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)

Certain benzodiazepines (BZs) like lorazepam, diazepam or clonazepam induce myoclonus jerks in photosensitive and non-photosensitive baboons. Papio papio, which are not accompanied by EEG paroxysmal discharges (type B). The effect of the selective BZ antagonist R0 15-1788 was evaluated in this myoclonus. Ro 15-1788 completely blocked type B myoclonus without decreasing the level of vigilance in the two types of baboons, and reversed the antiepileptic action of the BZs in the photosensitive ones, permitting the reappearance of myoclonus following EEG paroxysmal discharges (type A). L-5-hydroxytryptophan and progabide also blocked type B myoclonus, but the blockade was only transiently effective and was always accompanied by slight drowsiness.
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PMID:Differential effects of the benzodiazepine antagonist Ro 15-1788 on two types of myoclonus in baboon Papio papio. 613 45

A 42-year-old patient is reported who presented with marked daytime sleepiness and in whom the only major nocturnal polysomnographic abnormality was intense fragmentary (partial) myoclonus occurring with equal frequency in all stages of NREM sleep associated with some degree of sleep fragmentation. The myoclonus was very brief (less than 150 msec duration), aperiodic and recurred in asynchronous and asymmetrical fashion over the legs, arms and face. It appears unrelated to the clinically similar physiological myoclonus of REM sleep. Other main sleep disorders such as periodic movements, restless leg syndrome, sleep apnea and narcolepsy-cataplexy were excluded by history and polysomnography.
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PMID:Fragmentary pathological myoclonus in NREM sleep. 620 Feb 93

We describe a new syndrome, Rheumatic Pain Modulation Disorder (RPMD) ("fibrositis syndrome") with sleep-related myoclonus (involuntary periodic leg movements). Measures of sleepiness, fatigue and pain, before and after sleep, and aspects of sleep of nine subjects (Ss) with RPMD and sleep-related myoclonus were compared to nine subjects with excessive daytime somnolence and sleep-related myoclonus. In eight of the RPMD with sleep-related myoclonus and three of those with daytime sleepiness, an alpha (7.5-11 Hz) EEG Non-Rapid Eye Movement sleep disorder was demonstrated. The RPMD with sleep-related myoclonus group contained a greater number of women, more pain, morning fatigue, and disturbances in sleep (more stage changes and alpha EEG sleep prior to leg myoclonus); but in comparison to the sleep-related myoclonus, daytime somnolent group, there were no differences in evening and morning sleepiness, number of limb movements, movement arousals, awakenings after sleep onset, sleep duration, and percent sleep stages.
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PMID:Sleep-related myoclonus in rheumatic pain modulation disorder (fibrositis syndrome) and in excessive daytime somnolence. 658 52

In 3 patients with the syndrome of Unverricht-Lundborg's myoclonus-epilepsy electropolygraphic examinations were carried out during night sleep. A substantial disorganization of the sleep was revealed, the degree of which correlated with the gravity of the clinical picture. This disorganization manifested itself in pronounced changes of the electroencephalographic phenomenology of the sleep and disturbance of its structure with a prolongation of the 1st stage and the delta-sleep and a shortening of the 2nd stage and the quick sleep phase. An insufficient EEG desynchronization was noted in the periods of awakeness, drowsiness, and quick sleep: this pointed to defective functioning of the brain desynchronizing systems. In distinction from other forms of epilepsy the pathological paroxysmal activity was prevalent also in the period of the awakeness, and diminished in parallel with the depth of the sleep. The myoclonic hyperkinesis got also weaker at the stage of slow sleep, but became more intense at the quick sleep stage. The data obtained point to a pronounced dysfunction of the non-specific activating and deactivating systems of the brain in myoclonus-epilepsy. This dysfunction is associated with an organic affection of the trunco-diencephalic structures and the influence of the active epileptic process.
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PMID:[Sleep disorders in the Unverricht-Lundborg myoclonic epilepsy syndrome]. 681 Jun

