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)

A burst-suppression pattern on the EEG following anoxic insult is usually associated with a poor prognosis. Myoclonic jerks may accompany the electrographic burst. On rare occasions oral, ocular, or appendicular movements can be associated with bursts of EEG activity recorded following cerebral anoxic insult. At times these movements may cause confusion about the patient's state of consciousness or the purposefulness of the movements; they may mimic volitional movements in response to external stimuli. To better describe the variety of movements that may accompany bursts of EEG activity in comatose patients, we review 12 cases where movements occurred in association with the electrographic bursts.
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PMID:Clinical accompaniments of the burst-suppression EEG pattern. 916 10

It has been suggested that early myoclonic status after cardiorespiratory arrest is an agonal event. Here we describe three cases who developed early myoclonic status during a coma after cardiorespiratory arrest due to acute asthma. As consciousness improved, each patient developed Lance-Adams type multifocal myoclonus, but the eventual outcome was satisfactory. Only one patient needed assistance to walk, and all three were self caring. One patient had persistent dyscalculia. Early myoclonic status is not necessarily an agonal event, particularly when it follows arrest due to acute asthma or asphyxia.
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PMID:Early myoclonic status and outcome after cardiorespiratory arrest. 948 46

An 18-year-old female had common cold and insomnia in early March 1987. Later, abnormal speech and behavior, emotional incontinence, anorexia and consciousness disturbance appeared. On March 19, she was admitted to our hospital in semi-comatose state. Myoclonus-like movement on hands was observed, and epileptic attacks with tonic and clonic convulsions occasionally occurred. There were no neurological findings that suspected cerebral focal lesions. The respiration was assisted through tracheal intubation. Laboratory examinations showed inflammatory reactions (CRP+2, WBC 10,600) and transient high levels serum CK (6,215 IU). As she had bradycardia (30-40/min) with complete AV block on ECG, the pacemaker was implanted. The complication of myocarditis was suspected. EEG showed bilateral slow waves (3-6Hz), dominantly in frontal areas. Brain CT and CSF examinations were normal. After the combined administration of ara-A, dexamethasone and anti-convulsant, the consciousness level was recovered within a month. The serum antibody against coxsackie virus B4 alone was significantly increased. We concluded that coxsackie virus B4 caused acute encephalitis with mental symptoms and myocarditis with AV block. Recently, cytomegalovirus was reported to be the causative virus in a young female with non-HSV encephalitis who showed mental symptoms with good prognosis, but coxsackie virus B4 should also be considered as one of the causative viruses.
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PMID:[Coxsackie virus B4 encephalitis in a young female who developed mental symptoms, and consciousness disturbance, and completely recovered]. 959 14

Almost half of patients respond acutely to resuscitation but most die within the first several days after arrest. The incidence of survival to discharge from the hospital after cardiopulmonary arrest is about 15%; one third of those surviving have evidence of neurologic deficits. Although some prognostic variables are useful in determining which patients are most likely to die prior to discharge from the hospital, each patient needs to be evaluated on an individual basis and the various risk factors weighed carefully. As additional data accumulate, we may well be more effective at deciding which patients are more likely to benefit from CPR so that we can more judiciously apply this therapeutic modality. A number of studies have identified factors that contribute to poor outcome. Patients over 70 years of age usually fare poorly after CPR, but this is more a reflection of the number of coexisting diagnoses rather than years. Although initial survival may not be different from younger patients, fewer elderly patients live to discharge and more are likely to have neurologic sequelae. Concurrent diagnoses such as sepsis, AIDS, gastrointestinal bleeding, renal failure, cancer, and central nervous system disease have a universally poor response to CPR. If defibrillation occurs more than 6 minutes after arrest or on the general ward or if the resuscitative attempt lasts longer than 15 minutes, mortality is greater than 95%. If CPR continues for more than 30 minutes, there are no survivors. A low exhaled CO2 concentration (< 2%) during cardiac massage, asystole or EMD as the first identified rhythm, and recurrent arrest also carry a poor prognosis. On the other hand, at the time of arrest or during the immediate postarrest period, poor neurologic status is a less helpful predictor. The absence of spontaneous respiration is the only variable at the time of admission after out-of-hospital arrest that is particularly ominous. There is no evidence to suggest that the absence of spontaneous respiration implies any better prognosis for patients arresting in the hospital. Coma, hypoxic myoclonus, and absent reflexes, while not useful immediately following arrest, are of greater prognostic significance 48 hours later. Only 5% of patients who are unconscious 48 hours after arrest will have a full neurologic recovery. The Glasgow Coma Scale has also been used for prognostication.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Resuscitation: when is enough, enough? 1014 87

