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)

Following 4 weeks of treatment with ORF-8063 a polyfluorinated benzodiazepine derivative, 8 hospitalized patients manifesting a primary pathology of anxiety showed marked general improvement. 2 other persons were treated, but for shorter periods: 9 and 14 days. Both are included in the pre-post analysis. Mean optimal dosage was 66.5 mg. The five instruments used to measure therapeutic effect showed pre- to posttreatment change with high level of statistical significance in serveral of the pathological factors. When measures of change are considered, patients showed more improvement related to psychic than somatic components of anxiety. Change data also indicates more patients improvement in anxiety than depression. Side effects reported more were dizziness, faintness and insomnia; these were reported in 8 patients. 6 patients noted drowsiness, and 4 noted excitement. 5 persons tolerated optimum dosages with no extreme reactions; 5 others (including the 2 subjects who terminated treatment early) were unable to maintain optimum dosages because of side effects.
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PMID:The treatment of anxiety with a polyfluorinated benzodiazepine derivative. 2 34

In this multi-clinic double-blind study, patients suffering from insomnia were treated with triazolam 0.5 mg (Halcion) or placebo for 14 days. Four investigators treated 239 patients, 122 on triazolam and 117 on placebo. Thirty-nine patients, 10 on triazolam and 29 on placebo, dropped out for ineffectiveness of the medication and 32 patients, 16 in each group, dropped out for side effects. Analysis of pooled efficacy data showed that triazolam was significantly better than placebo on all efficacy parameters measured, including how much the medication helped the patients sleep, onset of sleep, duration of sleep, duration compared to usual, number of nocturnal awakenings, and feeling of restfulness in the morning. Triazolam did not produce evidence of tolerance development after 2 weeks of treatment. The same variety of side effects occurred on each treatment and primarily included drowsiness, grogginess, headaches, impaired coordination nausea, and dizziness.
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PMID:Multi-clinic double-blind comparison of triazolam (Halcion) and placebo administered for 14 consecutive nights in outpatients with insomnia. 2 13

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.
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PMID:Neuropsychiatric symptomatology with chronic renal insufficiency in the stage of compensated and decompensated retention. I. CNS disturbances. 5 91

Thirty-eight obese patients, resistant to conventional diet therapy, agreed to consume a 1.09 MJ (260 kcal)/day semi-synthetic diet consisting of 25 g egg albumin, 40 g oligosaccharides, vitamins and minerals, and were seen weekly as outpatients for eight weeks. At the beginning, the semi-synthetic diet was given with either the anorectic drug, mazindol (2 mg/day) or a placebo for four weeks and then changed over for the remaining four weeks; the study being conducted on a double-blind basis. The final treatment was a 4.2 MJ (1000 KCAL) conventional diet for a further four weeks without drug or placebo. Twenty-five patients completed the first eight weeks and 21 patients the final four weeks of the trial. The total mean weight losses were as follows: week 4, 9.3 kg; week 8, 13.7 kg; week 12, 12.2 kg. There was no significant difference in weight loss between mazindol treatment and placebo but the former group reported feeling less hungry. The chief side-effects observed were dizziness, nausea, dry mouth, insomnia and depression which were more frequent with mazindol. Six patients had to stop mazindol because of side-effects, but were able to continue the diet alone. It is concluded that a semi-synthetic diet containing 1.09 MJ (260 kcal) daily can be successfully employed in the treatment of obese outpatients, and is a practical therapeutic alternative to admission to hospital. There is no clinical advantage to be gained by the additional use of the anorectic drug, mazindol.
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PMID:A double-blind trial of mazindol using a very low calorie formula diet. 36 31

