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)

Myoclonus occasionally occurs in the perioperative setting and in patients on chronic opioid therapy. It appears to be dose-related in a unpredictable manner. Different mechanisms have been proposed to explain the occurrence of a series of neuromuscular disturbances probably sharing final common pathways. A neuroexcitatory opioid metabolite accumulation has been proposed to have a relevant role in determining myoclonus in patients treated with chronic opioid therapy for cancer pain, especially in the presence of renal impairment. The neurological status, previous oncologic treatment and concomitant therapy with neuroleptic drugs, the metabolic and hydration status should also have been considered. Adjuvant drugs, such as benzodiazepines or dantrolene may avoid the reduction of the opioid dose while maintaining an acceptable analgesia. Current practice suggests a change in opioid when pain control is not obtained at opioid doses resulting in unacceptable adverse effects, including myoclonus and hyperalgesia. A change in the type of opioid may be useful in patients who develop severe central adverse effects, even if these patients appear to have normal renal function or hydration status.
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PMID:Pathophysiology and treatment of opioid-related myoclonus in cancer patients. 951 54

Levofloxacin-induced-neurological adverse events such as convulsion, involuntary movement (tremor, myoclonus and chorea-like) and visual hallucination in two elderly patients are reported. A 67-year-old man with minor alcoholism and a past-history of gastrectomy and cholecystectomy was given 300 mg/day of oral levofloxacin and fulfenamic acid for an upper respiratory infection. On the 4th day, he reported gradual exacerbation of hand tremor which resembled chorea-like involuntary movement and gait disturbance. He also experienced visual hallucinations. On the 7th day, he suffered generalized convulsions and was admitted. Serum concentration of levofloxacin at this time (3 hours after last administration of a 100 mg tablet of levofloxacin) was 3.6 micrograms/ml. Cessation of the agents promoted complete recovery of these neurological adverse effects within a week. Another 85-year-old man with chronic bronchitis and slight renal impairment received long term administration of 200 mg/day of levofloxacin. On the 68th day of administration, gradual exacerbation of gait disturbance, dysarthria and chorea-like involuntary movement occurred. On the day of admission, 76 days after the start of administration, the serum level of levofloxacin was 2.55 micrograms/ml and that of spinal fluid was 1.12 micrograms/ml (3 hours after the last administration of a 100 mg tablet of levofloxacin). Cessation of the agents promoted complete recovery of these neurological adverse effects within the next two weeks. Both patients had no apparent neurological disorders except age-related brain atrophy. Age-related renal and brain impairment might have contributed to the neurological adverse effects of levofloxacin.
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PMID:[Levofloxacin-induced neurological adverse effects such as convulsion, involuntary movement (tremor, myoclonus and chorea like), visual hallucination in two elderly patients]. 1038 31

A 67-year-old woman with diabetes mellitus, chronic renal insufficiency, and recurrent urinary tract infections experienced encephalopathy and myoclonus while receiving cefepime. The adverse drug event was accompanied by elevated cefepime levels and abnormal electroencephalograms. This syndrome resolved after discontinuation of cefepime. Neurotoxicity is a known but possibly underreported adverse event associated with cefepime in patients with renal impairment who receive relatively excessive doses. Most cases reverse on drug cessation. In patients with renal disease, the maintenance dosage should be reduced and the patient monitored for neurotoxicity. Cefepime toxicity should be suspected whenever a patient receiving the drug experiences a change in mental status or myoclonus.
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PMID:Cefepime neurotoxicity: case report, pharmacokinetic considerations, and literature review. 1686 93

Impaired renal function increases the risk for cefepime-induced neurotoxicity. Symptoms include disorientation, myoclonus, status epilepticus, ataxia, gait disturbance, coma, and death. A high index of suspicion and early recognition of symptoms can minimize the risk of progression of symptoms to permanent neurologic impairment or death.
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PMID:Cefepime-induced neurotoxicity in a pediatric patient on chronic hemodialysis: a case report. 2922 28

Cefepime is a 4th generation cephalosporin often used for its ability to cover gram-positives, gram negatives, anaerobic bacteria, and, most importantly, pseudomonas. Prior to initiation of cefepime, the medication is dosed based on the renal function to avoid a multitude of its toxicity profiles, including encephalopathy, aphasia, myoclonus, seizures, and nonconvulsive status epilepticus. These risks are increased in the presence of renal impairment. We present a case of a 65-year-old woman who had presented to the emergency department (ED) two weeks after initiation of outpatient IV cefepime therapy with concerns of altered mentation and decreased oral intake. In the ED, the patient was noted to have a creatinine: 5.77 (baseline of 0.76) and urea: 94. During evaluation by the ED provider, the patient was noted to have transient slurring of speech, speech arrest, and tonic-clonic movements on the right. CT of the head, followed by CT angiography of the head and neck, demonstrated no acute intracranial pathology. Spot EEG revealed generalized slowing with unclear left-sided epileptiform discharges. There was a concern for complex partial seizures. Neurology and nephrology were consulted. The patient was given 1 g of levetiracetam, and emergent dialysis was performed. After dialysis, no other epileptiform activity was noted with the improvement of her encephalopathy. The patient returned to her baseline mentation. Here we emphasize the importance of recognizing cefepime's toxicity profile while triaging patients. In the rare event of toxicity, immediate treatment is discontinuing the offending agent and initiation of emergent hemodialysis.
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PMID:Cefepime-Induced Seizures: The Overlooked Outpatient Adverse Reaction. 3269 29

Movement disorders often emerge from the interplay of complex pathophysiological processes involving the kidneys and the nervous system. Tremor, myoclonus, ataxia, chorea, and parkinsonism can occur in the context of renal dysfunction (azotemia and electrolyte abnormalities) or they can be part of complications of its management (dialysis and renal transplantation). On the other hand, myoglobinuria from rhabdomyolysis in status dystonicus and certain drugs used in the management of movement disorders can cause nephrotoxicity. Distinct from these well-recognized associations, it is important to appreciate that there are several inherited and acquired disorders in which movement abnormalities do not occur as a consequence of renal dysfunction or vice versa but are manifestations of common pathophysiological processes affecting the nervous system and the kidneys. These disorders are the emphasis of this review. Increasing awareness of these conditions among neurologists may help them to identify renal involvement earlier, take timely intervention by anticipating complications and focus on therapies targeting common mechanisms in addition to symptomatic management of movement disorders. Recognition of renal impairment in a patient with complex neurological presentation may narrow down the differentials and aid in reaching a definite diagnosis.
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PMID:Movement Disorders and Renal Diseases. 3304 74