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)

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...
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PMID:Diving injuries to the inner ear. 40 82

Five subjects were compressed to 1000 ft (31 ATA) for 2 h breathing 3.2 ATA nitrogen, 0.5 ATA oxygen, and the remainder helium. The compression took 33 min with a 10-s stage at 50 ft (2.5 ATA), 1 MIN AT 320 FT (10.7 ATA), and 2 min at 700 ft (22 ATA). Hypothetically, this 1:10 ratio for nitrogen-helium partial pressures should induce neither nitrogen narcosis nor the High Pressure Nervous Syndrome (HPNS). Tests, therefore, were made during the experiment of postural tremor, spontaneous electroencephalogram, psychomotor and intellectual activities, and subjective sensations. One diver worked underwater for 40 min on a simulated engineering assembly while breathing with a closed-circuit breathing apparatus and wearing a battery-heated suit in water at 56 degrees F. Decompression was in 4 d using 0.8 ATA oxygen and helium. The performance tests indicated no narcosis and little or no signs of HPNS. No tremor or EEG changes were seen. The "wet" diver reported sensations of mild euphoria but the other four reported no difficulties. No nausea or dizziness of HPNS was reported. It is concluded that use of a ratio of 1:10::N2:He is effective in the control of narcosis and HPNS during rapid compression to 1000 ft (31 ATA).
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PMID:Optimal use of nitrogen to suppress the high pressure nervous syndrome. 111 94

Carbon monoxide (CO) poisoning is the commonest single cause of fatal poisoning in the U.K. (Broome & Pearson, 1988). The clinical features are numerous and include headache, fatigue, dizziness, confusion, memory loss, paraesthesia, chest pain, abdominal pain, nausea, and diarrhoea as well as coma, convulsions and death. Without adequate treatment many patients develop neuropsychiatric sequelae including headaches, irritability, memory loss, confusion and personality changes. The diagnosis of CO poisoning is often suggested only by circumstances surrounding the victim, and remains a challenge to the A&E department. Hyperbaric oxygen therapy (HBO) is internationally accepted as the most powerful form of treatment in severe cases (Drug & Therapeutics Bulletin, 1988; Lowe-Ponsford & Henry, 1989). However, in the U.K. treatment with HBO is often not considered due to lack of hyperbaric facilities (Meredith & Vale, 1988; Anand et al., 1988), and due to inadequate awareness on the part of hospital staff. We report a case of a patient deeply unconscious as a result of CO poisoning, in which serial treatments with HBO over a period of 14 days, produced dramatic results.
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PMID:Management of the moribund carbon monoxide victim. 811 Mar 42

The primary purpose of the study was to compare the response to bicycle ergometer exercise in children with and without juvenile rheumatoid arthritis (JRA). Heart rate, exercise duration, highest work load completed, and peak oxygen consumption (peak VO2) were compared. A secondary purpose of the study was to determine the relationship between peak VO2 and articular disease severity. Thirty children with JRA and 30 controls matched for age, sex, and body surface area (BSA) were the subjects. Peak VO2 was determined by an open-circuit computerized gas analysis system. Peak VO2, highest work load completed, exercise duration, and peak heart rate were significantly lower among the children with JRA than their respective controls. Submaximal heart rate was significantly higher for the children with JRA. There was no difference in resting heart rate between the two groups. There was no relationship between peak VO2 and articular disease severity among the children with JRA. The results suggest that aerobic conditioning programs may be indicated soon after diagnosis for patients with JRA, regardless of the severity of their articular disease. One subject with JRA and 2 control subjects reported light-headedness and dizziness, and 1 subject with JRA complained of increased knee swelling. We recommend that physical therapists monitor patients for signs of exercise intolerance and joint symptoms during exercise training sessions. [Jasso Giannini M, Protas EJ. Exercise response in children with and without juvenile rheumatoid arthritis: a case-comparison study.
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PMID:Exercise response in children with and without juvenile rheumatoid arthritis: a case-comparison study. 163 Dec 5

