to their medication regimen. MAIN OUTCOME MEASURES: The outcome measures were divided into two categories: subject self-report scales physician-administered scales. Subject self-report scales included the spasm frequency scale, spasm severity scale, interference with function scale, painful spasm scale, and global assessment scale. Physician-administered scales included the Modified Ashworth Scale, clonus scale, deep tendon reflexes, plantar stimulation response, and the Kurtzke Expanded Disability Status (EDSS) Scale. Digit Span and Digit Symbol subtests of the WAIS-R Intelligence Scale were administered to assess for possible impaired concentration. The Fatigue Impact Scale was administered to assess for changes in fatigue. The adjective generation technique was administered to assess for alterations in mood. RESULTS: A statistically significant reduction in the impairment of spasticity was found in the gabapentin-treated subjects compared with placebo as measured by the self-report scales of the spasm severity scale, interference with function scale, painful spasm scale, and global assessment scale and by the physician-administered scales of the Modified Ashworth and plantar stimulation response. No significant difference was noted in the Digit Span, Digit Symbol, adjective generation technique, and EDSS. CONCLUSION: Gabapentin reduces the impairment of spasticity, compared with placebo, without the side effects of worsening concentration and fatigue.
    • de Carvalho M (2001). Gabapentin for the treatment of spasticity in patients with amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord. 2: 47-8.
    • Dunevsky A and Perel AB (1998). Gabapentin for relief of spasticity associated with multiple sclerosis. Am J Phys Med Rehabil. 77: 451-4. Department of Rehabilitation Medicine, Kingsbrook Jewish Medical Center, Brooklyn, New York 11203, USA. The use of a recently released anticonvulsant, gabapentin, in the treatment of spasticity in two patients with multiple sclerosis is reported. Gabapentin was chosen because of its GABA-ergic effect and because previously reported studies have shown that it is well tolerated compared with other GABA-mimetic medication. Satisfactory release of spasticity with significant improvement of functional outcome was noted in both cases. Both patients were first treated with gabapentin for one month at 300 mg per day and then, with no reported side-effects, at 400 mg per day. Before treatment, spasticity (graded with modified Ashworth Scale) in one patient was 3 for left lower and 2 for right lower limbs, and Expanded Disability Status Scale (EDSS) was 7; ambulation was limited to a few steps with a standard walker. After two weeks of treatment, spasticity was 2 and 1 for the left and right lower limbs, respectively. At three-month intervals, spasticity was +1 for left and 1 for right lower limbs, and EDSS was 6; the patient could ambulate 75 to 100 m with a standard walker. In the second patient, spasticity before treatment was 2 for both lower and left upper limbs. EDSS was 5.5, and ambulation was confined to 100 m with a cane. Spasticity improved to +1 in lower and 1 in left upper limbs after two weeks and to 1 and normal after three months. At three months, EDSS was 3 and the patient could ambulate for long distances without an assistive device. We suggest that gabapentin can be used effectively to decrease spasticity without significant side effects in patients with multiple sclerosis.
    • Francisco GE, Kothari S and Huls C (2001). GABA agonists and gabapentin for spastic hypertonia. Phys Med Rehabil Clin N Am. 12: 875-88, viii. Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, University of Texas Sciences Center, Brain Injury Program, Institute for Rehabilitation and Research, Houston, Texas, USA. Spasticity is a result of an imbalance between the afferent excitatory and descending inhibitory pathways after central nervous system damage. Its pharmacologic control is believed to result from the antagonism of inhibitory mechanisms (gamma-aminobutyric acid [GABA] or glycine-mediated antagonism of excitatory mechanisms), or both. Because GABA receptor sites are widely present in the central nervous system, it is amenable to pharmacologic manipulation.
