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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dystonia refers to a specific clinical entity as well as movements occurring as a result of other syndromes. Dystonic movements are the most commonly misdiagnosed abnormal involuntary movements. Dystonia worsens under emotional or physical stress and with fatigue, lessens with rest, relaxation, hypnosis and sensory tricks, can have diurnal fluctuations and may disappear in sleep. Dystonia is often confused with chorea and myoclonus and considered to be voluntary, that is, psychogenic in origin, in part because of its unusual and varied clinical expression. The neuroscience nurse, cognizant of the natural history, phenomenology and genetics of dystonia, will be able to identify early signs and symptoms, inform colleagues and teach family members who care for children with primary dystonia.
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PMID:The primary dystonias of childhood. 183 82

Thirty-three patients with rheumatic pain modulation disorder (RPMD) were divided into 2 groups: RPMD with sleep related myoclonus (RPMD-SM) (n = 12) and RPMD only (n = 21). Both groups showed chronic nonarticular musculoskeletal pain, fatigue, tender points, and nonrestorative sleep with alpha (7.5-11 Hz) EEG sleep anomaly. RPMD-SM patients were older, had later onset of illness, showed disrupted sleep with periodic involuntary leg movements that were related to fatigue, and alpha EEG sleep related to fatigue and pain.
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PMID:Sleep related myoclonus in rheumatic pain modulation disorder (fibrositis syndrome). 346 Nov 58

Chronic musculoskeletal pain and fatigue of "fibrositis syndrome" are associated with a physiologic arousal disorder within sleep, the alpha (7.5 to 11 Hz) electroencephalographic, non-rapid-eye-movement sleep anomaly. In this nonrestorative sleep disorder, pain and mood symptoms may be mediated by psychologic distress (e.g., following a nonphysically injurious industrial or automobile accident), noxious environmental stimuli (e.g., noise), physiologic disturbance (e.g., sleep-related myoclonus, painful inflamed joints, i.e., rheumatoid arthritis), and altered central nervous system metabolism (e.g., disordered brain serotoninergic functions). Because such heterogeneous agents influence this hitherto poorly understood nonarticular rheumatic syndrome, the descriptive term "rheumatic pain modulation disorder" is suggested.
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PMID:Sleep and musculoskeletal pain. 346 14

A 30 year old female was exposed to chlordane through careless and excessive domestic use over a 1 to 4 week period. Early symptoms included circumoral numbness, anorexia, nausea, and fatigue. Myoclonic jerks occurred after a delay of one month. Malaise and anorexia became the dominant symptoms leading to referral at six months. Dysfunctional bleeding was attributed to hepatic enzyme induction by the chlordane and increased metabolism of contraceptive medication. Cholestyramine increased the stool elimination of chlordane.
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PMID:Subacute chlordane poisoning. 653 48

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

Nocturnal myoclonus has been identified as a cause of disturbed sleep and excessive daytime fatigue. To our knowledge, no therapy has heretofore been available to adequately control this problem. We identified this problem clinically in two patients; in one, the phenomenon was observed with a polygraphic sleep recording. Small doses of clonazepam, 1 mg, before retiring were found to specifically control the myoclonus and allow sleep patterns to return to normal.
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PMID:Clonazepam treatment of insomnia due to sleep myoclonus. 735 5

Of 842 consecutive patients with movement disorders seen over a 71 month period, 28 (3.3%) were diagnosed as having a documented or clinically established psychogenic movement disorder. Tremor was most common (50%) followed by dystonia, myoclonus, and parkinsonism. Clinical descriptions of various types are reviewed. Clinical characteristics common in these patients included distractability (86%), abrupt onset (54%), and selective disabilities (39%). Distractability seems to be most important in tremor and least important in dystonia. Other diagnostic clues included entrainment of tremor to the frequency of repetitive movements of another limb, fatigue of tremor, stimulus sensitivity, and previous history of psychogenic illness. On examination, 71% had other psychogenic features. Over 60% had a clear history of a precipitating event and secondary gain and 50% had a psychiatric diagnosis (usually depression). Twenty five per cent of patients presented with combined psychogenic movement disorder and organic movement disorder; 35% resolved and this subgroup had a shorter duration of disease than those who are unresolved. Psychogenic movement disorder represents an uncommon diagnosis among patients with movement disorders. The ability to make a diagnosis rests on the presence of a multitude of clinical clues and therapeutic action should be taken as early as possible.
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PMID:Psychogenic movement disorders: frequency, clinical profile, and characteristics. 756 21