Nifedipine antagonises influx of calcium through cell membrane slow channels, and sustained release formulations of the calcium channel blocker have been shown to be effective in the treatment of mild to moderate hypertension and both stable and variant angina pectoris. Preliminary findings also indicate that these formulations are effective in the treatment of Raynaud's phenomenon and hypertension in pregnancy, and that they reduce the frequency of ischaemic episodes in some patients with silent myocardial ischaemia. The exact mechanism of action of nifedipine in all of these disorders has not been defined. However, its potent peripheral and coronary arterial dilator properties, together with improvements in oxygen supply/demand, are of particular importance. A major goal of sustained release therapy is to permit reductions in the frequency of nifedipine administration, preferably to once daily, and thus improve patient compliance. Two new once-daily formulations--the nifedipine gastrointestinal therapeutic system (GITS) and a fixed combination capsule comprising sustained release nifedipine 20 mg and atenolol 50 mg--have exhibited marked antihypertensive efficacy. The GITS preparation has also been used effectively in the treatment of stable angina pectoris, and both formulations appear to be well tolerated. Sustained release nifedipine formulations are generally better tolerated than their conventionally formulated counterparts, particularly with regard to reflex tachycardia. Adverse effects seem to be dose related, are mainly associated with the drug's potent vasodilatory action, and include headache, flushing and dizziness. Generally, these effects are mild to moderate in severity and transient, usually diminishing with continued treatment. Thus, sustained release nifedipine formulations are useful and established cardiovascular therapeutic agents which have demonstrable efficacy in various forms of angina, mild to moderate hypertension and Raynaud's phenomenon. Further, promising results shown by the nifedipine GITS formulation, with its advantage of once daily administration suggest that it is likely to become one of the preferred nifedipine formulations for the treatment of hypertension and the various forms of angina.
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PMID:Sustained release nifedipine formulations. An appraisal of their current uses and prospective roles in the treatment of hypertension, ischaemic heart disease and peripheral vascular disorders. 171 8

Forty-two surgical patients were given epidural tramadol for control of postoperative pain. They were randomly assigned to three groups: group 1 (n = 15), in which 25 mg of tramadol were given; group 2 (n = 13), in which 50 mg of tramadol were given; and group 3 (n = 14), in which 75 mg of tramadol were given. When the patients complained of wound pain, epidural tramadol was given. Heart rate, blood pressure, respiratory rate, oxygen saturation (SpO2), sedation scale, motor blockade, verbal rating scale, subjective grading, and visual analogue pain scale (VAPS) were measured and recorded before the tramadol administration, at 5 and 15 min, and at 1, 2, 4, and 8 h after the tramadol administration. Only 26.6% of the patients in group 1 had significant relief of pain. The rest of them needed at least one incremental dose of 25 mg of tramadol. The baseline VAPS of the patients in group 2 was 8.9 +/- 2.0. It became 5.46 +/- 3.0 (p greater than 0.05) 15 min after tramadol was given, and dropped further to 1.9 +/- 1.8 (p greater than 0.05) 2 h later. The average duration of pain relief was 12.0 +/- 5.9 h. In group 3, the initial VAPS was 8.14 +/- 1.9. It decreased to 4.28 +/- 1.8 (p greater than 0.05) 15 min, and further dropped to 1.7 +/- 0.9 (p greater than 0.05) 2 h following tramadol administration. The average duration of pain relief was 11.3 +/- 4.8 h. The common side effects of tramadol such as dizziness, nausea, and dry mouth, were most frequently found in group 3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidural tramadol for postoperative pain relief. 175 61