    • Gruenthal M, Mueller M, Olson WL, Priebe MM, Sherwood AM and Olson WH (1997). Gabapentin for the treatment of spasticity in patients with spinal cord injury. Spinal Cord. 35: 686-9. Department of Neurology, University of Louisville School of Medicine, KY, USA. Our serendipitous observations suggested that some patients with spasticity appeared to have improved following the administration of the anticonvulsant drug gabapentin. As some patients with spasticity are either refractory to or intolerant of established medical treatments, we conducted this study to investigate the effect of gabapentin on spasticity in patients with spinal cord injury. Twenty-five patients with spinal cord injury and spasticity received oral gabapentin (2400 mg over 48 h) in a randomized, double blind, placebo-controlled crossover study. We assessed responses by measuring the Ashworth spasticity scale, muscle stretch reflexes, presence of clonus and reflex response to noxious stimuli. Patient ratings were obtained using a Likert Scale. Administration of gabapentin, but not placebo, was associated with an 11% reduction in spasticity as measured by the Ashworth Scale (P = 0.04) and by a 20% reduction in the Likert Scale (P = 0.0013). Significant changes were not obtained for the other measures. The data obtained suggest that gabapentin may be useful in the management of spasticity associated with spinal cord injury.
    • Hesse S and Mauritz KH (1997). Management of spasticity. Curr Opin Neurol. 10: 498-501. Berlin Clinic, Department of Neurological Rehabilitation, Free University Berlin, Germany. Recent open studies and two placebo-controlled studies confirm the potential role of Botulinum toxin A in the treatment of focal spasticity in adults and children. The effect of the toxin might not only be mediated by the paresis of extrafusal, but also intrafusal muscle fibres, thereby altering the afferent discharge. To enhance its effectiveness, an additional electrical stimulation seems promising. Most patients tolerate the neurolytic agent well. Two individuals, however, suffered from an intermittent tetraparesis after treatment. The repetitive magnetic stimulation and the use of gabapentin might be other new therapeutic options in the management of spasticity.
    • Jagustyn P and Romaniak A (2002). [GABApentin--new therapeutic possibilities]. Neurol Neurochir Pol. 36: 971-80. Kliniki Neurologii Wojskowego Instytutu Medycyny Lotniczej. The paper is a review of current experience with use of gabapentin--a new antiepileptic drug--in neurologic conditions others than epilepsy. Mechanism of action of the drug is not fully elucidated yet. However it proved to be effective in therapy of chronic pain, especially in neuropathic pain, neuralgia, low back pain, reflex sympathetic dystrophy and erythromelalgia. Gabapentin is also effective in pain and spasticity in multiple sclerosis. Clinical studies of gabapentin in movement disorders, such as Parkinson disease, essential tremor and atrophic lateral sclerosis are discussed in the paper. It can be summarized that gabapentin is a valuable medication and the use thereof in neurology is not limited to epilepsy.
    • Kita M and Goodkin DE (2000). Drugs used to treat spasticity. Drugs. 59: 487-95. Department of Neurology, University of California at San Francisco, School of Medicine UCSF/Mt Zion Multiple Sclerosis Center, 94115-1642, USA. kita@itsa.ucsf.edu. Spasticity is a common and disabling symptom for many patients with upper motor neuron dysfunction. It results from interruption of inhibitory descending spinal motor pathways, and although the pathophysiology of spasticity is poorly understood, the final common pathway is overactivity of the alpha motor neuron. Therapy for spasticity is symptomatic with the aim of increasing functional capacity and relieving discomfort. Any approach to treatment should be multidisciplinary, including physical therapy, and possibly surgery, as well as pharmacotherapy. It is important that treatment be tailored to the individual patient, and that both patient and care giver have realistic expectations. Pharmacotherapy is generally initiated at low dosages and then gradually increased in an attempt to avoid adverse effects. Optimal therapy is the lowest effective dosage. Baclofen, diazepam, tizanidine and dantrolene are currently approved for use in patients with spasticity. In addition, clonidine (usually as combination therapy), gabapentin and botulinum toxin have shown efficacy, however, more studies are required to confirm their place in therapy. Intrathecal baclofen, via a surgically implanted pump and reservoir, may provide relief in patients with refractory severe spasticity.
    • Krach LE (2001). Pharmacotherapy of spasticity: oral medications and intrathecal baclofen. J Child Neurol. 16: 31-6. Gillette Children's Specialty Healthcare, St. Paul, MN 55101, USA. lkrach@gillettechildrens.com. Spasticity is a common problem in children with neurologic impairment, particularly in those with cerebral palsy. Clinicians commonly make use of oral medications to attempt to reduce spasticity and increase function. Little has been published in the literature concerning the use of these medications in children and their effects on both muscle tone and function. This article is a review of the sites of action, side effects, and efficacy of benzodiazepines, baclofen, dantrolene sodium, alpha2-adrenergic agonists, and gabapentin. A brief review of intrathecal baclofen is included as well.