To contrast stimulus-sensitive generalized myoclonus with ensuing multifocal localized myoclonus in a patient with post-anoxic coma, we stressed the clinical as well as electroencephalographical differences between his initial generalized and subsequent focal myoclonus. While generalized myoclonus was presumably of extracortical origin and responsive to valproic acid, alternating Jacksonian seizures were definitely cortical and suppressed with phenytoin. These two different types of myoclonus should not be confused in post-anoxic coma.
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PMID:A case of post-anoxic encephalopathy with initial massive myoclonic status followed by alternating Jacksonian seizures. 1093 92

Serotonin syndrome is an underreported complication of pharmacotherapy that has been relatively ignored in the medical literature. We discuss 2 recent cases seen at our institution and 39 cases described in the English-language literature since 1995. We found that patients with serotonin syndrome most often (74.3%) presented within 24 hours of medication initiation, overdose, or change in dosage. The most common presenting symptoms and signs were confusion, agitation, diaphoresis, tachycardia, myoclonus, and hyperreflexia. The prevalences of hypertension, coma/unresponsiveness, seizures, and death were not as prominent in our study as previously reported, perhaps reflecting earlier recognition and intervention. The most common therapeutic intervention was supportive care alone (48% of patients). The use of 5-hydroxytryptamine (5-HT) antagonists such as cyproheptadine, however, has become more common and might reduce the duration of symptoms. Only 1 death occurred, and most patients (57.5%) had complete resolution of their symptoms within 24 hours of presentation. The increased use of serotonergic agents (alone and in combination) across multiple medical disciplines presents the possibility that the prevalence and clinical significance of this condition will rise in the future. Internists will need to be increasingly aware of and prepared for this pharmacologic complication. Prevention, early recognition of the clinical presentation, identification and removal of the offending agents, supportive care, and specific pharmacologic therapy are all important to the successful management of serotonin syndrome.
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PMID:Serotonin syndrome. Presentation of 2 cases and review of the literature. 1094 49

A patient comatose after acute anoxia developed bilaterally synchronous, periodic myoclonic jerks most prominently in the bilateral upper limbs. Although the myoclonus seemed to occur spontaneously, electrophysiological studies showed that the myoclonic jerks correlated in timing and size with arterial pulses, and was suppressed by massage over the carotid sinus. It is proposed that the present myoclonus is a variant of brainstem reflex myoclonus in which arterial pulses served as intrinsic trigger stimuli via the carotid sinus and the medullary reticular formation.
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PMID:Carotid brainstem reflex myoclonus after hypoxic brain damage. 1103 27

We report the clinical laboratory, electroencephalography (EEG), magnetic resonance imaging (MRI) and single photon emission computerized tomography (SPECT) findings in a 15 year-old euthyroid girl with autoimmune thyroiditis and encephalopathy. She had stupor, coma and generalized tonic clonic seizure preceded by tremor and myoclonus with a previous misdiagnosis of epilepsy and encephalitis. Response to steroid after the 3rd relapse was excellent. Another four children in the literature are also discussed.
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PMID:Tremor and myoclonus heralding Hashimoto's encephalopathy. 1108 93

A 37-year-old woman presented with acute cerebellar atrophy after ingesting toxic doses of tricyclic antidepressants in an attempt of suicide. Two hours after ingestion, she was comatose and showed myoclonus of the limbs, and eventually developed status epileptics. The patient underwent general anesthesia with thiopental, she had hyperpyrexia with elevated muscle enzymes and leukocytosis. These clinical and laboratory features suggested that she had serotonin syndrome (SS). After recovery from coma and hyperpyrexia that had lasted for 7 days, she showed cerebellar ataxia, and progressive cerebellar atrophy of CT scan. As well as neuroleptic malignant syndrome, the SS may cause cerebellar degeneration, probably due to sustained hyperpyrexia.
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PMID:[Progressive cerebellar atrophy following acute antidepressant intoxication]. 1129 69

