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

30 patients with delirium tremens were given in a double-blind trial--beside the basic treatment with chlormethiazol (Distraneurin)--aprotinin (Trasylol) or placebo. Duration of the delirium and the amount of chlormethiazol used were the criteria for successful treatment. It was shown that the additional application of aprotinin did neither shorten significantly the duration of the delirium not save the amount of chlormethiazol used. Methodologically, special attention was given to the question of duration of the delirium and of registering symptoms. A delirium-rating scale was devised and its analysis showed a good randomization of the items. One main question was as to what extent the individual items were good indicators of a delirium. An item intercorrelation showed that there were two clusters of symptoms: psychological and sympathetic nervous system symptoms. It could be shown that the items 'consciousness, orientation, hallucinations and short-term memory' were good indicators of the delirium, while items of the autonomous nervous system, as tremor of hands and body, facial muscular twitching and exteroceptive reflexes, were less indicative of delirium. The duration of the delirium seems to be the best criterion for the question as to whether a drug is effective or not in delirium tremens. There is a highly significant correlation between the degree of the severity of the delirium and its duration. Other significant predictors for the severity of the delirium were the maximal pulse rate and change in blood pressure. Age, duration of alcoholism and psychological or physical depravation showed no influence on the duration of the delirium.
 ...
PMID:[Criteria of the efficacy of therapeutic measures in alcoholic delirium. Study on the effectiveness of aprotinin in alcoholic delirium]. 80 70

The authors review the literature describing the neural symptoms induced by tricyclic antidepressants, especially tremor, seizures, akathisia, myoclonus, dyskinesia and delirium. Sedation, modifications of sleep, memory and appetite are also described. Tremor and myoclonus are the most frequent drug-induced neural symptoms. Delirium is most often caused by high-dosage treatments. The pathophysiology of akathisia and dyskinesia raises important questions concerning the mode of action of antidepressants.
 ...
PMID:Neural symptoms induced by tricyclic antidepressants: phenomenology and pathophysiology. 131 56

We report a 41-year-old male of citrullinemia associated with argininosuccinate acid synthetase deficiency. He was admitted to the Hitachi General Hospital because of finger tremor, restlessness and urinary incontinence. He had short stature and a poor appetite. Laboratory evaluation was summarized as follows: mild hypoglycemia, low plasma cortisol levels, delayed response of 17-OHCS and 17-KS to ACTH administration in urine, and delayed response of plasma ACTH level to insulin administration. In this case, ACTH deficiency is estimated to be a dysfunction of the hypothalamus. Replacement therapy of hydrocortisone improved his symptoms. He was readmitted to the hospital because of delirium and confusion, two weeks after the hydrocortisone administration. At that time, he had flapping tremor. Laboratory examination revealed hyperammonemia (NH3: 231 micrograms/dl) and mild elevation of GOT and GPT. Serum and urinary amino acid determination showed marked elevation of citrulline (478.1 nmol/ml in serum, 4681.2 mumol/day in urine). Lactulose administration, low protein diet and plasmapheresis were started, but he went into a coma. Without any improvement, he died on the 29th hospital day. Autopsy examination of the liver disclosed fatty change. Adrenal cortex depicted severe atrophy. Biochemical analysis of urea cycle enzymes of the liver and kidney showed decreased activity of argininosuccinate synthetase (liver: 0.0022 U/mg protein, 5% of that normal liver, kidney: 0.003 IU/mg protein, 20% of that in normal kidney). Citrullinemia associated with ACTH deficiency have not reported in the literature. It may be presumed that ACTH deficiency is concerned with the delayed onset of hyperammonemia. The relation between citrullinemia and endocrinological abnormalities is also discussed.
 ...
PMID:[A case of citrullinemia associated with isolated ACTH deficiency, rapidly developing coma]. 133 25

An autopsy case of ataxic form of Creutzfeldt-Jakob disease (Brownell and Oppenheimer, 1965) was reported. The patient, a 71-year-old male, noticed ataxic gait at the beginning of June in 1988, and was admitted to the Hiroshima City Hospital for the neurological examination at the end of June. He showed ataxia of the left arm and legs and diplopia. Gradually he became delirious at night. On July 16, tremor-like involuntary movement of the left hand was noticed. On July 20, he became somnolent and doubly incontinent. Myoclonus and paratonic rigidity were also observed. The EEG showed periodic synchronous discharge on July 25. The brain CT and MRI were normal. He became apallic gradually and died on October 28. The duration of illness was 5 months. At autopsy, brain weighed 1000gr. Cerebral atrophy and slight enlargement of the ventricles were observed. The cerebellum was also slightly atrophic. Histologically, the destruction of the cerebral cortical layer, slight sieve-like spongy state of the neuropil, slight neuronal loss of the thalamus and sieve-like spongy state of the striatum were observed. The cerebellar lesion was the most severe, where granular cell loss and gliosis of the cortex were observed.
 ...
PMID:[An autopsy case of ataxic form of Creutzfeldt-Jakob disease]. 156 39

