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)

The voltage-gated potassium channels Kv3.1 and Kv3.3 are widely expressed in the brain, including areas implicated in the control of motor activity and in areas thought to regulate arousal states. Although Kv3.1 and Kv3.3-single mutants show some physiological changes, previous studies revealed relatively subtle behavioral alterations suggesting that Kv3.1 and Kv3.3 channel subunits may be encoded by a pair of redundant genes. In agreement with this hypothesis, Kv3.1/Kv3.3-deficient mice display a 'strong' mutant phenotype that includes motor dysfunction (ataxia, myoclonus, tremor) and hyperactivity when exposed to a novel environment. In this paper we report that Kv3.1/Kv3.3-deficient mice are also constitutively hyperactive. Compared to wildtype mice, double mutants display 'restlessness' that is particularly prominent during the light period, when mice are normally at rest, characterized by more than a doubling of ambulatory and stereotypic activity, and accompanied by a 40% sleep reduction. When we reinvestigated both single mutants, we observed constitutive increases of ambulatory and stereotypic activity in conjunction with sleep loss in Kv3.1-single mutants but not in Kv3.3-single mutants. These findings indicate that the absence of Kv3.1-channel subunits is primarily responsible for the increased motor drive and the reduction in sleep time.
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PMID:Increased motor drive and sleep loss in mice lacking Kv3-type potassium channels. 1500 17

The effect of etomidate and alfentanil on heart rate, systolic arterial pressure, diastolic arterial pressure, and mean arterial pressure was compared with etomidate and placebo during electroconvulsive therapy (ECT). We also studied the influence of alfentanil on seizure duration using both the cuff method and 2-lead electroencephalographs on the prevention of myoclonus induction by etomidate, on duration of apnea and on postictal agitation after ECT. We enrolled 21 consecutive patients in a prospective placebo-controlled, within patient blocked randomized study. Alfentanil significantly reduced heart rate, diastolic arterial pressure, and mean arterial pressure both before and after the stimulus. The increase in these variables during the convulsion was not affected, compared with placebo. Alfentanil had no effect on seizure duration. However, apnea duration was prolonged during the alfentanil sessions as compared with placebo (73 seconds). Alfentanil did not significantly reduce the occurrence of myoclonus after etomidate as compared with placebo, nor did postictal agitation after ECT appear more often with alfentanil. Alfentanil could be useful to reduce tachycardia and hypertension during ECT in high-risk patients without effects on seizure duration. Alfentanil itself has no proconvulsive effect in combination with etomidate.
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PMID:Double-blind placebo controlled study of the effects of etomidate-alfentanil anesthesia in electroconvulsive therapy. 1516 27

Continuous parenteral hydromorphone is used to treat pain in palliative care. Case reports have suggested that neuroexcitatory symptoms, such as agitation, myoclonic activity, and even seizures may occur during administration. However, little information exists on the incidence of these side effects or their relationship to the dose or duration of parenteral hydromorphone. A retrospective chart review was performed on 48 terminally ill hospice patients who received continuous parenteral hydromorphone for pain control. Chart reviews were conducted searching for three neuroexcitatory symptoms: agitation, myoclonus, and seizures; the incidence and relationship of these symptoms were statistically compared to the maximal dose and number of days on continuous parenteral hydromorphone. We found that agitation, myoclonus, and seizures were not associated with the patients gender, age, or diagnosis but found that agitation was associated (p < 0.01) in patients with known metastatic disease. Agitation, myoclonus, and seizures were independently associated with the maximal dose (p < 0.05, p < 0.001, and p < 0.05) and with the duration (p < 0.01, p < 0.05, and p < 0.01) of continuous parenteral hydromorphone A possible mechanism for these findings is hydromorphone-3-glucoronide, a metabolic product of hydromorphone, which has been implicated in neuroexcitatory symptoms in laboratory investigations.
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PMID:Hydromorphone neuroexcitation. 1535 98

The susceptibility of red foxes (Vulpes vulpes) to European bat lyssavirus type 1 (EBLV-1) infection was examined. Eight foxes were inoculated intramuscularly (i.m.) with 10(4.9) foci-forming units (FFU) (n = 4) and 10(5.1) FFU (n = 4) and observed for up to 90 days. All foxes showed manifestations of a neurologic disorder (e.g. seizures, myoclonus, agitation), starting as early as 5 days post-infection (p.i.). Subsequently, all animals showed improvement followed by one or more relapses. One fox was killed 3 days after it recovered, 26 days post-infection. Two other foxes were also killed 38 and 54 days post-infection after severe neurologic signs returned. All foxes developed a humoral immune response against EBLV-1 as determined in serum and brain tissues. However, no rabies virus antigen was detected in the brain, other tissues and secretions examined (e.g. salivary gland, saliva, tonsils, lungs) by using different standard diagnostic techniques [fluorescent antibody test, reverse transcription polymerase chain reaction (RT-PCR), rabies tissue culture inoculation test], with the exception of one fox in which EBLV-1 RNA was detected by RT-PCR in only the spinal cord. Brain tissues showed moderate to severe multifocal, mononuclear encephalomyelitis in the three foxes that were killed during the observation period, although no EBLV-1 virus was detectable in these tissues.
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PMID:Rabies in red foxes (Vulpes vulpes) experimentally infected with European bat lyssavirus type 1. 1552 59

