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)

This paper reviews the main neurological complications of psychiatric drugs, in particular antipsychotics and antidepressants. Extrapyramidal syndromes include acute dystonia, parkinsonism, akathisia, tardive dyskinesia and tardive dystonia. Extrapyramidal symptoms (EPS) are less frequent with atypical than with conventional antipsychotics but remain common in clinical practice partly due to lack of screening by health professionals. Neuroleptic malignant syndrome (NMS) consists of severe muscle rigidity, pyrexia, change in conscious level and autonomic disturbance but partial forms also occur. NMS is particularly associated with the initiation and rapid increase in dose of high-potency antipsychotics but it has been reported with all the atypical antipsychotics and rarely with other drugs including antidepressants. Serotonin toxicity comprises altered mental state (agitation, excitement, confusion), neuromuscular hyperactivity (tremor, clonus, myoclonus, hyper-reflexia) and autonomic hyperactivity and occurs on a spectrum. Severe cases, termed serotonin syndrome, usually follow the co-prescription of drugs that increase serotonergic transmission by different pathways, for example a monoamine oxidase inhibitor (MAOI) and a selective serotonin reuptake inhibitor (SSRI). Most antipsychotics and antidepressants lower the seizure threshold and can cause seizures; the risk is greater with clozapine than with other atypical antipsychotics and greater with tricyclic antidepressants (TCAs) than with SSRIs. In randomised controlled trials in elderly patients with dementia atypical antipsychotics are associated with a higher risk of stroke and death than placebo. Cohort studies suggest that conventional drugs carry at least the same risk. Cessation of treatment with antipsychotics and antidepressants can lead to a wide range of discontinuation symptoms which include movement disorders and other neurological symptoms. Clinicians need to be familiar with strategies to reduce the risk of these adverse events and to manage them when they arise. Their occurrence needs to be balanced against the benefits of psychiatric drugs in terms of efficacy and improved quality of life in a range of disorders.
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PMID:Neurological complications of psychiatric drugs: clinical features and management. 1809 17

Fatal familial insomnia (FFI)--first reported in 1986--is a hereditary prion disease with autosomal-dominant inheritance, caused by a missense-mutation at codon 178 of the prion-protein gene (PRNP) on chromosome 20. A methionine-valine polymorphism at codon 129 of PRNP expresses different phenotypes. The clinical features of FFI are characterized by a disrupted sleep-wake cycle with resulting fluctuations of vigilance, autonomic hyperactivation, myoclonus, motor abnormalities and by cognitive disturbances. The age of onset is between middle to late adulthood (51 +/- 7.1 years), disease duration varies between 8 and 72 months (18.4 +/- 17.3 months) and is ultimately fatal. We report the case of a 57-year-old man with a diagnosed FFI by molecular-genetic investigation who suffered from increasing memory- and sleep-disturbance as well as physical restlessness and impotence for 9 months. Clinical features were motor symptoms, generalized myoclonus and hyperactivity with reduced attention and concentration. The neuropsychological findings were a severe disturbance of attention and memory as well as incipient deficits in executive functions. The cranial MRI and repeated EEG were normal; in detailed laboratory tests including CSF no abnormalities were detected. The clinical course was characterized by rapid decline of the motor and cognitive skills; the patient died 15 months after onset. Histological analysis showed the typical changes of FFI (spongiform changes at hippocampus and regio entorhinalis, severe gliosis in the thalamus and mild deposits of abnormal prion protein).
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PMID:[Fatal familial insomnia--a rare differential diagnosis in dementia]. 1818 21