    • Metz L (1998). Multiple sclerosis: symptomatic therapies. Semin Neurol. 18: 389-95. Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary and University of Calgary MS Clinic, Foothills Hospital, Alberta, Canada. Although new disease-altering treatments offer hope for those with multiple sclerosis, they are not appropriate for most. Management of symptoms, however, can help everyone with the disease. Several new therapies, including tizanidine, intrathecal baclofen, botulinum toxin injections, gabapentin, ondansitron, thalamic stimulation, and lamotrigine, increase our treatment options. Better understanding of the sleep disorders that commonly occur in those with multiple sclerosis will help us treat another disabling symptom. This chapter reviews the medical and surgical management of multiple sclerosis symptoms, including these new options.
    • Mueller ME, Gruenthal M, Olson WL and Olson WH (1997). Gabapentin for relief of upper motor neuron symptoms in multiple sclerosis. Arch Phys Med Rehabil. 78: 521-4. Department of Internal Medicine, University of Louisville School of Medicine, KY, USA. OBJECTIVE: To examine the efficacy of gabapentin in the treatment of spasticity and painful muscle spasms in patients with multiple sclerosis. DESIGN: Double-blind, placebo-controlled crossover study. SETTING: Free-standing, 93-bed, university-affiliated rehabilitation hospital. PARTICIPANTS: There were 15 patients between the ages of 18 and 50 who had laboratory-supported definite multiple sclerosis with spasticity and leg cramps severe enough to interfere with daily activities, including sleep. INTERVENTION: The patients received the placebo or 400mg gabapentin orally three times a day for 48 hours with an 11-day washout period. If the patients were on currently accepted modes of therapy, including oral baclofen, their current medication was not changed. MAIN OUTCOME MEASURES: The outcome measures were Visual Faces Scale rating, Kurtzke Disability Scale, quantitative surface electromyography, Ashworth Scale, presence or absence of clonus in response to rapid ankle dorsiflexion and wrist extension, presence or absence of reflex withdrawal in response to nailbed pressure to the first finger, and assessment of Babinski response. RESULTS: Statistically significant improvements for the gabapentin treated patients were found in the Ashworth Scale, Visual Faces Scale, and Kurtzke Disability Scale. CONCLUSIONS: At a dose of 400mg orally three times a day, gabapentin may be of value in the treatment of the spasticity and painful muscle cramping experienced by patients with multiple sclerosis.
    • Paisley S, Beard S, Hunn A and Wight J (2002). Clinical effectiveness of oral treatments for spasticity in multiple sclerosis: a systematic review. Mult Scler. 8: 319-29. The School of Health and Related Research, The University of Sheffield, UK. Spasticity is a common disabling feature of multiple sderosis. A variety of drugs are in regular use as oral treatment induding badofen, dantrolene, tizanidine, and diazepam. Published evidence of effectiveness is limited. Most trials are of small size, of short duration, and have not reported on functional outcomes. Studies have been published which suggest that badofen, tizanidine, and diazepam are all effective in reducing dinical measures of spasticity, but there is little evidence that they lead to an improvement in patient function. There is no evidence to suggest any difference in effectiveness between them. The evidence that dantrolene has any effect on spasticity is of poor quality. Diazepam and dantrolene are associated with more side effects than baclofen and tizanidine. There is evidence for the effectiveness of gabapentin in reducing spasticity and improving function in the short term, though longer-term studies are needed to establish its true value. One randomized controlled trial of threonine does not support its effectiveness.
