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)

Patients with end-stage renal disease undergoing regular dialysis are prone to encephalopathy, but the cause is often unclear. Dialysis patients are at risk for thiamine deficiency, which may mimic many uremic complications, including encephalopathy. To determine whether unexplained encephalopathy in regular dialysis patients is associated with thiamine deficiency, we conducted a prospective study that enrolled 30 consecutive dialysis patients with altered mental status admitted to a referred hospital during a 1-year period. A complete history, physical and neurological examinations, laboratory investigations, and computed tomographic scans or magnetic resonance imaging of the brain were obtained for each subject. In 10 of the 30 patients, diagnoses remained obscure after the initial workup. Manifestations included confusion, chorea, acute visual loss, rapidly progressive dementia, myoclonus, convulsions, and coma. Intravenous thiamine was administered to these 10 patients. All 10 patients had thiamine deficiency confirmed by a marked response to thiamine supplementation and/or a low serum thiamine concentration (35.3 +/- 6.0 nmol/L; normal, >50 nmol/L). Nine patients recovered, but one patient failed to respond because of delayed treatment. We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency. This condition is fatal if unrecognized and can be successfully treated with prompt thiamine replacement.
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PMID:Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. 1168 45

Propofol is an intravenous anaesthetic agent having anticonvulsant property. We report here a case in which propofol was effective in controlling myoclonus during rewarming in brain hypothermia patient. A 35-year-old male patient was admitted in a comatose state with right-sided hemiparesis, anisocoria and absence of bilateral light reflex. On admission, a head CT showed traumatic subarachnoid hemorrhage, left subdural hematoma, 10 mm midline shift and tentorial herniation with massive brain swelling together with extensive hypodensity in the frontal, temporal and occipital lobes bilaterally. Left decompressive hemicraniectomy, removal of hematoma and brain hypothermia therapy were started immediately. Postoperative head CT showed 15 mm midline shift. The temperature of the jugular bulb was maintained at 34 degrees C for 2 days together with sedation using midazolam under artificial ventilation. The patient was gradually rewarmed at a rate of 0.5 degree C per day from the third hospital day. Myoclonus of sudden onset developed on the patient's head and upper extremities on the third hospital day. An intravenous bolus injection of 10 mg midazolam and continued intravenous infusion of midazolam were given but they did not completely stop myoclonus. A bolus of propofol 60 mg was given intravenously and continuous intravenous infusion of propofol 2 mg.kg-1.hr-1 was started after which the progression of myoclonus disappeared. Myoclonus was kept controlled until the continuous intravenous infusion of midazolam and propofol was discontinued on the sixth hospital day, after which myoclonus occurred again after extubation on the seventh hospital day. The clinical course of this case suggests that propofol might be an alternative effective agent to suppress refractory myoclonus.
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PMID:[Efficacy of propofol in controlling myoclonus during rewarming in a brain hypothermia patient]. 1188 90

Hashimoto's encephalopathy (HE) is a rare neurological complication of chronic lymphocytic thyroiditis. As its clinical presentation is aspecific, other etiologies of acute encephalopathy have to be ruled out. We report the case of a 29-year old woman with neuropsychiatric signs preceding coma, myoclonus and epileptic seizures. Clinical and electroencephalographic features were consistent with the diagnosis of new variant of Creutzfeldt-Jakob disease. However, high titres of antithyroid antibodies in serum directed towards the diagnosis of HE. Despite oral steroids, the patient died five months later. Neuropathological findings ruled out spongiform encephalopathy and disclosed aspecific activated microglia. Our observation suggests that this process could be involved in the pathogenesis of HE. Even in the absence of clinical dysthyroidism, HE diagnosis has to be suspected in the settings of acute encephalopathy associated with seric antithyroid antibodies.
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PMID:[Hashimoto's encephalopathy: an anatomicoclinical observation]. 1198 89

