Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 70 years-old man was admitted at our hospital because of unstable angina pectoris. He had essential hypertension and right hemiplegia from a ischemic stroke two years before admission. On neurologic examination, it was found mental disorientation, unstable emotionality, right spastic hemiparesis with right Babinski sign, and segmental myoclonus affecting the superior lip and the palate (palatal nystagmus) on the right side. On the CT scan, a giant aneurysm of the basilar artery was detected. We conclude that the segmental myoclonus could be explained by ischemic lesions in the Guillain-Mollaret triangle.
 ...
PMID:Segmental myoclonus and basilar artery. Giant aneurysm. Case report. 130 61

A mother and two of her daughters had deafness and cortical reflex myoclonus; the mother also had mild truncal ataxia. Muscle and skin biopsy specimens revealed abundant ragged-red fibres and abnormal mitochondria. The son of one of the daughters had sensorineural deafness. Three other grandchildren were asymptomatic. The two daughters also had diabetes mellitus, hypertension and cardiomyopathy. Another daughter died of renal failure. The mother lost her hearing in her 70s, one daughter in her 30s, and the other daughter and the grandson in their 20s. The mother has had transient episodes (24-48 hours) of temporal disorientation, severe action myoclonus, and ataxia for about eight years. This is the first reported family with inherited deafness, myoclonus, and ataxia with mitochondrial pathology.
 ...
PMID:Abnormal muscle and skin mitochondria in family with myoclonus, ataxia, and deafness (May and White syndrome). 153 18

Ceftazidime, a beta-lactamase-stable, third-generation cephalosporin, is widely used for the treatment of serious gram-negative infections. Neurotoxicity has rarely been associated with the drug; however, two of our patients developed ceftazidime-induced neurotoxicity that produced confusion, disorientation, agitation, generalized weakness, and myoclonus. In both patients these symptoms cleared with either discontinuation or reduction of the dosage of ceftazidime. This emphasizes the importance of adjusting the dosage of ceftazidime in patients with renal insufficiency.
 ...
PMID:Neurotoxicity associated with ceftazidime therapy in geriatric patients with renal dysfunction. 192 20

A 66-year-old man with hepatic metastases from gastric adenocarcinoma was treated on two occasions with 5-fluoro-2-deoxyuridine (FUdR) via hepatic artery infusion (HAI). The patient developed neurologic signs and symptoms including disorientation, oculomotor defects, ataxia and multifocal myoclonus during both attempts at HAI. Systemic drug toxicity is unusual when FUdR is given via HAI, and neurologic toxicity has not previously been reported. We postulate individual hypersensitivity to FUdR or selective concentration of FUdR in brainstem structures to explain the toxicity in this case.
 ...
PMID:Neurologic toxicity associated with hepatic artery infusion HAI of FUdR. 294 26

In this article we report the case of a woman who survived an out-of-hospital cardiac arrest but was left with severe neuropsychological impairments due to anoxia. The deficits included anterograde and retrograde amnesia, dysphasia, disorientation, intellectual deterioration, visual impairments, ataxia, and myoclonus. Despite this degree of impairment the patient retained some insight into her condition which, in turn, created additional emotional problems. Rehabilitation and the problems of long-term care are considered.
 ...
PMID:Multiple neuropsychological deficits due to anoxic encephalopathy: a case study. 344 99

We present a 77-year-old woman with myoclonus and epilepsy. She was well until 35 years of age, when she noted an onset of trembling of the legs upon standing. Her symptom slowly progressed, and she felt a difficulty in standing when she was 39-year-old. She had a major motor seizure without an apparent focal onset when she was 46-year-old. She also developed tremor in her hands, and she felt difficulty in holding a glass filled with water. She was admitted to our service for the first time in 1965 when she was 51-year-old. She showed wide-based ataxic gait with truncal titubation. In finger to nose test, myoclonic jerks were induced in the upper extremities. Otherwise neurological examination was unremarkable. She was treated with primidone and phenobarbital, and was discharged for out patient follow up. Her symptoms slowly progressed, and gait and station became more difficult. Mentally she was sound. Three months prior to the present admission, she developed more difficulty in gait, and decrease in food intake. On the 14th of September in 1991, she was seen by a local physician who found an abnormal shadow in her chest X-ray, and she was admitted to our service for further work-up on September 18, 1991. On admission, the patient was a chronically ill and emaciated woman. Her blood pressure was 140/84 mmHg, heart rate 115/minutes and regular, and the body temperature 36.9 degrees C. The palpebral conjunctivae were anemic. No cervical adenopathy was noted. The lung fields were clear, and no heart murmur was audible. The abdomen was soft, and no organomegaly was present. On neurologic examination, she looked somnolent with disorientation to time and place. Her memory was poor, and she could not do well serial 7s. The disc was flat and the ocular movements appeared intact. Other cranial nerves were also unremarkable. She showed diffuse muscle wasting. She was unable to stand or walk. Maintaining the sitting position was also difficult. She was able to raise her arms, but almost unable to move her lower extremities. The precise muscle testing was impossible. No abnormal involuntary movement was seen. Finger to nose test could not be performed.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[A 77-year-old woman with myoclonus and epilepsy]. 812 9

