Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since its introduction into clinical practice in 1999, levetiracetam, the S enantiomer of piracetam, has rapidly found a secure place, initially in the therapy of partial onset seizures and subsequently in the treatment of idiopathic generalized epilepsies (IGE). It has many of the properties of an "ideal" antiepileptic drug, including rapid absorption, linear pharmokinetics, and sparse drug interactions. Tolerabiliy is generally excellent in both adults and children, although tiredness is a common dose-limiting adverse effect. Occasionally the drug can precipitate behavioral abnormalities, especially in patients with learning disability. There is a wide safety margin in overdose. In common with most antiepileptic drugs its mode of action remains uncertain. Levetiracetam binds to a specific site in the brain, influences intracellular calcium currents and reverses negative allosteric modulators of GABA- and glycine-gated currents in vitro. Its effectiveness has been demonstrated in animal models of epilepsy and in clinical trials of partial onset and IGE. Treatment of IGEs may be straightforward, with many patients demonstrating an excellent and robust response to valproate monotherapy. However, there remains a significant minority of patients for whom valproate is unsuitable, including those who experience unacceptable adverse effects (e.g., weight gain or hair loss) and women of childbearing age in whom the teratogenic potential of valproate is unacceptable. Therapeutic response to lamotrigine in this group is often disappointing, and many clinicians now are turning to the choice of levetiracetam. Efficacy in generalized tonic-clonic seizures and myoclonus is usually apparent and some patients experience improvement in typical absences. Experience of combinations of levetiracetam with other antiepileptic drugs is limited in IGE and the responses are largely anecdotal. In our hands, patients with refractory IGEs may respond to combinations of levetiracetam with valproate, lamotrigine, and phenobarbital, and adverse effects when they occur are usually limited to tiredness. Levetiracetam does not interact with the oral contraceptive pill, simplifying treatment in women of childbearing age. Although animal data look encouraging, questions over levetiracetam's teratogenic potential and overall safety in pregnancy will remain for many years to come.
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PMID:Levetiracetam in the treatment of idiopathic generalized epilepsies. 1630 90

The treatment of progressive myoclonic epilepsy (PME) is largely empirical, even though valproic acid (VPA) is usually considered the drug of first choice. However, VPA should be used with caution in PME due to mitochondrial dysfunction, i.e. in MERRF (myoclonic epilepsy with ragged red fibers) syndrome, because of its interaction with mitochondrial respiration and metabolism. Levetiracetam (LEV) treatment was started in combination with VPA in a patient with typical clinical, histological, and biochemical features of MERRF due to a mutation on the tRNA of Phenilalanine gene. The average myoclonus score improved dramatically, as well as the quality of life and no side effects were observed, even after having withdrawn VPA. LEV may benefit myoclonus in PME of mitochondrial origin without altering mitochondrial function, and it could be considered the drug of first choice for the treatment of myoclonus in MERRF.
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PMID:Antimyoclonic effect of levetiracetam in MERRF syndrome. 1641 77

We present three unrelated cases of genetically confirmed progressive myoclonic epilepsy of the Unverricht-Lundborg type who were treated with Levetiracetam as adjunctive therapy for their myoclonus. All cases responded with decrease of their myoclonus and improvement of quality of life. Two were able to return to or continue their employment. Patients tolerated the drug well without side effects reported. Levetiracetam appears to be a useful antimyoclonic agent in cases of progressive myoclonic epilepsy and should be considered for adjunctive therapy.
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PMID:Levetiracetam in three cases of progressive myoclonus epilepsy. 1724 59

Subacute sclerosing panencephalitis is a devastating progressive degenerative disease of the nervous system presumably caused by a persistent measles virus. Patients commonly present with myoclonia or encephalopathy. There are currently no known curative therapeutic options or effective symptomatic therapy. We treated a 12-year-old boy with subacute sclerosing panencephalitis who presented with acute encephalopathy and myoclonus. Electroencephalogram showed characteristic generalized periodic discharges. Levetiracetam produced dramatic improvement in both myoclonus and encephalopathy. The improvement was clear within 4 days. The electroencephalogram pattern showed improvement as well. Levetiracetam is a promising symptomatic therapy in subacute sclerosing panencephalitis for both the myoclonus and the encephalopathy. In this patient, it also appeared to improve the electroencephalographic pattern. We suggest that the generalized periodic discharges associated with the myoclonus contributed to the patient's encephalopathy.
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PMID:Successful treatment of encephalopathy and myoclonus with levetiracetam in a case of subacute sclerosing panencephalitis. 1915 68