We experienced a case of hypoxic brain damage induced by severe asthma who was successfully treated by hypothermia. A 20-year-old woman with a history of bronchial asthma suffered from severe respiratory distress and she stopped breathing for about 20 minutes. She was admitted to our hospital with respiratory arrest, deep coma, mydriasis and weak motor response to pain. She was intubated and mechanically ventilated with 100% oxygen. She was cooled down to 33 degrees C within 4 hours of her arrival. Her body temperature was maintained at about 33 degrees C for 2 days, and then gradually rewarmed. During hypothermia, PaCO2 was quite high(80-100 mmHg), but the intracranial pressure was kept low. After hypothermia therapy, she became free from consciousness disturbance and there were no neurological disorders except for mild myoclonus. Hypothermia has a possibility of effective therapy for patients with hypoxic brain damage after respiratory distress.
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PMID:[A case of hypoxic brain damage induced by severe asthma successfully treated by hypothermia therapy]. 1272 5

The authors report a case of area-specific stimulus-sensitive postanoxic myoclonus and discuss possible pathophysiology. A 71-year-old man sustained cardiorespiratory arrest that lasted 10 minutes and remained unresponsive. On the first EEG obtained 8 hours after the arrest there was no cerebral electrical activity before stimulation of the trigeminal-innervated areas. Periorbital stimulation was associated with bursts of spike-wave activity and generalized myoclonic jerks, whereas other types of stimulation did not elicit any response. A second EEG obtained 32 hours later showed a nonreactive alpha coma pattern. The patient died 7 days after the arrest. Area-specific stimulus-sensitive postanoxic myoclonus is very rare. The regularity of generalized bursts of spike-wave activity (cortical response) in response to stimulation of trigeminal-innervated areas suggests that the resting EEG electrocerebral silence may have been a result of cortical suppression with disinhibition of stimulus-sensitive brainstem-generated myoclonus.
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PMID:A case of area-specific stimulus-sensitive postanoxic myoclonus. 1276 83

The explosive RDX (hexogen, cyclonite) is usually used for the production of C-4 explosive. The rare occurrence of accidental and intentional RDX intoxications has been reported during manufacturing process or in wartime. In this article, the authors report 5 cases of accidental oral RDX poisoning. On admission, observed signs and symptoms included repetitive generalized tonic-clonic convulsions, postictal coma, lethargy, confusion, hyperreflexia, postictal amnesia, nausea, vomiting, abdominal tenderness, sinusal tachycardia, dysrhythmia with frequent ventricular premature beats, generalized muscle spasms, and myoclonus. Leukocytosis, mild anemia, methemoglobinemia, elevated levels of blood glucose, serum aspartate transaminase, alanine transaminase, lactic dehydrogenase, creatine phosphokinase, amilase, hypokalemia, metabolic acidosis, proteinuria, glucosuria, and myoglobinuria were also noted. Plasma RDX concentrations were 268 to 969 ng/mL at 3 hours of ingestion. For management, supportive and symptomatic measures were taken. Whole-bowel irrigation might have been an effective therapeutic procedure due to probable slow gastrointestinal absorption of RDX. Three patients who developed severe metabolic acidosis underwent urgent hemodialysis. All patients were discharged 7 to 21 days after admission without any sequelae. Plasma RDX levels were strongly correlated with the clinical and laboratory manifestations. The available toxicological data on this rare accidental poisoning are reviewed in light of the literature.
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PMID:Accidental oral poisoning caused by RDX (cyclonite): a report of 5 cases. 1518 66