    • Perlman SL (2000). Cerebellar Ataxia. Curr Treat Options Neurol. 2: 215-224. Department of Neurology, University of California at Los Angeles, 300 UCLA Medical Plaza, Suite B200, Los Angeles, CA 90095, USA. sperlman@ucla.edu. There is nothing more discouraging than for a patient to be given a specific diagnosis, then to be told that there is nothing that can be done. Physicians are equally disheartened to see exponential progress being made in the understanding of the pathophysiology of a complex disorder but few direct benefits resulting for their patients. Over the past 5 years, molecular genetic research has completely revolutionized the way in which the progressive cerebellar ataxias are classified and diagnosed, but it has yet to produce effective gene-based, neuroprotective, or neurorestorative therapies. The treatment of cerebellar ataxia remains primarily a neurorehabilitation challenge, employing physical, occupational, speech, and swallowing therapy; adaptive equipment; driver safety training; and nutritional counseling. Modest additional gains are seen with the use of medications that can improve imbalance, incoordination, or dysarthria (amantadine, buspirone, acetazolamide); cerebellar tremor (clonazepam, propranolol); and cerebellar or central vestibular nystagmus (gabapentin, baclofen, clonazepam). Many of the progressive cerebellar syndromes have associated features involving other neurologic systems (eg, spasticity, dystonia or rigidity, resting or rubral tremor, chorea, motor unit weakness or fatigue, autonomic dysfunction, peripheral or posterior column sensory loss, neuropathic pain or cramping, double vision, vision and hearing loss, dementia, and bowel, bladder, and sexual dysfunction), which can impede the treatment of the ataxic symptoms or can worsen with the use of certain drugs. Treatment of the associated features themselves may in turn worsen the ataxia either directly (as side effects of medication) or indirectly (eg, relaxation of lower limb spasticity that was acting as a stabilizer for an ataxic gait). Secondary complications of progressive ataxia can include deconditioning or immobility, weight loss or gain, skin breakdown, recurrent pulmonary and urinary tract infections, aspiration, occult respiratory failure, and obstructive sleep apnea, all of which can be life threatening. Depression in the patient and family members is common. Although no cures exist for most of the causes of cerebellar ataxia and there are as yet no proven ways to protect neurons from premature cell death or to restore neuronal populations that have been lost, symptomatic treatment can greatly improve the quality of life of these patients and prevent complications that could hasten death. Supportive interventions should always be offered-- education about the disease itself, genetic counseling, individual and family counseling, referral to support groups and advocacy groups, and guidance to online resources. Misinformation, fear, depression, hopelessness, isolation, and financial and interpersonal stress can often cause more harm to the patient and caregiver than the ataxia itself.
    • Priebe MM, Sherwood AM, Graves DE, Mueller M and Olson WH (1997). Effectiveness of gabapentin in controlling spasticity: a quantitative study. Spinal Cord. 35: 171-5. Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas, USA. The purpose of this investigation was to study the effectiveness of gabapentin in controlling spasticity in persons with spinal cord injury (SCI) using a surface EMG-based quantitative assessment technique called the brain motor control assessment (BMCA). Six men from a Veterans Affairs Medical Center with spasticity due to traumatic SCI were studied as part of a multi-center, placebo-controlled, cross-over, clinical trial of gabapentin. Spasticity was evaluated using multi-channel surface EMG recordings of muscles in the lower extremities, abdomen and low back before and during treatment with oral gabapentin or placebo. Gabapentin or placebo was given orally in doses 400 mg three times daily for 48 h. Following a 10 day wash-out period subjects were crossed-over to receive the medication not received the first time. This was followed by an elective open-label extension. Group results during the controlled trial did not reach statistical significance at the dosage used. One subject demonstrated a dramatic improvement in spasticity that was apparent both clinically and with the BMCA. Other subjects demonstrated modest improvements which were seen in the BMCA but not recognized clinically. During the open label extension, the four subjects who participated experienced important clinical improvements with higher doses (to 3600 mg/day). These improvements were often in components of spasticity in which the BMCA had detected subclinical changes during the cross-over trial. A seventh subject was studied using the BMCA at doses of 1200 mg T.I.D. gabapentin, off gabapentin and 800 mg T.I.D. gabapentin and demonstrated quantitatively a dose-related effect with higher doses of gabapentin which matched clinical observations. Gabapentin at doses of 400 mg T.I.D. may be effective in controlling some features of spasticity in persons with SCI. Higher doses provide greater control of spasticity, and controlled studies using higher doses are needed to evaluate gabapentin's efficacy.
    • Rosche J (2002). Treatment of spasticity. Spinal Cord. 40: 261-2.