A case of acute hepatic failure following ingestion of the veterinary euthanasia drug T61 is described. Presenting symptoms were drowsiness, disorientation, muscle hypertonia, and upper limb myoclonus, which faded within a few hours. Two days later, acute liver failure occurred, manifested as encephalopathy, jaundice, and a severe coagulopathy. The hepatic damage was thought to be due to the solvent dimethylformamide, which is the only known hepatotoxin included in the preparation utilized in the suicide attempt. High-dose (1.2 g/day) intravenous reduced glutathione was administered, with a rapid improvement of liver function. The patient was discharged after 17 days. Normalization of all liver function tests was achieved within two months. The favorable outcome in this case stands in contrast to the report of a previous case of lethal T61-induced hepatic failure. Although a different amount of dimethylformamide was ingested in each case (0.45 vs 0.60 ml/kg body wt) and individual differences in susceptibility to the effects of the hepatotoxic agent may have played a major role in these two cases, it is not unlikely that the infusion of high doses of glutathione to our patient contributed to her survival and hepatic recovery.
 ...
PMID:Severe hepatic failure occurring with T61 ingestion in an attempted suicide. Early recovery with the use of intravenous infusion of reduced glutathione. 846 75

The selective pharmacology of the selective serotonin reuptake inhibitors (SSRIs) results in a lower potential for pharmacodynamic drug interactions relative to other antidepressants such as the tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs). However, the SSRIs have been implicated in the development of the serotonin syndrome--a potentially life-threatening complication of treatment with psychotropic drugs. The syndrome is produced most often by the concurrent use of two or more drugs that enhance central nervous system serotonin activity and often goes unrecognized because of the varied and nonspecific nature of its clinical features. The serotonin syndrome is characterized by alterations in cognition (disorientation, confusion), behavior (agitation, restlessness), autonomic nervous system function (fever, shivering, diaphoresis, diarrhea), and neuromuscular (ataxia, hyperreflexia, myoclonus) activity. The difference between this syndrome and the occurrence of adverse effects caused by serotonin reuptake inhibitors alone is the clustering of the signs and symptoms, their severity, and their duration. There are important pharmacokinetic interactions between SSRIs and other serotonergic drugs due principally to their effects on the cytochrome P450(CYP) isoenzymes, the potential for which varies widely amongst the SSRI group, which may increase the likelihood of a pharmacodynamic interaction. The exceptionally long washout period required after fluoxetine discontinuation may cause additional problems and/or inconvenience. Patients with serotonin syndrome usually respond to discontinuation of drug therapy and supportive care alone, but they may also require treatment with antiserotonergic agent such as cyproheptadine, methysergide, and/or propranolol. To reduce the occurrence, morbidity, and mortality of the serotonin syndrome, it must be both prevented by prudent pharmacotherapy and given prompt recognition when it is present.
 ...
PMID:Selective serotonin reuptake inhibitor-induced serotonin syndrome: review. 916 67

A 50-year-old man was admitted to our hospital because of disorientation and nocturnal restlessness. The patient presented chronically progressive dementia. No myoclonus or periodic synchronous discharge (PSD) was found over time, with abnormal evidence in MRI-FLAIR (fluid-attenuated inversion recovery) images alone. Brain biopsy and prion protein gene analysis led to the final diagnosis of Creutzfeldt-Jakob disease (CJD) induced by the point mutation at codon 232 (Met to Arg). To date the cases of M232R mutation-induced CJD have been reported to present clinical symptoms and pathological evidences similar to sporadic CJD cases, and differential diagnosis between the types has been believed to be difficult. Our case suggests that some types of CJD induced by point mutation at codon 232 cannot be easily inferred from clinical findings.
 ...
PMID:[A case of codon 232 mutation-induced Creutzfeldt-Jakob disease visualized by the MRI-FLAIR images with atypical clinical symptoms]. 1082 2

Fever is one of the most frequent causes of hospital admission in patients with end-stage renal disease. Lack of an identified source of infection and/or lack of clinical response to the first empirical antibiotic treatment favour the use of broader spectrum antibiotics. The availability of fourth-generation cephalosporins (e.g. cefepime) and the increasing incidence of bacterial resistances to classical antibiotics has increased their use in the clinical practice. We present two cases of non-convulsive status epilepticus in patients with advanced chronic renal failure who received cefepime at doses corrected for the degree of renal function according to the manufacturer's instrument as. The clinical symptoms included shouthough, processes, disorientation, loss of attention, and the later appearance of myoclonus. In both cases the electroencephalogram (EEG) was compatible with non-convulsive epileptic status. After cefepime withdrawal there was a clinical remission of symptoms and normalization of the EEG. It is concluded that cefepime treatment can induce a non-convulsive epileptic status in patients with advanced chronic renal failure. Pharmacokinetic studies are urgently needed to clearly define the appropriate dose of cefepime in patients with advanced chronic renal failure.
 ...
PMID:[Non-convulsive status epilepticus secondary to adjusted cefepime doses in patients with chronic renal failure]. 1121 51


1 2 3 4 Next >>