dextromethorphan and Movement-Disorders

An 11-year-old girl with nonketotic hyperglycinemia who typically presented with a picture of early myoclonic encephalopathy in the neonatal period is presented in this article. Treated early with sodium benzoate and dextromethorphan, she became seizure-free, while myoclonus persisted. During examination, multifocal rhythmic myoclonic jerks in gamma frequency enhanced by motor activity were noted. Coherence analysis of the electroencephalography-electromyography relationship indicated a cortical origin of the myoclonic jerks. Observation of this case suggests that rhythmic cortical myoclonus may represent a late evolution of this rare disorder.

Topics: Anticonvulsants; Cerebral Cortex; Child; Child, Preschool; Dextromethorphan; Disease Progression; Electroencephalography; Epilepsies, Myoclonic; Female; Humans; Hyperglycinemia, Nonketotic; Infant; Infant, Newborn; Magnetic Resonance Imaging; Movement Disorders; Myoclonus; Sodium Benzoate; Survivors

Topics: Adrenergic Agents; Antitussive Agents; Child; Common Cold; Cough; Dextromethorphan; Drug Combinations; Drug-Related Side Effects and Adverse Reactions; Ephedrine; Histamine H1 Antagonists; Humans; Male; Movement Disorders; Pseudoephedrine; Pyridines

In animal models of Parkinson's disease (PD), glutamate antagonists diminish levodopa (LD)-associated motor fluctuations and dyskinesias. We sought to investigate if these preclinical observations can be extended to the human disease, by evaluating the effects of three non-competitive NMDA antagonists (dextrorphan, dextromethorphan and amantadine) on the motor response to LD in patients with advanced PD. In four separate trials, adjuvant therapy with these drugs reduced LD-induced dyskinesias and motor fluctuations. These findings support the view that drugs acting to inhibit glutamatergic transmission at the NMDA receptor can ameliorate LD associated motor response complications.

Topics: Amantadine; Clinical Trials as Topic; Controlled Clinical Trials as Topic; Dextromethorphan; Dextrorphan; Excitatory Amino Acid Antagonists; Glutamic Acid; Humans; Levodopa; Movement Disorders; Parkinson Disease; Psychomotor Performance; Receptors, N-Methyl-D-Aspartate

Dextromethorphan (DM, 40 or 80 mg/kg, i.p.) and MK-801 (3 or 10 mg/kg, i.p.) were compared in their ability to prevent the depletion of choline acetyltransferase (ChAT) activity in the rat striatum following intrastriatal injection of quinolinic acid. DM did not reduce striatal ChAT depletion following injection of either 300 or 150 nmol of quinolinic acid. Following injection of 300 nmol of quinolinic acid, MK-801 significantly reduced striatal ChAT depletion at a dose of 3 mg/kg and completely prevented striatal ChAT depletion at a dose of 10 mg/kg. In contrast to the potent neuroprotective action of MK-801, DM does not protect striatal cholinergic neurons from an acute challenge by an NMDA receptor agonist.

Topics: Animals; Choline O-Acetyltransferase; Corpus Striatum; Dextromethorphan; Dibenzocycloheptenes; Dizocilpine Maleate; Dose-Response Relationship, Drug; Levorphanol; Male; Movement Disorders; Pyridines; Quinolinic Acid; Quinolinic Acids; Rats; Rats, Inbred Strains