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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulatory regulation in response to postural changes follows mechanical rules, whereby the shifts in volume in the various organs of the body play an essential role. The change from the horizontal to the vertical position is accompanied by a decrease in pressure above the hydrostatic neutral point, i.e. in the cephalic vessels, whereas the capacious vessels in the caudal region are dilated and the venous return becomes sluggish. As a consequence of the different time courses followed by the various circulatory parameters in the wake of counter-regulatory measures, a distinction can be made between an early orthostatic instant regulatory response and a late orthostatic response. Prominent clinical features do not necessarily always consist of non-systemic dizziness, tinnitus, pallor cold sweat and, finally, orthostatic collapse, but general subjective symptoms such as deafness and tingling of the extremities, a chilly sensation and cardiac symptoms may frequently predominante. In the case of development of an autonomic neurotic symptom complex, psychoautonomic symptoms such as general sleep disturbance are observed. Apart from investigations carried out on a surgical tilting table in general practice, other procedures such as the Valsalva manoeuvre, the squatting test and, in most cases, the erect test are performed. Broadly speaking four different reaction types can be distinguished amongst cases of postural hypotension. Drugs with different therapeutic actions are selectively administered according to the pathophysiological characteristics of the individual patient and the sympathetic adrenal counter-regulatory response. Medico-mechanical measures and physical training should not be neglected.
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PMID:[Postural hypotension: pathophysiology and clinical features (author's transl)]. 1 41

Various reports have associated intravenous prostaglandins with gastrointestinal side effects. It is possible that prostaglandins may also cause contraction of the human gallbladder and precipitate side effects in patients with gallbladder disease. To find out, the authors studied the effects of prostaglandin E2 (PGE2) on the radiological size of the gallbladder during oral cholecystography with 16 g. of Solu-Biloptin (calcium ipodate). PGE2 was slowly injected, under fluoroscopic observation of the gallbladder, in 12 patients (8 female and 4 male) who had no signs of gallbladder disease in films taken before a fatty meal was given. The PG was given in doses of 20 mcg, 50 mcg, and 75 mcg (4 patients in each dose group). New films were taken 15 minutes and 30 minutes after PG injection. An ordinary fatty meal (200 ml of cream) and a 4th set of films was taken 30 minutes later. Previously described radiography and measurement of gallbladder volume were undertaken, and spontaneously reported side effects recorded. Intravenous PGE2, regardless of dose, did not change the form or size of the gallbladder. After the fatty meal, gallbladder contraction was the same as in untreated patients. The 50 mcg dosage resulted in temporary distress in 1 patient, while the 75 mcg dosage caused dizziness, nausea, and collapse in 3 patients. There was no reported side effects after the fatty meal. It was concluded that clinical doses of PGE do not cause gallbladder contraction, nor do they interfere with normal response of the gallbladder to a fatty meal.
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PMID:Letter: Intravenous prostaglandin and the gallbladder. 4 17

The authors describe side effects of Dimer X radiculography after premedication. The side effects in a study of hundred patients are divided in early complications (during the examination : dizziness, radicular pains and collapse) and in late complications (noted during the first day following the examination : headache, meningismus, myocloni, epileptic seizure, cauda syndrome, increase of radicular pains). After premedication with tiapride the rate of dizziness is decreased, the rate of headache is not diminished, but the headaches are very slight. Nausea and vomiting are suppressed by the premedication.
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PMID:[Secondary effects of Dimer X radiculography after premedication. A study of hundred patients (author's transl)]. 22

During Ramadan, Moslems are required strictly to avoid fluids and nourishment from dawn to sunset. Heat stress during such abstinence represents a substantial health hazard. In the Federal Republic of Germany (FRG) where numerous Moslems, particularly of Turkish origin, perform heat work and other heavy labour, we observed moderate to severe health disturbances in such labourers during Ramadan, e.g.: tachycardia, severe headaches, dizziness, nausea, vomiting and circulatory collapse. The severe dehydration of these workers was demonstrated by substantial increases in their hematocrit, serum protein, urea, creatinine, uric acid and electrolyte imbalance. Because of the evidence of the substantial health hazard to Islamic workers in such situations, we have strongly urged employers to refrain from assigning Islamic workers to heat work or heavy daytime work during Ramadan; we have therefore limited systematic studies of health problems during Ramadan to persons performing only moderate work. Even under these conditions signs of dehydration were found in the 32 labourers monitored. Some of these labourers also had to interrupt their observance of Ramadan due to health problems, e.g.: acute gout due to serum uric acid increase, or circulatory insufficiency. In light of the observed potentially harmful pathophysiological effects, the danger of dehydration of Islamic workers due to heat work during Ramadan should be taken very seriously.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The health risks of occupational stress in islamic industrial workers during the Ramadan fasting period. 181 40

