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 study was made in order to define risk factors for patients requiring spinal opioid therapy developing painful spastic muscle tone together with myoclonus and spinal jerking (MSJ). The case histories of 75 patients, all receiving morphine spinally, were retrospectively analysed and, of these, 10 suffered from the MSJ syndrome. The following were taken as evaluation criteria: age, sex, performance status, duration and dosage of previous systemic and current spinal morphine therapy, concomitant analgesic and co-analgesic medication, pretreatment of the dorsal column and neurological dysfunction due to damage either of the nerval plexus or of the medulla spinalis. As a result, high spinal morphine doses in conjunction with pathological changes within the spine were shown to be risk factors for this syndrome. Changing from spinal to systemic morphine application or reduction of spinal doses together with the addition of systemic morphine led to complete recovery from MSJ. As underlying mechanism, an imbalance between the activity of spinal and central opioid receptors and/or toxic morphine effects on the medulla spinalis are discussed. In conclusion, great care should be taken when applying morphine to the spine in patients with neurological dysfunction due to an apparent pathology of the medulla spinalis, especially if large amounts of morphine are likely to be required. Some systemic application of morphine might reduce the risk of patients developing MSJ syndrome.
Support Care Cancer 1994 Jul
PMID:Complications of spinal opioid therapy: myoclonus, spastic muscle tone and spinal jerking. 808 44

Eight cancer patients in the terminal stages of the disease treated with high doses of intravenous morphine developed hyperalgesia. All cases were retrospectively sampled from three different hospitals in Copenhagen. Five patients developed universal hyperalgesia and hyperesthesia which in 2 cases were accompanied by myoclonus. In 3 patients a pre-existing neuralgia increased to excruciating intensity and in 2 of these cases myoclonus occurred simultaneously. Although only few clinical descriptions of the relationship between hyperalgesia/myoclonus and high doses of morphine are available, experimental support from animal studies indicates that morphine, or its metabolites, plays a causative role for the observed behavioural syndrome. The possible mechanisms are discussed and treatment proposals given suggesting the use of more efficacious opioids with less excitatory potency in these situations.
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PMID:Hyperalgesia and myoclonus in terminal cancer patients treated with continuous intravenous morphine. 827 14

In advanced cancer patients close to death, delirium, multifocal myoclonus, and restlessness may occur. Multi-organ failure and related metabolic changes are mostly responsible for these symptoms. A pharmacologic approach to manage the delirium is necessary in the majority of cases. Benzodiazepines, neuroleptics, and barbiturates are the most common drugs used. In the case reported, propofol administered at very low doses provided good control of neuropsychiatric symptoms. After a loading dose of 20 mg, an infusion of 50-70 mg per hr was started. The patient died peacefully after 8 hr of propofol infusion, without requiring opioids. Propofol seems to be a promising drug in treating the terminal agitated state that can be associated with the dying process.
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PMID:Propofol in terminal care. 859 25

A neurologic paraneoplastic syndrome may be the first sign of an occult and treatable cancer. Some syndromes are associated with autoantibodies against neuronal antigens. Patients with cerebellar degeneration and ovarian or breast cancer have antibodies against 34 and 62 kilodalton (kDa) proteins in Purkinje cell cytoplasm: anti-Yo antibodies. Patients with encephalomyelitis or sensory neuronopathy and small cell lung cancer have antibodies against 35-40 kDa neuronal nuclear proteins: anti-Hu antibodies. Patients with opsoclonus-myoclonus and breast cancer have antibodies against 55 and 80 kDa neuronal nuclear proteins: anti-Ri antibodies. Patients with Lambert-Eaton myasthenic syndrome and small cell lung cancer have antibodies against voltage-gated calcium channels (anti-VGCC) in motor nerve terminals. The presence of anti-neuronal antibodies strongly indicates that a neurological syndrome is paraneoplastic, and often identify the site of an occult neoplasm. However, the absence of detectable antibodies does not rule out the presence of an underlying tumour.
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PMID:[Neurologic paraneoplastic syndromes and anti-neuronal antibodies]. 863 63

The opsoclonus-myoclonus syndrome (OMS) is a potentially devastating paraneoplastic or paraviral syndrome. Although it is a rare disorder, it has major implications for cancer, virology, immunology, developmental neurobiology, and molecular pharmacology. The mechanism of brain injury in OMS is unknown, but evidence suggests immune system dysregulation. This article surveys recent clinical and laboratory evidence for the autoimmune theory and discusses how some current therapies for OMS may exert their effects through immunomodulation. Specific testable hypotheses on the immunologic defect in OMS involving both B cells and T cells, the nature and mechanisms of brain injury, and their clinical correlations are proffered. The current therapeutic armamentarium provides a broad spectrum of nonselective immunotherapies, including noncytotoxic and cytotoxic drugs, intravenous immunoglobulins, and plasma exchange, some selected for induction and others for maintenance. The use of combination immunotherapies may allow steroid sparing, targeting of more than one immunologic effector pathway, and a mixture of early- and late-acting drugs. More selective immunotherapies, now available or in preclinical and clinical trials, have great potential for the treatment of OMS but require precise information on the underlying immunological problem. These data provide possible new directions for immunologic research and therapy in OMS.
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PMID:The immunopharmacology of the opsoclonus-myoclonus syndrome. 886 15