A case is reported in which tocainide, a relatively new cardiac antiarrhythmic for oral use, is believed to have caused a delirium. The patient had been admitted to a coronary intensive care unit for the treatment of ventricular arrhythmia and had developed confusion, impairment in concentration and severe anxiety. Her EEG was compatible with metabolic encephalopathy. The clinical picture varied with the use of tocainide so closely that it appeared to be the most likely cause of the delirium. Other factors were taken into consideration but did not seem to adequately disprove this impression. Tocainide has been known to cause minor, transient and treatable side effects in the form of gastrointestinal and central nervous symptoms--mainly nausea, tremor and dizziness. There have also been three case reports of paranoid psychoses. It is suggested that psychiatrists be aware of the above complications as they may have occasion to see patients taking tocainide, especially in consultation-liaison work. A table with the more common side effects and their frequencies is included.
 ...
PMID:Mental changes associated with tocainide, a new antiarrhythmic. 310 61

A mixture containing 3 g of boric acid and 300 mg of cinchocaine chloride prescribed due to painful dental protrusion was accidentally ingested by a 12-month-old girl. She developed violent vomiting and coughing. Irritability, tremor, seizures and a delirious reaction. She was treated with diazepam, intubated, sedated and ventilated. Her diuresis was stimulated with furosemide and fluid. Within the first 24 h she was treated with haemodialysis twice on femoral catheters. Her renal function was unaffected. In two days she fully recovered. The maximum measured levels of boric acid and cinchocaine chloride approximately 6 h after ingestion were 26 micrograms/ml and 71 ng/ml respectively. The plasma half-life of boric acid was 7.0 h and decreased to 3.6 and 4.4 h during the two haemodialyses. The total body clearance of boric acid increased correspondingly from 21 ml/min to 41 and 34 ml/min. The in vitro clearance of boric acid of the dialyser was later determined to be 18 ml/min. It is concluded that haemodialysis is valuable in the treatment of boric acid intoxication because it increases the elimination of the drug even in patients without any sign of renal toxicity.
 ...
PMID:Combined boric acid and cinchocaine chloride poisoning in a 12-month-old infant: evaluation of haemodialysis. 337 4

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
 ...
PMID:Pathogenesis of dialysis encephalopathy. 636 3

Five adults were treated successfully for severe theophylline poisoning due to intentional overdosage. Clinical features included nausea, tremor, delirium, hypotension and cardiac arrhythmias, metabolic acidosis, hyperglycemia, hypokalemia and hypophosphatemia. No seizures or deaths occurred despite very high serum theophylline concentrations (between 96 and 194 mug per ml). Extreme elevations of plasma catecholamines were documented and are implicated in the toxicity. beta-Blockade with intravenous administration of propranolol hydrochloride was the most effective therapy for theophylline-induced hypotension. All patients were treated with resin hemoperfusion, which resulted in significant clinical improvement and rapid lowering of the serum theophylline level.
 ...
PMID:Use of beta-blockade and hemoperfusion for acute theophylline poisoning. 650 85

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
 ...
PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

Cats were treated for 35 days with flurazepam, 5 mg/kg per day. The drug was administered through a gastric fistula. Ro15-1788, a benzodiazepine antagonist, caused an abstinence syndrome when administered through the gastric fistula 24 h after the last dose of chronic treatment. Abstinence signs included increased muscle tone, tremor, piloerection, pupillary dilation, panting, and excessive salivation. Neither convulsions nor delirium was seen. Severity of abstinence was similar after Ro15-1788 doses of 2-100 mg/kg, but lasted longer (8-10 h) after the higher dose. Readministering Ro15-1788 a week after the end of chronic treatment precipitated an attenuated abstinence syndrome, but was inactive after 2 weeks.
 ...
PMID:An antagonist-induced benzodiazepine abstinence syndrome. 681 Dec 90


1 2 3 4 5 6 Next >>