Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dementia, a syndrome of acquired intellectual deterioration, is an etiologically nonspecific condition that can be permanent or reversible. When evaluating demented patients, a careful exposure history will determine the possible role of drugs, metals, or toxins. Physical examination may reveal focal deficits in cases of intracranial mass lesions and spasticity or ataxia of the lower limbs if hydrocephalus is present. Coexistence of dementia and a peripheral neuropathy usually indicates the existence of a toxic or metabolic disorder. Depressed mood, sleep disturbance, anorexia, impotence, constipation, and psychomotor retardation indicate the presence of a depressive syndrome. Asterixis, myoclonus, and postural tremor are common in toxic-metabolic dementias, whereas resting tremor, choreoathetosis, or rigidity occur in progressive extrapyramidal disorder. EEG is focally abnormal in cases of cerebral mass lesions and shows generalized slowing in toxic-metabolic encephalopathies. CT will aid in the identification of hydrocephalus, subdural hematomas, and intracranial mass lesions. A thorough laboratory evaluation including complete blood count, erythrocyte sedimentation rate, electrolytes, blood urea nitrogen and blood sugar, liver and thyroid function tests, serum calcium and phosphorus levels, B12 and folate levels, serum copper and ceruloplasmin, VDRL, chest X-ray, electrocardiogram, and lumbar puncture may demonstrate treatable disorders that are adversely affecting intellectual function. Elderly individuals are particularly susceptible to the effects of toxic or metabolic disorders, and a mild dementia may be exaggerated by relatively minor fluctuations in metabolic status. Treatable causes of dementia should be sought in all demented patients.
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PMID:Treatable dementias. 635 58

This study was designed to evaluate the clinical tolerance to multiple IM injections of rDNA-produced human alpha-2 interferon (IFN) (Schering-Plough 30500) in patients with solid tumours. IFN was administered in escalating IM doses in separate groups of patients daily for 14 days and then twice weekly for a further 10 weeks. The dosage levels were 1, 3, 10, and 30 million U/injection. Subjective toxicity could be divided into two types, acute and chronic. The acute reactions took the form of an influenza-like syndrome consisting in chills, rigors, headache, tremor, nausea, vomiting, and myalgia. These symptoms were dose-related but tachyphylaxis developed with continued dosing. The chronic toxicity consisted of malaise, lethargy, fatigue, anorexia, and confusion. These symptoms were not so dose-dependent and tended to become more severe with prolonged treatment. Objective toxicity consisted of myelosuppression and liver dysfunction. Granulocyte counts below 1.0 X 10(9)/l were seen in three patients at the 30-million-U level, with platelet counts less than 100 X 10(9)/l in two of these. Elevation of the liver enzymes were seen in all five patients treated at 30 million U, but returned to normal after 1 week without IFN in all but one patient. A tolerable dose (IM) for phase II/III studies lies between 3 and 10 million U for daily scheduling and between 10 and 30 million U for twice-weekly injections.
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PMID:A phase I toxicity study of human rDNA interferon in patients with solid tumours. 646 93

Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.
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PMID:Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation. 663 51

Large intramuscular doses of a water-miscible preparation of vitamin A (500,000 I.U. retinyl acetate/ml), vitamin E (50 I.U./ml) and vitamin D2 (50,000 I.U./ml) were administered to young monkeys (Macacus fascicularis) weighing 1-1.8 kg. At vitamin A doses equivalent to 200 mg retinol/kg or higher, early signs of acute toxicity included yawning, apparent drowsiness, nausea and vomiting, head shaking, neck hyperextension, motor hyperactivity and coordination. These immediate signs were first noted 3-35 minutes after injection. Following apparent recovery at 1-2 hrs, longer term signs of toxicity, such as decreased activity, malaise, drowsiness, loss of appetite, loss of weight, and itchiness of the skin, appeared within 1-6 days, depending on the dose. Monkeys receiving the highest lethal doses became progressively weaker, showed labored breathing, lapsed into a coma, lost simple reflexes and then died. Respiratory failure usually preceded the cessation of heart beat. In some monkeys on a lower but lethal dose, death was preceded by generalized convulsive seizures. The time of onset of the first sign and survival time were inversely proportional to the dosage, but in individual monkeys no correlation existed between onset time and survival time. Female monkeys seemed to succumb faster to a lethal dose than male monkeys. All animals receiving the equivalent of 300 mg retinol/kg died. Under the conditions used, the LD50 was estimated to be 168 mg retinol (560 000 I>U.) per body weight.
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PMID:A lethal hypervitaminosis A syndrome in young monkeys (Macacus fascicularis) following a single intramuscular dose of a water-miscible preparation containing vitamins A, D2 and E. 697 50

The diazepam withdrawal syndrome was studied in 10 patients who had abused the drug for 3 to 14 years. In the previous 6 months their consumption of diazepam had ranged from 60 to 120 mg daily; none had used other drugs during this period. The withdrawal period lasted about 6 weeks. The intensity of the symptoms and signs was high initially, fell during the first 2 weeks, then rose again in the third week, before finally declining. Three groups of symptoms and signs were identified. Group A symptoms occurred throughout withdrawal and included tremor, anorexia, insomnia and myoclonus. Group B symptoms and signs were largely confined to the first 10 days and were those of a toxic psychosis. Group C symptoms reached a peak in the third and fourth weeks of withdrawal and were characterized by sense perceptions that were either heightened or lowered. The symptom groups, the presence of tremor and myoclonus, and the relief of symptoms by a test dose permit diazepam withdrawal to be distinguished from anxiety. The biphasic course of the symptoms is probably related to the pharmacokinetics of diazepam.
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PMID:Diazepam withdrawal syndrome: its prolonged and changing nature. 713 56

