Gene/Protein Disease Symptom Drug Enzyme Compound
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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

Symptoms of poisoning occurred in 19 persons in the Rhein-Main region in October 1976, after they had eaten mussels (Mytilus edulis) imported from Vigo, Spain. Mild oral paraesthesias, tingling in the fingertips and feet were followed by generalised numbness and dizziness. All symptoms disappeared within 48 hours. They had been caused by saxitoxin which is produced by a dinoflagellate and accumulated in the mussels, as confirmed by testing confiscated samples of mussels. Toxin concentration ranged from 6000 to 20 000 MU (mice units) per 100 g mussel meat.
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PMID:[Poisoning after ingestion of mussels (mytilus edulis) (author's transl)]. 89 97

Two groups of patients treated by short (Milan) and long (Newcastle) haemodialysis were compared for incidence of symptoms and biochemical control. Short dialysis corrected urea and creatinine as well but control of potassium and phosphate were similar. The only apparent penalties to be paid by short dialysis patients were a higher incidence of itching, tingling or numbness, impairment of vibratory sense and difficulty in controlling blood pressure. The short dialysis group had higher haemoglobin and less dyspnoea, muscle weakness and dizziness after dialysis.
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PMID:A comparison of short and long haemodialysis. 93 42

Ammonium persulfate is widely used to "boost" peroxide hair bleaches. These persulfates can produce a variety of cutaneous and respiratory responses, including allergic eczematous contact dermatitis, irritant dermatitis, localized edema, generalized urticaria, rhinitis, asthma, and syncope. Some of these reactions appear to be truly allergic while others appear to be due to the release of histamine on a nonallergic basis. Patch tests may be performed with 2% to 5% aqueous solution of ammonium persulfate. Scratch tests may result in asthma and syncope. In some patients, merely rubbing a saturated solution of ammonium persulfate into the skin will evoke a large urticarial wheal. Hairdressers should be made aware that these ammonium persulfate hair bleach preparations may provoke severe reactions and should seek medical attention if the client complains of severe itching, tingling, a burning sensation, hives, dizziness, or weakness.
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PMID:Persulfate hair bleach reactions. Cutaneous and respiratory manifestations. 96 35

Major findings from our work on exposures and effects from organophosphate-containing pesticides in selected occupational and community patients and groups in Israel are reviewed as a basis for recommending control measures. The worker groups were pilots, ground-crews, and field workers; exposed nonworkers were adults and children living in kibbutzim with drift exposures, and household residents in houses treated by pest exterminators. In all groups, evidence of exposure-illness associations was found even though persons with acute poisoning were not seen. Complaints (headache, dizziness, fatigue, nausea, breathing problems, abdominal cramps, and tingling in extremities) were associated with within-normal depressions in cholinesterase activity. Whole blood and plasma cholinesterase activity were slightly more sensitive indicators of mixed exposure than red blood cell cholinesterase activity. High alkyl phosphate levels and symptoms were seen in individuals with within-normal limit depressions in cholinesterase activity. Complaints of weakness and tingling in hands and feet, together with low-grade changes in nerve conduction, suggest the possible influence of agents with a neurotoxic esterase-type activity independent of cholinesterase activity. Transient in-season neuropsychological changes in tests of mood status and performance were associated with exposure. Recommendations for exposure reduction include: accelerating the already declining use of pesticides in general, and organophosphates in particular; promoting the shift from more to less toxic organophosphates and other pesticides; and introducing rigid performance specifications for closed systems in loading and mixing at end-user sites. Dermal protection remains a problem. Cholinesterase activity levels and symptom interviews are useful for monitoring workers at risk, but alkyl phosphate levels are the definitive measure of exposure, surveys, investigations and surveillance.
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PMID:Health effects from exposure to organophosphate pesticides in workers and residents in Israel. 133 Sep 77

