Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0426980 (motor symptom)
 471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The epileptic homozygotes of the Fayoumi strain of chickens (Fepi) are affected by photogenic reflex epilepsy with complete penetrance. Here we demonstrate that they are equally affected by audiogenic reflex epilepsy induced by intense sound stimulation. All the Fepi display sound-induced seizures from hatching to adulthood consisting of initial 'ictal arousal' and running fits usually followed by generalized clonico-tonic convulsions. A running fit is the preconvulsive motor symptom specifically induced by auditory stimulation while neck myoclonus is the preconvulsive motor symptom specifically induced by photic stimulation. The EEG interictal spikes and spike and waves are suppressed and replaced by a desynchronized trace during the seizures of both kinds. Viable neural chimeras were obtained by graft of embryonic brain vesicles from Fepi donors into normal chick embryos. Transfer of the complete audiogenic and photogenic phenotypes was obtained in chimeras resulting from embryonic substitution of both the prosencephalon and mesencephalon. The substitution of the prosencephalon alone resulted in transfer of interictal paroxysmal EEG activity accompanied by the sound and light-induced desynchronization and 'ictal arousal' with no motor seizures. Chimeras with embryonic substitution of the mesencephalon alone displayed running fits and convulsions induced by sound stimulation but only neck myoclonus following light stimulation. The conclusions are reached that: (i) the Fepi is a model of audiogenic and photogenic reflex epilepsy; (ii) in both types, the seizure initiator and the convulsion generator are localized in the brainstem, although reinforcement from telencephalic visual structures is needed to trigger photogenic generalized convulsions.
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PMID:Brain chimeras for the study of an avian model of genetic epilepsy: structures involved in sound and light-induced seizures. 779 53

Juvenile Huntington disease (JHD) patients are distinguished from adult patients by an age at onset of less than 20 years. Investigating patients in our own database, we examined the proposition derived from studies in world literature that JHD should not be viewed as a separate clinical entity but rather as a manifestation of the rigid variant of the disease. Of 53 patients with JHD recorded in the Leiden Roster for Huntington Disease, relationships between sex, age at onset, duration of illness, maternal or paternal inheritance, motor symptom, first clinical features, and characteristics during the disease course, were obtained from the patients' files, and investigated. Although chorea is present in JHD, patients more often developed rigidity. Paternal inheritance, early dementia, epilepsy/myoclonus, and tremor during the disease course are confined for the most part to the rigid cases. A shorter duration of illness was evident in male patients with rigid JHD who inherited the disease from their father and developed their first disease feature at a younger age. The recognition of JHD as a distinct clinical entity does not appear to be warranted. Therefore, we propose, in accordance with other investigators, that rigid JHD be considered a clinical variant with special features.
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PMID:Juvenile Huntington disease in the Netherlands. 930 74

Many pharmacological agents may induce a variety of movement disorders, including dystonia, tremor, parkinsonism, myoclonus and dyskinesia, with an acute, subacute or more chronic time course. Motor symptoms may be isolated or part of a more extensive cerebral or systemic condition, such as the neuroleptic malignant syndrome or the serotonin syndrome. Drug-induced movement disorders share a number of features that should make them easy to identify, including a clear temporal relationship between medication initiation and symptom onset, a dose-effect, and, with the exception of tardive syndromes, complete resolution after discontinuation of the offending agent. Diagnosis relies on a thorough medication history. Medications commonly involved include dopamine receptor blockers, antidepressants and anti-epileptics, among many others. Mechanisms underlying drug-induced movement disorders involve blockade, facilitation or imbalance of dopamine, serotonin, noradrenaline and cholinergic neurotransmission in the basal ganglia. The present review focuses on drug-induced movement disorders that typically develop as an acute (hours to days) or subacute (days to weeks) event, including acute dystonic reactions, akathisia, drug-induced parkinsonism, neuroleptic malignant syndrome, serotonin syndrome, parkinsonism-hyperpyrexia syndrome, drug-induced tremor, drug-induced hyperkinesias and movement disorders associated with the use of recreational drugs.
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PMID:Acute and subacute drug-induced movement disorders. 2426 59