A large number of reports have been devoted to the physiologic and toxic effects of methyl chloride, many of which are based on case histories involving occupational exposure. The detrimental actions of methyl chloride on the central and peripheral nervous systems are well established effects. It is a moderately severe narcotic and potentially severe nerve poison. Chronic intoxication is associated with damage to the central nervous system (CNS), kidneys, liver, bone marrow, cardiovascular system, respiratory system, and intestinal tract. The signs and symptoms range from the more severe medical dysfunctions such as cardiac irregularities, respiratory paralysis, nerve degeneration, and severe convulsions to the more subtle clinical observations such as CNS depression, nervousness and emotional instability, insomnia and anorexia, ataxia, blurred vision, light-headedness, nausea, dizziness, narcosis, and disorientation. The behavioral correlates of these and other neurotoxic effects of methyl chloride suggest that a gradual behavioral degradation occurs. Pharmacodynamic studies have shown the compound to be rapidly absorbed by the blood with most authors attributing the toxicity to an enzyme-catalyzed methylation reaction in the body. Despite the fact that several investigators have attempted to correlate such biological responses of methyl chloride with its toxicity, the present knowledge of the problem still lacks a detailed mechanism of action. Until such mechanisms are verified, adequate methods to assess subclinical neurological and behavioral changes must be effectively developed.
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PMID:Behavioral, neurological, and toxic effects of methyl chloride: a review of the literature. 38 67

A study was carried out in which 135 mildly or moderately depressed outpatients were randomly allocated to one of five groups receiving six weeks' treatment weith antidepressant drugs. The groups received a tricyclic antidepressant (trimipramine; mean dose 106 mg at night) or a monoamine oxidase inhibitor (MAOI) (phenelzine or isocarboxazid; mean doses 45 and 32 mg/day respectively), or a combination of the two (phenelzine plus trimipramine or isocarboxazid plus trimipramine). Various scales were used to measure depression before and at one, three, and six weeks of treatment, and results were assessed blindly. The tricyclic antidepressant was found to be consistently superior to the MAOIs and the combined treatments. Some differential indicators of response to the various antidepressants were found--for example, patients with initial complaints of dizziness, suicidal ideas, irritability, and insomnia and a longer duration of illness were more likely to respond to trimipramine--but these were of only modest significance. Side effects were not troublesome in any group. It is concluded that neither MAOIs nor MAOIs combined with tricyclic antidepressants are the treatment of first choice in unselected outpatients with mild or moderate depression.
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PMID:Controlled trial of trimipramine, monoamine oxidase inhibitors, and combined treatment in depressed outpatients. 39 42

The sympathomimetic agent ephedrine has potent thermogenic and anti-obesity properties in rodents. The effect is markedly enhanced by caffeine, while caffeine given alone has no effect. This study was undertaken to find out if a similar weight reducing synergism between ephedrine and caffeine is present in obese patients. In a randomized, placebo-controlled, double blind study, 180 obese patients were treated by diet (4.2 MJ/day) and either an ephedrine/caffeine combination (20mg/200mg), ephedrine (20 mg), caffeine (200 mg) or placebo three times a day for 24 weeks. Withdrawals were distributed equally in the four groups, and 141 patients completed the trial. Mean weight losses was significantly greater with the combination than with placebo from week 8 to week 24 (ephedrine/caffeine, 16.6 +/- 6.8 kg vs. placebo, 13.2 +/- 6.6 kg (mean +/- s.d.), P = 0.0015). Weight loss in both the ephedrine and the caffeine groups was similar to that of the placebo group. Side effects (tremor, insomnia and dizziness) were transient and after eight weeks of treatment they had reached placebo levels. Systolic and diastolic blood pressure fell similarly in all four groups. We conclude, that in analogy with animal studies, the ephedrine/caffeine combination is effective, while caffeine and ephedrine separately are ineffective for the treatment of human obesity.
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PMID:The effect and safety of an ephedrine/caffeine compound compared to ephedrine, caffeine and placebo in obese subjects on an energy restricted diet. A double blind trial. 131 81