Opsoclonus is a rare disorder of the saccadic system, in which fixation is continuously interrupted by multivectorial, back-to-back saccades that at times can be seen only with an ophthalmoscope. To diagnose it reliably, eye movement recording is required. Opsoclonus may be a harbinger of an occult malignancy, though many cases are postinfectious, toxic-metabolic or idiopathic. The underlying malignancy is usually neural crest tumors in children and lung, breast, or gynecologic cancer in adults. Opsoclonus can be accompanied by myoclonus and ataxia. Concurrent appearance of oscillations affecting eyes and limbs suggests a common brainstem generator. Dysfunction of the glycinergic omnipause neurons in the nucleus raphe interpositus has been proposed. Autoantibodies against neural epitopes shared with a tumor are implicated in the pathogenesis of opsoclonus in paraneoplastic cases. Because of the association with malignancies, full oncological work-up is indicated in every case. Coexisting opsoclonus carries a relatively good prognosis for the cancer; however, the neurologic disability may remain even if the tumor has been arrested. New, potentially effective immunoadsorption therapy for opsoclonus is currently under investigation.
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PMID:Opsoclonus. 887 53

The different pathogenic and clinical aspects of the paraneoplastic ophthalmological syndromes are discussed by the author. Opsoclonus-myoclonus, retinal degeneration are largely reviewed. It is possible that new modern immunological methods to elucidate the role of antibodies in the genesis of paraneoplastic syndrome and the role of these antigens in the functioning of nervous system. Recognising a ophthalmological syndrome as paraneoplastic will prompt a search for an early detection of a cancer and a more prompt treatment.
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PMID:Paraneoplastic ophthalmological syndromes. 891 42

Pain occurs in more than 80% of cancer patients before death. Because of the increase in the frequency of cancer deaths worldwide, it is imperative to address cancer pain as a public health problem. Until recently, educational efforts were focused on treatment issues rather than adequate assessment. The approach to pain intensity as a multidimensional construct has helped in focusing treatments and identifying prognostic factors. Valid tools have been developed that allow multidisciplinary assessment of these prognostic factors and their complex interrelationship with the analgesic response. As a result of increased opioid exposure, patients are currently developing newer toxicities, mostly central excitability including delirium, myoclonus, grand mal seizures, and hyperalgesia. The observation that more than 80% of patients will require alternate routes for opioid delivery before death led to the development of a number of novel and effective alternate routes for delivery. Finally, in recent years it has become evident that some specific pain syndromes need to be addressed using specific assessment and management techniques. Incidental pain, somatization, neuropathic pain, and cancer pain in patients with alcoholism and drug addiction are some of these syndromes.
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PMID:Cancer pain management. 906 Oct 98

A case of severe opioid toxicity is described in a 52-year-old cancer patient. The patient presented with classical clinical features of central hyperexcitability associated with opioid toxicity: delirium, myoclonus, hallucinations, hyperalgesia, and a possible seizure. This patient had a background of severe psychosocial distress and somatization in addition to a history of benzodiazepine dependence and alcohol abuse. The occurrence of opioid toxicity in this patient highlights the risks of a unidimensional approach to cancer pain, which ignores the non-organic components of pain, such as psychosocial distress, which will not respond to escalating doses of opioid medication.
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PMID:Severe opioid toxicity and somatization of psychosocial distress in a cancer patient with a background of chemical dependence. 920 57

While occasional myoclonic jerks are prevalent in cancer patients receiving opioids, severe myoclonic jerks and seizures due to opioids are uncommon. In this retrospective case series, we describe five cancer patients with refractory cancer pain and severe neuroexcitatory toxicity associated with extremely high-dose opioid therapy to characterize better the syndrome, its treatment, and its outcome. Two patients died following seizures, but three patients recovered following prompt treatment with parenteral midazolam infusions and rotation to alternative opioids. Possible mechanisms and treatment options for this potentially lethal clinical syndrome are reviewed. The authors conclude that severe multifocal myoclonus and seizures associated with extremely high-dose opioid therapy are life-threatening, and respond to parenteral midazolam infusion, rotation to alternative opioids, and aggressive supportive care.
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PMID:Strychnine-like multifocal myoclonus and seizures in extremely high-dose opioid administration: treatment strategies. 956 11


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