We report a case of serotonin syndrome that occurred in a patient with chronic heart failure associated with a panic disorder. The 39-year-old Japanese man had been treated with paroxetine at 20 mg/d for 1 1/2 years. He presented with rhabdomyolysis, renal failure, fulminant liver failure, cardiac conduction disturbance, and disseminated intravascular coagulation, as well as conventional symptoms of serotonin syndrome including alterations in cognition (disorientation, confusion) and behavior (restlessness), autonomic nervous system dysfunction (fever, shivering), and abnormal neuromuscular activity (ataxia, hyperreflexia, myoclonus). All medications prescribed before hospital admission were discontinued. After 24 hours of continuous venovenous hemofiltration, diuresis resumed and renal and liver function improved rapidly. Disorientation, restlessness, hyperreflexia, and myoclonus abated slowly over the next 72 hours. The patient's anxiety subsided more slowly, and he recovered completely 1 week later. The plasma concentration of paroxetine was elevated far above the upper limit of the therapeutic range. The patient had cytochrome P-450 (CYP) 2D6*1/*5, a heterozygosity of an inactivated allele of CYP2D6, which metabolizes paroxetine. The patient was determined to be an intermediate metabolizer who was potentially vulnerable to paroxetine, a major inhibitor of CYP2D6. Heart failure is often accompanied by psychiatric disorders. A wide range of drugs commonly prescribed for these conditions, including beta-blockers, antiarrhythmics, and antidepressants, are metabolized by CYP2D6. Genetic screening for CYP2D6 in patients with these conditions may prevent life-threatening drug intoxication.
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PMID:Life-threatening serotonin syndrome in a patient with chronic heart failure and CYP2D6*1/*5. 1554 25

Tardive dyskinesia is a movement disorder that develops after exposure to dopamine receptor blocking agents. Less well-appreciated are other, more recently described tardive syndromes that are phenomenologically distinct from tardive dyskinesia and respond to different treatments. Patients may simultaneously have more than one tardive syndrome. Major subtypes of tardive syndromes include tardive dyskinesia, characterized by orobuccolingual, truncal, or appendicular, choreiform movements; tardive dystonia, characterized by sustained, stereotyped muscle spasms of a twisting or turning character; and tardive akathisia, characterized by an inner sense of restlessness or unease. The sensation often is unpleasant and may be accompanied by repetitive, purposeless movements (stereotypies), such as pacing. Less common tardive syndromes include tardive myoclonus, tardive tourettism, and tardive tremor. Tardive syndromes often are a source of great distress and disability to patients and may be permanent, despite discontinuing the responsible medication. Prevention, early detection, and prompt management are the major clinical focus. When a patient develops a tardive syndrome appropriate actions include 1) review of the primary diagnosis that prompted starting a dopamine receptor blocking agent; 2) characterization of the movement disorder(s); 3) where possible, discontinuation of dopamine blocking agent or replacement with a less potent alternative agent; 4) gradual withdrawl of the offending drug because some patients have an exacerbation of a tardive syndrome after abrupt withdrawal; and 5) assessment of the severity of symptoms and development of a treatment plan based on the phenomenology, with the goal of maximizing patient comfort and function. Although tardive dyskinesia typically develops after chronic exposure to dopamine receptor blocking agents, it, and other variants (such as tardive dystonia) can develop very rapidly after treatment. There seems to be no minimal safe duration of exposure for the development of a tardive syndrome. It is important to recognize that anti-emetics, which are dopamine receptor blockers, such as prochlorperazine, promethazine and metoclopramide, can cause tardive syndromes. Clinicians should become familiar with antipsychotic agents that have a lower risk of causing tardive syndromes, such as clozapine, quetiapine, and olanzapine. We review treatment options for tardive dystonia.
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PMID:Tardive Dystonia. 1581 76