The specific sleep disorders of 97 patients 61-81 years old were compared with those of 264 middle-aged (41-60 years old) and 202 young (20-40 years old) patients. Sleep disorder diagnoses were made according to the Diagnostic Classification of the Association of Sleep Disorders Centers based on evaluations consisting of mental and physical examinations and all-night sleep recordings. Most young and middle-aged patients complained of excessive daytime sleepiness; the elderly complained of insomnia as often as excessive daytime sleepiness. The evaluations revealed objective findings in 93 per cent of the elderly, but only 77 per cent of younger patients. Nocturnal myoclonus or restless leg syndrome was the diagnosed cause of 23 per cent of elderly patients' sleep-wake problems, but only 11 per cent of middle-aged and 4 per cent of young patients had this problem. Respiratory disorders of sleep were found in 27 per cent of elderly, 35 per cent of middle-aged, and 20 per cent of young patients. Elderly patients (6 per cent) had psychiatric disorders diagnosed as the causes for their problems less frequently than did younger patients (22 per cent).
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PMID:Age-related sleep-wake disorders at a sleep disorder center. 685 47

The advances in research on sleep an biological rhythms have recently been applied to the diagnosis and treatment of sleep disorders. A new clinical specialty has developed with the establishment of sleep disorder centers and a diagnostic classification of sleep and arousal disorders. This new nosological approach has evolved from an extensive base of new scientific information concerning descriptive polygraphic and analysis of clinical case series. Four major categories have been defined: (a) disorders of initiating and maintaining sleep (insomnias), (b) disorders of excessive somnolence, (c) disorders of the sleep-wake schedule, and (d) dysfunctions associated with sleep. Within this comprehensive classification certain major pathophysiological advances are described for the "insomnias." These include polysomnographic identification of altered sleep stage patterns in the major effective illnesses, insomnias related to hypnotic drugs and alcohol, sleep disturbances associated with sleep-induced respiratory impairment, and sleep-related periodic movements during sleep (nocturnal myoclonus). Excessive daytime somnolence is primarily associated with the hypersomnia sleep-apnea syndrome and with narcolepsy. The relationship between biological rhythms (chronobiology) and disorders of the human sleep-wake schedules is very actively investigated. The recognition that sleep length, internal organization, and timing within neurophysiological circadian time-keeping systems has lead to better diagnosis of these sleep-wake disorders and new chronotherapeutic regimens. Finally, increasing identification and description of "parasomnias," i.e. dysfunctions associated with sleep, has led sleep research into important new areas that are of general physiological interest. It is now clear that sleep disorders medicine has become a new scientific and clinical discipline in its own right.
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PMID:Sleep and its disorders. 701 38

Sleep disruption is a common complaint in levodopa-treated parkinsonian patients. A survey of 100 parkinsonian patients revealed prominent sleep complaints in 74%. Sleep complaints were unrelated to patient age and the duration of disease but increased in prevalence with longer periods of levodopa therapy. Sleep abnormalities tended to increase in severity with continued treatment and insomnia tended to be followed by daytime somnolence, altered dream events, and episodic nocturnal vocalization and myoclonus. While dyskinetic side effects and on-off syndrome were encountered in patients with and without sleep complaints, 98% of patients experiencing psychiatric side effects also reported sleep disruption. It is suggested that sleep-related symptoms constitute an early stage of levodopa-induced dopaminergic psychiatric toxicity in the parkinsonian population. Clinical and experimental observations suggest that serotonergic mechanisms are important in this symptom complex.
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PMID:Sleep disruption in the course of chronic levodopa therapy: an early feature of the levodopa psychosis. 713 32