Sumatriptan succinate, a 5-HT1D receptor agonist, constricts human cranial arteries. Two parallel-group trials for treatment of acute migraines were conducted in the United States. Adult patients were randomized and given either 6 mg of sumatriptan succinate subcutaneously (n = 734) or placebo (n = 370). At 1 hour, sumatriptan was significantly more effective than placebo in reducing moderate or severe headache pain to mild or no pain (70% vs 22%), in completely relieving headaches (49% vs 9%), and in improving clinical disability (76% vs 34%). Sumatriptan also reduced nausea and photophobia significantly better than placebo. Patients with residual migraines received another injection; those who had originally received sumatriptan received either a second active injection (n = 187) or placebo (n = 178), while those who had received placebo received a second placebo injection (n = 335). Statistical evidence for benefit of second sumatriptan injection is absent. Adverse events associated with sumatriptan were tingling, dizziness, warm-hot sensations, and injection-site reactions. Sumatriptan is effective and well tolerated in patients with acute migraine.
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PMID:Treatment of acute migraine with subcutaneous sumatriptan. 165 6

Clinical symptoms were studied in 69 consecutive patients below the age of 40 years who were attending the emergency unit because of unexplained chest pain. In a structured interview a few weeks after the emergency visit, only one-third of the patients reported that they believed in the doctor's diagnosis; they believed in a psychological or cardiac origin of the pain more often than the doctors. The chest pain was most often described as oppressive and/or stabbing. In 95% of cases it was central or left-sided. Associated symptoms were commonly reported, breathlessness being most commonly reported by two-thirds of the patients, followed by dizziness, palpitation and numbness/tingling. Mental symptoms such as tiredness, anxiety and tension were frequently reported. On the basis of the background literature the aetiology is discussed. We conclude that immediate symptom analysis, including psychosomatic symptoms, particularly breathing problems, is of central importance.
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PMID:Clinical symptoms in young adults with atypical chest pain attending the emergency department. 189 50

To define glycemic thresholds for activation of counterregulatory hormone secretion, initiation of symptoms (autonomic and neuroglycopenic), and onset of deterioration of cognitive function, we measured indexes of these responses during glycemic plateaus of 90, 78, 66, 54, and 42 mg/dl in 10 normal volunteers, with the use of the hyperinsulinemic glucose clamp technique. Activation of glucagon, epinephrine, norepinephrine, and growth hormone secretion began at arterialized venous plasma glucose concentrations of 68 +/- 1, 68 +/- 1, 65 +/- 1, and 67 +/- 2 (SE) mg/dl, respectively. Autonomic symptoms (anxiety, palpitations, sweating, irritability, and tremor) began at 58 +/- 2 mg/dl, which was significantly (P = 0.0001) lower. Neuroglycopenic symptoms (hunger, dizziness, tingling, blurred vision, difficulty thinking, and faintness) and deterioration in cognitive function tests began at 51 +/- 3 and 49 +/- 2 mg/dl, respectively, values that were both significantly (P = 0.018 and 0.004, respectively) lower than that for initiation of autonomic symptoms. We therefore conclude that there is a distinct hierarchy of responses to decrements in plasma glucose, such that the threshold for activation of counterregulatory hormone secretion occurs at higher plasma glucose levels than that for initiation of autonomic warning symptoms, which in turn occurs at higher plasma glucose levels than that for onset of neuroglycopenic symptoms and deterioration in cerebral function. Such a hierarchy would maximize the opportunity to avoid incapacitating hypoglycemia.
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PMID:Hierarchy of glycemic thresholds for counterregulatory hormone secretion, symptoms, and cerebral dysfunction. 198 94

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

This study reports a total of 1677 patient days' experience with the use of Ethmozine to suppress ventricular premature depolarizations. A total of 39 patients were studied on three placebo-controlled protocols. Ethmozine, given at a mean total daily dose of 830 mg +/- 318 mg on a dosing schedule of every 8 hours, resulted in a mean plasma Ethmozine level of 0.42 micrograms/ml +/- 0.28 micrograms/ml. In addition to reducing ventricular premature depolarizations from 11,049/24 hr during placebo to 2231/24 hr during Ethmozine therapy (80% reduction), the drug also resulted in a 95% reduction in paired forms and a 99% reduction in total runs of ventricular tachycardia. Ethmozine is extraordinarily well tolerated with only mild side effects of dizziness, perioral tingling, and euphoria, with no serious toxicity requiring discontinuation of therapy. Ethmozine demonstrates great potential as an effective drug in suppressing ventricular premature depolarizations with minimal side effects or toxicity.
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PMID:Ethmozine suppression of single and repetitive ventricular premature depolarizations during therapy: documentation of efficacy and long-term safety. 634 45


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