  3. #3
    Hi Scott,
    I used neurontin for about 2 years for pain. Due to circumstances I quit neurontin (gradually) but there's been no increase in pain. First month in almost 4 years I'm not using pain medication and the pain isn't worse. I'm wondering why I've been taking it those years. There's no change in spasms.

  4. #4
    I take care of a C5-6, and she is on 600mg neurontin 3 times a day. It has helped with the spasms, but no real difference in pain. The spasms and tone were horrible before she started it. She also takes baclofen and valium.

  5. #5
    scott
    i use to take 600mg 3x a day, but ive cut back to 300mg 2x a day. if i dont take it at all, my spasms are bad. i dont feel any difference in pain. i stand on my staning frame for 1-2 hours a day and that has cut my spamsms down a whole lot. so your not the only one experiencing this! take care!

    Even if your body cannot move, you can still think and meditate ~Dalai Lama~

  6. #6
    It would be really interesting indeed if Neurontin helps with spasms. Most drugs such as baclofen is not useful for preventing spasms unless such high doses are taken that it weakens the muscles. However, neurontin does not cause weakness. This could presage a class of anti-epileptic drugs that could be useful for reducing spasms without causing weakness. Wise.

  7. #7
    i definitely noticed a decrease in spasms when my dose was doubled about 10 months ago (1200 to 2400mg/day). And I never noticed any pain relief, as I noticed no pain increase when I ran out of the medicine last week. Along the same lines, I noticed a drastic difference in spasms. The only drawback w/ the neurontin is the drowsiness.

    I want to try stepping back off my meds since I'm on so many (2400mgs neurontin, 90mgs baclofen, 4 mgs valium, 20 mgs ditropan per day), but at this point I'm going to try to step down from the valium 1st, then maybe cut back from the baclofen a bit, but I'll stay on the neurontin.

    My reasoning for this is b/c everything I've heard about neurontin is that it doesn't have bad side effects. But I've been told that high doses of baclofen works the liver really hard, and valium has a wide range of side effects.

    Does anyone have any thoughts on my "plan" of stepping off valium first, then a little baclofen maybe? Dr Young, do you agree that if I can choose b/t cutting back baclofen or neurontin that I should cut back baclofen first, since it has more negative side effects? Thanks!

  8. #8
    when i cut back on baclofen, i didnt notice any changes w/spasms, but i was on a low dose 10mg 3x a day and cut back 5-10mg a week and now i dont use it at all. when i started cutting back the neurontin, i noticed a major difference in spasms.

    Even if your body cannot move, you can still think and meditate ~Dalai Lama~

  9. #9
    Scott,
    I have been on Neurontin for spasticity for about six years now, I am 8 years post, after having no luck with baclofen and being unable to tolerate the sedation from zanaflex. It isn't a miracle drug for me, but if definitely helps, and is the sole routine anti-spasticity med that I use for daytime use (I still take zanaflex at bedtime, the sedation is welcome then, and use valium as necessary during the day for "bad" periods). I take 1200 mg three times a day. A neurologist handles my medications now, he treats a lot of MS patients, and thought it was worth trying when I was failing other medications. Six years ago I wasn't hearing about any other SCI patients using Neurontin for spasticity, but I am gradually hearing of more and more all the time now. I guess my neuro was ahead of his time. I have always known he was a sharp cookie (and a really nice guy to boot)! After seeing leading headache specialists, he was also the first doc to get my migraines under control, and give me some semblance of a quality life. Can you tell I love him?
    Laura

  10. #10
    This is rather off topic, but I wanted to add, being in the field, that another off-label use they have now found for neurontin is anxiety. Psychiatrists are finding that for some people it has rather significant anti-anxiety properties without the risk of dependence of the benzodiazepines like xanax, valium, klonopin, etc. It has turned out to be quite a nifty, albeit expensive, little drug.

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