The nocturnal myoclonus syndrome (NMS) consists of stereotyped, repetitive jerks of the lower limbs that occur during sleep or wakefulness. NMS is often related with restless-legs syndrome (RLS) and can cause severe sleep disturbances and daytime sleepiness. The efficacy of dopamine agonists in the treatment points to a dopaminergic dysfunction in NMS. We investigated the central dopamine D2-receptor occupancy with [123I] labeled (S)-2-hydroxy-3-iodo-6-methoxy-([1-ethyl-2-pyrrolidinyl]methyl) benzamide (IBZM) (a highly selective CNS D2 dopamine receptor ligand) ([123I]IBZM) and single photon emission tomography (SPET) in 20 patients with NMS and in 10 healthy controls. In most of the patients with NMS there was a lower [123I]IBZM binding in the striatal structures compared to controls. The results indicate that NMS is related to a decrease of central D2-receptor occupancy.
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PMID:Nocturnal myoclonus syndrome (periodic movements in sleep) related to central dopamine D2-receptor alteration. 778 13

A case of acute hepatic failure following ingestion of the veterinary euthanasia drug T61 is described. Presenting symptoms were drowsiness, disorientation, muscle hypertonia, and upper limb myoclonus, which faded within a few hours. Two days later, acute liver failure occurred, manifested as encephalopathy, jaundice, and a severe coagulopathy. The hepatic damage was thought to be due to the solvent dimethylformamide, which is the only known hepatotoxin included in the preparation utilized in the suicide attempt. High-dose (1.2 g/day) intravenous reduced glutathione was administered, with a rapid improvement of liver function. The patient was discharged after 17 days. Normalization of all liver function tests was achieved within two months. The favorable outcome in this case stands in contrast to the report of a previous case of lethal T61-induced hepatic failure. Although a different amount of dimethylformamide was ingested in each case (0.45 vs 0.60 ml/kg body wt) and individual differences in susceptibility to the effects of the hepatotoxic agent may have played a major role in these two cases, it is not unlikely that the infusion of high doses of glutathione to our patient contributed to her survival and hepatic recovery.
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PMID:Severe hepatic failure occurring with T61 ingestion in an attempted suicide. Early recovery with the use of intravenous infusion of reduced glutathione. 846 75

Primary Generalized Epilepsy (PGE) has been more hotly debated over the past decades than other forms of epileptic seizure disorder. The sudden synchronous appearance of bilateral spikes and spike-waves (mainly with myoclonus resp. absence) used to perplex the earliest generation of electroencephalographers, and the enigmatic genesis of these discharges (and seizures) has not ceased to fascinate the investigators of this phenomenon. A "centrencephalic" concept with paroxysmal discharges arising from thalamic structures and "projecting" to the cortex was championed for many years and eventually laid aside. More recently, the role of the thalamic level has been re-emphasized, mainly on the basis of experimental work. In this article, the bulk of experimental work is critically reviewed: the simian model (Papio papio), the feline, and the rodent models (Wistar rat, tottering mouse). Stress is being laid on fundamental differences between all of these models and human PGE. EEG evidence indicates a superior frontal origin of bilateral-synchronous spikes and spike-waves; depth EEG recordings in patients have failed to demonstrate primary thalamic spike generation. The heart of the matter in PGE appears to be the mechanism underlying paroxysmal discharges; above all the role of arousal. It is not awakening from sleep but the ensuing period that is critical in its epileptogenic thrust caused by alternating periods of return to drowsiness and arousing stimuli. This biphasic process gradually escalates EEG bursts to myoclonus (or absences) and possibly to a generalized tonic-clonic convulsion. Most conducive to this crescendo is the state of tiredness following a night of poor sleep. Bilateral synchrony is not precise and small time differences exist. The line between primary and secondary bilateral synchrony (with a primary cortical focus) can become blurred. Genetic predisposition to generalized paroxysms must always be considered, even in the face of a primary focus with secondary bilateral synchrony. Photosensitivity is a second paroxysm-inducing mechanism in PGE; it is much less common than the abnormal arousal ("dyshormia"); both mechanisms can be present in the same patient. Therapy and prevention of seizures in PGE are finally discussed. The concept of abnormal arousal mechanisms can be put into practice in order to prevent seizures: avoidance of sleepless nights, not always an easy task in adolescents and young adults.
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PMID:Primary (idiopathic) generalized epilepsy and underlying mechanisms. 871 97


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