Three patients presented with a 25-, 15-, and 5-year history of restless legs syndrome (RLS) and periodic limb movements during sleep (PLMS). For 1, 4, and 5 years, they reported additional involuntary trunk and limbs jerks preceding falling asleep and occasionally during intrasleep wakefulness. Videopolysomnography revealed jerks during relaxed wakefulness arising in axial muscles with a caudal and rostral propagation at a slow conduction velocity, characteristic of propriospinal myoclonus (PSM). Jerk-related EEG-EMG back-averaging did not disclose any preceding cortical potential. During relaxed wakefulness preceding falling asleep and during intrasleep wakefulness, PSM coexisted with motor restlessness and sensory discomfort in the limbs. PSM disappeared when spindles and K-complexes appeared on the EEG. At this time, typical PLMS appeared every 20 to 40 seconds, especially during light sleep stages. PLMS EMG activity was limited to leg, especially tibialis anterior muscles, and did not show propriospinal propagation. In one patient, alternating leg muscle activation was also present. Jerks with a PSM pattern represent another motor phenomenon associated with RLS and different from the more usual PLMS.
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PMID:Propriospinal myoclonus: a motor phenomenon found in restless legs syndrome different from periodic limb movements during sleep. 1600 57

There have been only a few reports of serotonin syndrome developing after mono-therapy with a selective serotonin reuptake inhibitor (SSRI). We report a case of serotonin syndrome caused by long-term therapy with fluvoxamine prior to treatment with paroxetine. An 18-year-old man with spinal cord injury (SCI) at thoracic level 2-3 presented with onset of serotonin syndrome after taking fluvoxamine (50 mg per day) for 8 weeks prior to treatment with paroxetine (10 mg per day) for 6 days. He had confusion, agitation, severe headache, tachycardia (124 beats/minute), hypertension (165/118 mmHg), high fever (39.1 degrees C), and myoclonus. All of the symptoms disappeared within 24 hours after discontinuation of administration of paroxetine. This is an interesting case of serotonin syndrome that developed after minimum doses of single therapy with an SSRI in a patient with SCI.
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PMID:Serotonin syndrome caused by minimum doses of SSRIS in a patient with spinal cord injury. 1699 52

The typical symptoms and signs of neuroleptic malignant syndrome (NMS) consist of fever muscle rigidity (stiffness, myoclonus, rod-like), alterations of consciousness (confusion, agitation, aggression, or catatonia), autonomic nervous system disturbances (i.e., hypertension, tachycardia, tachypnea, profuse sweating, and urine incontinence), abnormal blood tests such as low serum electrolytes, elevated serum creatinine phosphokinase (CPK) level, and leukocytosis. Muscle rigidity is often associated with myonecrosis, myoglobinuria, and elevated serum CPK. The mortality among NMS cases is in the 10 to 70% range depending on the severity of the symptoms and time of therapeutic approach. Mandatory therapy should include removal of causative agents, correction of body fluid and electrolytes, administration of benzodiazepine, clonazepam and bromocriptine (dopamine agonist), proved life-saving medications. The authors reported herein six cases with unusual clinical features of NMS. Four of them had been on antipsychotic for a year before becoming anorexic, dehydrated, agitated, and violent with paranoid delusion. One instance with underlying delirium tremens developed NMS after receiving haloperidol (30 mg IV) in addition to diazepam (200 mg IV) within 24 hours. Another patient was found to suffer from severe NMS after receiving bupropion (Dopamine inhibitor antidepressant) 300 mg/day. All patients displayed cardinal signs and symptoms of NMS in addition to dehydration and pallor. They were treated in the psychiatric ward and recovered rapidly from NMS after receiving clonazepam and bromocriptine and removal of the offending agents.
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PMID:Neuroleptic malignant syndrome: a review and report of six cases. 1721 72

Excess serotonin in the central nervous system leads to a condition commonly referred to as the serotonin syndrome, but better described as a spectrum of toxicity - serotonin toxicity. Serotonin toxicity is characterised by neuromuscular excitation (clonus, hyperreflexia, myoclonus, rigidity), autonomic stimulation (hyperthermia, tachycardia, diaphoresis, tremor, flushing) and changed mental state (anxiety, agitation, confusion). Serotonin toxicity can be: mild (serotonergic features that may or may not concern the patient); moderate (toxicity which causes significant distress and deserves treatment, but is not life-threatening); or severe (a medical emergency characterised by rapid onset of severe hyperthermia, muscle rigidity and multiple organ failure). Diagnosis of serotonin toxicity is often made on the basis of the presence of at least three of Sternbach's 10 clinical features. However, these features have very low specificity. The Hunter Serotonin Toxicity Criteria use a smaller, more specific set of clinical features for diagnosis, including clonus, which has been found to be more specific to serotonin toxicity. There are several drug mechanisms that cause excess serotonin, but severe serotonin toxicity only occurs with combinations of drugs acting at different sites, most commonly including a monoamine oxidase inhibitor and a serotonin reuptake inhibitor. Less severe toxicity occurs with other combinations, overdoses and even single-drug therapy in susceptible individuals. Treatment should focus on cessation of the serotonergic medication and supportive care. Some antiserotonergic agents have been used in clinical practice, but the preferred agent, dose and indications are not well defined.
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PMID:Serotonin toxicity: a practical approach to diagnosis and treatment. 1787 86


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