Triphasic waves are seen in the electro-encephalogram of adult patients with toxic-metabolic encephalopathies of various origins. Levetiracetam is a broad spectrum anti-epileptic drug with renal elimination and no hepatic metabolism. We describe the case of encephalopathy with triphasic waves concomitant with levetiracetam accumulation in a patient with chronic renal failure. The condition was reversible after down-titration of levetiracetam with no change of the renal function. Other causes of metabolic encephalopathy were excluded. Moreover, this patient suffered from a probable cortical myoclonus that relapsed after cessation of the drug but was well controlled by a low dosage adapted to the renal failure. In cases of metabolic encephalopathy with triphasic waves in a patient with renal failure taking levetiracetam, it is important to exclude toxic accumulation of levetiracetam among other causes.
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PMID:Levetiracetam accumulation in renal failure causing myoclonic encephalopathy with triphasic waves. 1920 20

Levetiracetam (LEV) has been shown to suppress myoclonus of various origins. Corticobasal degeneration (CBD), a progressive neurodegenerative disorder with Parkinsonian syndrome, is frequently accompanied by myoclonus. We investigated the effect of LEV on myoclonus in two CBD patients. LEV remarkably decreased the myoclonic activity in both patients already at 1,500 mg/day dose. This is the first report on LEV alleviating myoclonus in CBD. Our data indicate that it might be worthwhile to assess this effect in an appropriately designed study.
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PMID:Levetiracetam reduces myoclonus in corticobasal degeneration: report of two cases. 1975 67

Levetiracetam was approved for generalized and partial epilepsy in pediatric and adult population. It is also an effective antimyoclonus, but the evidence only supports its use as an adjunctive agent along with other antiepileptic drugs, such as sodium valproate, and it is commonly used in cases with juvenile myoclonic epilepsy. We report here 2 cases with juvenile myoclonic epilepsy who were switched from sodium valproate to levetiracetam to avoid the cosmetic or future teratogenic effect, but this switch was associated with exaggerated myoclonus despite escalating the dose of levetiracetam but resolved completely after reintroducing sodium valproate.
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PMID:Levetiracetam may worsen myoclonus in patients with juvenile myoclonic epilepsy: case reports. 2280 31

In this rare case, the patient presented with opsoclonus, myoclonus and ataxia. Serological and imaging studies revealed high glutamic acid decarboxylase antibody (GAD-Ab) levels. High-dose corticosteroids were of no benefit and subsequent intravenous immunoglobulin (IVIg) administration proved resolution of the condition. Levetiracetam proved useful in symptomatically controlling the myoclonus. Follow-up GAD-Ab levels were within normal limits.
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PMID:Presentation of opsoclonus myoclonus ataxia syndrome with glutamic acid decarboxylase antibodies. 2287 89

Levetiracetam can suppress sialidosis-related myoclonus but its effects on cerebral metabolism warrant elucidation. In this report, fluorodeoxyglucose-positron emission tomography was conducted before and after levetiracetam in a sialidosis patient. By subtracting the drug "off" from "on" signals, regions of enhanced metabolism were shown to be allocated mostly in the bilateral fronto-temporal regions whereas regions of reduced metabolism were distributed mainly in the occipital areas. Imaging changes suggest that the effects of levetiracetam may be different in different brain regions. The drug may also elicit fronto-temporal inhibitory impulses to suppress the vigorous myoclonus in sialidosis.
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PMID:Functional neuroimages of cortical myoclonus altered by levetiracetam in a patient with sialidosis. 2315 44

Myoclonus creates significant disability for patients. This symptom or sign can have many different etiologies, presentations, and pathophysiological mechanisms. A thorough evaluation for the myoclonus etiology is critical for developing a treatment strategy. The best etiological classification scheme is a modified version from that proposed by Marsden et al. in 1982. Clinical neurophysiology, as assessed by electromyography and electroencephalography, can be used to classify the pathophysiology of the myoclonus using a neurophysiology classification scheme. If the etiology of the myoclonus cannot be reversed or treated, then symptomatic treatment of the myoclonus itself may be warranted. Unfortunately, there are few controlled studies for myoclonus treatments. The treatment strategy for the myoclonus is best derived from the neurophysiology classification scheme categories: 1) cortical, 2) cortical-subcortical, 3) subcortical-nonsegmental, 4) segmental, and 5) peripheral. A cortical physiology classification is most common. Levetiracetam is suggested as first-line treatment for cortical myoclonus, but valproic acid and clonazepam are commonly used. Cortical-subcortical myoclonus is the physiology demonstrated by myoclonic seizures, such as in primary epileptic myoclonus (e.g., juvenile myoclonic epilepsy). Valproic acid has demonstrated efficacy in such epileptic syndromes with other medications providing an adjunctive role. Clonazepam is used for subcortical-nonsegmental myoclonus, but other treatments, depending on the syndrome, have been used for this physiological type of myoclonus. Segmental myoclonus is difficult to treat, but clonazepam and botulinum toxin are used. Botulinum toxin is used for focal examples of peripheral myoclonus. Myoclonus treatment is commonly not effective and/or limited by side effects.
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PMID:Treatment of myoclonus. 2403 28


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