Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

80 strictly selected patients with chronic renal insufficiency with plasma creatinine values of 1.4--14.5 mg% were examined according to a fixed scheme to determine the presence of symptoms and signs of renal encephalopathy. The general cerebral symptoms complained of were headache in 33.4% of the patient material, dizziness in 30.3%, easy fatigability in 62.5%, giddiness in 18.8% and insomnia in 37.5%. The most prominent neurological findings were hyperactive deep reflexes in 30% and action tremor in 23.8%. The symptoms of organic brain syndrome were impairment of memory in 32.5%, weakness of concentration in 28.8% and lability of affect in 63.7%. Diffuse EEG abnormalities were found in 26.2%. While the clinical neuropsychiatric symptoms did not show any statistically significant correlation with the various internal medical data, a trend was observed in the greater number of pathological EEGs with an increase in the impairment of renal function. Furthermore, there was a statistically significant correlation, (alpha less than or equal to0.015) between the occurrence of pathological EEGs and the plasma creatinine and BUN values. It is remarkable that the patients with abnormal EEGs had a relatively low mean creatinine level of 5.89 mg%. The strict dietetic management of the patients is regarded as one of the deciding factors for the relatively low frequency of neuropsychiatric symptoms in the material studied.
 ...
PMID:Neuropsychiatric symptomatology with chronic renal insufficiency in the stage of compensated and decompensated retention. I. CNS disturbances. 5 91

Two hundred and twenty three cases of acute carbon monoxide poisoning were observed during acute stage and followed-up subsequently for three months. Through single factor and multiple factors analyses, six out of 97 observed factors were demonstrated as risk factors for the development of delayed encephalopathy, namely, elderliness, mental work, previously with hypertension, coma lasting for 2-3 days, long standing dizziness and fatigue after regaining consciousness and mental stimulation during recovery. Based on these factors, a regression equation for predicting the probability of developing delayed encephalopathy in individual patient with acute carbon monoxide poisoning has been established In order to minimize the development of delayed encephalopathy, it is advisable to keep the patients of acute carbon monoxide poisoning with above mentioned related factors under constant monitoring and surveillance.
 ...
PMID:[Related factors for the development of delayed encephalopathy following acute carbon monoxide poisoning]. 160 69

A 38 year-old laborer experienced solvent intoxication during each of two spray paintings of a dump truck and other heavy equipment in an enclosed, unventilated garage. The paint base consisted primarily of toluene and methyl ethyl ketone. Nausea, headaches, dizziness, respiratory difficulty and other symptoms began after exposures. Over the next several days he developed impaired concentration, memory loss and cerebellar signs including an intention tremor, gait ataxia and dysarthria. MRI of the brain and EGG early in the work-up were normal, although later MRIs demonstrated fluid collection over the left parietal area. Examination by a toxicologist and neurologist revealed likely toxic encephalopathy with dementia and cerebellar ataxia. Three formal neuropsychological assessments over 2 1/2 years quantified cognitive, motor and behavioral changes. Despite similar findings in chronic exposure to these solvents, lasting sequelae following acute exposure have not been widely reported.
 ...
PMID:Chronic neuropsychological and neurological impairment following acute exposure to a solvent mixture of toluene and methyl ethyl ketone (MEK). 174 49

The purpose of this review has been to discuss human and environmental factors which may influence the acute irritative and neurotoxic effects of organic solvents. The review is based on a field study and on four human experimental studies. Several studies have shown that printers and other workers exposed to mixtures of solvents experience an increased frequency of work related irritative and neurological symptoms although the exposure has been far below the occupational exposure limits. A series of controlled human exposure studies was carried out. Different groups of persons were exposed to the most frequent solvent, toluene. Toluene in alveolar air and the urinary excretion of the metabolites were measured and the acute effects of toluene were assessed by the performance in a series of test of the perceptual and psychomotor functions as well as a standardized registration of annoyance and symptoms. The pharmacokinetics of toluene is complex and there is a large individual variation in the excretion of the metabolites. This variation can only to a limited extend be related to known variables. Intake of alcohol during exposure inhibits the metabolism of toluene and increases the internal dose. Normal therapeutic doses of cimetidine or propranolol have no measurable effect on toluene metabolism. Exposure to 100 ppm during 7 h causes irritation in the eyes and airways as well as feeling of intoxication, dizziness, and headache. There are signs of impairment in the performance in test concerning visual perception, colour vision, vigilance as well as the psychomotor functions. However, the influence on the performance tests was not seen in all studies. Variations in the air concentration of toluene with peaks op to 300 ppm causes fluctuation in the alveolar concentrations, but no acute effect of these peaks or of increased physical activity during exposure could be detected. However, the importance of peek concentrations and of workload for the development of chronic solvent encephalopathy is still unknown. The influence of a 9-25 years occupational exposure to solvents was investigated. A group of printers occupationally exposed to mixtures of solvents were compared with a matched unexposed control group. There was no difference between printers and controls in the performance in the psychological test, but in two of the tests there were tendencies to increased sensitivity to toluene in the group of printers. It is concluded that exposure to toluene corresponding to the occupational limit in several countries cause irritative and prenarcotic symptoms and possibly a lowered performance.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Human solvent exposure. Factors influencing the pharmacokinetics and acute toxicity. 203 Oct 44