Serotonin syndrome is a potentially life-threatening adverse drug reaction caused by excessive serotonergic agonism in central and peripheral nervous system serotonergic receptors (Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-1120). Symptoms are characterized by a triad of neuron-excitatory features, which include (a) neuromuscular hyperactivity -- tremor, clonus, myoclonus, hyperreflexia and, in advanced stages, pyramidal rigidity; (b) autonomic hyperactivity -- diaphoresis, fever, tachycardia and tachypnea; (c) altered mental status -- agitation, excitement and, in advanced stages, confusion (Gillman PK. Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. Br J Anaesth 2005;95:434-441). It arises when pharmacological agents increase serotonin neurotransmission at postsynaptic 5-hydroxytryptamine 1A and 5-hydroxytryptamine 2A receptors through increased serotonin synthesis, decreased serotonin metabolism, increased serotonin release, inhibition of serotonin reuptake or direct agonism of the serotonin receptors (Houlihan D. Serotonin syndrome resulting from coadministration of tramodol, venlafaxine, and mirtazapine. Ann Pharmacother 2004;38:411-413). The etiology is often the result of therapeutic drug use, intentional overdosing of serotonergic agents or complex interactions between drugs that directly or indirectly modulate the serotonin system (Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-1120). Due to the increasing availability of agents with serotonergic activity, physicians need to more aware of serotonin syndrome. The following case highlights the complex nature in which serotonin syndrome can arise, as well as the proper recognition and treatment of a potentially life-threatening yet easily avoidable condition.
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PMID:Serotonin syndrome: a complex but easily avoidable condition. 1843 63

Haloperidol has long been used to manage agitation in dementia, but it is associated with increased side effects. We report the first case of a patient with severe Alzheimer's disease who presented with non-epileptic myoclonus just after haloperidol treatment was initiated.
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PMID:Multifocal myoclonus induced by haloperidol. 1952 95

The serotonin syndrome is a toxic state largely attributable to changes in sensitivity of serotonin receptor system in the brainstem and spinal cord resulting from increased serotonergic activity in central neurologic system, due to use of serotonergic agents either in overdose or in combination. Serotonin syndrome may present with neuromuscular (clonus, myoclonus, tremor, hyperreflexia) and autonomic (fever, mydriasis, tachycardia, tachypnea) symptoms and mental status changes (confusion, agitation) and may result in death in severe cases. The risk for the development of serotonin syndrome is increased with the combined use of agents from different groups such as selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs). The growing use of SSRIs for depression and the introduction of pharmacological agents newly developed for the treatment of various medical disorders increases the risk of drug-drug interactions and toxic states like serotonin syndrome. In the presented case clinical presentation and outcome of the serotonin syndrome which has developed as a consequence of concomitant linezolid use in a young patient who was already on an SSRI antidepressant is discussed. Linezolid is an oxazolidinone antibiotic which has MAOI-like properties. This case is presented to inform psychiatrists especially working in consultation-liaison settings about the risk of drug-drug interactions and possible prevention of these.
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PMID:[Serotonin syndrome associated with linezolid use: a case report]. 2001 32

The serotonin toxicity (ST) is a potentially life-threatening adverse drug reaction results from therapeutic drug use, intentional self-poisoning, or inadvertent interactions between drugs. ST can be caused by a single or a combination of drugs with serotonergic activity due to excessive serotonergic agonism on central nervous system and peripheral serotonergic receptors (monoamine oxidase inhibitors, tricyclic antidepressants, SSRIs, opiate analgesics, over-the-counter cough medicines, antibiotics, weight-reduction agents, antiemetics, antimigraine agents, drugs of abuse, H2-antagonist and herbal products). The serotonin toxicity is often described as a clinical triad of mental-status changes (agitation and excitement with confusion), autonomic hyperactivity (diaphoresis, fever, tachycardia, and tachypnea), neuromuscular abnormalities (tremor, clonus, myoclonus, and hyperreflexia) and, in the advanced stage, spasticity; not all of these findings are consistently present. In this article, we describe two cases of ST due to interaction between Citalopram and two CYP2D6 inhibitors: Cimetidine and Topiramate and their clinical resolution after treatment discontinuation.
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PMID:Serotonin toxicity: a short review of the literature and two case reports involving citalopram. 2149 Oct 99

