myoclonus/seizures

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Epileptic negative myoclonus as the presenting seizure type in rolandic epilepsy.

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Epileptic negative myoclonus is an uncommon seizure type characterized by a sudden, brief loss of muscle tone that may lead to falling. It has been associated largely with benign childhood epilepsy with centrotemporal spikes (rolandic epilepsy), although it may also be a feature of other epileptic

Benign neonatal sleep myoclonus: frequently misdiagnosed as neonatal seizures.

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18 neonates aged 5-60 days with Benign neonatal sleep myoclonus were identified. Fifteen neonates had been misdiagnosed as neonatal seizures before referral. All treatments were withdrawn once the diagnosis of benign neonatal sleep myoclonus was made. Benign neonatal sleep myoclonus should be

Action Myoclonus and Seizure in Kufor-Rakeb Syndrome.

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Kufor-Rakeb syndrome (KRS) is a rare autosomal recessive neurologic disease with diverse phenotypic features. Herein we report an Iranian KRS family with seizure and action myoclonus in addition to other typical manifestations of this

Efficacy of lacosamide on seizures and myoclonus in a patient with epilepsia partialis continua.

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A 39-year-old male with epilepsia partialis continua, refractory to first- and second-line antiepileptic drugs, is described. Lacosamide produced a progressive antiepileptic effect on Jacksonian motor seizures and subsequently on positive myoclonus, which developed into negative myoclonus before

Efhc1 deficiency causes spontaneous myoclonus and increased seizure susceptibility.

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Mutations in EFHC1 gene have been previously reported in patients with epilepsies, including those with juvenile myoclonic epilepsy. Myoclonin1, also known as mRib72-1, is encoded by the mouse Efhc1 gene. Myoclonin1 is dominantly expressed in embryonic choroid plexus, post-natal ependymal cilia,

Febrile myoclonus: an underreported, benign condition in infancy often misinterpreted as febrile seizures.

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Massive myoclonic jerks, often presenting in a dramatic fashion during a febrile illness, have rarely been reported and have usually been related to as febrile seizures. Febrile myoclonus is usually a benign phenomenon with no neurological sequelae. However, it may be impressive enough to provoke

Early visual seizures and progressive myoclonus epilepsy in neuronopathic Gaucher disease due to a rare compound heterozygosity (N188S/S107L).

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OBJECTIVE Gaucher disease, the inherited deficiency of the lysosomal enzyme glucocerebrosidase, is characterized by genotypic and phenotypic heterogeneity. We recently characterized the glucocerebrosidase alleles of a patient with an unusual clinical presentation of type 3 Gaucher

[Negative myoclonus; a simple partial seizure].

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Negative myoclonus in a 4-year-old boy was analyzed by polygraphic study, which lead to the diagnosis of simple partial seizure. He had irregularly trembling movements of right upper limb when he held some objects with his right hand. There were also coarse trembling movements in his body and lower

Myoclonic jerks are commonly associated with absence seizures in early-onset absence epilepsy.

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Typical absence seizures are observed in various epilepsy syndromes, however, few series have focused on early-onset absence epilepsy (EOAE). We aimed to evaluate the occurrence of this seizure type in children under 4 years of age in order to evaluate their electroclinical characteristics and

Prevention of cysteamine-induced myoclonus blocks the long-term inhibition of kindled seizures.

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In kindled rats, the administration of cysteamine (CSH, 200 mg/kg, i.p.) 4 h prior to a kindled seizure leads to long-term (up to 10 days) inhibition of kindled seizures. CSH (200 mg/kg, i.p.) also induces myoclonic seizures in kindled rats. We suggest that the long-term inhibition of kindled

Legionnaire's disease presenting with encephalitis, myoclonus, and seizures: Successful treatment with doxycycline.

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Legionnaire's disease (LD) is a non-zoonotic atypical community acquired pneumonia (CAP) with several characteristic extra-pulmonary findings. Pending diagnostic test results, selected characteristic findings when considered together are the basis of clinical syndromic diagnosis and the basis of

Ketogenic diet prevents seizure and reduces myoclonic jerks in rats with cardiac arrest-induced cerebral hypoxia.

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Although the mechanism underlying the anti-epileptic effects of a ketogenic diet (KD) is not known, KD is reported to be an effective treatment for intractable epilepsy, in particular among children. Here, we evaluated whether a KD can reduce posthypoxic seizure and myoclonic jerks in a rat model of

Biotin-responsive encephalopathy with myoclonus, ataxia, and seizures.

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Prominent neurological abnormalities, including myoclonus, seizures, ataxia, and hearing loss, have been noted in juvenile-onset biotin-responsive MCD. The underlying defect in many of these patients, who generally present in the first year of life, appears to be a deficiency of biotinidase. We have

Strychnine-like multifocal myoclonus and seizures in extremely high-dose opioid administration: treatment strategies.

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While occasional myoclonic jerks are prevalent in cancer patients receiving opioids, severe myoclonic jerks and seizures due to opioids are uncommon. In this retrospective case series, we describe five cancer patients with refractory cancer pain and severe neuroexcitatory toxicity associated with

Anticonvulsant activity of two orally active competitive N-methyl-D-aspartate antagonists, CGP 37849 and CGP 39551, against sound-induced seizures in DBA/2 mice and photically induced myoclonus in Papio papio.

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Two novel N-methyl-D-aspartate (NMDA) antagonists, DL-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid CPG 37849 and the corresponding 1-ethyl ester CGP 39551, were tested as anticonvulsants in DBA/2 mice and photosensitive Senegalese baboons, Papio papio. In DBA/2 mice, CGP 37849 is more potent

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