In guinea-pigs, the oral and subcutaneous LD50 values were very similar (cf. 0,173 mg/kg over 48 h with 0,116 mg/kg over 24 and 48 h). When dosed subcutaneously, a cumulative effect was observed. Intravenous administration of cotyledoside to anaesthetized guinea-pigs resulted in: dyspnoea, increased heart rates and blood pressures, and electrocardiagraphic changes typical of cardiac glycoside poisoning. A positive cardiac inotropic effect was succeeded by a positive chronotropic one. In sheep, acute and subacute intoxication resulted in ruminal, respiratory and cardiac changes. The signs included ruminal stasis, cyanosis, cardiac arrhythmia, ectopic foci and AV dissociation, followed by hypotension and progressive respiratory and cardiac failure. The skeletal muscles were affected in only 1 sheep vide infra. In chronically intoxicated sheep typical clinical signs of "krimpsiekte" developed, e.g. weakness, reluctance to stand, unsteadiness on feet, tremor and paresis of hindquarter muscles, paresis of the neck, arching of the back and standing with the feet close together. Respiratory function was affected in all 3 cases; ruminal stasis, with concomitant loss of appetite occurring in one, and a transient change in heart function in another. The syndrome induced by acute cotyledoside poisoning is similar to that of other cardiac glycosides, but the paretic signs of chronic intoxication resemble "krimpsiekte", a disease associated only with intoxication with the plants of the family Crassulaceae.
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PMID:Studies on South African cardiac glycosides. II. Observations on the clinical and haemodynamic effects of cotyledoside. 718 41

A 69-year-old woman was admitted because of severe dehydration due to anorexia. Consciousness disturbance was found to be due to severe abnormalities of serum electrolyte balance, but recovered quickly by correcting the hyperosmolality. While the initial serum sodium value of 186 mEq/L was corrected to 139 mEq/L in 5 days, locked-in syndrome, bilateral hand tremor and tetraparesis appeared. Brain magnetic resonance imaging (MRI) revealed symmetrically high signal intensity areas on T2-weighted images and low signal intensity areas on T1-weighted images in central part of pons and bilateral middle cerebellar peduncles. One and a half month later, these neurologic symptoms were improved and the MRI abnormalities also disappeared. Auditory brain stem responses which showed prolongations of III to V wave peak to peak latency at the onset returned to normal. It is noted in this case that central pontine myelinolysis (CPM) and extrapontine myelipolysis (EPM) appeared during the period of rapid correction of hypernatremia. Although it is known CPM and EPM are caused by hypernatremia or the rapid correction of hyponatremia, there has been reported only one case of CPM and EPM after rapid correction of hypernatremia. According to the hypothesis of Norenberg, rapid rise in serum sodium may cause CPM and EPM, but if CPM and EPM are caused by the rapid correction of hypernatremia in this case, CPM and EPM may be caused by another pathogenesis of the disorder.
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PMID:[A case of central pontine myelinolysis and extrapontine myelinolysis during rapid correction of hypernatremia]. 772 94

External application of picoTesla range magnetic fields (MF) has been reported recently to be efficacious in the treatment of patients with Parkinson's disease (PD) including those who manifest levodopa-related dyskinesias. In the present communication, we present four additional Parkinsonian patients who showed, within a brief period of time, marked improvement in motor symptoms after therapy with MF. Three of the patients had been maintained on antiParkinsonian medication during treatment with MF while the fourth patient had never received pharmacotherapy. Improvement with magnetic therapy was noted not only in the motor sphere (resting tremor, gait apraxia, postural instability), but also in nonmotor aspects of the disease including mood, sleep, pain, anorexia, autonomic, and cognitive functions attesting to the unique efficacy of external picoTesla range MF in the treatment of Parkinsonism. Poverty of facial expression (hypomimia, "masked facies"), which correlates with the degree of striatal dopaminergic deficiency, is one of the clinical hallmarks of PD reflecting the severity of hypokinesia and rigidity in the orofacial musculature. In this report, we emphasize the effects of MF on the hypomimia of PD and provide visual documentation illustrating the changes in the patients' facial expression which follow treatment with MF.
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PMID:Further observations on the unique efficacy of picoTesla range magnetic fields in Parkinson's disease. 808 4

Between January 1982 and December 1989 more than 5,000 clinical cases of bovine parasitic otitis were examined. Clinical signs were mild in early cases and were characterised by dullness, anorexia and occasional head shaking, but were severe in long standing cases where the major presenting clinical signs were dark brown aural discharges which soiled the hair below and in front of the ear, emaciation, central nervous signs, recumbency and death.
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PMID:Clinical observations on bovine parasitic otitis in Tanzania. 846 37

To obtain some insight into the toxicity of paraquat (PQ) in humans, PQ dichloride at 250 ppm in the diet was administered to both normal (NO) rats and ODS-od/od (OD) rats which are unable to synthesize ascorbic acid (AsA). Firstly, OD rats and NO rats treated with PQ were compared with untreated NO rats (CO). Only OD rats displayed several symptoms of PQ poisoning such as anorexia, hypokinesia, diarrhea, epistaxis, tremor and their pili became rough about 9 days after. Their cysteine proteinase inhibitor level in plasma and lung increased to 2- and 6-fold, respectively, of CO. In contrast, NO rats treated with PQ resembled CO rats, and their cysteine proteinase inhibitor levels were unchanged until 11 days. After this period they began to display symptoms. Secondly, OD rats fed with different amounts of AsA were compared. Excess AsA delayed the onset of symptoms by only 1 day. Thirdly, the day of onset of symptoms was found to be influenced with the weight of rats.
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PMID:Effect of dietary paraquat on a rat mutant unable to synthesize ascorbic acid. 882 87


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