D-Lactate-associated encephalopathy is a rare clinical syndrome characterized by dizziness, ataxia, confusion, headaches, memory loss, lethargy, and aggressiveness which may progress to frank but reversible coma. It occurs in patients with profound dysfunction of the short-bowel syndrome and is believed to result from massive carbohydrate malabsorption with resultant over-production of D-lactate and other organic anions by the colonic flora. Extremely elevated serum levels of D-lactate (but not L-lactate) confirm the diagnosis, but currently D-lactate is not clearly established as the putative neurotoxin. We describe a patient who repeatedly developed D-lactate encephalopathy after surgical removal of nearly the entire jejunum and ileum. Markedly elevated D-lactate serum levels were documented during an encephalopathic episode. Potential pathophysiologic mechanisms and the treatment rationale are discussed.
 ...
PMID:D-lactate-associated encephalopathy after massive small-bowel resection. 276 Apr 34

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

Sixty-two patients with chronic toxic encephalopathy diagnosed in 1976-1981 were considered for reexamination in 1983-1984. Thirteen were found to have other diseases that might contribute to brain dysfunction. Seventeen were unwilling or unable to participate. The final group consisted of 32 men 33 to 63 (median 55) years of age who were physically and psychometrically reexamined with the same methods used in the initial investigation. The interval between the first and present examination was 21-88 (median 48) months, and exposure to solvents had ceased. The subjects reported some improvement in their neurasthenic problems. In particular they suffered less from fatigue, headache, and dizziness. When diagnosed they had an average of seven out of ten typical neurasthenic symptoms included in the toxic encephalopathy syndrome. At the time of the follow-up the mean number of symptoms had decreased significantly to five. The psychometric retesting showed significant deterioration in verbal memory, improvement in visual memory, and unchanged results on the other tests. In conclusion, these toxic encephalopathy patients improved subjectively when exposure stopped. Psychometrically they performed very close to the initial testing, which excluded progressive brain disease or subacute pharmacological solvent intoxication.
 ...
PMID:Prospective clinical and psychometric investigation of patients with chronic toxic encephalopathy induced by solvents. 335 95

In patients with portal hypertension and tense ascites, large-volume paracentesis improves patient comfort and may improve systemic hemodynamics. However, it has been avoided in nonedematous patients because of concern for complications, including intravascular volume depletion. In this study, 12 nonedematous patients with chronic liver disease, portal hypertension and tense ascites underwent 14 large-volume (5-liter) paracenteses for the relief of discomfort and/or respiratory distress. Plasma volume was measured directly by a dilution method with 125I-labeled human serum albumin prior to and at 24 or 48 hr after 13 of the paracenteses. All patients felt better postparacentesis. No dizziness, hypotension, tachycardia, encephalopathy or change in mean serum sodium, creatinine or blood urea nitrogen occurred. Two patients experienced a decrease in hematocrit, which was not explained by blood loss or increase in plasma volume. Mean plasma volume was 3,713 +/- 129 ml (55.1 +/- 1.5 ml per kg ideal body weight) preparacentesis and 3,684 +/- 136 ml postparacentesis, the difference being -0.78% (p = 0.48, NS). Our results suggest that 5-liter paracentesis in nonedematous patients with tense portal hypertension-related ascites improves patient comfort and is not associated with a decrease in measured plasma volume.
 ...
PMID:Large-volume paracentesis in nonedematous patients with tense ascites: its effect on intravascular volume. 335

Fifty-four consecutive patients were treated with amiodarone for symptomatic ventricular tachycardia or ventricular fibrillation refractory to treatment with conventional antiarrhythmic drugs. A reversible neurologic syndrome of tremor, ataxia, and occasionally peripheral neuropathy without nystagmus, dizziness, encephalopathy, or long-tract signs developed in 54% of the patients and was the most common reason for altering or discontinuing drug therapy. Neurologic side effects improved or resolved within 2 days to 4 weeks of decreasing or discontinuing amiodarone. Frequent neurologic toxicity is a hitherto undescribed complication of amiodarone therapy. Wider recognition of this syndrome will avoid unnecessary and costly diagnostic evaluation.
 ...
PMID:Frequent neurologic toxicity associated with amiodarone therapy. 653 58

A short review is given of the pharmacokinetic characteristics and side effects of the nitroimidazoles: metronidazole, tinidazole and ornidazole. The drugs are well absorbed from the gastrointestinal tract, maximum plasma levels generally being obtained 1 to 4 h after oral intake. Metronidazole has been shown to be absorbed after rectal administration; vaginal absorption is documented for all three drugs. The nitroimidazoles are widely distributed in the body, cross the placenta and appear in breast milk. Therapeutically effective concentrations of e.g. metronidazole have been demonstrated in e.g. the central nervous system, middle ear discharges, bile, peritoneal fluid, and fluids and tissues of the female genital tract. The binding to plasma proteins is less than 20%. Available data suggest that the elimination half-lives of these drugs differ, being 7-8 h for metronidazole, about 12 h for tinidazole and 14-15 h for ornidazole. Both metronidazole and ornidazole, but not tinidazole, seem to be extensively metabolized before elimination. The nature and frequency of adverse reactions to this drug include encephalopathy in a few patients treated with doses between 5 and 10 g daily as an adjunct to radiotherapy, and peripheral neuropathy observed in patients treated for prolonged periods with high doses. Among the common side effects of the nitroimidazoles are symptoms from the gastrointestinal tract such as nausea, anorexia, vomiting and metallic or bitter taste. Dizziness, ataxia and headache have been reported. When given together with alcohol, a disulfiram-like intolerance reaction can be obtained.
 ...
PMID:Pharmacokinetics of nitroimidazoles. Spectrum of adverse reactions. 694 57


1 2 3 4 5 6 7 8 Next >>