Thyrotropin-releasing hormone (TRH) stimulates pituitary thyrotropin synthesis and release and also regulates autonomic nervous system functions by acting as a neuromodulator and neurotransmitter. In experimental animals a stimulation of ventilation by thyrotropin-releasing hormone was shown when applied at central nervous system sites that affect respiratory motor output. It was the goal of our study to investigate the respiratory properties of thyrotropin-releasing hormone on basal and stimulated (i.e. CO2-rebreathing) conditions following systemic thyrotropin-releasing hormone application in healthy humans. Thyrotropin-releasing hormone (200 micrograms, 400 micrograms intravenous) initiated a rapid short lasting rise of minute volume, ventilatory air-flow and alveolar oxygen tension under steady state breathing (P less than 0.001). Breathing frequency was less affected, heart rate rose concomitantly (P less than 0.001). While breathing with increasing concentrations of carbon dioxide, minute volume was higher under thyrotropin-releasing hormone than under placebo alone. Further effects (e.g. nausea, dizziness, palpitations) mostly appeared later than respiratory changes and thus may not be responsible for their initiation. Our findings prove systemic thyrotropin-releasing hormone to be a strong respiratory stimulant in man. Response in respiratory output was also accompanied by central nervous system-effects (e.g. dizziness, restlessness, augmented vigilance). The mode of thyrotropin-releasing hormone effects on respiration after peripheral administration is still speculative. An augmented sympathetic output or a direct receptor mediated action at central nervous system sites may be responsible, while a peripheral effect cannot be excluded.
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PMID:Thyrotropin-releasing hormone has stimulatory effects on ventilation in humans. 190 74

Forty-one patients suffering from sudden hearing loss were studied by the following method. Twenty patients (group A) were treated with oral administration of prednisolone, intravenous administration of vitamin B and C, furosemide and stellate ganglion block. Another 21 patients (group B) were treated with oral administration of these drugs, stellate ganglion block and oxygen inhalation. Forty six percent of all these patients, 35 percent of group A and 57 percent of group B, regained less than 20 dB of their normal hearing level. The patients who are younger, having shorter duration from first finding of symptoms to starting of therapy and smaller average deficiency of hearing, without dizziness are easy to recover. Oxygen inhalation with drug therapy and stellate ganglion block is a useful treatment for sudden hearing loss.
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PMID:[The effect of drug therapy and stellate ganglion block with or without oxygen inhalation on sudden hearing loss]. 192 Aug 4

Five patients presented to the emergency department (ED) following exposure in an enclosed space to methylene chloride (dichloromethane), used for removing paint. Two workers and three rescuers were involved. Two rescuers complained only of dizziness and mild nausea, and were subsequently discharged from the ED. One rescuer was asymptomatic. Worker no. 1 arrived in cardiac arrest and eventually died in the ED despite resuscitation efforts. Worker no. 2 also presented to the ED in cardiac arrest, and was successfully resuscitated to pulse and blood pressure. However, he never regained consciousness or spontaneous respirations, and died on the fourth day. Of interest is that worker no. 2's carboxyhemoglobin level increased from 2% to 8% over the 9 hours following admission, despite administration of 40% to 50% oxygen by endotracheal tube. Among the conclusions that can be drawn are (1) the cause of death in these patients was not carbon monoxide poisoning, but solvent-induced narcosis; (2) carboxyhemoglobin levels may continue to rise following cessation of exposure, despite administration of high flow oxygen; (3) rescuers can easily become victims if proper protective clothing and respirators are not worn.
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PMID:Methylene chloride: report of five exposures and two deaths. 222

Ten intensive care patients and five healthy volunteers each received a bolus injection of lidocaine HCl (100 mg, 2%) over an injection period of 5 s. After 0.5, 1, 2, 4, 8, 15 and 25 min arterial, central venous and peripheral venous blood samples were collected. In four of the volunteers, arterial and central venous samples were also taken about 10 s after the end of injection. The fluorescence polarization method by means of the Abbott-TDx system was used, and plasma concentrations of lidocaine were determined. The measurements showed that lidocaine levels in central venous plasma 10 s after the end of administration were higher than those in arterial plasma. By 30 s after administration the opposite situation had developed, so that arterial concentrations were higher than those in central venous plasma. This relation did not change throughout the study, though the two levels became closer, as is shown by the ratios (Table 3, Fig. 2). Concentrations in peripheral venous plasma increased more slowly but remained far below those in arterial and central venous plasma, at least for the first 8 min. After 15 min lidocaine levels were almost the same in all three samples. During the entire study there were no ECG changes, and neither heart rate nor blood pressure showed any significant deviation from the values obtained at the beginning. The volunteers had minor toxic manifestations, such as dizziness, tinnitus and a metallic taste in the mouth; one person had a sensation of pressure in his chest, which improved following oxygen administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The concentration of free lidocaine in arterial, central venous and peripheral vein plasma following intravenous injection]. 233 Apr 29


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