Some factors have been identified as contributing to medical errors such as labels, appearance, and location of ampules. In this case report, inadvertent intrathecal injection of 80 mg tranexamic acid was followed by severe pain in the back and the gluteal region, myoclonus on lower extremities and agitation. General anesthesia was induced to complete surgery. At the end of anesthesia, patient developed polymyoclonus and seizures needing supportive care of the hemodynamic, and respiratory systems. He developed ventricular tachycardia treated with Cordarone infusion. The patient's condition progressively improved to full recovery 2 days after. Confusion between hyperbaric bupivacaine and tranexamic acid was due to similarities in appearance between both ampules.
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PMID:Inadvertent intrathecal injection of tranexamic acid. 2165 27

Sleep bruxism is a sleep-related movement disorder that can be responsible for various pains and dysfunctions in the orofacial region. The aim of the current case-control association study was to investigate the association of genetic, psychological and behavioral factors with sleep bruxism in a Japanese population. Non-related participants were recruited and divided into either a sleep bruxism group (n = 66) or control group (n = 48) by clinical diagnoses and 3-night masseter electromyographic recordings by means of a portable miniature device. The Epworth Sleepiness Scale, Temperament and Character Inventory, NEO-Five Factor Inventory and custom-made questionnaires that asked about familial aggregation, alcohol intake, caffeine intake, cigarette smoking, past stressful life events, daytime tooth-contacting habit, temporomandibular disorder, daily headache, snoring, apnea/hypopnea symptoms, leg-restlessness symptoms and nocturnal-myoclonus symptoms were administered. In addition, 13 polymorphisms in four genes related to serotonergic neurotransmission (SLC6A4, HTR1A, HTR2A and HTR2C) were genotyped. These factors were compared between case (sleep bruxism) and control groups in order to select potential predictors of sleep-bruxism status. The statistical procedure selected five predictors: Epworth Sleepiness Scale, leg-restlessness symptoms, rs6313 genotypes, rs2770304 genotypes and rs4941573 genotypes. A multivariate stepwise logistic regression analysis between the selected predictors and sleep-bruxism status was then conducted. This analysis revealed that only the C allele carrier of HTR2A single nucleotide polymorphism rs6313 (102C>T) was associated significantly with an increased risk of sleep bruxism (odds ratio = 4.250, 95% confidence interval: 1.599-11.297, P = 0.004).This finding suggests a possible genetic contribution to the etiology of sleep bruxism.
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PMID:Association of genetic, psychological and behavioral factors with sleep bruxism in a Japanese population. 2254 12

Morphine has been widely used for the treatment of acute, chronic, and cancer pain and is considered the strongest analgesic in clinical care. Conversely, morphine-induced analgesia may be accompanied by several side effects. Animal studies have demonstrated that low doses of morphine administered intrathecally can produce reliable analgesia for thermal, mechanical, and chemical nociceptive stimulation. On the other hand, high doses of morphine administered intrathecally may induce spontaneous nociceptive responses such as scratching, biting, and licking in mice as well as agitation and vocalization in rats. In addition, similar nociceptive responses including hyperalgesia, allodynia, and myoclonus have been observed in humans following intrathecal or systemic administration of high-dose morphine. It has been suggested that the spontaneous nociceptive behaviors evoked by high-dose morphine may be mediated by a non-opioid mechanism that is not yet fully understood. This review describes the mechanisms of spontaneous nociceptive behaviors evoked by high-dose morphine focusing on the neurotransmitters/neuromodulators released from primary afferent fibers.
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PMID:[Mechanism of spinal pain transmission and its regulation]. 2545 39

Progressive encephalomyelitis with rigidity and myoclonus (PERM) is a rare disease. PERM consists of the same symptoms as stiff person syndrome, in addition to sensory, brainstem and autonomic features. We herein report a case of PERM in a 48-year-old woman who initially presented with spasticity of the lower limbs and subsequently developed upper limb spasticity, perioral myoclonus and restlessness after three months. The onset of potentially fatal dysautonomia was observed at the peak of the disease. Treatment with high-dose immunoglobulin (400 mg/kg, 5 days), levetiracetam and azathioprine resulted in a drastic and sustained improvement of these symptoms. This is an interesting case of PERM in which the patient showed a dramatic improvement following immune moderation.
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PMID:Successful immune moderation treatment for progressive encephalomyelitis with rigidity and myoclonus. 2574 16


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