Paraneoplastic syndromes related to soft tissue tumors are very uncommon and an association of paraneoplastic diseases with a malignant fibrous histiocytoma (MFH) has not been reported so far. Opsoclonus-myoclonus is a rare paraneoplastic nervous system syndrome, that was well documented in adult patients with neoplasms particularly of the lung and breast. A 77-year-old woman developed typical opsoclonus-myoclonus syndrome and rapidly progressed to coma. The opsoclonus and generalized myoclonus continued until the patient's death seven months later. An autopsy examination identified a pleomorphic MFH in the retroperitoneum without a metastatic spread. Microscopic examination of the cerebellum revealed an atrophy of the granular layer along with a marked patchy loss of Purkinje cells, and a loss of neurons in the cerebellar nuclei accompanied by distinct peridental demyelination and astrogliosis. A moderate loss of neurons and neuronal chromatolysis were observed also in the inferior olivary nuclei. However, the omnipause neurons of the nucleus raphe interpositus, that are supposed to be responsible for opsoclonus generation under pathological conditions, as well as ocular brain stem nuclei were all intact. We failed to prove the presence of known antineuronal anti-Yo, anti-Hu or anti-Ri autoantibodies in both serum and cerebrospinal fluid (CSF) of the patient. However, the confirmation of the intrathecal IgG synthesis by oligoclonal bands in CSF and the immunohistochemical detection of IgG deposits on membranes of Purkinje cells, neurons of cerebellar granular layer and in cerebellar nuclei in our case support the presumed autoimmune nature of the disease.
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PMID:Paraneoplastic opsoclonus-myoclonus syndrome associated with malignant fibrous histiocytoma: neuropathological findings. 1523 19

We describe the clinical and electroencephalographic features of a comatose patient with severe anoxic encephalopathy who experienced acute reflex myoclonus precipitated by passive eye opening/closure and painful stimulation. Acute stimulus-sensitive postanoxic myoclonus is an underdiagnosed epileptic condition. Shortly after the anoxic insult, the diagnosis should be based on EEG evaluation and various types of stimulation. These should include passive eye opening/closure and painful stimuli.
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PMID:Acute stimulus-sensitive postanoxic myoclonus: description of a case. 1612 56

A 47-year-old woman developed confusion, incoordination, and hypertension after she was given linezolid in addition to sertraline for 5 days. Her symptoms resolved within 4 days of discontinuing linezolid. One and a half months later, she received a second course of linezolid; sertraline was discontinued on day 1 of linezolid therapy. On day 9 of therapy, the patient developed confusion, myoclonus, and incoordination, and cardiopulmonary arrest occurred, leaving the patient in a coma. Diarrhea, hypertension, and tachycardia developed after cardiopulmonary arrest. Linezolid was discontinued on day 10, and cyproheptadine was given. Linezolid is a weak monoamine oxidase inhibitor and has been reported to interact with selective serotonin reuptake inhibitors (SSRIs). Several cases of serotonin syndrome in patients taking linezolid and SSRIs have been reported, including two reports with sertraline, one with paroxetine, four with citalopram, and two with fluoxetine. One abstract of a retrospective analysis reported that serotonin syndrome did not occur in patients who received linezolid and fluoxetine, paroxetine, or sertraline. Because of several limitations, however, no conclusions can be drawn from that retrospective analysis. A drug interaction involving escitalopram and linezolid has not been documented. Caution should be used when linezolid is used in patients receiving an SSRI. Other antibiotic options should be considered first, and linezolid should be reserved as the last resort if possible. If the infection requires linezolid, the SSRI should be discontinued, and the patient should be monitored closely for serotonin syndrome.
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PMID:Drug interactions between linezolid and selective serotonin reuptake inhibitors: case report involving sertraline and review of the literature. 1646 32

Hypoxic-ischemic encephalopathy accompanying cardiac arrest is a common cause of long-term neurological dysfunction. With the improvement in prehospital emergency systems, larger numbers of people are resuscitated from cardiac arrests, although with the increased prospect of neurological sequelae. Neurological impairment after cardiac arrest is dependent on the degree of brain damage suffered during the arrest. Although the duration and severity of brain ischemia is often difficult to determine, clinicians are often faced with difficult issues related to predicting outcome related to awakening and long-term neurological deficits after the arrest. Neurological impairments range from mild cognitive deficits to severe motor and cognitive deficits that preclude independence in many activities of daily living. Several neurological syndromes have been described in patients who awaken from hypoxic-ischemic coma with lasting motor and cognitive deficits. This review will address many of the common syndromes after hypoxic-ischemic encephalopathy, including persistent vegetative states, seizures, myoclonus, movement disorders, cognitive dysfunction, and other neurological abnormalities.
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PMID:Long-term neurological complications after hypoxic-ischemic encephalopathy. 1696 43


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