Mortality from coronary artery disease is a common problem in treated hypertensive patients, and these people have a high prevalence of elevated cholesterol levels. A study was undertaken to determine whether cholesterol could be lowered effectively without major side effects in patients with treated hypertension. Forty-nine patients (mean age 67.6 years) with cholesterol greater than 5.5 mmol/l were placed on a reduced-fat (less than 30% of calories from fat with a ratio of polyunsaturated to saturated fats of less than 1) diet for 3 months. If the cholesterol was between 5.5 and 7.5 mmol/l and total cholesterol divided by high-density lipoprotein cholesterol was greater than 4.5, the patients were randomly allocated either to the simvastatin (24 patients) or the placebo group (25 patients). Diet and placebo caused minor and insignificant falls in cholesterol and no change in triglycerides or lipids. Treatment with simvastatin reduced cholesterol levels from 6.85 to 4.75 mmol/l (P less than 0.001), triglycerides from 2.7 to 2.1 mmol/l (P less than 0.01), low-density lipoproteins from 4.6 to 2.6 mmol/l (P less than 0.001) and high-density lipoproteins rose from 1.09 to 1.18 mmol/l (P less than 0.01). Total cholesterol divided by high-density lipoprotein cholesterol fell from 6.3 to 4.0 (P less than 0.001). The drug was well tolerated and the side-effect profile did not differ from the placebo in clinical or biochemical events. The active drug was stopped in one patient (abdominal pain, dizziness, headache, tiredness) and in two patients taking the placebo (elevated creatine phosphokinase, cardiovascular collapse). Simvastatin effectively lowered total cholesterol and improved the lipoprotein profile. The dose required in most patients was 40 mg/day. Simvastatin may be an acceptable drug to improve the lipoprotein profile in order to determine whether this improves the prognosis in patients treated for hypertension.
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PMID:Simvastatin in the treatment of hypercholesterolaemia in patients with essential hypertension. 233 14

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Normal cochlear function was preserved in a patient after excision of the membranous canal from a huge fistula at revision surgery eight years after the primary procedure. A recurrent cholesteatoma had eroded the entire prominence of the horizontal canal and surrounded its membranous portion. The cholesteatoma, including the membranous canal, was removed in a one-stage procedure. The open ends of the bony canal were sealed with a fascia soaked in fibrin glue. After initial dizziness and severely reduced hearing, the patient quickly recovered, with normal bone conduction and a stable 30-dB hearing level by air conduction. The lumen of the membranous canal was patent, and only the ampullar end was atretic. Presumably, the fistula became separated from fluid spaces by formation of perilymphatic partitions and by collapse of the membranous labyrinth adjacent to the fistula.
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PMID:Preservation of hearing after removal of the membranous canal with a cholesteatoma. 374 67

A study of 20 asymptomatic elderly people living at home or in residential care and 20 symptomatic elderly subjects (with falls, 'collapse', dizziness, 'funny turns' etc.) revealed that cardiac arrhythmias are common in both groups. Only three of the asymptomatic group and two of the symptomatic group had sinus rhythm throughout their 24-hour electrocardiographic recordings. In the symptomatic group, the arrhythmias bore no relation to the symptoms. Clinical follow-up of up to 6-9 months revealed that elderly people with rhythm abnormalities noted on 24-hour electrocardiographic recording do not develop symptoms.
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PMID:Cardiac arrhythmias in the elderly. 710 71

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

A 68-year-old female on two-year chronic hemodialysis for chronic renal failure due to chronic pyelonephritis, was admitted to hospital for weakness, dulled sensorium and dizziness. On examination the patient was in a state of circulatory collapse, the electrocardiogram showed an accelerated idioventricular rhythm and laboratory analysis revealed extreme hyperkalemia (K+ 10.1 mmol/l). There were no common causes of shock, such as hypovolemia, sepsis, heart failure and presence of vasodilator drugs. The patient was treated with calcium gluconate, sodium bicarbonate and sodium chloride (to oppose the effects of hyperkalemia on the cell membrane to minimize cardiac and neuromuscular toxicity), insulin and dextrose (to increase the transport of K+ from the extracellular to the intracellular compartment), and hemodialysis (to remove K+ from the body). At the end of the hemodialysis session, the patient was in a clinically good condition, blood pressure was 160/90 mm Hg and the serum K+ concentration was normal. The case appeared to suggest that extreme hyperkalemia may have direct effects on vascular resistance, causing hypotension and shock.
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PMID:A life-threatening complication of extreme hyperkalemia in a patient on maintenance hemodialysis. 748 41


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