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)

We describe acute movement disorders in 92 children, aged 5 days to 15 years, from an Indian tertiary hospital. Eighty-nine children had hyperkinetic movement disorders, with myoclonus in 25, dystonia in 21, choreoathetosis in 19, tremors in 15, and tics in 2. Tetany and tetanus were seen in 5 and 2 children, respectively. Hypokinetic movement disorders included acute parkinsonism in 3 children. Noninflammatory and inflammatory etiology were present in 60 and 32 children, respectively. Benign neonatal sleep myoclonus in 16 and opsoclonus myoclonus syndrome in 7 accounted for the majority of myoclonus cases. Vitamin B12 deficiency in 13 infants was the most common cause of tremors. Rheumatic fever and encephalitis were the most common causes of acute choreoathetosis. Acute dystonia had metabolic etiology in 6 and encephalitis and drugs in 3 each. Psychogenic movement disorders were seen in 4 cases only, although these patients may be underreported.
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PMID:Acute movement disorders in children: experience from a developing country. 2529 19

Cortical reflex myoclonus is a typical feature of progressive myoclonic epilepsy (PME) in which it is accompanied by other types of mostly drug-resistant seizures and progressive neurological signs. Although PME is characterized by cortical hyperexcitability, studies have demonstrated atrophy and degenerative changes in the brainstem in various types of PME. Thus, we have questioned whether any stimuli may trigger a hyperactive response of brainstem reticular formation in PME and investigated the startle reflex in individuals with PME. We recorded the auditory startle response (ASR) and the startle response to somatosensory inputs (SSS) in patients with PME, and compared the results with healthy volunteers and patients with other types of drug-resistant epilepsy. All patients were using antiepileptic drugs (AEDs), 12 were on multiple AEDs. The probability of ASR was significantly lower and mean onset latency was longer in patients with PME compared with other groups. SSS responses over all muscles were low in both the PME and drug-resistant epilepsy groups; however, the differences were not statistically significant. The presence of a response over the biceps brachii muscle was zero in the PME group and showed a borderline difference compared with the other groups. Decreased probability and prolonged latencies of ASR in PME indicate inhibition of reflex circuit. A trend for decreased responses of SSS suggests hypoactive SSS in both PME and other epilepsy groups. Hypoactive ASR in PME and hypoactive SSS in both PME and other epilepsies may be attributed to the degeneration of pontine reticular nuclei in PME and functional inhibition by AEDs in both disorders.
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PMID:Startle Response in Progressive Myoclonic Epilepsy. 2717 Jun 68