We made a long term prospective study of 66 patients with juvenile myoclonic epilepsy (JME). Prevalence was 10.2% among 672 patients with epilepsies. Sex distribution was equal. Sixty-three were not diagnosed on referral; JME was not initially recognized in the epilepsy clinic in 22. Clinical typical absence seizures were reported in 33.3%, myoclonic jerks in 97% and generalized tonic-clonic seizures (GTC) in 78.8% of the patients. Mean age (+/- SD) at onset was 10.5 +/- 3.4 years (range 5-16 years) for absence seizures, 15 +/- 3.5 years (range 8-26 years) for myoclonic jerks, and 16 +/- 3.5 years (9-28) years (range 1-9 years) and GTC by 4.4 +/- 2.7 years (range 1-8 years) in 14 (21.2%) patients who manifested all three types of seizure. Absence were never antedated by myoclonic jerks or GTC. Myoclonic jerks occurred on awakening in 87.5% of the patients. GTC occurred mainly on awakening, but other patients had nocturnal or diurnal GTC with no circadian distribution. Neurologic examination was normal for all patients except for tremor of the hands similar to essential tremor, noted in 35% of patients. Computed tomography (CT) brain scans were normal: 93% of patients had precipitating factors: sleep deprivation (89.5%), fatigue (73.7%), photosensitivity (36.8%; television and video games 8.8%), menstruation (24.1% of women), mental concentration (22.8%), and stress (12.3%). Incidence of JME among siblings (13 of 41 examined families) implies an autosomal recessive mode of inheritance for this Arab population. EEGs were frequently normal in treated patients. At least one abnormal EEG was recorded in 56 (84.9%) patients. Abnormalities consisted mainly of generalized discharges of spike/double spike and/or polyspike and slow wave. Frequent multiple spikes and discharge fragmentations varied from 0.5- to 20-s duration (mean 6.8 s). Twenty (30.3%) had focal abnormalities, and 18 (27.3%) had photoconvulsive discharges. Eighty-eight percent of patients remained seizure-free for > or = 3 years of follow-up. Effective treatment was achieved with valproate (VPA); control of myoclonic jerks was improved with clonazepam (CZP). CZP monotherapy did not consistently prevent GTC. Adding small doses of CZP with simultaneous reduction of VPA was the most effective and better tolerated form of medication, particularly in patients demonstrating an adverse reaction or requiring a large VPA dosage. VPA dosage was successfully reduced in 15 patients who were seizure-free for > 2 years and had infrequent seizures before treatment, but 9 of 11 patients relapsed after VPA discontinuation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Juvenile myoclonic epilepsy: a 5-year prospective study. 815 46

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

Nearly two-thirds of polio survivors report abnormal movements in sleep, with 52% reporting that their sleep is disturbed by these movements. Sleep studies were performed in seven polio survivors to document objectively abnormal movements in sleep. Two patients demonstrated generalized random myoclonus, with brief contractions and even ballistic movements of the arms and legs, slow repeated grasping movements of the hands, slow flexion of the arms, and contraction of the shoulder and pectoral muscles. Two other patients demonstrated periodic movements in sleep with muscle contractions and ballistic movements of the legs, two had periodic movements in sleep plus restless legs syndrome, and one had sleep starts involving only contraction of the arm muscles. Abnormal movements in sleep occurred in Stage II sleep in all patients, in Stage I in some patients, and could significantly disturb sleep architecture even though patients were totally unaware of muscle contractions. Poliovirus-induced damage to the spinal cord and brain is presented as a possible cause of abnormal movements in sleep. The diagnosis of post-polio fatigue, evaluation of abnormal movements in sleep, and management of abnormal movements in sleep using benzodiazepines or dopamimetic agents are described.
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PMID:Abnormal movements in sleep as a post-polio sequelae. 971 25


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