The postconcussion syndrome refers to a large number of symptoms and signs that may occur alone or in combination following usually mild head injury. The most common complaints are headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of consciousness and memory, and noise sensitivity. Mild head injury is a major public health concern because the annual incidence is about 150 per 100,000 population, accounting for 75% or more of all head injuries. The postconcussion syndrome has been recognized for at least the last few hundred years and has been the subject of intense controversy for more than 100 years. The Hollywood head injury myth has been an important contributor to persisting skepticism and might be countered by educational efforts and counter-examples from boxing. The organicity of the postconcussion syndrome has now become well documented. Abnormalities following mild head injury have been reported in neuropathologic, neurophysiologic, neuroimaging, and neuropsychologic studies. There are multiple sequelae of mild head injury, including headaches of multiple types, cranial nerve symptoms and signs, psychologic and somatic complaints, and cognitive impairment. Rare sequelae include hematomas, seizures, transient global amnesia, tremor, and dystonia. Neuroimaging and physiologic and psychologic testing should be used judiciously based on the problems of the particular patient rather than in a cookbook fashion. Prognostic studies clearly substantiate the existence of a postconcussion syndrome. Manifestations of the postconcussion syndrome are common, with resolution in most patients by 3 to 6 months after the injury. Persistent symptoms and cognitive deficits are present in a distinct minority of patients for additional months or years. Risk factors for persisting sequelae include age over 40 years; lower educational, intellectual, and socioeconomic level; female gender; alcohol abuse; prior head injury; and multiple trauma. Although a small minority are malingerers, frauds, or have compensation neurosis, most patients have genuine complaints. Contrary to a popular perception, most patients with litigation or compensation claims are not cured by a verdict. Treatment is individualized depending on the specific complaints of the patient. Although a variety of medication and psychologic treatments are currently available, ongoing basic and clinical research of all aspects of mild head injury are crucial to provide more efficacious treatment in the future.
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PMID:The postconcussion syndrome and the sequelae of mild head injury. 143 59

Somatic symptoms are one of the leading reasons for medical outpatient clinic visits, with the most common symptoms having a prevalence of 10% or more. However, the usual diagnostic workups are often unproductive, with less than 1 in 5 symptoms having an organic explanation after the initial physical examination and laboratory testing. Therapy appears more effective for some symptoms than for others. Of patients with unspecified pain or gastrointestinal complaints, greater than 70% state that some type of treatment has been helpful, whereas less than 50% of individuals with fatigue, dizziness, numbness, insomnia, sexual dysfunction, anxiety, or depression report any relief. Future educational efforts and research need to focus on that majority of symptoms that are either psychiatric or unexplained, in order to improve our current evaluation and management strategies.
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PMID:Symptoms in medical patients: an untended field. 173 31

Fifty-four patients with advanced malignancies were treated on this phase I trial of coumarin and cimetidine. The dose of coumarin was escalated, with three patients treated at each dose level, while the cimetidine dose was held constant at 300 mg four times daily. Patients received coumarin alone as a single daily oral dose for 14 days; on day 15, cimetidine was added and both drugs were continued until progression of disease. This trial was initiated with patients receiving coumarin at 400 mg daily and closed at 7 g daily with four of five patients on this dose experiencing nausea and vomiting. Treatment was generally well tolerated over a wide range of coumarin doses. Symptomatic side effects were few, mild, and usually self limited. Side effects included insomnia, nausea, vomiting, diarrhea, and dizziness. Two patients withdrew from therapy because of daily nausea and vomiting. Typically, nausea, vomiting, and dizziness occurred 2.5-3 hours after a dose of coumarin. In most patients, these side effects abated spontaneously with continuation of therapy. There was no significant hematologic or renal toxicity. Hepatotoxicity occurred in only one patient and was manifested by asymptomatic abnormal elevations of serum hepatic transaminases. This toxicity was reversible upon interruption of therapy. Objective tumor regressions were observed in six patients with renal cell carcinoma. Responses occurred at coumarin doses ranging from 600 mg to 5 g daily. Coumarin is a relatively nontoxic, oral, outpatient therapy that warrants further investigations for the treatment of human malignancies. Because of its low toxicity, there is potential for combining coumarin with chemotherapeutic and/or biological agents in an attempt to improve on efficacy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I evaluation of coumarin (1,2-benzopyrone) and cimetidine in patients with advanced malignancies. 176 68


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