We report a 56-year-old woman with progressive gait disturbance. Her mother had Parkinson's disease with onset at age 70. She died at age 74 and the post-mortem examination confirmed the diagnosis of Lewy body positive Parkinson's disease. The patient was well until the age of 50(1995) when she noted an onset of resting tremor and difficulty of gait. She also developed delusional ideation and was admitted to a psychiatric service of another hospital, where a major tranquilizer was given. The delusion disappeared but she developed marked rigidity. The major tranquilizer was discontinued and an anticholinergic and amantadine HCl were given. She showed marked improvement to Hoehn and Yahr stage II and was discharged. In 1995, when she was 52 years of the age, she developed delusion again and a major tranquilizer was given. She developed marked parkinsonism again and became Hoehn and Yahr stage V. The major tranquilizer was discontinued and she was treated with levodopa/carbidopa, trihexyphenidyl, bromocriptine, and dops. She improved remarkably to stage II. She was admitted to our service on October 8, 1996 for drug adjustment. She was alert and not demented. She was anxious but delusion or hallucination was noted. Higher cerebral functions were intact. Cranial nerve functions were also intact except for masked face and small voice. Her posture was stooped and steps were small. She showed retropulsion and moderate bradykinesia. Resting tremor was noted in her left hand. Rigidity was noted in both legs. No cerebellar ataxia or weakness was noted. Deep tendon reflexes were within normal range and sensation was intact. Her cranial MRI revealed some atrophic changes in the putamen, in which a T 2-high signal linear lesion was seen along the lateral border of the putamen bilaterally. In addition, posterior part of the putamen showed T 2-low signal intensity change. She was treated with 1.6 mg of talipexole, 6 mg of trihexyphenidyl, and 100 mg of L-dops. She was in stage III of Hoehn and Yahr. She developed neurogenic bladder with a large amount of residual urine for which she required catheterization. She was transferred to another hospital. Despite drug adjustment, she lost response to levodopa and her parkinsonism deteriorated gradually. She also developed syncope orthostatic hypotension. In April of 1998, she developed intracerebral hemorrhage and was admitted again on April 19, 1998. She was unable to stand and showed marked akinesia and rigidity. She was in stage V of Hoehn and Yahr. Her cranial CT scan revealed bilateral high-density lesions in the posterior parietal lobes. She developed dysphagia for which she required gastrostomy. She was transferred to another hospital but her clinical condition deteriorated further. On December 22, 1999, she developed fever and dyspnea and was admitted to our service again. She developed cardial arrest at the emergency room from hypoxia. She was resuscitated; however, she was comatose with loss of brain stem reflexes. Later on she developed generalized myoclonus. She developed cardiac arrest and pronounced dead on December 28, 1999. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had striatonigral degeneration because of poor response to levodopa in the later course, autonomic failures, and MRI changes. Some other participants thought that the patient had a form of familial Parkinson's disease. Opinions were divided into these two possibilities. Post-mortem examination revealed that the substantia nigra showed intense neuronal loss and gliosis, however, no Lewy bodies were seen. In addition, intracytoplasmic inclusions were seen in oligodendrocytes. The putamen was markedly atrophic in its posterior part with marked gliosis and neuronal loss. The ventromedial part of the pontine nucleus also showed neuronal loss and intracytoplasmic glial inclusions. Pathologic diagnosis was multiple system atrophy. In the parietal lobe, an arteriovenous malformation with bleeding was noted. This is very unique case. Although her mother had Lewy body-positive Parkinson's disease, the patient had Lewy body-negative multiple system atrophy with a-synuclein-positive glial inclusions. Whether this is just a coincidental occurrence or the presence of a genetic load for Parkinson's disease might triggered her multiple system atrophy is an interesting question to be answered in future.
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PMID:[A-56-year-old woman with parkinsonism, whose mother had Parkinson's disease]. 1142 77


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